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Test bank for Pharmacology for Nursing Care 8th Edition by Richard A. Lehne

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Test bank for Pharmacology for Nursing Care 8th Edition by Richard A. Lehne

Test bank for Pharmacology for Nursing Care 8th Edition by Richard A. Lehne

A favorite among nursing students, Pharmacology for Nursing Care, 8th Edition, features a uniquely engaging writing style, clear explanations, and unmatched clinical precision and currency to help you gain a solid understanding of key drugs and their implications — as opposed to just memorization of certain facts. Compelling features such as a drug prototype approach, use of large and small print to distinguish need-to-know versus nice-to-know content, and a focus on major nursing implications save you study time by directing your attention on the most important, need-to-know information. The new edition also features an abundance of content updates to keep you ahead of the curve in school and in professional practice.

 

Front Matter
Dedication
About the author
Contributors and reviewers
Welcome to our eighth edition
What’s new in the book?
New drugs
New special interest topics
Restructured content
Canadian trade names
Learning supplements for students
Evolve student resources
Pharmacology online
Study guide
Teaching supplements for instructors
Evolve instructor resources
Please write
Preface
Laying foundations in basic principles
Reviewing physiology and pathophysiology
Teaching through prototypes
Large print and small print: a way to focus on essentials
Using clinical reality to prioritize content
Nursing implications: demonstrating the application of pharmacology in nursing practice
About dosage calculations
Ways to use this textbook
Acknowledgments
Interactive Review – Pharmacology for Nursing Care
I Introduction
Interactive Review – I: Introduction
CHAPTER 1 Orientation to pharmacology
Four basic terms
Drug.
Pharmacology.
Clinical pharmacology.
Therapeutics.
Properties of an ideal drug
The big three: effectiveness, safety, and selectivity
Effectiveness.
Safety.
Selectivity.
Additional properties of an ideal drug
Reversible action.
Predictability.
Ease of administration.
Freedom from drug interactions.
Low cost.
Chemical stability.
Possession of a simple generic name.
Because no drug is ideal . . .
Figure 1–1 ▪ Factors that determine the intensity of drug responses.
The therapeutic objective
Factors that determine the intensity of drug responses
Administration
Pharmacokinetics
Pharmacodynamics
Sources of individual variation
Summary
Key points
CHAPTER 2 Application of pharmacology in nursing practice
Evolution of nursing responsibilities regarding drugs
Application of pharmacology in patient care
Preadministration assessment
Collecting baseline data.
Identifying high-risk patients.
Dosage and administration
Evaluating and promoting therapeutic effects
Evaluating therapeutic responses.
Promoting patient adherence.
Implementing nondrug measures.
Minimizing adverse effects
Minimizing adverse interactions
Making PRN decisions
Managing toxicity
Application of pharmacology in patient education
Dosage and administration
Drug name.
Dosage size and schedule of administration.
Technique of administration.
Duration of drug use.
Drug storage.
Promoting therapeutic effects
Minimizing adverse effects
Minimizing adverse interactions
Application of the nursing process in drug therapy
Review of the nursing process
Assessment.
Analysis: nursing diagnoses.
Planning.
Implementation (intervention).
Evaluation.
Applying the nursing process in drug therapy
Preadministration assessment
Baseline data needed to evaluate therapeutic effects.
Baseline data needed to evaluate adverse effects.
Identification of high-risk patients.
Assessment of the patient’s capacity for self-care.
TABLE 2–1 ▪ Examples of Nursing Diagnoses That Can Be Derived from Knowledge of Adverse Drug Effects
Analysis and nursing diagnoses
Planning
Defining goals.
Setting priorities.
Identifying interventions.
Establishing criteria for evaluation.
Implementation
Evaluation
Use of a modified nursing process format to summarize nursing implications in this text
Preadministration assessment.
TABLE 2–2 ▪ Modified Nursing Process Format Used for Summarizing Nursing Implications in This Text
Implementation: administration.
Implementation: measures to enhance therapeutic effects.
Ongoing evaluation and interventions.
Patient education.
What about diagnosis and planning?
Summary
Key points
CHAPTER 3 Drug regulation, development, names, and information
Landmark drug legislation
New drug development
The randomized controlled trial
Use of controls.
TABLE 3–1 ▪ Steps in New Drug Development
Randomization.
Blinding.
Stages of new drug development
Preclinical testing
Clinical testing
Phase I.
Phases II and III.
Phase IV: postmarketing surveillance.
Limitations of the testing procedure
Limited information in women and children
Women.
TABLE 3–2 ▪ Some New Drugs That Were Withdrawn from the U.S. Market for Safety Reasons
Children.
Failure to detect all adverse effects
TABLE 3–3 ▪ The Three Types of Drug Names
Exercising discretion regarding new drugs
Drug names
The three types of drug names
Chemical name.
Generic name.
Trade name.
TABLE 3–4 ▪ Generic Drug Names Whose Final Syllables Indicate Pharmacologic Class
Which name to use, generic or trade?
The little problems with generic names
TABLE 3–5 ▪ Generic Names and Trade Names of Some Common Drugs
TABLE 3–6 ▪ Some OTC Products That Share the Same Trade Name
The big problems with trade names
A single drug can have multiple trade names.
Over-the-counter (OTC) products with the same trade name may have different active ingredients.
TABLE 3–7 ▪ Products from the United States and Canada That Have the Same Trade Name but Different Active Ingredients in Other Countries
Trade names can endanger international travelers.
What if peas were marketed like drugs?
Generic products versus brand-name products
Are generic products and brand-name products therapeutically equivalent?
TABLE 3–8 ▪ Some Important Drug References
Would a difference between brand-name and generic products justify the use of trade names?
Conclusion regarding generic names and trade names
Over-the-counter drugs
Sources of drug information
People
Clinicians and pharmacists.
Poison control centers.
Pharmaceutical sales representatives.
Published information
Text-like books
Newsletters
Reference books
The internet
Key points
II Basic Principles of Pharmacology
Interactive Review – II: Basic Principles of Pharmacology
CHAPTER 4 Pharmacokinetics
Application of pharmacokinetics in therapeutics
A note to chemophobes
Figure 4–1 ▪ The four basic pharmacokinetic processes. Dotted lines represent membranes that must be crossed as drugs move throughout the body.
Passage of drugs across membranes
Membrane structure
Three ways to cross a cell membrane
Channels and pores
Transport systems
Figure 4–2 ▪ Structure of the cell membrane. The cell membrane consists primarily of a double layer of phospholipid molecules. The large globular structures represent protein molecules imbedded in the lipid bilayer.
P-glycoprotein.
Direct penetration of the membrane
Polar molecules
Figure 4–3 ▪ Polar molecules. A, Stippling shows the distribution of electrons within the water molecule. As indicated, water’s electrons spend more time near the oxygen atom than near the hydrogen atoms, making the area near the oxygen atom somewhat negative and the area near the hydrogen atoms more positive. B, Kanamycin is a polar drug. The 2 –OH groups of kanamycin attract electrons, thereby causing the area around these groups to be more negative than the rest of the molecule.
Figure 4–4 ▪ Quaternary ammonium compounds. A, The basic structure of quaternary ammonium compounds. Because the nitrogen atom has bonds to four organic radicals, quaternary ammonium compounds always carry a positive charge. Because of this charge, quaternary ammonium compounds are not lipid soluble and cannot cross most membranes. B, Tubocurarine is a representative quaternary ammonium compound. Note that tubocurarine contains two “quaternized” nitrogen atoms.
Ions
Quaternary ammonium compounds
PH-dependent ionization
Figure 4–5 ▪ Ionization of weak acids and weak bases. The extent of ionization of weak acids (A) and weak bases (B) depends on the pH of their surroundings. The ionized (charged) forms of acids and bases are not lipid soluble and hence do not readily cross membranes. Note that acids ionize by giving up a proton and that bases ionize by taking on a proton.
Ion trapping (pH partitioning)
Absorption
Factors affecting drug absorption
Rate of dissolution.
Surface area.
Blood flow.
Lipid solubility.
Figure 4–6 ▪ Ion trapping of drugs. This figure demonstrates ion trapping using aspirin as an example. Because aspirin is an acidic drug, it will be nonionized in acid media and ionized in alkaline media. As indicated, ion trapping causes molecules of orally administered aspirin to move from the acidic (pH 1) environment of the stomach to the more alkaline (pH 7.4) environment of the plasma, thereby causing aspirin to accumulate in the blood. In the figure, aspirin (acetylsalicylic acid) is depicted as ASA with its COOH (carboxylic acid) group attached. Step 1: Once ingested, ASA dissolves in the stomach contents, after which some ASA molecules give up a proton and become ionized. However, most of the ASA in the stomach remains nonionized. Why? Because the stomach is acidic, and acidic drugs don’t ionize in acidic media. Step 2: Because most ASA molecules in the stomach are nonionized (and therefore lipid soluble), most ASA molecules in the stomach can readily cross the membranes that separate the stomach lumen from the plasma. Because of the concentration gradient that exists between the stomach and the plasma, nonionized ASA molecules will begin moving into the plasma. (Note that, because of their charge, ionized ASA molecules cannot leave the stomach.) Step 3: As the nonionized ASA molecules enter the relatively alkaline environment of the plasma, most give up a proton (H+) and become negatively charged ions. ASA molecules that become ionized in the plasma cannot diffuse back into the stomach. Step 4: As the nonionized ASA molecules in the plasma become ionized, more nonionized molecules will pass from the stomach to the plasma to replace them. This movement occurs because the laws of diffusion demand equal concentrations of diffusible substances on both sides of a membrane. Because only the nonionized form of ASA is able to diffuse across the membrane, it is this form that the laws of diffusion will attempt to equilibrate. Nonionized ASA will continue to move from the stomach to the plasma until the amount of ionized ASA in plasma has become large enough to prevent conversion of newly arrived nonionized molecules into the ionized form. Equilibrium will then be established between the plasma and the stomach. At equilibrium, there will be equal amounts of nonionized ASA in the stomach and plasma. However, on the plasma side, the amount of ionized ASA will be much larger than on the stomach side. Because there are equal concentrations of nonionized ASA on both sides of the membrane but a much higher concentration of ionized ASA in the plasma, the total concentration of ASA in plasma will be much higher than in the stomach.
PH partitioning.
Characteristics of commonly used routes of administration
TABLE 4–1 ▪ Properties of Major Routes of Drug Administration
Intravenous
Barriers to absorption.
Absorption pattern.
Advantages.
Rapid onset.
Control.
Permits use of large fluid volumes.
Permits use of irritant drugs.
Disadvantages.
High cost, difficulty, and inconvenience.
Irreversibility.
Figure 4–7 ▪ Drug movement at typical capillary beds. In most capillary beds, “large” gaps exist between the cells that compose the capillary wall. Drugs and other molecules can pass freely into and out of the bloodstream through these gaps. As illustrated, lipid-soluble compounds can also pass directly through the cells of the capillary wall.
Fluid overload.
Infection.
Embolism.
The importance of reading labels.
Intramuscular
Barriers to absorption.
Absorption pattern.
Advantages.
Disadvantages.
Subcutaneous
Oral
Barriers to absorption.
Absorption pattern.
Drug movement following absorption.
Advantages.
Disadvantages.
Variability.
Inactivation.
Figure 4–8 ▪ Movement of drugs following GI absorption. All drugs absorbed from sites along the GI tract—stomach, small intestine, and large intestine (but not the oral mucosa or distal rectum)—must go through the liver, via the portal vein, on their way to the heart and then the general circulation. For some drugs, passage is uneventful. Others undergo extensive hepatic metabolism. And still others undergo enterohepatic recirculation, a repeating cycle in which a drug moves from the liver into the duodenum (via the bile duct) and then back to the liver (via the portal blood). As discussed in the text under Enterohepatic Recirculation, the process is limited to drugs that have first undergone hepatic glucuronidation.
Patient requirements.
Local irritation.
Comparing oral administration with parenteral administration
Pharmaceutical preparations for oral administration
Tablets.
Enteric-coated preparations.
Sustained-release preparations.
Additional routes of administration
Distribution
Blood flow to tissues
Exiting the vascular system
Typical capillary beds
The blood-brain barrier
Figure 4–9 ▪ Drug movement across the blood-brain barrier. Tight junctions between cells that compose the walls of capillaries in the CNS prevent drugs from passing between cells to exit the vascular system. Consequently, in order to reach sites of action within the brain, a drug must pass directly through cells of the capillary wall. To do this, the drug must be lipid soluble or be able to use an existing transport system.
Placental drug transfer
Protein binding
Figure 4–10 ▪ Placental drug transfer. To enter the fetal circulation, drugs must cross membranes of the maternal and fetal vascular systems. Lipid-soluble drugs can readily cross these membranes and enter the fetal blood, whereas ions and polar molecules are prevented from reaching the fetal blood.
Figure 4–11 ▪ Protein binding of drugs. A, Albumin is the most prevalent protein in plasma and the most important of the proteins to which drugs bind. B, Only unbound (free) drug molecules can leave the vascular system. Bound molecules are too large to fit through the pores in the capillary wall.
Entering cells
Metabolism
Hepatic drug-metabolizing enzymes
Therapeutic consequences of drug metabolism
Accelerated renal drug excretion.
Drug inactivation.
Increased therapeutic action.
Activation of prodrugs.
Increased or decreased toxicity.
Special considerations in drug metabolism
Age.
Induction of drug-metabolizing enzymes.
First-pass effect.
Figure 4–12 ▪ Therapeutic consequences of drug metabolism. (See text for details.)
Nutritional status.
Competition between drugs.
Enterohepatic recirculation
Figure 4–13 ▪ Renal drug excretion. (MW = molecular weight.)
Excretion
Renal drug excretion
Steps in renal drug excretion
Glomerular filtration.
Passive tubular reabsorption.
Active tubular secretion.
Factors that modify renal drug excretion
PH-dependent ionization.
Competition for active tubular transport.
Age.
Nonrenal routes of drug excretion
Breast milk
Other nonrenal routes of excretion
Time course of drug responses
Plasma drug levels
Clinical significance of plasma drug levels
Figure 4–14 ▪ Single-dose time course.
Two plasma drug levels defined
Minimum effective concentration.
Toxic concentration.
Therapeutic range
Single-dose time course
Drug half-life
Figure 4–15 ▪ Drug accumulation with repeated administration. This figure illustrates the accumulation of a hypothetical drug during repeated administration. The drug has a half-life of 1 day. The dosing schedule is 2 gm given once a day on days 1 through 9. Note that plateau is reached at about the beginning of day 5 (ie, after four half-lives). Note also that, when administration is discontinued, it takes about 4 days (four half-lives) for most (94%) of the drug to leave the body.
Drug levels produced with repeated doses
The process by which plateau drug levels are achieved
Time to plateau
Techniques for reducing fluctuations in drug levels
Loading doses versus maintenance doses
Decline from plateau
Key points
Enterohepatic Recirculation (read text)
Cytochrome P450 Drug Metabolism (read text)
Cytochrome P450 Mechanism (read text)
Half-Life (read text)
CHAPTER 5 Pharmacodynamics
Dose-response relationships
Basic features of the dose-response relationship
Maximal efficacy and relative potency
Maximal efficacy
Figure 5–1 ▪ Basic components of the dose-response curve. A, A dose-response curve with dose plotted on a linear scale. B, The same dose-response relationship shown in A but with the dose plotted on a logarithmic scale. Note the three phases of the dose-response curve: Phase 1, The curve is relatively flat; doses are too low to elicit a significant response. Phase 2, The curve climbs upward as bigger doses elicit correspondingly bigger responses. Phase 3, The curve levels off; bigger doses are unable to elicit a further increase in response. (Phase 1 is not indicated in A because very low doses cannot be shown on a linear scale.)
Figure 5–2 ▪ Dose-response curves demonstrating efficacy and potency. A, Efficacy, or “maximal efficacy,” is an index of the maximal response a drug can produce. The efficacy of a drug is indicated by the height of its dose-response curve. In this example, meperidine has greater efficacy than pentazocine. Efficacy is an important quality in a drug. B, Potency is an index of how much drug must be administered to elicit a desired response. In this example, achieving pain relief with meperidine requires higher doses than with morphine. We would say that morphine is more potent than meperidine. Note that, if administered in sufficiently high doses, meperidine can produce just as much pain relief as morphine. Potency is usually not an important quality in a drug.
Relative potency
Figure 5–3 ▪ Interaction of drugs with receptors for norepinephrine. Under physiologic conditions, cardiac output can be increased by the binding of norepinephrine (NE) to receptors (R) on the heart. Norepinephrine is supplied to these receptors by nerves. These same receptors can be acted on by drugs, which can either mimic the actions of endogenous NE (and thereby increase cardiac output) or block the actions of endogenous NE (and thereby reduce cardiac output).
Drug-receptor interactions
Introduction to drug receptors
Figure 5–4 ▪ The four primary receptor families. 1, Cell membrane–embedded enzyme. 2, Ligand-gated ion channel. 3, G protein–coupled receptor system (G = G protein). 4, Transcription factor. (See text for details.)
The four primary receptor families
Cell membrane–embedded enzymes.
Ligand-gated ion channels.
G protein–coupled receptor systems.
Transcription factors.
Receptors and selectivity of drug action
Figure 5–5 ▪ Interaction of acetylcholine with its receptor. A, Three-dimensional model of the acetylcholine molecule. B, Binding of acetylcholine to its receptor. Note how the shape of acetylcholine closely matches the shape of the receptor. Note also how the positive charges on acetylcholine align with the negative sites on the receptor.
Figure 5–6 ▪ Model of simple occupancy theory. The simple occupancy theory states that the intensity of response to a drug is proportional to the number of receptors occupied; maximal response is reached with 100% receptor occupancy. Because the hypothetical cell in this figure has only four receptors, maximal response is achieved when all four receptors are occupied.
Theories of drug-receptor interaction
Simple occupancy theory
Modified occupancy theory
Affinity.
Intrinsic activity.
Agonists, antagonists, and partial agonists
Agonists
Antagonists
Noncompetitive versus competitive antagonists.
Noncompetitive (insurmountable) antagonists.
Competitive (surmountable) antagonists.
Figure 5–7 ▪ Dose-response curves in the presence of competitive and noncompetitive antagonists. A, Effect of a noncompetitive antagonist on the dose-response curve of an agonist. Note that noncompetitive antagonists decrease the maximal response achievable with an agonist. B, Effect of a competitive antagonist on the dose-response curve of an agonist. Note that the maximal response achievable with the agonist is not reduced. Competitive antagonists simply increase the amount of agonist required to produce any given intensity of response.
Partial agonists
Regulation of receptor sensitivity
Drug responses that do not involve receptors
Interpatient variability in drug responses
Figure 5–8 ▪ Interpatient variation in drug responses. A, Data from tests of a hypothetical acid suppressant in 100 patients. The goal of the study is to determine the dosage required by each patient to elevate gastric pH to 5. Note the wide variability in doses needed to produce the target response for the 100 subjects. B, Frequency distribution curve for the data in A. The dose at the middle of the curve is termed the ED50—the dose that will produce a predefined intensity of response in 50% of the population.
Measurement of interpatient variability
The ED50
Clinical implications of interpatient variability
Figure 5–9 ▪ The therapeutic index. A, Frequency distribution curves indicating the ED50 and LD50 for drug “X.” Because its LD50 is much greater than its ED50, drug X is relatively safe. B, Frequency distribution curves indicating the ED50 and LD50 for drug “Y.” Because its LD50 is very close to its ED50, drug Y is not very safe. Also note the overlap between the effective-dose curve and the lethal-dose curve.
The therapeutic index
Key points
CHAPTER 6 Drug interactions
Drug-drug interactions
Consequences of drug-drug interactions
Intensification of effects
Increased therapeutic effects.
Increased adverse effects.
Reduction of effects
Reduced therapeutic effects.
Reduced adverse effects.
Creation of a unique response
Basic mechanisms of drug-drug interactions
Direct chemical or physical interactions
Pharmacokinetic interactions
Altered absorption.
Altered distribution.
Competition for protein binding.
Alteration of extracellular pH.
Altered metabolism.
Induction of CYP isozymes.
TABLE 6–1 ▪ Drugs That Are Important Substrates, Inhibitors, or Inducers of Specific CYP Isozymes
Inhibition of CYP isozymes.
Altered renal excretion.
Interactions that involve P-glycoprotein.
Pharmacodynamic interactions
Interactions at the same receptor.
Interactions resulting from actions at separate sites.
Combined toxicity
Clinical significance of drug-drug interactions
Minimizing adverse drug-drug interactions
Drug-food interactions
Impact of food on drug absorption
Decreased absorption.
Increased absorption.
TABLE 6–2 ▪ Some Drugs Whose Levels Can Be Increased by Grapefruit Juice
Impact of food on drug metabolism: the grapefruit juice effect
Impact of food on drug toxicity
Impact of food on drug action
Timing of drug administration with respect to meals
Drug-supplement interactions
Key points
Competition for Protein Binding (read text)
Inhibition of Drug Metabolism (read text)
Renal “Active Secretion” (read text)
CHAPTER 7 Adverse drug reactions and medication errors
Adverse drug reactions
Scope of the problem
Definitions
Side effect
Toxicity
Allergic reaction
Idiosyncratic effect
Iatrogenic disease
Physical dependence
Carcinogenic effect
Teratogenic effect
Organ-specific toxicity
Hepatotoxic drugs
TABLE 7–1 ▪ Some Hepatotoxic Drugs
QT interval drugs
Identifying adverse drug reactions
TABLE 7–2 ▪ Drugs That Prolong the QT Interval, Induce Torsades de Pointes, or Both
Adverse reactions to new drugs
Figure 7–1 ▪ Form for reporting adverse drug events to the FDA.
Ways to minimize adverse drug reactions
Medication guides, boxed warnings, and REMS
Medication guides
Boxed warnings
TABLE 7–3 ▪ Types of Medication Errors
Risk evaluation and mitigation strategies
Medication errors
What’s a medication error and who makes them?
Types of medication errors
Causes of medication errors
TABLE 7–4 ▪ Causes of Medication Errors
Ways to reduce medication errors
TABLE 7–5 ▪ Examples of Drugs with Names That Sound Alike or Look Alike*
TABLE 7–6 ▪ Sixteen Ways to Cut Medication Errors*
BOX 7–1 ▪ SPECIAL INTEREST TOPIC
MEDICATION RECONCILIATION
What is medication reconciliation and when is it done?
How is medication reconciliation conducted?
Does medication reconciliation reduce medication errors?
Should medication reconciliation be conducted at discharge?
How to report a medication error
TABLE 7–7 ▪ Abbreviations, Symbols, and Dose Designations That Can Promote Medication Errors
Key points
CHAPTER 8 Individual variation in drug responses
Body weight and composition
Age
Pathophysiology
Kidney disease
Figure 8–1 ▪ Effect of renal failure on kanamycin half-life. Kanamycin was administered at time “0” to two patients, one with healthy kidneys and one with renal failure. Note that drug levels declined very rapidly in the patient with healthy kidneys and extremely slowly in the patient with renal failure, indicating that renal failure greatly reduced the capacity to remove this drug from the body. (T1/2 = half-life.)
Figure 8–2 ▪ Altered drug distribution in response to altered plasma pH. Lower curve, Plasma (extracellular) pH. Note the decline in pH in response to inhalation of CO2. Upper curve, Plasma levels of phenobarbital. Note the decline in plasma drug levels during the period of extracellular acidosis. This decline results from the redistribution of phenobarbital into cells. (See text for details.)
Liver disease
Acid-base imbalance
Altered electrolyte status
Tolerance
Pharmacodynamic tolerance
TABLE 8–1 ▪ Development of Metabolic Tolerance as a Result of Repeated Pentobarbital Administration
Metabolic tolerance
Tachyphylaxis
Placebo effect
Variability in absorption
BOX 8–1 ▪ SPECIAL INTEREST TOPIC
HAS THE PLACEBO LOST ITS EFFECT?
Bioavailability
Other causes of variable absorption
Genetics and pharmacogenomics
Genetic variants that alter drug metabolism
TABLE 8–2 ▪ Examples of How Genetic Variations Can Affect Drugs Responses
Genetic variants that alter drug targets
Genetic variants that alter immune responses to drugs
Gender
Race
Drug interactions
Diet
Failure to take medicine as prescribed
Key points
III Drug Therapy Across the Life Span
Interactive Review – III: Drug Therapy Across the Life Span
CHAPTER 9 Drug therapy during pregnancy and breast-feeding
Drug therapy during pregnancy: basic considerations
Physiologic changes during pregnancy and their impact on drug disposition and dosing
Placental drug transfer
Adverse reactions during pregnancy
Drug therapy during pregnancy: teratogenesis
Incidence and causes of congenital anomalies
Teratogenesis and stage of development
Identification of teratogens
Figure 9–1 ▪ Effects of teratogens at various stages of development of the fetus.
TABLE 9–1 ▪ Drugs That Should Be Avoided During Pregnancy Because of Proven or Strongly Suspected Teratogenicity*
TABLE 9–2 ▪ FDA Pregnancy Risk Categories
FDA pregnancy risk categories
Minimizing the risk of drug-induced teratogenesis
Responding to teratogen exposure
TABLE 9–3 ▪ Drugs That Are Contraindicated During Breast-Feeding
TABLE 9–4 ▪ Drugs of Choice for Breast-Feeding Women*
Drug therapy during breast-feeding
Key points
CHAPTER 10 Drug therapy in pediatric patients
Pharmacokinetics: neonates and infants
Figure 10–1 ▪ Comparison of plasma drug levels in adults and infants. A, Plasma drug levels following IV injection. Dosage was adjusted for body weight. Note that plasma levels remain above the minimum effective concentration (MEC) much longer in the infant. B, Plasma drug levels following subQ injection. Dosage was adjusted for body weight. Note that both the maximum drug level and the duration of action are greater in the infant.
Absorption
Oral administration.
Intramuscular administration.
Transdermal absorption.
Distribution
Protein binding.
Blood-brain barrier.
Hepatic metabolism
TABLE 10–1 ▪ Comparison of the Metabolism and Effect of Hexobarbital in Adult Versus Newborn Animals
TABLE 10–2 ▪ Renal Function in Adults Versus Infants
TABLE 10–3 ▪ Adverse Drug Reactions Unique to Pediatric Patients
Renal excretion
Pharmacokinetics: children 1 year and older
Adverse drug reactions
Dosage determination
Promoting adherence
Key points
CHAPTER 11 Drug therapy in geriatric patients
Pharmacokinetic changes in the elderly
Absorption
Distribution
TABLE 11–1 ▪ Physiologic Changes That Can Affect Pharmacokinetics in the Elderly
Metabolism
Excretion
Pharmacodynamic changes in the elderly
Adverse drug reactions and drug interactions
Promoting adherence
TABLE 11–2 ▪ Some Drugs to Generally Avoid in the Elderly
TABLE 11–3 ▪ Factors That Contribute to Poor Adherence in the Elderly
Key points
IV Peripheral Nervous System Drugs
Interactive Review – IV: Peripheral Nervous System Drugs
Introduction
CHAPTER 12 Basic principles of neuropharmacology
How neurons regulate physiologic processes
Figure 12–1 ▪ How neurons regulate other cells. There are two basic steps in the process by which neurons elicit responses from other cells: (1) axonal conduction and (2) synaptic transmission. (T = neurotransmitter.)
Figure 12–2 ▪ Steps in synaptic transmission. Step 1, Synthesis of transmitter (T) from precursor molecules (Q, R, and S). Step 2, Storage of transmitter in vesicles. Step 3, Release of transmitter: In response to an action potential, vesicles fuse with the terminal membrane and discharge their contents into the synaptic gap. Step 4, Action at receptor: Transmitter binds (reversibly) to its receptor on the postsynaptic cell, causing a response in that cell. Step 5, Termination of transmission: Transmitter dissociates from its receptor and is then removed from the synaptic gap by (a) reuptake into the nerve terminal, (b) enzymatic degradation, or (c) diffusion away from the gap.
Basic mechanisms by which neuropharmacologic agents ACT
Sites of action: axons versus synapses
Axonal conduction
Synaptic transmission
Receptors
Steps in synaptic transmission
Step 1: transmitter synthesis.
Step 2: transmitter storage.
Step 3: transmitter release.
Step 4: receptor binding.
TABLE 12–1 ▪ Effects of Drugs on Synaptic Transmission and the Resulting Impact on Receptor Activation
Step 5: termination of transmission.
Effects of drugs on the steps of synaptic transmission
Transmitter synthesis.
Transmitter storage.
Figure 12–3 ▪ Multiple drug receptors and selective drug action. Mort, All of Mort’s organs are regulated through activation of type A receptors. Drugs that affect type A receptors on one organ will affect type A receptors on all other organs. Hence, selective drug action is impossible. Merv, Merv has four types of receptors (A, B, C, and D) to regulate his four organs. A drug that acts at one type of receptor will not affect the others. Hence, selective drug action is possible.
Transmitter release.
Receptor binding.
Termination of transmitter action.
Multiple receptor types and selectivity of drug action
An approach to learning about peripheral nervous system drugs
Key points
CHAPTER 13 Physiology of the peripheral nervous system
Divisions of the nervous system
Overview of autonomic nervous system functions
Functions of the parasympathetic nervous system
Figure 13–1 ▪ Opposing effects of parasympathetic and sympathetic nerves.
Functions of the sympathetic nervous system
Basic mechanisms by which the autonomic nervous system regulates physiologic processes
Patterns of innervation and control
Feedback regulation
Figure 13–2 ▪ Feedback loop of the autonomic nervous system.
Figure 13–3 ▪ The basic anatomy of the parasympathetic and sympathetic nervous systems and the somatic motor system.
Baroreceptor reflex.
Autonomic tone
Anatomic considerations
Parasympathetic nervous system
Sympathetic nervous system
Somatic motor system
Introduction to transmitters of the peripheral nervous system
Introduction to receptors of the peripheral nervous system
Primary receptor types: cholinergic receptors and adrenergic receptors
Subtypes of cholinergic and adrenergic receptors
Figure 13–4 ▪ Transmitters employed at specific junctions of the peripheral nervous system. Summary: 1.All preganglionic neurons of the parasympathetic and sympathetic nervous systems release acetylcholine as their transmitter. 2.All postganglionic neurons of the parasympathetic nervous system release acetylcholine as their transmitter. 3.Most postganglionic neurons of the sympathetic nervous system release norepinephrine as their transmitter. 4.Postganglionic neurons of the sympathetic nervous system that innervate sweat glands release acetylcholine as their transmitter. 5.Epinephrine is the principal transmitter released by the adrenal medulla. 6.All motor neurons to skeletal muscles release acetylcholine as their transmitter.
Exploring the concept of receptor subtypes
What do we mean by the term receptor subtype?
How do we know that receptor subtypes exist?
TABLE 13–1 ▪ Responses of Skeletal Muscle and Ciliary Muscle to a Series of Drugs
Figure 13–5 ▪ Drug structure and receptor selectivity. These cartoon figures illustrate the relationship between structure and receptor selectivity. The structure of acetylcholine allows this transmitter to interact with both receptor subtypes. In contrast, because of their unique structures, nicotine and muscarine are selective for the cholinergic receptor subtypes whose structure complements their own.
How can drugs be more selective than natural transmitters at receptor subtypes?
Why do receptor subtypes exist?
Do receptor subtypes matter to us? you bet!
Locations of receptor subtypes
Functions of cholinergic and adrenergic receptor subtypes
Functions of cholinergic receptor subtypes
Figure 13–6 ▪ Locations of cholinergic and adrenergic receptor subtypes. Summary: 1. NicotinicN receptors are located on the cell bodies of all postganglionic neurons of the parasympathetic and sympathetic nervous systems. NicotinicN receptors are also located on cells of the adrenal medulla. 2. NicotinicM receptors are located on skeletal muscle. 3. Muscarinic receptors are located on all organs regulated by the parasympathetic nervous system (ie, organs innervated by postganglionic parasympathetic nerves). Muscarinic receptors are also located on sweat glands. 4. Adrenergic receptors—alpha, beta, or both—are located on all organs (except sweat glands) regulated by the sympathetic nervous system (ie, organs innervated by postganglionic sympathetic nerves). Adrenergic receptors are also located on organs regulated by epinephrine released from the adrenal medulla.
Functions of adrenergic receptor subtypes
Alpha1 receptors
Alpha2 receptors
TABLE 13–2 ▪ Functions of Peripheral Cholinergic Receptor Subtypes
Beta1 receptors
Beta2 receptors
TABLE 13–3 ▪ Functions of Peripheral Adrenergic Receptor Subtypes
Dopamine receptors
Receptor specificity of the adrenergic transmitters
Figure 13–7 ▪ Life cycle of acetylcholine. Note that transmission is terminated by enzymatic degradation of ACh and not by uptake of intact ACh back into the nerve terminal. (Acetyl CoA = acetylcoenzyme A, ACh = acetylcholine, AChE = acetylcholinesterase.)
TABLE 13–4 ▪ Receptor Specificity of Adrenergic Transmitters*
Transmitter life cycles
Life cycle of acetylcholine
Figure 13–8 ▪ Life cycle of norepinephrine. Note that transmission mediated by NE is terminated by reuptake of NE into the nerve terminal, and not by enzymatic degradation. Be aware that, although postsynaptic cells may have alpha1, beta1, and beta2 receptors, NE can only activate postsynaptic alpha1 and beta1 receptors; physiologic activation of beta2 receptors is done by epinephrine. (DA = dopamine, MAO = monoamine oxidase, NE = norepinephrine.)
Life cycle of norepinephrine
Life cycle of epinephrine
Key points
Autonomic Neurotransmitters (read text)
Epinephrine (read text)
AChE (read text)
Introduction to Cholinergic Drugs
Introduction to Cholinergic Drugs
TABLE 1 ▪ Categories of Cholinergic Drugs
TABLE 2 ▪ Summary of Cholinergic Drugs and Their Receptors
CHAPTER 14 Muscarinic agonists and antagonists
Muscarinic agonists
Bethanechol
Mechanism of action
Pharmacologic effects
Pharmacokinetics
Therapeutic uses
Urinary retention.
Investigational GI uses.
Figure 14–1 ▪ Structures of muscarinic agonists. Note that, with the exception of pilocarpine, all of these agents are quaternary ammonium compounds, and hence always carry a positive charge. Because of this charge, these compounds cross membranes poorly.
Adverse effects
Cardiovascular system.
Alimentary system.
Urinary tract.
Exacerbation of asthma.
Dysrhythmias in hyperthyroid patients.
Preparations, dosage, and administration
Other muscarinic agonists
Cevimeline
Actions and uses.
Adverse effects.
Drug interactions.
Preparations, dosage, and administration.
Pilocarpine
Acetylcholine
Muscarine
Toxicology of muscarinic agonists
Sources of muscarinic poisoning.
Symptoms.
Treatment.
Muscarinic antagonists (anticholinergic drugs)
Atropine
Mechanism of action
Pharmacologic effects
Heart.
Exocrine glands.
Smooth muscle.
TABLE 14–1 ▪ Relationship Between Dosage and Responses to Atropine
Eye.
Central nervous system (cns).
Dose dependency of muscarinic blockade.
Pharmacokinetics
Therapeutic uses
Preanesthetic medication.
Disorders of the eye.
Bradycardia.
Intestinal hypertonicity and hypermotility.
Muscarinic agonist poisoning.
Peptic ulcer disease.
Asthma.
Biliary colic.
Adverse effects
Xerostomia (dry mouth).
Blurred vision and photophobia.
Elevation of intraocular pressure.
Urinary retention.
Constipation.
Anhidrosis.
Tachycardia.
Asthma.
Drug interactions
Preparations, dosage, and administration
General systemic therapy.
AtroPen for cholinesterase inhibitor poisoning.
Ophthalmology.
Muscarinic antagonists for overactive bladder
Overactive bladder: characteristics and overview of treatment
TABLE 14–2 ▪ Muscarinic Receptor Subtypes
Introduction to anticholinergic therapy of OAB
Specific anticholinergic drugs for OAB
TABLE 14–3 ▪ Anticholinergic Drugs for Overactive Bladder
Oxybutynin.
Immediate-release tablets.
Syrup.
Extended-release tablets.
Transdermal patch.
Topical gel.
Darifenacin.
Solifenacin.
Tolterodine.
Immediate-release tablets.
Extended-release capsules.
Fesoterodine.
Trospium.
Immediate-release tablets.
Extended-release capsules.
Other muscarinic antagonists
Scopolamine.
Ipratropium bromide.
Antisecretory anticholinergics.
Dicyclomine.
Pirenzepine and telenzepine.
Mydriatic cycloplegics.
Centrally acting anticholinergics.
Toxicology of muscarinic antagonists
Sources of antimuscarinic poisoning.
Symptoms.
Treatment.
Warning.
Key points
Atropine (read text)
Atropine Therapy for Sinus Bradycardia (read text)
Summary of Major Nursing Implications*
Bethanechol
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Route
Administration
Ongoing evaluation and interventions
Evaluating therapeutic effects
Minimizing adverse effects
Management of acute toxicity
Atropine and other muscarinic antagonists (anticholinergic drugs)
Preadministration assessment
Therapeutic goal
Identifying high-risk patients
Implementation: administration
Routes
Administration
Ongoing evaluation and interventions
Minimizing adverse effects
Xerostomia (dry mouth).
Blurred vision.
Photophobia.
Urinary retention.
Constipation.
Hyperthermia.
Tachycardia.
Minimizing adverse interactions
Management of acute toxicity
Symptoms.
Treatment.
CHAPTER 15 Cholinesterase inhibitors and their use in myasthenia gravis
Reversible cholinesterase inhibitors
Neostigmine
Chemistry
Mechanism of action
Pharmacologic effects
Figure 15–1 ▪ Structural formulas of reversible cholinesterase inhibitors. Note that neostigmine and edrophonium are quaternary ammonium compounds, but physostigmine is not. What does this difference imply about the relative abilities of these drugs to cross membranes, including the blood-brain barrier?
Figure 15–2 ▪ Hydrolysis of acetylcholine by cholinesterase.
Figure 15–3 ▪ Inhibition of cholinesterase by reversible and “irreversible” inhibitors. (See text for details.)
Muscarinic responses.
Neuromuscular effects.
Central nervous system.
Pharmacokinetics
Therapeutic uses
Myasthenia gravis.
Reversal of competitive (nondepolarizing) neuromuscular blockade.
Adverse effects
Excessive muscarinic stimulation.
Neuromuscular blockade.
Precautions and contraindications
Drug interactions
Muscarinic antagonists.
Competitive neuromuscular blockers.
Depolarizing neuromuscular blockers.
Acute toxicity
Symptoms.
Treatment.
Preparations, dosage, and administration
Preparations.
Dosage and administration.
TABLE 15–1 ▪ Clinical Applications of Cholinesterase Inhibitors
Other reversible cholinesterase inhibitors
Physostigmine
Ambenonium, edrophonium, and pyridostigmine
Drugs for alzheimer’s disease
“Irreversible” cholinesterase inhibitors
Basic pharmacology
Chemistry
Figure 15–4 ▪ Structural formulas of “irreversible” cholinesterase inhibitors. Note that irreversible cholinesterase inhibitors contain an atom of phosphorus. Because of this atom, these drugs are known as organophosphate cholinesterase inhibitors. With the exception of echothiophate, all of these drugs are highly lipid soluble, and therefore move throughout the body with ease.
Mechanism of action
Pharmacologic effects
Therapeutic uses
Toxicology
Sources of poisoning.
Symptoms.
Treatment.
Pralidoxime.
Myasthenia gravis
Pathophysiology
Treatment with cholinesterase inhibitors
Beneficial effects.
Side effects.
Dosage adjustment.
Myasthenic crisis and cholinergic crisis.
Myasthenic crisis.
Cholinergic crisis.
Distinguishing myasthenic crisis from cholinergic crisis.
Use of identification by the patient.
Key points
Summary of Major Nursing Implications*
Reversible cholinesterase inhibitors
Preadministration assessment
Therapeutic goal
Baseline data
Myasthenia gravis.
Identifying high-risk patients
Implementation: administration
Routes
Administration and dosage in myasthenia gravis
Administration.
Optimizing dosage.
Reversing competitive (nondepolarizing) neuromuscular blockade
Treating muscarinic antagonist poisoning
Implementation: measures to enhance therapeutic effects
Myasthenia gravis
Promoting compliance.
Using identification.
Ongoing evaluation and interventions
Evaluating therapeutic effects
Myasthenia gravis.
Minimizing adverse effects
Excessive muscarinic stimulation.
Cholinergic crisis.
CHAPTER 16 Drugs that block nicotinic cholinergic transmission: neuromuscular blocking agents and ganglionic blocking agents
Neuromuscular blocking agents
Control of muscle contraction
Basic concepts: polarization, depolarization, and repolarization
Steps in muscle contraction
Figure 16–1 ▪ The depolarization-repolarization cycle of the motor end-plate and muscle membrane.
Figure 16–2 ▪ Steps in excitation-contraction coupling.
Competitive (nondepolarizing) neuromuscular blockers
Group properties
Chemistry
Mechanism of action
Figure 16–3 ▪ Structural formulas of representative neuromuscular blocking agents.
Pharmacologic effects
Muscle relaxation.
Hypotension.
Central nervous system.
Pharmacokinetics
Figure 16–4 ▪ Mechanism of competitive neuromuscular blockade. Pancuronium, a competitive blocker, competes with acetylcholine (ACh) for binding to nicotinicM receptors on the motor end-plate. Binding of pancuronium does not depolarize the end-plate, and therefore does not cause contraction. At the same time, the presence of pancuronium prevents ACh from binding to the receptor, and hence contraction is prevented.
Therapeutic uses
Adverse effects
Respiratory arrest.
Hypotension.
Precautions and contraindications
Myasthenia gravis.
Electrolyte disturbances.
Drug interactions
General anesthetics.
Antibiotics.
Cholinesterase inhibitors.
TABLE 16–1 ▪ Properties of Competitive and Depolarizing Neuromuscular Blockers
Toxicity
Properties of individual agents
Atracurium.
Cisatracurium.
Pancuronium.
Rocuronium.
Vecuronium.
Depolarizing neuromuscular blockers: succinylcholine
Mechanism of action
Pharmacologic effects
Muscle relaxation.
Central nervous system.
Pharmacokinetics
Therapeutic uses
Adverse effects
Prolonged apnea in patients with low pseudocholinesterase activity.
Malignant hyperthermia.
Postoperative muscle pain.
Hyperkalemia.
Drug interactions
Cholinesterase inhibitors.
Antibiotics.
Toxicology
Preparations, dosage, and administration
Therapeutic uses of neuromuscular blockers
Muscle relaxation during surgery
Facilitation of mechanical ventilation
Endotracheal intubation
Adjunct to electroconvulsive therapy
Diagnosis of myasthenia gravis
Ganglionic blocking agents
Mechanism of action
Pharmacologic effects
Therapeutic use
Adverse effects
Antimuscarinic effects.
Orthostatic hypotension.
CNS effects.
Ask yourself.
TABLE 16–2 ▪ Predominant Autonomic Tone and Responses to Ganglionic Blockade
Key points
Summary of Major Nursing Implications*
Neuromuscular blocking agents
Preadministration assessment
Therapeutic goal
Identifying high-risk patients
Implementation: administration
Routes
Intravenous.
Intramuscular.
Administration
Implementation: measures to enhance therapeutic effects
Ongoing evaluation and interventions
Minimizing adverse effects
Apnea.
Hypotension.
Malignant hyperthermia.
Hyperkalemia with cardiac arrest.
Muscle pain.
Minimizing adverse interactions
Antibiotics.
Cholinesterase inhibitors.
Adrenergic Drugs
CHAPTER 17 Adrenergic agonists
Mechanisms of adrenergic receptor activation
Direct receptor binding.
Promotion of NE release.
TABLE 17–1 ▪ Mechanisms of Adrenergic Receptor Activation
Inhibition of NE reuptake.
Inhibition of NE inactivation.
Overview of the adrenergic agonists
Chemical classification: catecholamines versus noncatecholamines
Catecholamines
Noncatecholamines
Receptor specificity
Figure 17–1 ▪ Structures of representative catecholamines and noncatecholamines. Catecholamines: Note that all of the catecholamines share the same basic chemical formula. Because of their biochemical properties, the catecholamines cannot be used orally, cannot cross the blood-brain barrier, and have short half-lives (owing to rapid inactivation by MAO and COMT). Noncatecholamines: Although structurally similar to catecholamines, noncatecholamines differ from catecholamines in three important ways: they can be used orally; they can cross the blood-brain barrier; and, because they are not rapidly metabolized by MAO or COMT, they have much longer half-lives.
Therapeutic applications and adverse effects of adrenergic receptor activation
TABLE 17–2 ▪ Receptor Specificity of Representative Adrenergic Agonists
Clinical consequences of alpha1 activation
Therapeutic applications of alpha1 activation
Hemostasis.
Nasal decongestion.
Adjunct to local anesthesia.
Elevation of blood pressure.
Mydriasis.
Adverse effects of alpha1 activation
Hypertension.
Necrosis.
Bradycardia.
Clinical consequences of alpha2 activation
Clinical consequences of beta1 activation
Therapeutic applications of beta1 activation
Heart failure.
Shock.
Atrioventricular heart block.
Cardiac arrest caused by asystole.
Adverse effects of beta1 activation
Altered heart rate or rhythm.
Angina pectoris.
Clinical consequences of beta2 activation
Therapeutic applications of beta2 activation
Asthma.
Delay of preterm labor.
Adverse effects of beta2 activation
Hyperglycemia.
Tremor.
Clinical consequences of dopamine receptor activation
Multiple receptor activation: treatment of anaphylactic shock
Pathophysiology of anaphylaxis.
Treatment.
Properties of representative adrenergic agonists
Epinephrine
Therapeutic uses
BOX 17–1 ▪ SPECIAL INTEREST TOPIC
THE EPIPEN: DON’T LEAVE HOME WITHOUT IT!
EpiPen description and dosage
EpiPen storage and replacement
Who should carry an EpiPen and when should they use it?
What’s the self-injection procedure?
What should be done after the injection?
Does IM epinephrine have side effects?
TABLE 17–3 ▪ Epinephrine Solutions: Concentrations for Different Routes of Administration
Pharmacokinetics
Absorption.
Inactivation.
Adverse effects
Hypertensive crisis.
Dysrhythmias.
Angina pectoris.
Necrosis following extravasation.
Hyperglycemia.
Drug interactions
MAO inhibitors.
Tricyclic antidepressants.
General anesthetics.
Alpha-adrenergic blocking agents.
Beta-adrenergic blocking agents.
Preparations, dosage, and administration
Norepinephrine
Isoproterenol
Therapeutic uses
Cardiovascular.
Bronchospasm.
Asthma.
Adverse effects
Drug interactions
Preparations and administration
Dopamine
Receptor specificity
Therapeutic uses
Shock.
Heart failure.
Acute renal failure.
Adverse effects
Drug interactions
Preparations, dosage, and administration
Preparations.
Dosage.
Administration.
TABLE 17–4 ▪ Discussion of Adrenergic Agonists in Other Chapters
Dobutamine
Actions and uses.
Adverse effects.
Drug interactions.
Preparations, dosage, and administration.
Phenylephrine
Albuterol
Therapeutic uses
Asthma.
Adverse effects
Ephedrine
Discussion of adrenergic agonists in other chapters
Key points
Epinephrine and CPR (read text)
Summary of Major Nursing Implications
Epinephrine
Preadministration assessment
Therapeutic goal
Identifying high-risk patients
Implementation: administration
Routes
Administration
Ongoing evaluation and interventions
Evaluating therapeutic effects
Minimizing adverse effects
Cardiovascular effects.
Necrosis.
Hyperglycemia.
Minimizing adverse interactions
MAO inhibitors and tricyclic antidepressants.
General anesthetics.
Dopamine
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Route
Administration
Ongoing evaluation and interventions
Evaluating therapeutic effects
Minimizing adverse effects
Cardiovascular effects.
Necrosis.
Minimizing adverse interactions
MAO inhibitors.
Tricyclic antidepressants.
General anesthetics.
Dobutamine
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Route
Administration
Ongoing evaluation and interventions
Evaluating therapeutic effects
Minimizing adverse effects
Minimizing adverse interactions
MAO inhibitors.
Tricyclic antidepressants.
General anesthetics.
CHAPTER 18 Adrenergic antagonists
Alpha-adrenergic antagonists
Therapeutic and adverse responses to alpha blockade
Therapeutic applications of alpha blockade
Essential hypertension.
TABLE 18–1 ▪ Receptor Specificity of Adrenergic Antagonists
Reversal of toxicity from alpha1 agonists.
Benign prostatic hyperplasia.
Pheochromocytoma.
Raynaud’s disease.
Adverse effects of alpha blockade
Adverse effects of alpha1 blockade
Orthostatic hypotension.
Reflex tachycardia.
Nasal congestion.
Inhibition of ejaculation.
Sodium retention and increased blood volume.
Adverse effects of alpha2 blockade
Properties of individual alpha blockers
Prazosin
Actions and uses.
Pharmacokinetics.
Adverse effects.
Preparations, dosage, and administration.
Terazosin
Actions and uses.
Pharmacokinetics.
Adverse effects.
Preparations, dosage, and administration.
Doxazosin
Actions and uses.
Pharmacokinetics.
Adverse effects.
Preparations, dosage, and administration.
Dosage using cardura.
Dosage using cardura xl.
Tamsulosin
Actions and uses.
Pharmacokinetics.
Adverse effects.
Drug interactions.
Preparations, dosage, and administration.
Alfuzosin
Actions and uses.
Pharmacokinetics.
Adverse effects.
Drug interactions.
Preparations, dosage, and administration.
Silodosin
Actions and uses.
Adverse effects.
Preparations, dosage, and administration.
Phentolamine
Actions and uses.
Adverse effects.
Preparations, dosage, and administration.
Phenoxybenzamine
Actions and uses.
Adverse effects.
Preparations, dosage, and administration.
Beta-adrenergic antagonists
Therapeutic and adverse responses to beta blockade
Therapeutic applications of beta blockade
Angina pectoris.
Hypertension.
Cardiac dysrhythmias.
Myocardial infarction.
Reduction of perioperative mortality.
Heart failure.
Hyperthyroidism.
Migraine prophylaxis.
Stage fright.
Pheochromocytoma.
Glaucoma.
Adverse effects of beta blockade
Adverse effects of beta1 blockade
Bradycardia.
Reduced cardiac output.
Precipitation of heart failure.
AV heart block.
Rebound cardiac excitation.
Adverse effects of beta2 blockade
Bronchoconstriction.
Hypoglycemia from inhibition of glycogenolysis.
Adverse effects in neonates from beta1 and beta2 blockade
Properties of individual beta blockers
Propranolol
Pharmacologic effects
Pharmacokinetics
Therapeutic uses
Adverse effects
Bradycardia.
AV heart block.
Heart failure.
Rebound cardiac excitation.
TABLE 18–2 ▪ Clinical Pharmacology of the Beta-Adrenergic Blocking Agents
Bronchoconstriction.
Inhibition of glycogenolysis.
CNS effects.
Effects in neonates.
Precautions, warnings, and contraindications
Severe allergy.
Diabetes.
TABLE 18–3 ▪ Beta-Adrenergic Blocking Agents: Summary of Therapeutic Uses*
Cardiac, respiratory, and psychiatric disorders.
Drug interactions
Calcium channel blockers.
Insulin.
Preparations, dosage, and administration
General dosing considerations.
Preparations.
Dosage.
Metoprolol
Pharmacologic effects.
Pharmacokinetics.
Therapeutic uses.
Adverse effects.
Precautions, warnings, and contraindications.
Preparations, dosage, and administration.
Other beta-adrenergic blockers
Receptor specificity.
Pharmacokinetics.
Therapeutic uses.
Adverse effects.
Intrinsic sympathomimetic activity (partial agonist activity).
Vasodilation.
Dosage and administration.
Key points
Summary of Major Nursing Implications*
Alpha1-adrenergic antagonists
Preadministration assessment
Therapeutic goal
Doxazosin, prazosin, terazosin.
Doxazosin, terazosin, alfuzosin, silodosin, tamsulosin.
Baseline data
Essential hypertension.
Benign prostatic hyperplasia.
Identifying high-risk patients
Implementation: administration
Route
Administration
Ongoing evaluation and interventions
Evaluating therapeutic effects
Essential hypertension.
Benign prostatic hyperplasia.
Minimizing adverse effects
Orthostatic hypotension.
First-dose effect.
Beta-adrenergic antagonists
Preadministration assessment
Therapeutic goal
Baseline data
All patients.
Hypertension.
Angina pectoris.
Cardiac dysrhythmias.
Identifying high-risk patients
Implementation: administration
Routes
Oral.
Intravenous.
Administration
Ongoing evaluation and interventions
Evaluating therapeutic effects
Hypertension.
Angina pectoris.
Cardiac dysrhythmias.
Minimizing adverse effects
Bradycardia.
AV heart block.
Heart failure.
Rebound cardiac excitation.
Postural hypotension.
Bronchoconstriction.
Effects in diabetic patients.
Effects in neonates.
CNS effects.
Minimizing adverse interactions
Calcium channel blockers.
Insulin.
CHAPTER 19 Indirect-acting antiadrenergic agents
Centrally acting alpha2 agonists
Clonidine
Mechanism of antihypertensive action
Pharmacologic effects
Pharmacokinetics
Therapeutic uses
Adverse effects
Drowsiness.
Xerostomia.
Rebound hypertension.
Use in pregnancy.
Abuse.
Other adverse effects.
Preparations, dosage, and administration
Preparations.
Dosage and administration.
Oral.
Transdermal.
Guanabenz and guanfacine
Methyldopa and methyldopate
Mechanism of action
Pharmacologic effects
Therapeutic use
Adverse effects
Positive coombs’ test and hemolytic anemia.
Hepatotoxicity.
Other adverse effects.
Preparations, dosage, and administration
Preparations.
Oral therapy with methyldopa.
Intravenous therapy with methyldopate.
Adrenergic neuron-blocking agents
Reserpine
Mechanism of action
Pharmacologic effects
Peripheral effects.
Figure 19–1 ▪ Mechanism of reserpine action. Reserpine depletes neurons of norepinephrine (NE) by two mechanisms. (1) As indicated in this figure, reserpine blocks the uptake of dopamine (DA) into vesicles, thereby preventing NE synthesis. (2) Reserpine also displaces NE from vesicles, thereby allowing degradation of NE by monoamine oxidase present in the nerve terminal (not shown).
Effects on the CNS.
Therapeutic uses
Hypertension.
Psychotic states.
Adverse effects
Depression.
Cardiovascular effects.
GI effects.
Preparations, dosage, and administration
Key points
Summary of Major Nursing Implications*
Clonidine
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Routes
Administration
Oral.
Transdermal.
Ongoing evaluation and interventions
Evaluating therapeutic effects
Minimizing adverse effects
Drowsiness and sedation.
Xerostomia.
Rebound hypertension.
Abuse.
Methyldopa
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Routes
Oral.
Intravenous.
Administration
Ongoing evaluation and interventions
Evaluating therapeutic effects
Minimizing adverse effects
Hemolytic anemia.
Hepatotoxicity.
V Central Nervous System Drugs
Interactive Review – V: Central Nervous System Drugs
Introduction
CHAPTER 20 Introduction to central nervous system pharmacology
Transmitters of the CNS
The blood-brain barrier
TABLE 20–1 ▪ Neurotransmitters of the CNS
How do CNS drugs produce therapeutic effects?
Adaptation of the CNS to prolonged drug exposure
Increased therapeutic effects.
Decreased side effects.
Tolerance and physical dependence.
Development of new psychotherapeutic drugs
Approaching the study of CNS drugs
Key points
Drugs for Neurodegenerative Disorders
CHAPTER 21 Drugs for Parkinson’s disease
Pathophysiology that underlies motor symptoms
Figure 21–1 ▪ A model of neurotransmission in the healthy striatum and parkinsonian striatum. A, In the healthy striatum, dopamine (DA) released from neurons originating in the substantia nigra inhibits the firing of neurons in the striatum that release gamma-aminobutyric acid (GABA). Conversely, neurons located within the striatum, which release acetylcholine (ACh), excite the GABAergic neurons. Hence, under normal conditions, the inhibitory actions of DA are balanced by the excitatory actions of ACh, and controlled movement results. B, In Parkinson’s disease, the neurons that supply DA to the striatum degenerate. In the absence of sufficient DA, the excitatory effects of ACh go unopposed, and disturbed movement results.
Overview of motor symptom management
Therapeutic goal
Drugs employed
TABLE 21–1 ▪ Dopaminergic Agents for Parkinson’s Disease
Clinical guidelines
Drug selection
Initial treatment.
Management of motor fluctuations.
Neuroprotection.
TABLE 21–2 ▪ Drugs for Motor Complications of Levodopa Therapy
Pharmacology of the drugs used for motor symptoms
Levodopa
Use in Parkinson’s disease
Beneficial effects.
Acute loss of effect.
Mechanism of action
Pharmacokinetics
Adverse effects
Nausea and vomiting.
Figure 21–2 ▪ Steps leading to alteration of CNS function by levodopa. To produce its beneficial effects in PD, levodopa must be (1) transported across the blood-brain barrier; (2) taken up by dopaminergic nerve terminals in the striatum; (3) converted into dopamine; (4) released into the synaptic space; and (5) bound to dopamine receptors on striatal GABAergic neurons, causing them to fire at a slower rate. Note that dopamine itself is unable to cross the blood-brain barrier, and hence cannot be used to treat PD.
Figure 21–3 ▪ Conversion of levodopa to dopamine. Decarboxylases present in the brain, liver, and intestine convert levodopa into dopamine. Pyridoxine (vitamin B6) accelerates the reaction.
Dyskinesias.
Cardiovascular effects.
Psychosis.
BOX 21–1 ▪ SPECIAL INTEREST TOPIC
SURGICAL AND ELECTRICAL TREATMENTS FOR PARKINSON’S DISEASE
Deep brain stimulation (DBS)
Pallidotomy
Cell implants
TABLE 21–3 ▪ Major Drug Interactions of Levodopa
Other adverse effects.
Drug interactions
First-generation antipsychotic drugs.
Monoamine oxidase inhibitors.
Anticholinergic drugs.
Pyridoxine.
Food interactions
Preparations
Levodopa/carbidopa
Mechanism of action
Advantages of carbidopa
Disadvantages of carbidopa
Preparations, dosage, and administration
Levodopa/carbidopa: sinemet.
Levodopa/carbidopa: parcopa.
Carbidopa alone.
Dopamine agonists
Figure 21–4 ▪ Fate of levodopa in the presence and absence of carbidopa. In the absence of carbidopa, 98% of an administered dose of levodopa is metabolized in intestinal and peripheral tissues—either by decarboxylases or COMT—leaving only 2% for actions in the brain. Hence, in order to deliver 10 mg of levodopa to the brain, the dose of levodopa must be large (500 mg). By inhibiting intestinal and peripheral decarboxylases, carbidopa increases the percentage of levodopa available to the brain. Hence, the dose needed to deliver 10 mg is greatly reduced (to 100 mg in this example). Since carbidopa cannot cross the blood-brain barrier, it does not suppress conversion of levodopa to dopamine in the brain. Furthermore, since carbidopa reduces peripheral production of dopamine (from 140 mg to 50 mg in this example), peripheral toxicity (nausea, cardiovascular effects) is greatly reduced.
Pramipexole
Actions and uses.
Pharmacokinetics.
Adverse effects and interactions.
Preparations, dosage, and administration.
Parkinson’s disease.
Restless legs syndrome.
Ropinirole
Actions, uses, and adverse effects.
Preparations, dosage, and administration.
Parkinson’s disease.
Restless legs syndrome.
Apomorphine
Actions and therapeutic use.
Pharmacokinetics.
Adverse effects.
Combined use with an antiemetic.
Preparations, dosage, and administration.
Ergot derivatives: bromocriptine and cabergoline
Bromocriptine.
Cabergoline.
COMT inhibitors
Entacapone
Actions and therapeutic use.
Pharmacokinetics.
Adverse effects.
Drug interactions.
Preparations, dosage, and administration.
Tolcapone
Actions and therapeutic use.
Pharmacokinetics.
Adverse effects.
Liver failure.
Other adverse effects.
Preparations, dosage, and administration.
Levodopa/carbidopa/entacapone
MAO-B inhibitors
Selegiline
Actions and use.
Pharmacokinetics.
Tablets and capsules.
Orally disintegrating tablets.
Adverse effects.
Hypertensive crisis.
Drug interactions.
Levodopa.
Meperidine.
Fluoxetine.
Preparations, dosage, and administration.
Tablets and capsules.
Orally disintegrating tablets.
Transdermal system.
Rasagiline
Actions and therapeutic use.
Pharmacokinetics.
Adverse effects.
Drug and food interactions.
Preparations, dosage, and administration.
Amantadine
Actions and uses.
Adverse effects.
Preparations, dosage, and administration.
Centrally acting anticholinergic drugs
Nonmotor symptoms and their management
Autonomic symptoms.
Sleep disturbances.
Depression.
Dementia.
Psychosis.
Key points
Summary of Major Nursing Implications*
Levodopa/carbidopa [sinemet, parcopa]
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Route
Administration
Ongoing evaluation and interventions
Evaluating therapeutic effects
Managing acute loss of effect
Minimizing adverse effects
Nausea and vomiting.
Dyskinesias.
Dysrhythmias.
Orthostatic hypotension.
Psychosis.
Minimizing adverse interactions
First-generation antipsychotic drugs.
MAO inhibitors.
Anticholinergic drugs.
High-protein meals.
Dopamine agonists
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Route
Oral.
Subcutaneous.
Administration
Ongoing evaluation and interventions
Evaluating therapeutic effects
Minimizing adverse effects
Nausea and vomiting.
Orthostatic hypotension.
Dyskinesias.
Hallucinations.
Sleep attacks.
Fetal injury.
Impulse control disorders.
CHAPTER 22 Alzheimer’s disease
Pathophysiology
Degeneration of neurons
Reduced cholinergic transmission
Beta-amyloid and neuritic plaques
Neurofibrillary tangles and tau
Figure 22–1 ▪ Histologic changes in Alzheimer’s disease. A, Healthy neuron. B, Neuron affected by Alzheimer’s disease, showing characteristic intracellular neurofibrillary tangles. Note also extracellular neuritic plaques.
Apolipoprotein E4
Endoplasmic reticulum–associated binding protein
Homocysteine
Risk factors, symptoms, biomarkers, and diagnosis
Risk factors
Symptoms
TABLE 22–1 ▪ Symptoms of Alzheimer’s Disease
Biomarkers
Diagnosis
Preclinical AD.
Probable dementia due to AD.
TABLE 22–2 ▪ Diagnostic Criteria for All-Cause Dementia, Probable Dementia Due to Alzheimer’s Disease, and Mild Cognitive Impairment Due to Alzheimer’s Disease
Mild cognitive impairment due to AD.
Drugs for cognitive impairment
TABLE 22–3 ▪ Drugs for Cognitive Impairment
Cholinesterase inhibitors
Group properties
Mechanism of action.
Therapeutic effect.
Adverse effects.
Drug interactions.
Dosage and duration of treatment.
Properties of individual cholinesterase inhibitors
Tacrine.
Donepezil.
Rivastigmine.
Galantamine.
Memantine
Figure 22–2 ▪ Memantine mechanism of action. A, Normal physiology. In the resting postsynaptic neuron, magnesium occupies the NMDA receptor channel, blocking calcium entry. Binding of glutamate to the receptor displaces magnesium, allowing calcium to enter. When glutamate dissociates from the receptor, magnesium returns to the channel and blocks further calcium inflow. The brief period of calcium entry constitutes a “signal” in the learning and memory process. B, Pathophysiology. Slow but steady leakage of glutamate from the presynaptic neuron keeps the NMDA receptor in a constantly activated state, thereby allowing excessive calcium influx, which can impair memory and learning, and can eventually cause neuronal death. C, Effect of memantine. Memantine blocks calcium entry when extracellular glutamate is low, and thereby stops further calcium entry, which allows intracellular calcium levels to normalize. When a burst of glutamate is released in response to an action potential, the resulting high level of glutamate is able to displace memantine, causing a brief period of calcium entry. Not shown: When glutamate diffuses away, memantine reblocks the channel, and thereby stops further calcium entry, despite continuing low levels of glutamate in the synapse.
Therapeutic effects.
Mechanism of action.
Pharmacokinetics.
Adverse effects.
Drug interactions.
Dosage and administration.
Drugs for neuropsychiatric symptoms
Can we prevent alzheimer’s disease or delay cognitive decline?
TABLE 22–4 ▪ Interventions to Delay the Onset of Alzheimer’s Disease or Slow Cognitive Decline
Key points
CHAPTER 23 Drugs for multiple sclerosis
Overview of MS and its treatment
Pathophysiology
What’s the primary pathology of ms?
How does inflammation occur?
What initiates the autoimmune process?
What happens when an acute attack is over?
Figure 23–1 ▪ Symptom patterns that define the four subtypes of MS.
Does MS injure the myelin sheath of peripheral neurons?
Signs and symptoms
MS subtypes
Relapsing-remitting MS.
Secondary progressive MS.
Primary progressive MS.
Progressive-relapsing MS.
Diagnosis
TABLE 23–1 ▪ 2010 Revised McDonald Criteria for Diagnosis of MS
TABLE 23–2 ▪ Disease-Modifying Drugs for MS
Drug therapy overview
Disease-modifying therapy
Relapsing-remitting MS.
Secondary progressive MS.
Progressive-relapsing MS.
Primary progressive MS.
Treating an acute episode (relapse)
Drug therapy of symptoms
Disease-modifying drugs I: immunomodulators
Interferon beta preparations
Description and mechanism
Therapeutic use
Adverse effects and drug interactions
Flu-like reactions.
Hepatotoxicity.
Myelosuppression.
Injection-site reactions.
Depression.
Neutralizing antibodies.
Drug interactions.
Preparations, dosage, and administration
Avonex (interferon beta-1a for IM use).
Rebif (interferon beta-1a for subq use).
Betaseron and extavia (interferon beta-1b for subq use).
Glatiramer acetate
Therapeutic use.
Description and mechanism.
Adverse effects and drug interactions.
Preparations, dosage, and administration.
Natalizumab
Therapeutic uses
Multiple sclerosis.
Crohn’s disease.
Mechanism of action
Adverse effects
Progressive multifocal leukoencephalopathy.
Hepatotoxicity.
Hypersensitivity reactions.
Neutralizing antibodies.
Drug interactions
Preparations, dosage, and administration
Fingolimod
Pharmacokinetics
Mechanism of action
Adverse effects
Bradycardia.
Macular edema.
Liver injury.
Infection.
Fetal harm.
Use during breast-feeding.
Reduced lung function.
Drug interactions
Ketoconazole.
Cardiac drugs.
Vaccines.
Drugs that suppress immune function.
Preparations, dosage, and administration
Disease-modifying drugs II: immunosuppressants
Mitoxantrone
Therapeutic use
Mechanism of action
Pharmacokinetics
Adverse effects
Myelosuppression.
Cardiotoxicity.
Fetal harm.
Other adverse effects.
Monitoring summary
Preparations, dosage, and administration
Disease-modifying drugs III: investigational agents
Drugs used to manage MS symptoms
TABLE 23–3 ▪ Investigational Disease-Modifying Drugs for MS
Bladder dysfunction
Bowel dysfunction
Fatigue
Depression
Sexual dysfunction
Neuropathic pain
Dalfampridine to improve walking
Actions and uses.
Pharmacokinetics.
Adverse effects.
Preparations, dosage, and administration.
Ataxia and tremor
Spasticity
Cognitive dysfunction
Dizziness and vertigo
Key points
Summary of Major Nursing Implications*
Interferon beta
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Routes
Intramuscular.
Subcutaneous.
Administration
Avonex.
Rebif.
Betaseron and extavia.
Ongoing evaluation and interventions
Evaluating therapeutic effects
Minimizing adverse effects
Flu-like reactions.
Hepatotoxicity.
Myelosuppression.
Injection-site reactions.
Minimizing adverse interactions
Hepatotoxic and myelosuppressant drugs.
Glatiramer acetate
Preadministration assessment
Therapeutic goal
Implementation: administration
Route
Administration
Ongoing evaluation and interventions
Evaluating therapeutic effects
Minimizing adverse effects
Injection-site reactions.
Immediate postinjection reaction.
Natalizumab
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Route
Administration
Ongoing evaluation and interventions
Evaluating therapeutic effects
Minimizing adverse effects
Progressive multifocal leukoencephalopathy.
Hepatotoxicity.
Hypersensitivity reactions.
Drug interactions
Fingolimod
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Route
Administration
Ongoing evaluation and interventions
Evaluating therapeutic effects
Monitoring summary
Minimizing adverse effects
Bradycardia.
Macular edema.
Liver injury.
Infection.
Fetal harm.
Use during breast-feeding.
Reduced lung function.
Minimizing adverse interactions
Ketoconazole.
Cardiac drugs.
Drugs that suppress immune function.
Vaccines.
Mitoxantrone
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Route
Administration
Ongoing evaluation and interventions
Evaluating therapeutic effects
Monitoring summary
Minimizing adverse effects
Myelosuppression.
Cardiotoxicity.
Fetal harm.
Urine and tissue discoloration.
Neurologic Drugs
CHAPTER 24 Drugs for epilepsy
Seizure generation
TABLE 24–1 ▪ Drugs for Specific Types of Seizures
Types of seizures
Partial seizures
Simple partial seizures.
Complex partial seizures.
Secondarily generalized seizures.
Generalized seizures
Tonic-clonic seizures (grand mal).
Absence seizures (petit mal).
Atonic seizures.
Myoclonic seizures.
Status epilepticus.
Febrile seizures.
Mixed seizures: Lennox-Gastaut syndrome
How antiepileptic drugs work
Suppression of sodium influx.
Suppression of calcium influx.
Promotion of potassium efflux.
Antagonism of glutamate.
Potentiation of GABA.
Basic therapeutic considerations
Therapeutic goal and treatment options
Diagnosis and drug selection
BOX 24–1 ▪ SPECIAL INTEREST TOPIC
NONDRUG THERAPIES FOR EPILEPSY: NEUROSURGERY, VAGUS NERVE STIMULATION, AND THE KETOGENIC DIET
Neurosurgery: the cure that’s rarely used
Vagus nerve stimulation: fighting impulses with impulses
The ketogenic diet: it’s tough but it works
Drug evaluation
Monitoring plasma drug levels
Promoting patient adherence
Withdrawing antiepileptic drugs
TABLE 24–2 ▪ Clinical Pharmacology of the Oral Antiepileptic Drugs (AEDs)
Suicide risk with antiepileptic drugs
TABLE 24–3 ▪ Comparison of Traditional and Newer Antiepileptic Drugs
Classification of antiepileptic drugs
Traditional antiepileptic drugs
Phenytoin
Mechanism of action
Figure 24–1 ▪ Relationship between dose and plasma level for phenytoin compared with most other drugs. A, Within the therapeutic range, small increments in phenytoin dosage produce sharp increases in plasma drug levels. This relationship makes it difficult to maintain plasma phenytoin levels within the therapeutic range. B, Within the therapeutic range, small increments in dosage of most drugs produce small increases in drug levels. With this relationship, moderate fluctuations in dosage are unlikely to result in either toxicity or therapeutic failure.
Pharmacokinetics
Absorption.
Metabolism.
Therapeutic uses
Epilepsy.
Cardiac dysrhythmias.
Adverse effects
Effects on the CNS.
Gingival hyperplasia.
Dermatologic effects.
Effects in pregnancy.
Cardiovascular effects.
Purple glove syndrome.
Other adverse effects.
Drug interactions
Interactions resulting from induction of hepatic drug-metabolizing enzymes.
Drugs that increase plasma levels of phenytoin.
Drugs that decrease plasma levels of phenytoin.
CNS depressants.
Preparations, dosage, and administration
Preparations.
Dosage.
Administration.
Carbamazepine
Mechanism of action
Pharmacokinetics
Therapeutic uses
Epilepsy.
Bipolar disorder.
Trigeminal and glossopharyngeal neuralgias.
Adverse effects
CNS effects.
Hematologic effects.
Birth defects.
Hypo-osmolarity.
Dermatologic effects.
TABLE 24–4 ▪ Oral Preparations of Valproic Acid and Its Derivatives
Drug-drug and drug-food interactions
Induction of drug-metabolizing enzymes.
Phenytoin and phenobarbital.
Grapefruit juice.
Preparations, dosage, and administration
Valproic acid
Nomenclature
Mechanism of action
Pharmacokinetics
Therapeutic uses
Seizure disorders.
Bipolar disorder.
Migraine.
Adverse effects
Gastrointestinal effects.
Hepatotoxicity.
Pancreatitis.
Pregnancy-related harm.
Hyperammonemia.
Other adverse effects.
Drug interactions
Phenobarbital.
Phenytoin.
Topiramate.
Carbapenem antibiotics.
Preparations, dosage, and administration
Preparations.
Oral dosage and administration.
Ethosuximide
Therapeutic use.
Mechanism of action.
Pharmacokinetics.
Adverse effects and drug interactions.
Preparations, dosage, and administration.
Phenobarbital
Mechanism of antiseizure action
Pharmacokinetics
Therapeutic uses
Epilepsy.
Sedation and induction of sleep.
Adverse effects
Neuropsychologic effects.
Physical dependence.
Exacerbation of intermittent porphyria.
Use in pregnancy.
Other adverse effects.
Toxicity
Drug interactions
Induction of drug-metabolizing enzymes.
CNS depressants.
Valproic acid.
Drug withdrawal
Preparations, dosage, and administration
Preparations.
Dosage.
Administration.
Primidone
Pharmacokinetics.
Therapeutic uses.
Adverse effects.
Drug interactions.
Preparations, dosage, and administration.
Newer antiepileptic drugs
Oxcarbazepine
Actions and uses.
Pharmacokinetics.
Adverse effects.
Use in pregnancy and breast-feeding.
Drug interactions.
Preparations, dosage, and administration.
Lamotrigine
Therapeutic uses.
Mechanism of action.
Pharmacokinetics.
Drug interactions.
Adverse effects.
Preparations, dosage, and administration.
Gabapentin
Therapeutic uses.
Mechanism of action.
Pharmacokinetics.
Drug interactions.
Adverse reactions.
Preparations, dosage, and administration.
Gabapentin enacarbil
Pregabalin
Therapeutic uses.
Mechanism of action.
Pharmacokinetics.
Adverse effects.
Abuse potential and physical dependence.
Reproductive toxicity.
Drug interactions.
Preparations, dosage, and administration.
Neuropathic pain associated with diabetic peripheral neuropathy.
Postherpetic neuralgia.
Epilepsy.
Fibromyalgia.
Levetiracetam
Topiramate
Actions and uses.
Pharmacokinetics.
Adverse effects.
Drug interactions.
Preparations, dosage, and administration.
Tiagabine
Actions and uses.
Pharmacokinetics.
Adverse effects.
Drug interactions.
Preparations, dosage, and administration.
Zonisamide
Actions and uses.
Pharmacokinetics.
Adverse effects.
Use in pregnancy and breast-feeding.
Drug and food interactions.
Preparations, dosage, and administration.
Felbamate
Mechanism of action.
Pharmacokinetics.
Therapeutic uses.
Adverse effects.
Drug interactions.
Preparations, dosage, and administration.
Lacosamide
Actions and uses.
Pharmacokinetics.
Adverse effects.
Drug interactions.
Preparations, dosage, and administration.
Rufinamide
Actions and uses.
Pharmacokinetics.
Adverse effects.
Drug interactions.
Preparations, dosage, and administration.
Vigabatrin
Actions and uses.
Pharmacokinetics.
Adverse effect: vision loss.
Other adverse effects.
Drug interactions.
Preparations, dosage, and administration.
Ezogabine
Management of epilepsy during pregnancy
Management of generalized convulsive status epilepticus
Key points
Summary of Major Nursing Implications*
Nursing implications that apply to all antiepileptic drugs
Preadministration assessment
Therapeutic goal
Baseline data
Implementation: administration
Dosage determination
Promoting adherence
Ongoing evaluation and interventions
Evaluating therapeutic effects
Minimizing danger from uncontrolled seizures
Minimizing adverse effects
CNS depression.
Withdrawal seizures.
Usage in pregnancy.
Suicidal thoughts and behavior.
Minimizing adverse interactions
CNS depressants.
Phenytoin
Preadministration assessment
Therapeutic goal
Identifying high-risk patients
Implementation: administration
Routes
Administration
Oral.
Intravenous.
Ongoing evaluation and interventions
Minimizing adverse effects
CNS effects.
Gingival hyperplasia.
Use in pregnancy.
Dermatologic reactions.
Withdrawal seizures.
Minimizing adverse interactions
CNS depressants.
Warfarin and oral contraceptives.
Carbamazepine
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Route
Administration
Ongoing evaluation and interventions
Minimizing adverse effects
CNS effects.
Hematologic effects.
Birth defects.
Severe skin reactions.
Minimizing adverse interactions
Interactions due to induction of drug metabolism.
Phenytoin and phenobarbital.
Grapefruit juice.
Valproic acid
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Routes
Administration
Ongoing evaluation and interventions
Minimizing adverse effects
Gastrointestinal effects.
Hepatotoxicity.
Pancreatitis.
Pregnancy-related harm.
Hyperammonemia.
Minimizing adverse interactions
Antiepileptic drugs.
Topiramate.
Carbapenem antibiotics.
Phenobarbital
Preadministration assessment
Therapeutic goal
Identifying high-risk patients
Implementation: administration
Routes
Administration
Oral.
Intravenous.
Ongoing evaluation and interventions
Minimizing adverse effects
Neuropsychologic effects.
Exacerbation of intermittent porphyria.
Use in pregnancy.
Withdrawal seizures.
Minimizing adverse interactions
Interactions caused by induction of drug metabolism.
CNS depressants.
Valproic acid.
CHAPTER 25 Drugs for muscle spasm and spasticity
Drug therapy of muscle spasm: centrally acting muscle relaxants
Mechanism of action
TABLE 25–1 ▪ Drugs for Muscle Spasm: Centrally Acting Muscle Relaxants
Figure 25–1 ▪ Structural similarity between baclofen and gamma-aminobutyric acid (GABA).
Therapeutic use
Adverse effects
CNS depression.
Hepatic toxicity.
Physical dependence.
Other adverse effects.
Dosage and administration
Drugs for spasticity
Baclofen
Mechanism of action
Therapeutic use
Adverse effects
CNS effects.
Withdrawal.
Other adverse effects.
Preparations, dosage, and administration
Oral.
Intrathecal.
Diazepam
Actions.
Adverse effects.
Preparations, dosage, and administration.
Dantrolene
Mechanism of action
Therapeutic uses
Spasticity.
Malignant hyperthermia.
Adverse effects
Hepatic toxicity.
Other adverse effects.
Preparations, dosage, and administration
Preparations.
Use in spasticity.
Use in malignant hyperthermia.
Preoperative prophylaxis.
Treatment of an ongoing crisis.
Key points
Summary of Major Nursing Implications*
Drugs used to treat muscle spasm: centrally acting skeletal muscle relaxants
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Routes
Oral.
Parenteral.
Dosage
Implementation: measures to enhance therapeutic effects
Ongoing evaluation and interventions
Minimizing adverse effects
CNS depression.
Hepatic toxicity.
Minimizing adverse interactions
CNS depressants.
Avoiding withdrawal reactions
Baclofen
Preadministration assessment
Therapeutic goal
Baseline data
Implementation: administration
Routes
Administration
Ongoing evaluation and interventions
Evaluating therapeutic effects
Minimizing adverse effects
CNS depression.
Minimizing adverse interactions
CNS depressants.
Avoiding withdrawal reactions
Oral baclofen.
Intrathecal baclofen.
Dantrolene
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Route
Administration
Ongoing evaluation and interventions
Summary of monitoring
Therapeutic effects.
Adverse effects.
Minimizing adverse effects
CNS depression.
Hepatic toxicity.
Muscle weakness.
Minimizing adverse interactions
CNS depressants.
Diazepam
Drugs for Pain
CHAPTER 26 Local anesthetics
Basic pharmacology of the local anesthetics
Classification
Mechanism of action
Selectivity of anesthetic effects
Time course of local anesthesia
Figure 26–1 ▪ Structural formulas of representative local anesthetics.
TABLE 26–1 ▪ Contrasts Between Ester and Amide Local Anesthetics
Use with vasoconstrictors
Fate in the body
Absorption and distribution.
Metabolism.
Adverse effects
Central nervous system.
Cardiovascular system.
Allergic reactions.
Use in labor and delivery.
Methemoglobinemia.
Properties of individual local anesthetics
Procaine
Preparations.
Lidocaine
Preparations.
Cocaine
Anesthetic use.
CNS effects.
TABLE 26–2 ▪ Topical Local Anesthetics: Trade Names, Indications, and Time Course of Action
Cardiovascular effects.
Preparations and administration.
Other local anesthetics
Clinical use of local anesthetics
Topical administration
Therapeutic uses.
Systemic toxicity.
TABLE 26–3 ▪ Injectable Local Anesthetics: Trade Names and Time Course of Action
Administration by injection
Infiltration anesthesia
Nerve block anesthesia
Intravenous regional anesthesia
Epidural anesthesia
Spinal (subarachnoid) anesthesia
Technique.
Adverse effects.
Key points
Summary of Major Nursing Implications*
Topical local anesthetics
Preadministration assessment
Therapeutic goal
Identifying high-risk patients
Implementation: administration
Routes
Administration
Ongoing evaluation and interventions
Minimizing adverse effects
Systemic toxicity.
Allergic reactions.
Injected local anesthetics
Preadministration assessment
Therapeutic goal
Identifying high-risk patients
Implementation: administration
Preparation of the patient
Administration
Ongoing evaluation and interventions
Minimizing adverse effects
Systemic reactions.
Allergic reactions.
Labor and delivery.
Self-inflicted injury.
Spinal headache and urinary retention.
CHAPTER 27 General anesthetics
Inhalation anesthetics
Basic pharmacology
Properties of an ideal inhalation anesthetic
Balanced anesthesia
TABLE 27–1 ▪ Properties of the Major Inhalation Anesthetics
Molecular mechanism of action
Minimum alveolar concentration
Pharmacokinetics
Uptake and distribution
Uptake.
Distribution.
Elimination
Export in the expired breath.
Metabolism.
Adverse effects
Respiratory and cardiac depression.
Sensitization of the heart to catecholamines.
Malignant hyperthermia.
Aspiration of gastric contents.
Hepatotoxicity.
Toxicity to operating room personnel.
Drug interactions
Adjuncts to inhalation anesthesia
Preanesthetic medications
Benzodiazepines.
Opioids.
TABLE 27–2 ▪ Classification of the Inhalation Anesthetics
Alpha2-adrenergic agonists.
Anticholinergic drugs.
Neuromuscular blocking agents
Postanesthetic medications
Analgesics.
Antiemetics.
Muscarinic agonists.
Dosage and administration
Classification of inhalation anesthetics
Properties of individual inhalation anesthetics
Halothane
Anesthetic properties
Potency.
Time course.
Analgesia.
Muscle relaxation.
Adverse effects
Hypotension.
Respiratory depression.
Promotion of dysrhythmias.
Malignant hyperthermia.
Hepatotoxicity.
Other adverse effects.
Elimination
Isoflurane
Enflurane
Desflurane
Sevoflurane
Nitrous oxide
Obsolete inhalation anesthetics
Intravenous anesthetics
Short-acting barbiturates (thiobarbiturates)
Thiopental.
Benzodiazepines
Diazepam.
Midazolam.
Propofol
Actions and uses.
Adverse effects.
Abuse.
Fospropofol
Etomidate
Ketamine
Anesthetic effects.
Adverse psychologic reactions.
Who should receive ketamine.
Therapeutic uses.
Neuroleptic-opioid combination: droperidol plus fentanyl
Key points
Summary of Major Nursing Implications
All inhalation anesthetics
Preoperative patients: counseling, assessment, and medicating
Counseling
Assessment
Medication history.
Respiratory and cardiovascular function.
Preoperative medication
Postoperative patients: ongoing evaluation and interventions
Evaluations and interventions that pertain to specific organ systems
Cardiovascular and respiratory systems.
Central nervous system.
Gastrointestinal tract.
Urinary tract.
Management of postoperative pain
CHAPTER 28 Opioid (narcotic) analgesics, opioid antagonists, and nonopioid centrally acting analgesics
Opioid analgesics
Introduction to the opioids
Terminology
Endogenous opioid peptides
Opioid receptors
Mu receptors.
TABLE 28–1 ▪ Important Responses to Activation of Mu and Kappa Receptors
TABLE 28–2 ▪ Drug Actions at Mu and Kappa Receptors
Kappa receptors.
Classification of drugs that act at opioid receptors
Pure opioid agonists.
Agonist-antagonist opioids.
Pure opioid antagonists.
Basic pharmacology of the opioids
Morphine
Source
Overview of pharmacologic actions
Therapeutic use: relief of pain
Figure 28–1 ▪ Structural similarity between morphine and met-enkephalin. In the morphine structural formula, highlighting indicates the part of the molecule thought responsible for interaction with opioid receptors. In the met-enkephalin structural formula, highlighting indicates the region of structural similarity with morphine.
TABLE 28–3 ▪ Opioid Analgesics: Abuse Liability and Maximal Pain Relief
Mechanism of analgesic action.
Adverse effects
Respiratory depression.
Constipation.
Orthostatic hypotension.
Urinary retention.
Cough suppression.
Biliary colic.
Emesis.
Elevation of intracranial pressure.
Euphoria/dysphoria.
Sedation.
Miosis.
Birth defects.
Neurotoxicity.
Adverse effects from prolonged use.
Pharmacokinetics
Tolerance and physical dependence
Tolerance.
Physical dependence.
Abuse liability
Precautions
Decreased respiratory reserve.
Labor and delivery.
Neonatal opioid dependence.
Head injury.
TABLE 28–4 ▪ Interactions of Morphine-Like Drugs with Other Drugs
Other precautions.
Drug interactions
CNS depressants.
Anticholinergic drugs.
Hypotensive drugs.
Monoamine oxidase inhibitors.
Agonist-antagonist opioids.
Opioid antagonists.
Other interactions.
Toxicity
Clinical manifestations.
Treatment.
Preparations
Morphine alone.
Morphine/naltrexone [embeda].
Dosage and administration
General guidelines.
Routes and dosages.
Oral.
Intramuscular and subcutaneous.
Intravenous.
Epidural and intrathecal.
Other strong opioid agonists
Fentanyl
Parenteral.
TABLE 28–5 ▪ Clinical Pharmacology of Pure Opioid Agonists
Transdermal system.
Transmucosal.
Lozenge on a stick.
Soluble buccal film.
Buccal tablets.
Sublingual tablets.
Intranasal.
Alfentanil and sufentanil
Remifentanil
Meperidine
Methadone
Heroin
Hydromorphone, oxymorphone, and levorphanol
Basic pharmacology.
Preparations, dosage, and administration.
Hydromorphone.
Oxymorphone.
Levorphanol.
Figure 28–2 ▪ Biotransformation of heroin into morphine. Heroin, as such, is biologically inactive. After crossing the blood-brain barrier, heroin is converted to monoacetylmorphine (MAM) and then into morphine itself. MAM and morphine are responsible for the effects elicited by injection of heroin.
Moderate to strong opioid agonists
Codeine
Preparations, dosage, and administration.
Oxycodone
Hydrocodone
Tapentadol
Actions and uses.
Pharmacokinetics.
Adverse effects.
Drug interactions.
Preparations, dosage, and administration.
Propoxyphene
Agonist-antagonist opioids
TABLE 28–6 ▪ Clinical Pharmacology of Opioid Agonist-Antagonists
Pentazocine
Actions and uses.
Preparations, dosage, and administration.
Parenteral.
Oral.
Nalbuphine
Butorphanol
Buprenorphine
Basic pharmacology.
Preparations.
Transdermal patch.
Solution for injection.
Sublingual tablets and sublingual film.
Clinical use of opioids
Dosing guidelines
Pain assessment
Dosage determination
Figure 28–3 ▪ Fluctuation in opioid blood levels seen with three dosing procedures. Note that with PRN dosing, opioid levels can fluctuate widely, going from subtherapeutic to excessive and back again. In contrast, when opioids are administered with a PCA device or on a fixed schedule, levels stay within the therapeutic range, allowing continuous pain relief with minimal adverse effects.
Dosing schedule
Avoiding a withdrawal reaction
Physical dependence, abuse, and addiction as clinical concerns
Definitions
Physical dependence.
Abuse.
Addiction.
Minimizing fears about physical dependence
Minimizing fears about addiction
Balancing the need to provide pain relief with the desire to minimize abuse
Patient-controlled analgesia
PCA devices.
Drug selection and dosage regulation.
Comparison of PCA with traditional IM therapy.
Patient education.
Using opioids for specific kinds of pain
Postoperative pain.
Obstetric analgesia.
Myocardial infarction.
Head injury.
Cancer-related pain.
Chronic noncancer pain.
REMS to reduce opioid-related morbidity, mortality, and abuse
Opioid antagonists
Naloxone
Mechanism of action
Pharmacologic effects
Pharmacokinetics
Therapeutic uses
Reversal of opioid overdose.
Reversal of postoperative opioid effects.
Reversal of neonatal respiratory depression.
Preparations, dosage, and administration
Preparations and routes.
Opioid overdose.
Postoperative opioid effects.
Neonatal respiratory depression.
Other opioid antagonists
Methylnaltrexone
Actions and therapeutic use.
Pharmacokinetics.
Adverse effects, precautions, and drug interactions.
Preparations, dosage, and administration.
Alvimopan
Naltrexone
Nonopioid centrally acting analgesics
Tramadol
Mechanism of action.
Therapeutic use.
Pharmacokinetics.
Adverse effects.
Drug interactions.
Abuse liability.
Warning: suicide.
Preparations, dosage, and administration.
Clonidine
Mechanism of pain relief.
Analgesic use.
Pharmacokinetics.
Adverse effects.
Hypotension.
Bradycardia.
Rebound hypertension.
Catheter-related infection.
Other adverse effects.
Contraindications.
Preparations, dosage, and administration.
Ziconotide
Mechanism of action.
Clinical trials.
Pharmacokinetics.
Adverse effects.
Drug interactions.
Preparations, dosage, and administration.
Dexmedetomidine
Actions and therapeutic use.
Pharmacokinetics.
Adverse effects.
Drug interactions.
Preparations, dosage, and administration.
Key points
Opiate Intoxication (read text)
Summary of Major Nursing Implications*
Pure opioid agonists
Preadministration assessment
Therapeutic goal
Baseline data
Pain assessment.
Vital signs.
Identifying high-risk patients
Implementation: administration
Routes
Dosage
General guidelines.
Dosage in patients with cancer.
Discontinuing opioids.
Administration
Ongoing evaluation and interventions
Evaluating therapeutic effects
Minimizing adverse effects
Respiratory depression.
Sedation.
Orthostatic hypotension.
Constipation.
Urinary retention.
Biliary colic.
Emesis.
Cough suppression.
Miosis.
Neurotoxicity.
Birth defects.
Opioid dependence in the neonate.
Dysrhythmias.
Minimizing adverse interactions
CNS depressants.
Anticholinergic drugs.
Hypotensive drugs.
Opioid antagonists.
Agonist-antagonist opioids.
MAO inhibitors.
CYP3A4 inhibitors.
Agonist-antagonist opioids
Therapeutic goal
Routes
Differences from pure opioid agonists
Naloxone
Therapeutic goal
Routes
Dosage
CHAPTER 29 Pain management in patients with cancer
Pathophysiology of pain
What is pain?
Neurophysiologic basis of painful sensations
TABLE 29–1 ▪ Barriers to Cancer Pain Management
Nociceptive pain versus neuropathic pain
Pain in cancer patients
Management strategy
Assessment and ongoing evaluation
Figure 29–1 ▪ Flow chart for pain management in patients with cancer. NSAID = nonsteroidal anti-inflammatory drug. (Adapted from Jacox A, Carr DB, Payne R, et al: Management of Cancer Pain [Clinical Practice Guideline No. 9; AHCPR Publication No. 94-0592]. Rockville, MD: Agency for Health Care Policy and Research, 1994.)
Comprehensive initial assessment
Assessment of pain intensity and character: the patient self-report
Physical and neurologic examinations
Diagnostic tests
Psychosocial assessment
Pain intensity scales
Ongoing evaluation
Figure 29–2 ▪ Linear pain intensity scales. If used as a graphic rating scale, a 10-cm baseline is recommended.
Figure 29–3 ▪ Wong-Baker FACES pain rating scale. Explain to the patient that the first face represents a person who feels happy because he or she has no pain, and that the other faces represent people who feel sad because they have pain, ranging from a little to a lot. Explain that face 10 represents a person who hurts as much as you can imagine, but that you don’t have to be crying to feel this bad. Ask the patient to choose the face that best reflects how he or she is feeling. The numbers below the faces correspond to the values in the numeric pain scale shown in Figure 29–2.
Barriers to assessment
Figure 29–4 ▪ The WHO analgesic ladder for cancer pain management. Note that steps represent pain intensity. Accordingly, if a patient has intense pain at the outset, then treatment can be initiated with an opioid (step 2), rather than trying a nonopioid first (step 1).
Drug therapy
Nonopioid analgesics
Nonsteroidal anti-inflammatory drugs
TABLE 29–2 ▪ Drugs That Are Not Recommended for Treating Cancer Pain
Acetaminophen
TABLE 29–3 ▪ Dosages for Nonopioid Analgesics: Acetaminophen and Selected NSAIDs
Opioid analgesics
Mechanism of action and classification
Tolerance and physical dependence
Tolerance.
TABLE 29–4 ▪ Equianalgesic Doses of Pure Opioid Agonists and Tramadol
Physical dependence.
Addiction
Drug selection
Preferred opioids.
Opioid rotation.
Opioids to use with special caution.
Opioids to avoid.
Dosage
Routes of administration
Oral.
Rectal.
Transdermal.
Intravenous and subcutaneous.
Intramuscular.
Intraspinal.
Intraventricular.
Patient-controlled analgesia.
Managing breakthrough pain
Managing side effects
Respiratory depression.
Constipation.
Sedation.
Nausea and vomiting.
Other side effects.
Adjuvant analgesics
Antidepressants
Tricyclic antidepressants.
Other antidepressants.
Antiseizure drugs
TABLE 29–5 ▪ Adjuvant Drugs for Cancer Pain
Local anesthetics/antidysrhythmics
CNS stimulants
Antihistamines
Glucocorticoids
Bisphosphonates
Nondrug therapy
Invasive procedures
Neurolytic nerve block
Neurosurgery
Tumor surgery
Radiation therapy
Physical and psychosocial interventions
Physical interventions
Heat.
Cold.
Massage.
Exercise.
Acupuncture and transcutaneous electrical nerve stimulation.
Psychosocial interventions
Relaxation and imagery.
Cognitive distraction.
Peer support groups.
Pain management in special populations
The elderly
Heightened drug sensitivity.
Undertreatment of pain.
Increased risk of side effects and adverse interactions.
Young children
Assessment
Verbal children.
Preverbal and nonverbal children.
Treatment
Opioid abusers
Patient education
General issues
Drug therapy
Nondrug therapy
The joint commission pain management standards
Key points
CHAPTER 30 Drugs for headache
TABLE 30–1 ▪ Characteristics of Major Headache Syndromes
TABLE 30–2 ▪ Factors That Can Precipitate Migraine Headache
Migraine headache
Characteristics, pathophysiology, and overview of treatment
Characteristics
Pathophysiology
Overview of treatment
TABLE 30–3 ▪ Migraine Headache: Drugs for Abortive Therapy
Abortive therapy
Analgesics
Aspirin-like drugs
Opioid analgesics
Ergot alkaloids
Ergotamine
Mechanism of antimigraine action.
Therapeutic uses.
BOX 30–1 ▪ SPECIAL INTEREST TOPIC
MEDICATION OVERUSE HEADACHE: TOO MUCH OF A GOOD THING
Pharmacokinetics.
Adverse effects.
Overdose.
Drug interactions.
Triptans.
CYP3A4 inhibitors.
Physical dependence.
Contraindications.
Preparations, dosage, and administration.
Sublingual.
Oral.
Rectal.
Dihydroergotamine
Therapeutic uses.
Pharmacologic effects.
Pharmacokinetics.
Drug interactions.
Contraindications.
Parenteral administration.
Intramuscular and subcutaneous.
Intravenous.
Intranasal administration.
Oral inhalation.
Serotonin1b/1d receptor agonists (triptans)
Sumatriptan
Mechanism of action.
Therapeutic use.
Pharmacokinetics.
Adverse effects.
Chest symptoms.
Coronary vasospasm.
Teratogenesis.
Other adverse effects.
Drug interactions.
Ergot alkaloids and other triptans.
Monoamine oxidase inhibitors.
Table 30–4 ▪ Clinical Pharmacology of the Triptans
Selective serotonin reuptake inhibitors (SSRIs) and serotonin/norepinephrine reuptake inhibitors (SNRIS).
Preparations, dosage, and administration.
Subcutaneous, using a needle.
Subcutaneous, using a needle-free device.
Oral.
Nasal spray.
Transdermal.
Other serotonin1B/1D receptor agonists
Zolmitriptan.
Naratriptan.
Rizatriptan.
Almotriptan.
Frovatriptan.
Eletriptan.
Other abortive agents
Sumatriptan/naproxen.
Haloperidol.
Telcagepant.
Preventive therapy
TABLE 30–5 ▪ Migraine Headache: Drugs for Preventive Therapy
Beta blockers
Antiepileptic drugs
Divalproex.
Topiramate.
Tricyclic antidepressants
Estrogens and triptans for menstrual migraine
TABLE 30–6 ▪ Drugs Used for Prophylaxis of Cluster Headache
Other drugs for prophylaxis
Calcium channel blockers
Botulinum toxin
Angiotensin-converting enzyme inhibitors (aceis) and angiotensin II receptor blockers (ARBs)
Supplements
Riboflavin.
Coenzyme Q-10.
Butterbur.
Cluster headaches
Characteristics
Drug therapy
Prophylaxis.
Treatment.
Tension-type headache
Characteristics
Treatment
Key points
Summary of Major Nursing Implications*
Ergotamine and dihydroergotamine
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Routes
Ergotamine alone.
Ergotamine plus caffeine.
Dihydroergotamine.
Dosage and administration
Implementation: measures to enhance therapeutic effects
Ongoing evaluation and interventions
Evaluating therapeutic effects
Minimizing adverse effects
Nausea and vomiting.
Ergotism.
Physical dependence.
Abortion.
Minimizing adverse interactions
Inhibitors of CYP3A4.
Serotonin1b/1d receptor agonists (triptans)
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Routes
Oral.
Subcutaneous.
Intranasal.
Dosage and administration
Implementation: measures to enhance therapeutic effects
Ongoing evaluation and interventions
Evaluating therapeutic effects
Minimizing adverse effects
Coronary vasospasm.
Teratogenesis.
Minimizing adverse interactions
Ergot alkaloids and other triptans.
SSRIs and SNRIS.
MAOIs.
CYP3A4 inhibitors.
Propranolol.
Psychotherapeutic Drugs
CHAPTER 31 Antipsychotic agents and their use in schizophrenia
Schizophrenia: clinical presentation and etiology
Clinical presentation
Three types of symptoms
Positive symptoms and negative symptoms.
TABLE 31–1 ▪ DSM-5 Diagnostic Criteria for Schizophrenia
Table 31–2 ▪ Positive and Negative Symptoms of Schizophrenia
Cognitive symptoms.
Acute episodes
Residual symptoms
Long-term course
Etiology
First-generation (conventional) antipsychotics
Group properties
Classification
Classification by potency
Chemical classification
Mechanism of action
Therapeutic uses
Schizophrenia.
Table 31–3 ▪ Antipsychotic Drugs: Relative Potency and Incidence of Selected Side Effects
Table 31–4 ▪ Antipsychotic Drugs: Routes and Dosages
Bipolar disorder (manic-depressive illness).
Tourette’s syndrome.
Prevention of emesis.
Other applications.
Adverse effects
Table 31–5 ▪ Receptor Blockade and Side Effects of Antipsychotic Drugs
Table 31–6 ▪ Extrapyramidal Side Effects of Antipsychotic Drugs
Extrapyramidal symptoms
Acute dystonia.
Parkinsonism.
Akathisia.
Tardive dyskinesia.
Other adverse effects
Neuroleptic malignant syndrome.
Anticholinergic effects.
Orthostatic hypotension.
Sedation.
Neuroendocrine effects.
Seizures.
Sexual dysfunction.
Agranulocytosis.
Severe dysrhythmias.
Effects in elderly patients with dementia.
Signs of withdrawal and extrapyramidal symptoms in neonates.
Dermatologic effects.
Physical and psychologic dependence
Drug interactions
Anticholinergic drugs.
CNS depressants.
Levodopa and direct dopamine receptor agonists.
Toxicity
Properties of individual agents
High-potency agents
Haloperidol
Actions and uses.
Pharmacokinetics.
Adverse effects.
Preparations.
Dosage and administration.
Oral.
Intramuscular.
Other high-potency agents
Fluphenazine.
Trifluoperazine.
Thiothixene.
Pimozide.
Medium-potency agents
Loxapine.
Perphenazine.
Low-potency agents
Chlorpromazine
Therapeutic uses.
Pharmacokinetics.
Adverse effects.
Drug interactions.
Preparations, dosage, and administration.
Oral therapy.
Parenteral therapy.
Thioridazine
Second-generation (atypical) antipsychotics
Clozapine
Mechanism of action
Therapeutic use
Schizophrenia.
Levodopa-induced psychosis.
Pharmacokinetics
Adverse effects and interactions
Agranulocytosis.
Metabolic effects: weight gain, diabetes, and dyslipidemia.
Seizures.
Extrapyramidal symptoms.
Myocarditis.
Orthostatic hypotension.
Effects in elderly patients with dementia.
Drug interactions.
Preparations, dosage, and administration
Other second-generation antipsychotics
Risperidone
Mechanism of action.
Pharmacokinetics.
Therapeutic effects.
Adverse effects.
Preparations, dosage, and administration.
Schizophrenia, oral therapy.
Schizophrenia, intramuscular therapy.
Bipolar disorder.
Irritability associated with autism spectrum disorder.
Paliperidone
Olanzapine
Mechanism of action.
Pharmacokinetics.
Therapeutic uses.
Schizophrenia.
Bipolar disorder.
Adverse effects with oral olanzapine.
Adverse effects with long-acting IM olanzapine.
Preparations.
Dosage and administration.
Schizophrenia.
Bipolar disorder.
Treatment-resistant major depression.
Ziprasidone
Mechanism of action.
Pharmacokinetics.
Adverse effects.
Drug interactions.
Preparations.
Dosage and administration.
Schizophrenia, oral.
Schizophrenia, intramuscular.
Bipolar disorder.
Quetiapine
Actions and uses.
Pharmacokinetics.
Adverse effects.
Drug interactions.
Preparations.
Dosage and administration.
Schizophrenia.
Major depression.
Bipolar disorder.
Aripiprazole
Contrasts with other atypical antipsychotic agents.
Mechanism of action.
Pharmacokinetics.
Adverse effects.
Drug interactions.
Preparations.
Dosage and administration.
Schizophrenia.
Major depressive disorder.
Bipolar disorder.
Irritability associated with autism spectrum disorder.
Agitation associated with schizophrenia or bipolar mania.
Asenapine
Therapeutic use.
Mechanism of action.
Pharmacokinetics.
Adverse effects.
Drug interactions.
Preparations, dosage, and administration.
Iloperidone
Actions and therapeutic use.
Pharmacokinetics.
Adverse effects.
Drug interactions.
Preparations, dosage, and administration.
Lurasidone
Actions and therapeutic use.
Pharmacokinetics.
Adverse effects.
Drug interactions.
Preparations, dosage, and administration.
Depot antipsychotic preparations
Management of schizophrenia
Drug therapy
Drug selection
Table 31–7 ▪ Depot Antipsychotic Preparations
Dosing
Routes
Oral.
Sublingual.
Intramuscular.
Initial therapy
Maintenance therapy
Adjunctive drugs
Promoting adherence
Nondrug therapy
Key points
Summary of Major Nursing Implications*
First-generation (conventional) antipsychotics
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Routes
Administration
Dosing.
Oral liquids.
Intramuscular.
Implementation: measures to enhance therapeutic effects
Promoting adherence
Nondrug therapy
Ongoing evaluation and interventions
Evaluating therapeutic effects
Minimizing adverse effects
Early EPS: acute dystonia, parkinsonism, and akathisia.
Late EPS: tardive dyskinesia.
Neuroleptic malignant syndrome.
Anticholinergic effects.
Orthostatic hypotension.
Sedation.
Seizures.
Sexual dysfunction.
Dermatologic effects.
Neuroendocrine effects.
Agranulocytosis.
Severe dysrhythmias.
Signs of withdrawal and extrapyramidal symptoms in neonates.
Death in elderly dementia patients.
Minimizing adverse interactions
Anticholinergics.
CNS depressants.
Levodopa and direct dopamine receptor agonists.
QT-prolonging drugs.
Second-generation (atypical) antipsychotics
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Routes
Dosing
Implementation: measures to enhance therapeutic effects
Promoting adherence
Ongoing evaluation and interventions
Evaluating therapeutic effects
Minimizing adverse effects
Orthostatic hypotension and anticholinergic effects.
Agranulocytosis.
Leukopenia/neutropenia.
Metabolic effects: weight gain, diabetes, and dyslipidemia.
Seizures.
Sedation.
Extrapyramidal symptoms.
Myocarditis.
Dysrhythmias.
Signs of withdrawal and extrapyramidal symptoms in neonates.
Death in elderly dementia patients.
Cataracts.
Minimizing adverse interactions
CNS depressants.
Levodopa and direct dopamine receptor agonists.
Myelosuppressive drugs.
QT-prolonging drugs.
Inducers and inhibitors of CYP3A4.
CHAPTER 32 Antidepressants
Major depression: clinical features, pathogenesis, and treatment overview
TABLE 32–1 ▪ DSM-5 Diagnostic Criteria for Major Depression
BOX 32–1 ▪ SPECIAL INTEREST TOPIC
POSTPARTUM DEPRESSION
Clinical features
Pathogenesis
Treatment overview
Drugs used for depression
TABLE 32–2 ▪ Antidepressant Classes and Adult Dosages
Basic considerations
Time course of response
Drug selection
Managing treatment
Suicide risk with antidepressant drugs
Selective serotonin reuptake inhibitors (SSRIs)
Fluoxetine
Mechanism of action
TABLE 32–3 ▪ Therapeutic Uses of Selective Serotonin Reuptake Inhibitors
Figure 32–1 ▪ Mechanism of action of selective serotonin reuptake inhibitors. A, Under drug-free conditions, the actions of serotonin are terminated by active uptake of the transmitter back into the nerve terminals from which it was released. B, By inhibiting the reuptake pump for serotonin, the SSRIs cause the transmitter to accumulate in the synaptic space, thereby intensifying transmission.
Therapeutic uses
Pharmacokinetics
Adverse effects
Sexual dysfunction.
Weight gain.
Serotonin syndrome.
Withdrawal syndrome.
Neonatal effects from use in pregnancy.
Teratogenesis.
Suicide risk.
Extrapyramidal side effects.
Bruxism.
Bleeding disorders.
Hyponatremia.
Other adverse effects.
Drug interactions
MAOIs and other drugs that increase the risk of serotonin syndrome.
Tricyclic antidepressants and lithium.
Antiplatelet drugs and anticoagulants.
TABLE 32–4 ▪ Drugs That Promote Activation of Serotonin Receptors
Drugs that are substrates for or inhibitors of CYP2D6.
Preparations, dosage, and administration
Preparations.
Dosage for depression.
Daily dosing.
Weekly dosing.
Withdrawal.
Other SSRIs
Sertraline
Fluvoxamine
Paroxetine
Citalopram
Escitalopram
Serotonin/norepinephrine reuptake inhibitors (SNRIS)
Venlafaxine
Desvenlafaxine
Duloxetine
Mechanism of action and therapeutic uses.
Figure 32–2 ▪ Structural similarities between tricyclic antidepressants and phenothiazine antipsychotics. Except for the areas highlighted, the phenothiazine nucleus is nearly identical to that of TCAs. Because of their structural similarities, TCAs and phenothiazines have several pharmacologic properties in common.
Pharmacokinetics.
Adverse effects.
Effects in pregnancy and lactation.
Drug interactions.
Preparations, dosage, and administration.
Tricyclic antidepressants (TCAs)
Chemistry
Mechanism of action
TABLE 32–5 ▪ Antidepressants: Adverse Effects and Impact on Neurotransmitters
Pharmacokinetics
Therapeutic uses
Depression.
Bipolar disorder.
Fibromyalgia syndrome.
Other uses.
Adverse effects
Orthostatic hypotension.
Anticholinergic effects.
Diaphoresis.
Sedation.
Cardiac toxicity.
Seizures.
Hypomania.
Suicide risk.
Yawngasm.
Drug interactions
Monoamine oxidase inhibitors.
Direct-acting sympathomimetic drugs.
Indirect-acting sympathomimetic drugs.
Anticholinergic agents.
CNS depressants.
Toxicity
Clinical manifestations.
Treatment.
Dosage and routes of administration
Dosage.
Preparations and drug selection
Preparations.
Drug selection.
Monoamine oxidase inhibitors (MAOIs)
Oral MAOIs
Mechanism of action
Figure 32–3 ▪ Mechanism of action of monoamine oxidase inhibitors. A, Under drug-free conditions, much of the norepinephrine or serotonin that undergoes reuptake into nerve terminals becomes inactivated by MAO. Inactivation helps maintain an appropriate concentration of transmitter within the terminal. B, MAO inhibitors prevent inactivation of norepinephrine and serotonin, thereby increasing the amount of transmitter available for release. Release of supranormal amounts of transmitter intensifies transmission.
Therapeutic uses
Depression.
Other psychiatric uses.
Adverse effects
CNS stimulation.
Orthostatic hypotension.
Hypertensive crisis from dietary tyramine.
Figure 32–4 ▪ Interaction between dietary tyramine and MAOIs. A, In the absence of MAOIs, much of ingested tyramine is inactivated by MAO in the intestinal wall (not shown in the figure). Any dietary tyramine that is not metabolized in the intestinal wall is transported directly to the liver, where it undergoes immediate inactivation by hepatic MAO. No tyramine reaches the general circulation. B, Three events occur in the presence of MAOIs: (1) Inhibition of neuronal MAO raises levels of norepinephrine in sympathetic nerve terminals. (2) Inhibition of intestinal and hepatic MAO allows dietary tyramine to pass through the intestinal wall and liver to enter the systemic circulation intact. (3) Upon reaching peripheral sympathetic nerve terminals, tyramine promotes the release of accumulated norepinephrine stores, thereby causing massive vasoconstriction and excessive stimulation of the heart.
TABLE 32–6 ▪ Foods That Can Interact with MAO Inhibitors
Drug interactions
Indirect-acting sympathomimetic agents.
Interactions secondary to inhibition of hepatic MAO.
Tricyclic antidepressants.
Serotonergic drugs.
Antihypertensive drugs.
Meperidine.
Preparations, dosage, and administration
Transdermal MAOI: selegiline
Atypical antidepressants
Bupropion
Actions and uses.
Pharmacokinetics.
Adverse effects.
Drug interactions.
Preparations, dosage, and administration.
Preparations for depression.
Dosage for major depression.
Dosage for seasonal affective disorder.
Preparations for smoking cessation.
Mirtazapine
Other atypical antidepressants
Nefazodone
Trazodone
Vilazodone
Amoxapine
Reboxetine
Nonconventional drugs for depression
Ketamine
St. john’s wort
S-adenosylmethionine
Somatic (nondrug) therapies for depression
Electroconvulsive therapy
Transcranial magnetic stimulation
Vagus nerve stimulation
Light therapy
Key points
Summary of Major Nursing Implications*
Implications that apply to all antidepressants
Psychologic assessment
Reducing the risk of suicide
Promoting adherence
Nondrug therapy
Evaluating therapeutic effects
Selective serotonin reuptake inhibitors
Preadministration assessment
Therapeutic goal
Alleviation of symptoms of major depression.
Other goals.
Identifying high-risk patients
Implementation: administration
Route
Administration
Ongoing evaluation and interventions
Minimizing adverse effects
Suicide risk.
CNS stimulation.
Serotonin syndrome.
Sexual dysfunction.
Dizziness and fatigue.
Rash.
Weight gain.
Neonatal abstinence syndrome (nah) and persistent pulmonary hypertension of the newborn (pphn).
Teratogenesis.
Dysrhythmias.
GI bleeding.
Hyponatremia.
Bruxism.
Minimizing adverse interactions
MAOIs and other drugs that increase the risk of serotonin syndrome.
TCAs and lithium.
Antiplatelet drugs and anticoagulants.
Drugs that are substrates for or inhibitors of CYP2D6.
Tricyclic antidepressants
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Routes
Administration
Ongoing evaluation and interventions
Minimizing adverse effects
Suicide risk.
Orthostatic hypotension.
Anticholinergic effects.
Diaphoresis.
Sedation.
Cardiotoxicity.
Seizures.
Hypomania.
Minimizing adverse interactions
MAO inhibitors.
Sympathomimetic agents.
Anticholinergic agents.
CNS depressants.
Monoamine oxidase inhibitors
Preadministration assessment
Therapeutic goal
Identifying high-risk patients
Implementation: administration
Routes
Oral.
Transdermal.
Administration
All MAOIs.
Transdermal selegiline.
Ongoing evaluation and interventions
Minimizing adverse effects
Suicide risk.
Hypertensive crisis.
Orthostatic hypotension.
Skin rash.
Minimizing adverse interactions
All drugs.
Indirect-acting sympathomimetics.
Tricyclic antidepressants.
Serotonergic drugs.
Antihypertensive drugs.
Meperidine.
CHAPTER 33 Drugs for bipolar disorder
Characteristics of bipolar disorder
Types of mood episodes seen in BPD
Pure manic episode (euphoric mania).
Hypomanic episode (hypomania).
Major depressive episode (depression).
Mixed episode.
Patterns of mood episodes
TABLE 33–1 ▪ Proposed DSM-5 Criteria for a Manic Episode
Etiology
Treatment of bipolar disorder
Drug therapy
Types of drugs employed
Mood stabilizers.
Antipsychotics.
Antidepressants.
TABLE 33–2 ▪ Initial Treatment of First Manic Episode
Drug selection
Acute therapy: manic episodes.
Acute therapy: depressive episodes.
Long-term preventive treatment.
Promoting adherence
Nondrug therapy
Education and psychotherapy
BOX 33–1 ▪ SPECIAL INTEREST TOPIC
OMEGA-3 FATTY ACIDS FOR BIPOLAR DISORDER: A FISH STORY WITH A HAPPY ENDING
Electroconvulsive therapy
Mood-stabilizing drugs
Lithium
Chemistry
Therapeutic uses
Bipolar disorder.
Other uses.
TABLE 33–3 ▪ Toxicities Associated with Excessive Plasma Level of Lithium
Mechanism of action
Pharmacokinetics
Absorption and distribution.
Excretion.
Monitoring plasma lithium levels.
Adverse effects
Adverse effects that occur when lithium levels are excessive.
TABLE 33–4 ▪ Lithium Carbonate Preparations
Adverse effects that occur at therapeutic levels of lithium.
Early adverse effects.
Tremor.
Polyuria.
Renal toxicity.
Goiter and hypothyroidism.
Teratogenesis.
Use in lactation.
Other side effects.
Drug interactions
Diuretics.
Nonsteroidal anti-inflammatory drugs (NSAIDs).
Anticholinergic drugs.
Preparations, dosage, and administration
Preparations and administration.
TABLE 33–5 ▪ Adult Oral Dosages for Atypical Antipsychotics Used in Bipolar Disorder
Dosing.
Antiepileptic drugs
Divalproex sodium (valproate)
Carbamazepine
Lamotrigine
Antipsychotic drugs
Key points
Summary of Major Nursing Implications*
Lithium
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Route
Administration
Promoting adherence
Ongoing evaluation and interventions
Monitoring summary
Lithium levels.
Other parameters to monitor.
Evaluating therapeutic effects
Minimizing adverse effects
Effects caused by excessive drug levels.
Tremor.
Hypothyroidism and goiter.
Renal toxicity.
Polyuria.
Use in pregnancy and lactation.
Minimizing adverse interactions
Diuretics.
Anticholinergic drugs.
Nonsteroidal anti-inflammatory drugs.
CHAPTER 34 Sedative-hypnotic drugs
Benzodiazepines
Overview of pharmacologic effects
Central nervous system.
Figure 34–1 ▪ Schematic model of the GABA receptor–chloride channel complex showing binding sites for benzodiazepines and barbiturates. The GABA receptor–chloride channel complex, which spans the neuronal cell membrane, can exist in an open or closed configuration. Binding of GABA to its receptor on the complex causes the chloride channel to open. The resulting inward flow of chloride ions hyperpolarizes the neuron (makes the cell highly negative inside) and thereby decreases its ability to fire. Hence GABA is an inhibitory neurotransmitter. Binding of a benzodiazepine to its receptor on the complex increases the frequency of channel opening, thereby increasing chloride influx. Hence, benzodiazepines enhance the inhibitory effects of GABA. In the absence of GABA, benzodiazepines have no effect on channel opening. The benzodiazepine-like drugs (zolpidem, zaleplon, and eszopiclone) have actions much like those of the benzodiazepines. Effects of barbiturates on the chloride channel are dose dependent: at low doses, barbiturates enhance the actions of GABA (by prolonging the duration of channel opening); at high doses, barbiturates directly mimic the actions of GABA.
TABLE 34–1 ▪ Contrasts Between Benzodiazepines and Barbiturates
Cardiovascular system.
Respiratory system.
Molecular mechanism of action
Pharmacokinetics
Absorption and distribution.
TABLE 34–2 ▪ Applications of the Benzodiazepines
Metabolism.
Time course of action.
Therapeutic uses
Anxiety.
Insomnia.
Seizure disorders.
Muscle spasm.
Alcohol withdrawal.
Perioperative applications.
Adverse effects
CNS depression.
Anterograde amnesia.
Sleep driving and other complex sleep-related behaviors.
Paradoxical effects.
Respiratory depression.
Abuse.
Use in pregnancy and lactation.
Other adverse effects.
Drug interactions
CNS depressants.
Tolerance and physical dependence
Tolerance.
Physical dependence.
Acute toxicity
Oral overdose.
Intravenous toxicity.
General treatment measures.
Treatment with flumazenil.
Preparations, dosage, and administration
Preparations and dosage.
Routes.
Oral.
Intravenous.
Intramuscular.
Benzodiazepine-like drugs
Zolpidem
Zaleplon
Eszopiclone
Ramelteon: a melatonin agonist
BOX 34–1 ▪ SPECIAL INTEREST TOPIC
MELATONIN, KEEPER OF THE CIRCADIAN CLOCK
Therapeutic use.
Mechanism of action.
Pharmacokinetics.
Adverse effects.
TABLE 34–3 ▪ Characteristics of Barbiturate Subgroups
Physical dependence and abuse.
Drug interactions.
Precautions.
Use in pregnancy and breast-feeding.
Preparations, dosage, and administration.
Barbiturates
Classification
Mechanism of action
Pharmacologic effects
CNS depression.
Cardiovascular effects.
Induction of hepatic drug-metabolizing enzymes.
Figure 34–2 ▪ Induction of hepatic microsomal enzymes by barbiturates. By increasing synthesis of porphyrin, barbiturates increase production of cytochrome P450, a key component of the hepatic drug-metabolizing system.
Tolerance and physical dependence
Tolerance.
Physical dependence.
Figure 34–3 ▪ Development of tolerance to the toxic and subjective effects of barbiturates. With prolonged barbiturate use, tolerance develops. However, less tolerance develops to toxic effects than to desired effects. Consequently, as duration of use increases, the difference between the dose producing desirable effects and the dose producing toxicity becomes progressively smaller, thereby increasing the risk of serious harm.
Pharmacokinetics
Therapeutic uses
Seizure disorders.
Induction of anesthesia.
Insomnia.
Other uses.
Adverse effects
Respiratory depression.
Suicide.
Abuse.
Use in pregnancy.
Exacerbation of intermittent porphyria.
Hangover.
Paradoxical excitement.
Hyperalgesia.
Drug interactions
CNS depressants.
Interactions resulting from induction of drug-metabolizing enzymes.
Acute toxicity
Symptoms.
Treatment.
Administration
Oral.
Intravenous.
Intramuscular.
Miscellaneous sedative-hypnotics
Basic pharmacologic profile
Chloral hydrate
Meprobamate
Management of insomnia
Sleep phases
Basic principles of management
Cause-specific therapy
Nondrug therapy
TABLE 34–4 ▪ Rules for Sleep Fitness
Therapy with hypnotic drugs
Major hypnotics used for treatment
Benzodiazepines
TABLE 34–5 ▪ Major Drugs for Insomnia
Benzodiazepine-like drugs: zolpidem, zaleplon, and eszopiclone
Ramelteon
Other hypnotics
Antidepressants
Trazodone.
Doxepin.
Antihistamines
Alternative medicines
Key points
Summary of Major Nursing Implications*
Benzodiazepines
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Routes
Oral.
IM and IV.
Rectal.
Administration
Oral.
Intravenous.
Implementation: measures to enhance therapeutic effects
Ongoing evaluation and interventions
Evaluating therapeutic effects
Minimizing adverse effects
CNS depression.
Sleep driving and other complex sleep-related behaviors.
Paradoxical effects.
Physical dependence.
Abuse.
Use in pregnancy and lactation.
Minimizing adverse interactions
CNS depressants.
CHAPTER 35 Management of anxiety disorders
TABLE 35–1 ▪ First-Line Drugs for Anxiety Disorders
TABLE 35–2 ▪ Proposed DSM-5 Diagnostic Criteria for Generalized Anxiety Disorder
Generalized anxiety disorder
Characteristics
Treatment
Benzodiazepines
TABLE 35–3 ▪ Dosages of Benzodiazepines Approved for Anxiety
Buspirone
Actions and therapeutic use.
Pharmacokinetics.
Adverse effects.
Drug and food interactions.
Tolerance, dependence, and abuse.
Preparations, dosage, and administration.
Antidepressants: venlafaxine, paroxetine, escitalopram, and duloxetine
Panic disorder
Characteristics
Treatment
Antidepressants
Selective serotonin reuptake inhibitors.
Venlafaxine.
Tricyclic antidepressants.
Monoamine oxidase inhibitors.
Benzodiazepines.
Obsessive-compulsive disorder
Characteristics
Treatment
Selective serotonin reuptake inhibitors
TABLE 35–4 ▪ Proposed DSM-5 Diagnostic Criteria for Obsessive-Compulsive Disorder
Clomipramine
Deep brain stimulation
Social anxiety disorder (social phobia)
Characteristics
TABLE 35–5 ▪ Proposed DSM-5 Diagnostic Criteria for Social Anxiety Disorder (Social Phobia)
Treatment
TABLE 35–6 ▪ Proposed DSM-5 Diagnostic Criteria for Post-Traumatic Stress Disorder*
Post-traumatic stress disorder
Characteristics
Treatment
Key points
CHAPTER 36 Central nervous system stimulants and attention-deficit/hyperactivity disorder
Central nervous system stimulants
Amphetamines
Chemistry
Dextroamphetamine and levamphetamine.
Amphetamine.
Lisdexamfetamine.
Methamphetamine.
Figure 36–1 ▪ Structural formulas of the amphetamines. “Amphetamine” is a 50:50 mixture of dextroamphetamine and levamphetamine. Note that dextroamphetamine and levamphetamine are simply mirror images of each other. Both compounds contain the same atomic components.
Mechanism of action
Pharmacologic effects
Central nervous system.
Cardiovascular system.
Tolerance
Physical dependence
Abuse
Adverse effects
CNS stimulation.
Weight loss.
Cardiovascular effects.
Psychosis.
Acute toxicity
Symptoms.
Treatment.
Therapeutic uses
Attention-deficit/hyperactivity disorder.
Narcolepsy.
Obesity.
Preparations, dosage, and administration
Dextroamphetamine sulfate.
Short duration.
Long duration.
Amphetamine/dextroamphetamine mixture. amphetamine mixture is available in sd and ld formulations. both are used for adhd.
Short duration.
Long duration.
Lisdexamfetamine.
Methamphetamine.
Methylphenidate and dexmethylphenidate
Methylphenidate
Figure 36–2 ▪ Structural formulas of the methylxanthines.
Preparations, dosage, and administration
Short duration.
Intermediate duration.
Long duration.
Concerta.
Metadate CD.
Biphentin.
Ritalin LA.
Daytrana.
Dexmethylphenidate
Methylxanthines
TABLE 36–1 ▪ Dietary Caffeine
Caffeine
Dietary sources
Mechanism of action
Pharmacologic effects
Central nervous system.
Heart.
Blood vessels.
Bronchi.
Kidney.
Reproduction.
Pharmacokinetics
Therapeutic uses
Neonatal apnea.
Promoting wakefulness.
Other applications.
Acute toxicity
Preparations, dosage, and administration
For promoting wakefulness.
For neonatal apnea.
Theophylline
Theobromine
Miscellaneous CNS stimulants
Modafinil
Therapeutic use.
Mechanism of action.
Pharmacokinetics.
Adverse effects.
Drug interactions.
Preparations, dosage, and administration.
Armodafinil
Strychnine
Strychnine poisoning
Causes.
Symptoms.
Treatment.
Doxapram
Cocaine
BOX 36–1 ▪ SPECIAL INTEREST TOPIC
DID KISSES KILL CALVIN?
Attention-deficit/hyperactivity disorder
Basic considerations
ADHD in children
Signs and symptoms
Etiology
Management overview
ADHD in adults
Drugs used for ADHD
CNS stimulants
TABLE 36–2 ▪ Proposed DSM-5 Diagnostic Criteria for ADHD
Specify based on current presentation
TABLE 36–3 ▪ Major Drugs for Attention-Deficit/Hyperactivity Disorder
Nonstimulants
Atomoxetine, a norepinephrine uptake inhibitor
Description and therapeutic effects.
Mechanism of action.
Pharmacokinetics.
Adverse effects.
Drug interactions.
Role in ADHD therapy.
Preparations, dosage, and administration.
Alpha2-adrenergic agonists
Guanfacine.
Clonidine.
Antidepressants
Tricyclic antidepressants.
Bupropion.
Key points
Summary of Major Nursing Implications*
Amphetamines, methylphenidate, and dexmethylphenidate
Preadministration assessment
Therapeutic goal
Baseline data
Children with ADHD.
Narcolepsy.
Identifying high-risk patients
Implementation: administration
Routes
Oral.
Transdermal.
Administration
Oral.
Transdermal.
Ongoing evaluation and interventions
Evaluating therapeutic effects
Children with ADHD.
Minimizing adverse effects
Excessive CNS stimulation.
Weight loss.
Cardiovascular effects.
Psychosis.
Withdrawal reactions.
Hypersensitivity reactions.
Minimizing abuse
Caffeine
General considerations
Minimizing adverse effects
Cardiovascular effects.
Excessive CNS stimulation.
Drug Abuse
CHAPTER 37 Drug abuse I: basic considerations
Definitions
Drug abuse
Addiction
Other definitions
APA diagnostic criteria regarding drugs of abuse
Factors that contribute to drug abuse
Reinforcing properties of drugs
TABLE 37–1 ▪ American Psychiatric Association Diagnostic Criteria Pertaining to Drugs of Abuse
Physical dependence
Psychologic dependence
Social factors
Drug availability
Vulnerability of the individual
Neurobiology of addiction
Principles of addiction treatment
The controlled substances act
Record keeping
DEA schedules
Prescriptions
Schedule II.
TABLE 37–2 ▪ Principles of Drug-Addiction Treatment
Schedules III and IV.
TABLE 37–3 ▪ Drug Enforcement Agency Classification of Controlled Substances
Schedule v.
Labeling
State laws
Key points
CHAPTER 38 Drug abuse II: alcohol
Basic pharmacology of alcohol
Central nervous system effects
Acute effects.
TABLE 38–1 ▪ Central Nervous System Responses at Various Blood Alcohol Levels
Chronic effects.
Impact on cognitive function.
Effect on sleep.
Other pharmacologic effects
Cardiovascular system.
Glucose metabolism.
Bone health.
Respiration.
Liver.
Stomach.
Kidney.
Pancreas.
Sexual function.
Cancer.
Pregnancy.
Lactation.
Impact on longevity
Figure 38–1 ▪ Ethanol metabolism and the effect of disulfiram. Conversion of ethanol into acetaldehyde takes place slowly (about 15 mL/hr). Consumption of more than 15 mL/hr will cause ethanol to accumulate. Effects of disulfiram result from accumulation of acetaldehyde secondary to inhibition of aldehyde dehydrogenase.
TABLE 38–2 ▪ People Who Should Avoid Alcohol*
Pharmacokinetics
Absorption.
Distribution.
Metabolism.
Blood levels of alcohol.
TABLE 38–3 ▪ Alcohol Content of Beer, Wine, and Whiskey
Tolerance
Physical dependence
Drug interactions
CNS depressants.
Nonsteroidal anti-inflammatory drugs.
Acetaminophen.
Disulfiram.
Antihypertensive drugs.
Acute overdose
Summary of precautions and contraindications
Therapeutic uses
Topical.
Oral.
Intravenous.
Local injection.
Alcohol use disorder
TABLE 38–4 ▪ American Psychiatric Association Diagnostic Criteria Pertaining to Alcohol Use
TABLE 38–5 ▪ Screening Instrument: The Alcohol Use Disorders Identification Test (AUDIT)
Drugs for alcohol use disorder
TABLE 38–6 ▪ Drugs Used to Facilitate Alcohol Withdrawal
Drugs used to facilitate withdrawal
Benzodiazepines
Adjuncts to benzodiazepines
Drugs used to maintain abstinence
Disulfiram aversion therapy
Therapeutic effects.
Mechanism of action.
Pharmacologic effects.
Patient selection.
Patient education.
Preparations, dosage, and administration.
Naltrexone
Acamprosate
Therapeutic use.
Mechanism of action.
Pharmacokinetics.
Adverse effects and drug interactions.
Preparations, dosage, and administration.
Topiramate
Ondansetron
Nutritional support, fluid replacement, and antibiotics
Key points
Summary of Major Nursing Implications*
Disulfiram
Preadministration assessment
Therapeutic goal
Patient selection
Identifying high-risk patients
Implementation: administration
Route
Administration
Implementation: measures to enhance therapeutic effects
CHAPTER 39 Drug abuse III: nicotine and smoking
Basic pharmacology of nicotine
Mechanism of action
TABLE 39–1 ▪ Average Annual Smoking-Attributable Mortality (United States, 2000–2004)*
Pharmacokinetics
Pharmacologic effects
Cardiovascular effects.
GI effects.
CNS effects.
Effects during pregnancy and lactation.
Tolerance and dependence
Tolerance.
Dependence.
Acute poisoning
Symptoms.
Treatment.
Chronic toxicity from smoking
BOX 39–1 ▪ SPECIAL INTEREST TOPIC
SMOKING CESSATION DURING PREGNANCY
Pharmacologic aids to smoking cessation
TABLE 39–2 ▪ Pharmacologic Aids for Smoking Cessation
TABLE 39–3 ▪ Internet-Based Resources for Smoking Cessation
Nicotine replacement therapy
Nicotine chewing gum (nicotine polacrilex)
Nicotine lozenges (nicotine polacrilex)
TABLE 39–4 ▪ Nicotine Transdermal Systems (Patches)
Nicotine transdermal systems (patches)
Nicotine inhaler
Nicotine nasal spray
Bupropion SR
Varenicline
Mechanism of action.
Pharmacokinetics.
Adverse effects.
Drug interactions.
Preparations, dosage, and administration.
Nortriptyline and clonidine
Nicotine conjugate vaccine
Products that are not recommended
Key points
CHAPTER 40 Drug abuse IV: major drugs of abuse other than alcohol and nicotine
Heroin, oxycodone, and other opioids
Patterns of use
Figure 40–1 ▪ Structural formulas of representative drugs of abuse. (LSD = d-lysergic acid diethylamide; THC = tetrahydrocannabinol.)
TABLE 40–1 ▪ Pharmacologic Categorization of Abused Drugs
Subjective and behavioral effects
Preferred drugs and routes of administration
Heroin.
TABLE 40–2 ▪ Some Street Names for Abused Drugs
Oxycodone.
Meperidine.
Tolerance and physical dependence
Tolerance.
Physical dependence.
Treatment of acute toxicity
Detoxification
Methadone substitution.
Buprenorphine.
Clonidine-assisted withdrawal.
Rapid and ultrarapid withdrawal.
Drugs for long-term management of opioid addiction
TABLE 40–3 ▪ Drugs for Long-Term Management of Opioid Addiction
Methadone.
Buprenorphine.
Naltrexone.
Sequelae of compulsive opioid use
General CNS depressants
Barbiturates
Tolerance.
Physical dependence and withdrawal techniques.
BOX 40–1 ▪ SPECIAL INTEREST TOPIC
DATE-RAPE DRUGS: ROHYPNOL AND GHB
Rohypnol
GHB
Acute toxicity.
Benzodiazepines
Psychostimulants
Cocaine
Forms.
Routes of administration.
Subjective effects and addiction.
Acute toxicity: symptoms and treatment.
Chronic toxicity.
Use during pregnancy.
Tolerance, dependence, and withdrawal.
Treatment of cocaine addiction.
Methamphetamine
Description and routes.
Patterns of use.
Subjective and behavioral effects.
Adverse psychologic effects.
Adverse cardiovascular effects.
Other adverse effects.
Tolerance, dependence, and withdrawal.
Treatment.
Marijuana and related preparations
Cannabis sativa, the source of marijuana
Psychoactive component
Mechanism of action
Pharmacokinetics
Administration by smoking.
Oral administration.
Behavioral and subjective effects
Effects of low to moderate doses.
High-dose effects.
Effects of chronic use.
Role in schizophrenia.
Physiologic effects
Cardiovascular effects.
Respiratory effects.
Effects on reproduction.
Altered brain structure.
Tolerance and dependence
Therapeutic use
Approved uses for cannabinoids.
Suppression of emesis.
Appetite stimulation.
Relief of neuropathic pain.
Unapproved uses for cannabinoids.
Glaucoma.
Multiple sclerosis.
Medical research on marijuana.
Legal status of medical marijuana.
United States.
Canada.
Comparison of marijuana with alcohol
Psychedelics
D-lysergic acid diethylamide (lsd)
History.
Mechanism of action.
Time course.
Subjective and behavioral effects.
Physiologic effects.
Tolerance and dependence.
Toxicity.
Potential therapeutic uses.
Salvia
Mescaline, psilocin, psilocybin, and dimethyltryptamine
Dissociative drugs
Phencyclidine
Chemistry and pharmacokinetics
Chemistry.
Pharmacokinetics.
Mechanism of action
Subjective and behavioral effects
Effects of low to moderate doses.
High-dose (toxic) effects.
Managing toxicity.
Ketamine
Dextromethorphan
3,4-methylenedioxymethamphetamine (MDMA, ecstasy)
Time course and dosage.
Who uses MDMA and why?
Adverse effects.
Potential medical use.
Inhalants
Anesthetics
Volatile nitrites
Organic solvents
Administration.
Acute pharmacologic effects.
Chronic toxicity.
Management.
Anabolic steroids
Key points
VI Drugs that Affect Fluid and Eletrolyte Balance
Interactive Review – VI: Drugs that Affect Fluid and Electrolyte Balance
CHAPTER 41 Diuretics
Review of renal anatomy and physiology
Anatomy
Physiology
Overview of kidney functions
The three basic renal processes
Filtration.
Reabsorption.
Figure 41–1 ▪ Schematic representation of a nephron and collecting duct.
Active tubular secretion.
Processes of reabsorption that occur at specific sites along the nephron
Proximal convoluted tubule.
Loop of Henle.
Distal convoluted tubule (early segment).
Figure 41–2 ▪ Schematic diagram of a nephron showing sites of sodium absorption and diuretic action. The percentages indicate how much of the filtered sodium and chloride is reabsorbed at each site.
Distal nephron: late distal convoluted tubule and collecting duct.
Sodium-potassium exchange.
Regulation of urine concentration by ADH.
Introduction to diuretics
How diuretics work
Adverse impact on extracellular fluid
Classification of diuretics
High-ceiling (loop) diuretics
Furosemide
Mechanism of action
Pharmacokinetics
Therapeutic uses
Adverse effects
Hyponatremia, hypochloremia, and dehydration.
Hypotension.
Hypokalemia.
Ototoxicity.
Hyperglycemia.
Hyperuricemia.
Use in pregnancy.
Impact on lipids, calcium, and magnesium.
Drug interactions
Digoxin.
Ototoxic drugs.
Potassium-sparing diuretics.
Lithium.
Antihypertensive agents.
Nonsteroidal anti-inflammatory drugs (NSAIDs).
Preparations, dosage, and administration
Oral.
Parenteral.
Other high-ceiling diuretics
TABLE 41–1 ▪ High-Ceiling (Loop) Diuretics: Routes, Time Course, and Dosage
Thiazides and related diuretics
Hydrochlorothiazide
Mechanism of action
Pharmacokinetics
Therapeutic uses
Essential hypertension.
Edema.
Diabetes insipidus.
Protection against postmenopausal osteoporosis.
Adverse effects
Hyponatremia, hypochloremia, and dehydration.
Hypokalemia.
Use in pregnancy and lactation.
TABLE 41–2 ▪ Thiazides and Related Diuretics: Dosages and Time Course of Effects
Hyperglycemia.
Hyperuricemia.
Impact on lipids and magnesium.
Drug interactions
Preparations, dosage, and administration
Other thiazide-type diuretics
Potassium-sparing diuretics
TABLE 41–3 ▪ Potassium-Sparing Diuretics: Names, Dosages, and Time Course of Effects
Spironolactone
Mechanism of action
Therapeutic uses
Hypertension and edema.
Heart failure.
Other uses.
Adverse effects
Hyperkalemia.
Endocrine effects.
Benign and malignant tumors.
Drug interactions
Thiazide and loop diuretics.
Agents that raise potassium levels.
Preparations, dosage, and administration
Triamterene
Mechanism of action
Therapeutic uses
Adverse effects
Hyperkalemia.
Other adverse effects.
Preparations, dosage, and administration
Amiloride
Pharmacologic properties.
Preparations, dosage, and administration.
Mannitol, an osmotic diuretic
Mechanism of diuretic action
Pharmacokinetics
Therapeutic uses
Prophylaxis of renal failure.
Reduction of intracranial pressure.
Reduction of intraocular pressure.
Adverse effects
Edema.
Other adverse effects.
Preparations, dosage, and administration
Key points
Aldosterone Regulation Mechanism (read text)
Diuretics (read text)
Furosemide (read text)
Summary of Major Nursing Implications*
High-ceiling (loop) diuretics
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Routes
Furosemide and bumetanide.
Ethacrynic acid and torsemide.
Administration
Oral.
Parenteral.
Promoting adherence
Ongoing evaluation and interventions
Evaluating therapeutic effects
Minimizing adverse effects
Hyponatremia, hypochloremia, and dehydration.
Hypotension.
Hypokalemia.
Ototoxicity.
Hyperglycemia.
Hyperuricemia.
Minimizing adverse interactions
Digoxin.
Lithium.
Ototoxic drugs.
Thiazides and related diuretics
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Routes
Oral.
Intravenous.
Administration
Promoting adherence
Ongoing evaluation and interventions
Evaluating therapeutic effects
Minimizing adverse effects
Minimizing adverse interactions
Potassium-sparing diuretics
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Route
Administration
Ongoing evaluation and interventions
Evaluating therapeutic effects
Minimizing adverse effects
Hyperkalemia.
Endocrine effects.
Minimizing adverse interactions
Drugs that raise potassium levels.
CHAPTER 42 Agents affecting the volume and ion content of body fluids
Disorders of fluid volume and osmolality
Volume contraction
Isotonic contraction
Definition and causes.
Treatment.
Hypertonic contraction
Definition and causes.
Treatment.
Hypotonic contraction
Definition and causes.
Treatment.
Volume expansion
Acid-base disturbances
Respiratory alkalosis
Causes.
Treatment.
Respiratory acidosis
Causes.
Treatment.
Metabolic alkalosis
Causes.
Treatment.
Metabolic acidosis
Causes.
Treatment.
Potassium imbalances
Regulation of potassium levels
Hypokalemia
Causes and consequences
Prevention and treatment
Oral potassium chloride.
Uses, dosage, and preparations.
Adverse effects.
Intravenous potassium chloride.
Contraindications to potassium use.
Hyperkalemia
Causes.
Consequences.
Treatment.
Magnesium imbalances
Hypomagnesemia
Causes and consequences
Prevention and treatment
Magnesium hydroxide.
Magnesium sulfate.
Uses, administration, and dosage.
Adverse effects.
Hypermagnesemia
Key points
VII Drugs that Affect the Heart, Blood Vessels, and Blood
Interactive Review – VII: Drugs that Affect the Heart, Blood Vessels, and Blood
CHAPTER 43 Review of hemodynamics
Overview of the circulatory system
Components of the circulatory system
Distribution of blood
What makes blood flow?
Figure 43–1 ▪ Distribution of blood in the circulatory system. Note that a large percentage of the blood resides in the venous system.
Figure 43–2 ▪ Forces that promote and impede flow of blood. Blood flows from the point of higher pressure toward the point of lower pressure. Resistance to flow is determined by vessel diameter, vessel length, and blood viscosity.
Figure 43–3 ▪ Distribution of pressure within the systemic circulation. Note that pressure is highest when blood leaves the left ventricle, falls to only 18 mm Hg as blood exits capillaries, and reaches negative values within the right atrium.
How does blood get back to the heart?
Regulation of cardiac output
Determinants of cardiac output
Figure 43–4 ▪ Venous valves and the auxiliary venous “pump.” A, Veins and their one-way valves in the leg. Note that the configuration of these valves ensures that blood will move toward the heart. B, Contraction of skeletal muscle pumps venous blood toward the heart.
Heart rate.
Stroke volume.
Preload.
Afterload.
Control of stroke volume by venous return
Starling’s law of the heart
Figure 43–5 ▪ The Starling relationship between myocardial fiber length and contractile force. Note that an increase in fiber length produces a corresponding increase in contractile force. Fiber length increases as the ventricles enlarge during filling. Increased contractile force is reflected by increased stroke volume.
Figure 43–6 ▪ Systemic-pulmonary imbalance that develops when the output of the left and right ventricles is not identical. In this example, the output of the left ventricle (LV) is 1% less than the output of the right ventricle (RV). Hence, while the right ventricle pumps 5000 mL/min, the left pumps only 4950 mL/min—50 mL/min less than the right side. This causes blood to back up in the pulmonary circulation. After 20 minutes, 1000 mL of blood has shifted from the systemic circulation to the pulmonary circulation. Death would ensue in less than 40 minutes. (The 2 days are an allowance for the undertaker and clergy.) Numbers in the pulmonary and systemic circulations indicate volume of blood in liters.
Factors that determine venous return
Starling’s law and maintenance of systemic-pulmonary balance
Regulation of arterial pressure
Overview of control systems
Steady-state control by the ANS
Rapid control by the ANS: the baroreceptor reflex
The Renin-Angiotensin-Aldosterone system
Renal retention of water
Postural hypotension
Natriuretic peptides
Key points*
Renin-Angiotensin in Control of Blood Pressure (read text)
CHAPTER 44 Drugs acting on the Renin-Angiotensin-Aldosterone system
Physiology of the Renin-Angiotensin-Aldosterone system
Types of angiotensin
Actions of angiotensin II
Vasoconstriction.
Release of aldosterone.
Alteration of cardiac and vascular structure.
Figure 44–1 ▪ Regulation of blood pressure by the renin-angiotensin-aldosterone system. In addition to the mechanisms depicted, angiotensin II can raise blood pressure by (1) acting on the distal nephron to promote reabsorption of sodium and (2) increasing vasoconstriction by three mechanisms: promoting release of norepinephrine from sympathetic nerves; promoting release of epinephrine from the adrenal medulla; and acting in the central nervous system to increase sympathetic outflow to blood vessels. (ARBs = angiotensin receptor blockers.)
Actions of aldosterone
Regulation of blood volume and blood pressure.
Pathologic cardiovascular effects.
Formation of angiotensin II by renin and angiotensin-converting enzyme
Renin
Regulation of renin release.
Angiotensin-converting enzyme (kinase II)
Regulation of blood pressure by the Renin-Angiotensin-Aldosterone system
Tissue (local) angiotensin II production
Figure 44–2 ▪ Overview of ACE inhibitor actions and pharmacologic effects. Angiotensin-converting enzyme (ACE) and kinase II are two names for the same enzyme. When angiotensin II is the substrate, we call the enzyme ACE; when bradykinin is the substrate, we call it kinase II. Inhibition of this enzyme decreases production of angiotensin II (thereby reducing angiotensin II levels), and decreases breakdown of bradykinin (thereby increasing bradykinin levels).
Angiotensin-converting enzyme inhibitors
Mechanism of action and overview of pharmacologic effects
Pharmacokinetics
Therapeutic uses
Hypertension.
TABLE 44–1 ▪ ACE Inhibitors: Approved Indications and Adult Dosages
Heart failure.
Myocardial infarction.
Diabetic and nondiabetic nephropathy.
Figure 44–3 ▪ Elevation of glomerular filtration pressure by angiotensin II. Angiotensin II increases filtration pressure by (1) increasing pressure in the afferent arteriole (secondary to increasing systemic arterial pressure), and by (2) constricting the efferent arteriole, thereby generating back-pressure in the glomerulus.
Prevention of MI, stroke, and death in patients at high cardiovascular risk.
Diabetic retinopathy.
Adverse effects
First-dose hypotension.
Cough.
Hyperkalemia.
Renal failure.
Fetal injury.
Angioedema.
Dysgeusia and rash.
Neutropenia.
Drug interactions
Diuretics.
Antihypertensive agents.
Drugs that raise potassium levels.
Lithium.
Nonsteroidal anti-inflammatory drugs (NSAIDs).
Preparations, dosage, and administration
Angiotensin II receptor blockers
Mechanism of action and overview of pharmacologic effects
Therapeutic uses
Hypertension.
Heart failure.
Diabetic nephropathy.
Myocardial infarction.
Stroke prevention.
Prevention of MI, stroke, and death in patients at high cardiovascular risk.
Diabetic retinopathy.
TABLE 44–2 ▪ Angiotensin II Receptor Blockers: Approved Indications and Adult Dosages
Migraine headache.
Adverse effects
Angioedema.
Fetal harm.
Renal failure.
Cancer.
Drug interactions
Preparations, dosage, and administration
Aliskiren, a direct renin inhibitor
Mechanism of action
Therapeutic use
Pharmacokinetics
Adverse effects
Angioedema and cough.
Gastrointestinal effects.
Hyperkalemia.
Fetal injury and death.
Drug interactions
Preparations, dosage, and administration
Aldosterone antagonists
Eplerenone
Mechanism of action
Therapeutic use
Hypertension.
Heart failure.
Pharmacokinetics
Adverse effects
Hyperkalemia.
Drug interactions
Preparations, dosage, and administration
Spironolactone
Key points
Summary of Major Nursing Implications*
Angiotensin-converting enzyme inhibitors
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Routes
Oral.
Intravenous.
Dosage and administration
Ongoing evaluation and interventions
Monitoring summary
Evaluating therapeutic effects
Hypertension.
Heart failure.
Diabetic nephropathy.
Minimizing adverse effects
First-dose hypotension.
Cough.
Hyperkalemia.
Fetal injury.
Angioedema.
Renal failure.
Dysgeusia and rash (mainly with captopril).
Neutropenia (mainly with captopril).
Minimizing adverse interactions
Diuretics.
Antihypertensive agents.
Drugs that elevate potassium levels.
Lithium.
Nonsteroidal anti-inflammatory drugs.
Angiotensin II receptor blockers
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Route
Dosage and administration
Ongoing evaluation and interventions
Evaluating therapeutic effects
Hypertension.
Heart failure.
Diabetic nephropathy.
Minimizing adverse effects
Angioedema.
Fetal injury.
Renal failure.
Cancer.
Minimizing adverse interactions
Antihypertensive agents.
Aliskiren, a direct renin inhibitor
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Route
Dosage and administration
Ongoing evaluation and interventions
Minimizing adverse effects
Hyperkalemia.
Fetal injury.
Angioedema.
Minimizing adverse interactions
Drugs that elevate potassium levels.
Antihypertensive agents.
CHAPTER 45 Calcium channel blockers
Calcium channels: physiologic functions and consequences of blockade
Vascular smooth muscle
Heart
Myocardium.
SA node.
AV node.
Coupling of cardiac calcium channels to beta1-adrenergic receptors.
Calcium channel blockers: classification and sites of action
Classification
Figure 45–1 ▪ Coupling of cardiac calcium channels with beta1-adrenergic receptors. In the heart, beta1 receptors are coupled to calcium channels. As a result, when cardiac beta1 receptors are activated, calcium influx is enhanced. The process works as follows. Binding of an agonist (eg, norepinephrine) causes a conformational change in the beta receptor, which in turn causes a change in G protein, converting it from an inactive state (in which GDP is bound to the alpha subunit) to an active state (in which GTP is bound to the alpha subunit). (G protein is so named because it binds guanine nucleotides: GDP and GTP.) Following activation, the alpha subunit dissociates from the rest of G protein and activates adenylyl cyclase, an enzyme that converts ATP to cyclic AMP (cAMP). cAMP then activates protein kinase, an enzyme that phosphorylates proteins—in this case, the calcium channel. Phosphorylation changes the channel such that calcium entry is enhanced when the channel opens. (Opening of the channel is triggered by a change in membrane voltage [ie, by passage of an action potential].) The effect of calcium entry on cardiac function is determined by the type of cell involved. If the cell is in the SA node, heart rate increases; if the cell is in the AV node, impulse conduction through the node accelerates; and if the cell is part of the myocardium, force of contraction is increased. Because binding of a single agonist molecule to a single beta receptor stimulates the synthesis of many cAMP molecules, with the subsequent activation of many protein kinase molecules, causing the phosphorylation of many calcium channels, this system can greatly amplify the signal initiated by the agonist.
Sites of action
Verapamil and diltiazem: agents that act on vascular smooth muscle and the heart
Verapamil
TABLE 45–1 ▪ Calcium Channel Blockers: Classification, Sites of Action, and Indications
Hemodynamic effects
Direct effects.
Indirect (reflex) effects.
Net effect.
Pharmacokinetics
Therapeutic uses
Angina pectoris.
Essential hypertension.
Cardiac dysrhythmias.
Migraine.
Adverse effects
Common effects.
Cardiac effects.
Other effects.
Drug and food interactions
Digoxin.
Beta-adrenergic blocking agents.
Grapefruit juice.
Toxicity
Clinical manifestations.
Treatment.
General measures.
Hypotension.
Bradycardia and AV block.
Ventricular tachydysrhythmias.
Preparations, dosage, and administration
Oral.
Intravenous.
Diltiazem
Actions and uses.
Pharmacokinetics.
Adverse effects.
Drug and food interactions.
Preparations, dosage, and administration.
Dihydropyridines: agents that act mainly on vascular smooth muscle
Nifedipine
TABLE 45–2 ▪ Comparisons and Contrasts Between Nifedipine and Verapamil
Hemodynamic effects
Direct effects.
Indirect (reflex) effects.
Net effect.
Pharmacokinetics
Therapeutic uses
Angina pectoris.
Hypertension.
Investigational uses.
Adverse effects
Drug interactions
Beta-adrenergic blockers.
Toxicity
Preparations, dosage, and administration
Other dihydropyridines
Nicardipine.
Amlodipine.
Isradipine.
Felodipine.
Nimodipine.
Nisoldipine.
Clevidipine.
Key points
Summary of Major Nursing Implications*
Verapamil and diltiazem
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Routes
Administration
Oral.
Intravenous.
Ongoing evaluation and interventions
Evaluating therapeutic effects
Angina pectoris.
Essential hypertension.
Minimizing adverse effects
Cardiosuppression.
Peripheral edema.
Constipation.
Minimizing adverse interactions
Digoxin.
Beta blockers.
Grapefruit juice.
Managing acute toxicity
Dihydropyridines
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Route
Oral.
Intravenous.
Administration
Ongoing evaluation and interventions
Evaluating therapeutic effects
Minimizing adverse effects
Reflex tachycardia.
Peripheral edema.
Managing acute toxicity
CHAPTER 46 Vasodilators
Basic concepts in vasodilator pharmacology
Selectivity of vasodilatory effects
Overview of therapeutic uses
TABLE 46–1 ▪ Types of Vasodilators
TABLE 46–2 ▪ Vasodilator Selectivity
Adverse effects related to vasodilation
Postural hypotension
Reflex tachycardia
Expansion of blood volume
Pharmacology of individual vasodilators
Hydralazine
Cardiovascular effects
Pharmacokinetics
Absorption and time course of action.
Metabolism.
Therapeutic uses
Essential hypertension.
Hypertensive crisis.
Heart failure.
Adverse effects
Reflex tachycardia.
Increased blood volume.
Systemic lupus erythematosus–like syndrome.
Other adverse effects.
Drug interactions
Preparations, dosage, and administration
Preparations.
Oral therapy.
Parenteral therapy.
Minoxidil
Cardiovascular effects
Pharmacokinetics
Therapeutic uses
Adverse effects
Reflex tachycardia.
Sodium and water retention.
Hypertrichosis.
Figure 46–1 ▪ Structure and metabolism of sodium nitroprusside. Note the five cyanide (CN) groups in nitroprusside and their liberation during metabolism. Note also the release of nitric oxide (NO), the active component of nitroprusside.
Pericardial effusion.
Other adverse effects.
Preparations, dosage, and administration
Sodium nitroprusside
Cardiovascular effects
Mechanism of action
Metabolism
Therapeutic uses
Hypertensive emergencies.
Other uses.
Adverse effects
Excessive hypotension.
Cyanide poisoning.
Thiocyanate toxicity.
Preparations, dosage, and administration
Drugs acting on the Renin-Angiotensin-Aldosterone system
Angiotensin-converting enzyme (ACE) inhibitors.
Angiotensin II receptor blockers (ARBs).
Direct renin inhibitors (dris).
Organic nitrates
Calcium channel blockers
Sympatholytic drugs
Alpha-adrenergic blocking agents.
Ganglionic blocking agents.
Adrenergic neuron blocking agents.
Centrally acting agents.
Nesiritide
Drugs for pulmonary arterial hypertension
Key points
CHAPTER 47 Drugs for hypertension
TABLE 47–1 ▪ Classification of Blood Pressure for Adults Age 18 and Older
TABLE 47–2 ▪ Types of Hypertension and Their Frequency
Basic considerations in hypertension
Classification of blood pressure
Normal.
Prehypertension.
Hypertension.
Types of hypertension
Primary (essential) hypertension
Secondary hypertension
BOX 47–1 ▪ SPECIAL INTEREST TOPIC
ISOLATED SYSTOLIC HYPERTENSION: THE REAL KILLER OF AGING AMERICANS
Consequences of hypertension
Management of chronic hypertension
Basic considerations
Diagnosis
TABLE 47–3 ▪ Overview of Blood Pressure Management in Adults 18 Years and Older
Benefits of lowering blood pressure
Patient evaluation
Hypertension with a treatable cause.
Factors that increase cardiovascular risk.
Diagnostic tests.
Treatment goals
Therapeutic interventions
Lifestyle modifications
Weight loss.
Sodium restriction.
The DASH eating plan.
Alcohol restriction.
Aerobic exercise.
Smoking cessation.
Maintenance of potassium and calcium intake.
Figure 47–1 ▪ Primary determinants of arterial blood pressure.
Drug therapy
Review of blood pressure control
Principal determinants of blood pressure
Cardiac output.
Peripheral vascular resistance.
Systems that help regulate blood pressure
Sympathetic baroreceptor reflex.
Renin-Angiotensin-Aldosterone system.
Renal regulation of blood pressure.
Figure 47–2 ▪ Sites of action of antihypertensive drugs. Note that some antihypertensive agents act at more than one site: beta blockers act at sites 4 and 8a, and thiazides act at sites 6 and 7. The hemodynamic consequences of drug actions at the sites depicted are summarized in Table 47–4. (ACE = angiotensin-converting enzyme, ARB = angiotensin II receptor blocker.) No longer available in the United States.
Antihypertensive mechanisms: sites of drug action and effects produced
1—brainstem.
TABLE 47–4 ▪ Summary of Antihypertensive Effects Elicited by Drug Actions at Specific Sites
2—sympathetic ganglia.
3—terminals of adrenergic nerves.
4—beta1-adrenergic receptors on the heart.
5—alpha1-adrenergic receptors on blood vessels.
6—vascular smooth muscle.
7—renal tubules.
Components of the Renin-Angiotensin-Aldosterone system (8a to 8e)
8a—beta1 receptors on juxtaglomerular cells.
8b—renin.
8c—angiotensin-converting enzyme.
8d—angiotensin ii receptors.
TABLE 47–5 ▪ Drugs for Chronic Hypertension
8e—aldosterone receptors.
Classes of antihypertensive drugs
Diuretics
Thiazide diuretics.
High-ceiling (loop) diuretics.
TABLE 47–6 ▪ Combination Products for Chronic Hypertension
BOX 47–2 ▪ SPECIAL INTEREST TOPIC
AND THE BEST DRUG IS . . . THE CHEAP ONE!
Postscript
Potassium-sparing diuretics.
Sympatholytics (antiadrenergic drugs)
Beta-adrenergic blockers.
Alpha1 blockers.
Alpha/beta blockers: carvedilol and labetalol.
Centrally acting alpha2 agonists.
Adrenergic neuron blockers.
Direct-acting vasodilators: hydralazine and minoxidil
Calcium channel blockers
Drugs that suppress the RAAS
ACE inhibitors.
Angiotensin II receptor blockers.
Direct renin inhibitors.
Aldosterone antagonists.
Fundamentals of hypertension drug therapy
Treatment algorithm
Figure 47–3 ▪ Algorithm for treating hypertension.
TABLE 47–7 ▪ Classes of Antihypertensive Drugs Recommended for Initial Therapy of Hypertension in Patients with Certain High-Risk Comorbid Conditions
Initial drug selection
Patients without compelling indications.
Patients with compelling indications.
Adding drugs to the regimen
Rationale for drug selection.
Benefits of multidrug therapy.
Dosing
Step-down therapy
Individualizing therapy
Patients with comorbid conditions
Renal disease.
Diabetes.
Patients in special populations
African americans.
TABLE 47–8 ▪ Comorbid Conditions That Require Cautious Use or Complete Avoidance of Certain Antihypertensive Drugs
Children and adolescents.
The elderly.
Minimizing adverse effects
Promoting adherence
Why adherence is often hard to achieve
Ways to promote adherence
Patient education.
Teach self-monitoring.
Minimize side effects.
Establish a collaborative relationship.
Simplify the regimen.
Other measures.
Drugs for hypertensive emergencies
Sodium nitroprusside.
Fenoldopam.
Labetalol.
Clevidipine.
Drugs for hypertensive disorders of pregnancy
Chronic hypertension
Preeclampsia and eclampsia
Key points
Summary of Major Nursing Implications*
Antihypertensive drugs
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Routes
Dosage
Implementation: measures to enhance therapeutic effects
Lifestyle modifications
Weight reduction.
Sodium restriction.
Dash diet.
Alcohol restriction.
Exercise.
Smoking cessation.
Promoting adherence
Provide patient education.
Encourage self-monitoring.
Minimize adverse effects.
Establish a collaborative relationship.
Simplify the regimen.
Other measures.
Ongoing evaluation and interventions
Evaluating treatment
Minimizing adverse effects
General considerations.
Adverse effects of specific drugs.
Minimizing adverse interactions
CHAPTER 48 Drugs for heart failure
Pathophysiology of heart failure
Cardiac remodeling
Physiologic adaptations to reduced cardiac output
Figure 48–1 ▪ Relationship of ventricular diameter to contractile force. In the normal heart and the failing heart, increased fiber length produces increased contractile force. However, for any given fiber length, contractile force in the failing heart is much less than in the healthy heart. By increasing cardiac contractility, digoxin shifts the relationship between fiber length and stroke volume in the failing heart toward that in the normal heart.
Cardiac dilation.
Increased sympathetic tone.
Water retention and increased blood volume.
Consequences.
Natriuretic peptides.
Figure 48–2 ▪ The vicious cycle of maladaptive compensatory responses to a failing heart.
The vicious cycle of “compensatory” physiologic responses
Signs and symptoms of heart failure
Classification of heart failure severity
Overview of drugs used to treat heart failure
Diuretics
Figure 48–3 ▪ American College of Cardiology/American Heart Association (ACC/AHA) Stage and New York Heart Association (NYHA) Classification of Heart Failure.
Thiazide diuretics.
High-ceiling (loop) diuretics.
Potassium-sparing diuretics.
Drugs that inhibit the RAAS
ACE inhibitors
Hemodynamic benefits.
TABLE 48–1 ▪ Inhibitors of the Renin-Angiotensin-Aldosterone System Used in Heart Failure
Impact on cardiac remodeling.
Adverse effects.
Dosage.
Angiotensin II receptor blockers
Aldosterone antagonists
Direct renin inhibitors
Beta blockers
Digoxin
Inotropic agents (other than digoxin)
Sympathomimetic drugs: dopamine and dobutamine
Dopamine.
Dobutamine.
Phosphodiesterase inhibitors
Inamrinone.
Milrinone.
Vasodilators (other than ACE inhibitors and ARBs)
Isosorbide dinitrate plus hydralazine
Intravenous vasodilators for acute care
Nitroglycerin.
Sodium nitroprusside.
Nesiritide.
Mechanism of action.
Pharmacokinetics.
Adverse effects.
Preparations, dosage, and administration.
Digoxin, a cardiac glycoside
Chemistry
BOX 48–1 ▪ SPECIAL INTEREST TOPIC
ATTENTION LADIES: DIGOXIN MAY BE HAZARDOUS TO YOUR HEALTH
Mechanical effects on the heart
Mechanism of inotropic action.
Relationship of potassium to inotropic action.
Figure 48–4 ▪ Ion fluxes across the cardiac cell membrane. During the action potential, Na+ and Ca++ enter the cardiac cell and K+ exits. Following the action potential, Na+, K+-ATPase pumps Na+ out of the cell and takes up K+. Ca++ leaves the cell in exchange for the uptake of Na+. By inhibiting Na+,K+-ATPase, digoxin prevents the extrusion of Na+, causing Na+ to accumulate inside the cell. The resulting buildup of intracellular Na+ suppresses the Na+-Ca++ exchange process, thereby causing intracellular levels of Ca++ to rise.
Hemodynamic benefits in heart failure
Increased cardiac output.
Consequences of increased cardiac output.
Decreased sympathetic tone.
Increased urine production.
Decreased renin release.
Summary of hemodynamic effects.
Neurohormonal benefits in heart failure
Electrical effects on the heart
Mechanisms for altering electrical activity of the heart.
Effects on specific regions of the heart.
Adverse effects I: cardiac dysrhythmias
Mechanism of ventricular dysrhythmia generation.
Predisposing factors.
Hypokalemia.
Elevated digoxin levels.
Heart disease.
Diagnosing digoxin-induced dysrhythmias.
Managing digoxin-induced dysrhythmias.
TABLE 48–2 ▪ Drug Interactions with Digoxin
Adverse effects II: noncardiac adverse effects
Adverse effects III: measures to reduce adverse effects
Drug interactions
Diuretics.
ACE inhibitors and ARBs.
Sympathomimetics.
Quinidine.
Verapamil.
Pharmacokinetics
Absorption.
Distribution.
Elimination.
Half-life and time to plateau.
Single-dose time course.
A note on plasma digoxin levels.
Preparations, dosage, and administration
Preparations.
Administration.
Dosage in heart failure.
Digitalization.
Management of heart failure
Stage A
Stage B
Stage C
Drug therapy
Diuretics.
ACE inhibitors and ARBs.
Aldosterone antagonists.
Beta blockers.
Digoxin.
Isosorbide dinitrate/hydralazine.
Drugs to avoid
Device therapy
Implanted cardioverter-defibrillators.
Cardiac resynchronization.
Exercise training
Evaluating treatment
Stage D
Key points
Summary of Major Nursing Implications*
Digoxin
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Routes
Administration
Oral.
Intravenous.
Promoting adherence
Implementation: measures to enhance therapeutic effects
Ongoing evaluation and interventions
Evaluating therapeutic effects
Minimizing adverse effects
Cardiotoxicity.
Noncardiac effects.
Minimizing adverse interactions
Diuretics.
ACE inhibitors and ARBs.
Sympathomimetic agents.
Quinidine.
CHAPTER 49 Antidysrhythmic drugs
Introduction to cardiac electrophysiology, dysrhythmias, and the antidysrhythmic drugs
Electrical properties of the heart
Figure 49–1 ▪ Cardiac conduction pathways.
Impulse conduction: pathways and timing
SA node.
AV node.
His-Purkinje system.
Cardiac action potentials
Fast potentials
Phase 0.
Phase 1.
Phase 2.
Phase 3.
Figure 49–2 ▪ Ion fluxes during cardiac action potentials and effects of antidysrhythmic drugs. A, Fast potential of the His-Purkinje system and atrial and ventricular myocardium. Blockade of sodium influx by class I drugs slows conduction in the His-Purkinje system. Blockade of calcium influx by beta blockers and calcium channel blockers decreases contractility. Blockade of potassium efflux by class III drugs delays repolarization and thereby prolongs the effective refractory period. B, Slow potential of the sinoatrial (SA) node and atrioventricular (AV) node. Blockade of calcium influx by beta blockers, calcium channel blockers, and adenosine slows AV conduction. Beta blockers and calcium channel blockers decrease SA nodal automaticity (phase 4 depolarization); the ionic basis of this effect is not understood.
Phase 4.
Slow potentials
Figure 49–3 ▪ The electrocardiogram.
Phase 0.
Phases 1, 2, and 3.
Phase 4.
The electrocardiogram
Generation of dysrhythmias
Disturbances of automaticity
Disturbances of conduction
Atrioventricular block.
Figure 49–4 ▪ Reentrant activation: mechanism and drug effects. A, In normal conduction, impulses from the branched Purkinje fiber stimulate the strip of ventricular muscle in two places. Within the muscle, waves of excitation spread from both points of excitation, meet between the Purkinje fibers, and cease further travel. B, In the presence of one-way block, the strip of muscle is excited at only one location. Impulses spreading from this area meet no impulses coming from the left and, therefore, can travel far enough to stimulate branch 1 of the Purkinje fiber. This stimulation passes back up the fiber, past the region of one-way block, and then stimulates branch 2, causing reentrant activation. C, Elimination of reentry by a drug that improves conduction in the sick branch of the Purkinje fiber. D, Elimination of reentry by a drug that further suppresses conduction in the sick branch, thereby converting one-way block into two-way block.
Reentry (recirculating activation).
Classification of antidysrhythmic drugs
Class I: sodium channel blockers
Class II: beta blockers
Class III: potassium channel blockers (drugs that delay repolarization)
Class IV: calcium channel blockers
Other antidysrhythmic drugs
TABLE 49–1 ▪ Vaughan Williams Classification of Antidysrhythmic Drugs
Prodysrhythmic effects of antidysrhythmic drugs
Overview of common dysrhythmias and their treatment
Supraventricular dysrhythmias
Atrial fibrillation.
Atrial flutter.
Sustained supraventricular tachycardia (SVT).
Ventricular dysrhythmias
Sustained ventricular tachycardia.
Ventricular fibrillation.
Ventricular premature beats (vpbs).
Digoxin-induced ventricular dysrhythmias.
Torsades de pointes.
Principles of antidysrhythmic drug therapy
Balancing risks and benefits
Properties of the dysrhythmia to be considered
Sustained versus nonsustained dysrhythmias.
Asymptomatic versus symptomatic dysrhythmias.
Supraventricular versus ventricular dysrhythmias.
Phases of treatment
TABLE 49–2 ▪ Properties of Antidysrhythmic Drugs
Long-term treatment: drug selection and evaluation
Minimizing risks
Pharmacology of the antidysrhythmic drugs
Class I: sodium channel blockers
Class IA agents
Quinidine
Chemistry and source.
Effects on the heart.
Effects on the ECG.
Therapeutic uses.
Pharmacokinetics.
Adverse effects.
Diarrhea.
Cinchonism.
Cardiotoxicity.
Arterial embolism.
Other adverse effects.
Drug interactions.
Digoxin.
Other interactions.
Preparations, dosage, and administration.
Preparations.
Dosage.
Administration.
Procainamide
Effects on the heart and ECG.
Therapeutic uses.
Pharmacokinetics.
Adverse effects.
Systemic lupus erythematosus–like syndrome.
Blood dyscrasias.
Cardiotoxicity.
Other adverse effects.
Preparations, dosage, and administration.
Oral.
Parenteral.
Disopyramide
Effects on the heart and ECG.
Adverse effects.
Therapeutic uses.
Preparations, dosage, and administration.
Class IB agents
Lidocaine
Effects on the heart and ECG.
Pharmacokinetics.
Antidysrhythmic use.
Adverse effects.
Preparations, dosage, and administration.
Intravenous.
Intramuscular.
Phenytoin
Effects on the heart and ECG.
Pharmacokinetics.
Adverse effects and interactions.
Antidysrhythmic applications.
Dosage and administration.
Mexiletine
Class IC agents
Flecainide
Propafenone
Class II: beta blockers
Propranolol
Effects on the heart and ECG.
Therapeutic use.
Adverse effects.
Dosage and administration.
Acebutolol
Esmolol
Class III: potassium channel blockers (drugs that delay repolarization)
Amiodarone
Oral therapy
Therapeutic use.
Effects on the heart and ECG.
Pharmacokinetics.
Adverse effects.
Pulmonary toxicity.
Cardiotoxicity.
Thyroid toxicity.
Liver toxicity.
Opthalmic effects.
Toxicity in pregnancy and breast-feeding.
Dermatologic toxicity.
Other adverse effects.
Drug interactions.
Dosage.
Intravenous therapy
Therapeutic use.
Effects on the heart and ECG.
Adverse effects.
Dosage.
Dronedarone
Effects on the heart and ECG.
Pharmacokinetics.
Adverse effects.
Cardiac effects.
Liver toxicity.
Toxicity in pregnancy and breast-feeding.
Drug interactions.
Summary of contraindications.
Preparations, dosage, and administration.
Sotalol
Actions and uses.
Pharmacokinetics.
Adverse effects.
Preparations, dosage, and administration.
Dofetilide
Therapeutic use.
Effects on the heart and ECG.
Pharmacokinetics.
Adverse effects.
Drug interactions.
Preparations, dosage, and administration.
Ibutilide
Class IV: calcium channel blockers
Effects on the heart and ECG.
Therapeutic uses.
Adverse effects.
Drug interactions.
Preparations, dosage, and administration.
Verapamil.
Diltiazem.
Other antidysrhythmic drugs
Adenosine
Effects on the heart and ECG.
Therapeutic use.
Pharmacokinetics.
Adverse effects.
Drug interactions.
Preparations, dosage, and administration.
Digoxin
Effects on the heart.
Effects on the ECG.
Adverse effects and interactions.
Antidysrhythmic uses.
Atrial fibrillation and atrial flutter.
Supraventricular tachycardia.
Dosage and administration.
Nondrug treatment of dysrhythmias
Implantable cardioverter-defibrillators
Radiofrequency catheter ablation
Key points
Normal Electrophysiology of the Heart (read text)
Beta Blockers (read text)
Calcium Channel Blockers (read text)
Diltiazem Injection, Cardiac Effects (read text)
Adenosine Infusion, Cardiac Effects (read text)
Amiodarone Treatment for Ventricular Fibrillation (read text)
Amiodarone Treatment for Ventricular Tachycardia (read text)
Summary of Major Nursing Implications*
Quinidine
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Routes
Usual route.
Rare routes.
Administration
Ongoing evaluation and interventions
Evaluating therapeutic effects
Minimizing adverse effects
Diarrhea.
Cinchonism.
Cardiotoxicity.
Arterial embolism.
Minimizing adverse interactions
Digoxin.
Procainamide
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Routes
Administration
Ongoing evaluation and interventions
Evaluating therapeutic effects
Minimizing adverse effects
Sle-like syndrome.
Blood dyscrasias.
Cardiotoxicity.
Arterial embolism.
Lidocaine
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Routes
Usual.
Emergencies.
Administration
Intravenous.
Intramuscular.
Ongoing evaluation and interventions
Evaluating therapeutic effects
Minimizing adverse effects
Amiodarone
Preadministration assessment
Therapeutic goal
Oral therapy.
Intravenous therapy.
Baseline data
Identifying high-risk patients
Implementation: administration
Routes
Oral.
Intravenous.
Administration and dosage
Oral.
Intravenous.
Ongoing evaluation and interventions
Evaluating therapeutic effects
Minimizing adverse effects
Pulmonary toxicity.
Cardiotoxicity.
Liver toxicity.
Thyroid toxicity.
Toxicity in pregnancy and breast-feeding.
Ophthalmic effects.
Dermatologic effects.
Minimizing adverse interactions
Drugs whose levels can be increased by amiodarone.
Drugs that can reduce amiodarone levels.
Drugs that can increase the risk of dysrhythmias.
Drugs that can cause bradycardia.
Grapefruit juice.
CHAPTER 50 Prophylaxis of coronary heart disease: drugs that help normalize cholesterol and triglyceride levels
Figure 50–1 ▪ Basic structure of plasma lipoproteins.
TABLE 50–1 ▪ Morbidity and Mortality from Cardiovascular Disease in General, and Coronary Heart Disease in Particular, United States
Cholesterol
Plasma lipoproteins
Structure and function of lipoproteins
Function.
Basic structure.
Apolipoproteins.
Classes of lipoproteins
TABLE 50–2 ▪ Properties of the Plasma Lipoproteins That Affect Atherosclerosis
Very-low-density lipoproteins
Low-density lipoproteins
High-density lipoproteins
LDL cholesterol versus HDL cholesterol
Role of LDL cholesterol in atherosclerosis
Detection, evaluation, and treatment of high cholesterol: recommendations from ATP III
Cholesterol screening
Adults
Children and adolescents
Figure 50–2 ▪ Progression of atherosclerosis. A, Damaged endothelium. B, Diagram of fatty streak and lipid core formation. C, Diagram of fibrous plaque. Raised plaques are visible: some are yellow and some are white. D, Diagram of a complicated lesion, showing a thrombus (in red) and collagen (in blue).
TABLE 50–3 ▪ Health Classification of Blood Cholesterol and Triglyceride Levels*
TABLE 50–4 ▪ NCEP Classification of Cholesterol Levels for Children and Adolescents*
TABLE 50–5 ▪ Major Risk Factors (Other Than High LDL Cholesterol) That Modify LDL Treatment Goals
CHD risk assessment
Factors in risk assessment
Identifying CHD risk factors.
Calculating 10-year CHD risk.
BOX 50–1 ▪ SPECIAL INTEREST TOPIC
INFLAMMATION, C-REACTIVE PROTEIN, AND CARDIOVASCULAR RISK
Identifying CHD risk equivalents.
Identifying an individual’s chd risk category
Final note: each type of dyslipidemia a patient has contributes independently to CHD risk
Figure 50–3 ▪ Tables for calculating Framingham Risk Prediction Scores. To determine an individual’s 10-year risk of developing clinical coronary disease, simply circle the appropriate points for each of the five risk factors considered (age, total cholesterol, smoking status, HDL cholesterol, and systolic blood pressure) and then add up the points. The point total indicates the 10-year risk. For example, a total of 13 points indicates a 10-year risk of 12% for men.
TABLE 50–6 ▪ LDL Cholesterol Goals and Therapeutic Interventions for People in Specific CHD Risk Categories
Treatment of high LDL cholesterol
Therapeutic lifestyle changes
The TLC diet.
Weight control.
TABLE 50–7 ▪ Nutrient Composition of the TLC Diet Described in ATP III
Exercise.
Smoking cessation.
Drug therapy
Secondary treatment targets
Metabolic syndrome
TABLE 50–8 ▪ Recommended Dietary Modifications to Lower Serum Cholesterol
TABLE 50–9 ▪ Drugs Used to Improve Plasma Levels of LDL, HDL, and Triglycerides
High triglycerides
Drugs and other products used to improve plasma lipid levels
HMG-CoA reductase inhibitors (statins)
Beneficial actions
Reduction of LDL cholesterol.
TABLE 50–10 ▪ HMG-CoA Reductase Inhibitors: Selected Aspects of Clinical Pharmacology
Elevation of HDL cholesterol.
Reduction of triglyceride levels.
Nonlipid beneficial cardiovascular actions.
Increased bone formation.
Mechanism of cholesterol reduction
Clinical trials
Secondary prevention studies.
Primary prevention studies.
Primary prevention in patients with normal cholesterol levels.
Prevention in patients with diabetes.
TABLE 50–11 ▪ HMG-CoA Reductase Inhibitors: FDA-Approved Indications
Therapeutic uses
Hypercholesterolemia.
Primary and secondary prevention of CV events.
Primary prevention in people with normal LDL levels.
Post-MI therapy.
Diabetes.
Potential uses.
Pharmacokinetics
Adverse effects
Myopathy/rhabdomyolysis.
Hepatotoxicity.
Drug interactions
With other lipid-lowering drugs.
With drugs that inhibit CYP3A4.
Use in pregnancy
Preparations, dosage, and administration
Drug selection
LDL goal.
Drug interactions.
Kidney function.
Safety in asians.
Price.
Niacin (nicotinic acid)
Effect on plasma lipoproteins.
Mechanism of action.
The aim-high trial.
Therapeutic use.
TABLE 50–12 ▪ HMG-CoA Reductase Inhibitors: Preparations, Dosage, and Administration
Adverse effects.
Preparations, dosage, and administration.
Bile-acid sequestrants
Colesevelam
Effect on plasma lipoproteins.
Pharmacokinetics.
Mechanism of action.
Therapeutic use.
Adverse effects.
Drug interactions.
Preparations, dosage, and administration.
Older agents: cholestyramine and colestipol
Ezetimibe
Mechanism of action and effect on plasma lipoproteins.
Therapeutic use.
Pharmacokinetics.
Adverse effects.
Drug interactions.
Statins.
Fibrates.
Bile-acid sequestrants.
Cyclosporine.
Caution.
Preparations, dosage, and administration.
Fibric acid derivatives (fibrates)
Gemfibrozil
Effect on plasma lipoproteins.
Mechanism of action.
Therapeutic use.
Adverse effects.
Gallstones.
Myopathy.
Liver injury.
Drug interactions.
Preparations, dosage, and administration.
Fenofibrate
Actions and uses.
Pharmacokinetics.
Adverse effects and drug interactions.
Preparations, dosage, and administration.
Fenofibric acid
Drug combinations
Lovastatin/niacin [advicor]
Actions and uses.
Adverse effects.
Preparations, dosage, and administration.
Simvastatin/niacin [simcor]
Actions and uses.
Adverse effects.
Preparations, dosage, and administration.
Simvastatin/ezetimibe [vytorin]
Actions and uses.
Adverse effects and drug interactions.
Preparations, dosage, and administration.
Pravastatin/aspirin [pravigard pac]
Figure 50–4 ▪ Structures of omega-3 fatty acids in fish oil.
Atorvastatin/amlodipine [caduet]
Simvastatin/sitagliptin [juvisync]
Fish oil
Lovaza.
Plant stanol and sterol esters
Estrogen
Cholestin
Key points
Cholesterol-Lowering Medications (read text)
Summary of Major Nursing Implications*
Implications that apply to all drugs that lower LDL cholesterol
Preadministration assessment
Baseline data
Identifying CHD risk factors
Measures to enhance therapeutic effects
Diet modification
Exercise
Reduction of CHD risk factors
Promoting compliance
HMG-CoA reductase inhibitors (statins)
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Route
Administration
Ongoing evaluation and interventions
Evaluating therapeutic effects
Minimizing adverse effects
Hepatotoxicity.
Myopathy.
Minimizing adverse interactions
Use in pregnancy
Niacin (nicotinic acid)
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Formulations
Route
Administration
Measures to enhance therapeutic effects
Dietary therapy
Ongoing evaluation and interventions
Evaluating therapeutic effects
Minimizing adverse effects
Flushing.
Hepatotoxicity.
Hyperglycemia.
Hyperuricemia.
Bile-acid sequestrants
Preadministration assessment
Therapeutic goal
Baseline data
Implementation: administration
Route
Administration
Ongoing evaluation and interventions
Evaluating therapeutic effects
Minimizing adverse effects
Constipation.
Vitamin deficiency.
Minimizing adverse interactions.
Gemfibrozil
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Route
Administration
Ongoing evaluation and interventions
Evaluating therapeutic effects
Minimizing adverse effects
Gallstones.
Myopathy.
Liver disease.
Minimizing adverse interactions
Warfarin.
Statins.
CHAPTER 51 Drugs for angina pectoris
Determinants of cardiac oxygen demand and oxygen supply
Oxygen demand.
Oxygen supply.
Angina pectoris: pathophysiology and treatment strategy
Chronic stable angina (exertional angina)
Pathophysiology.
Figure 51–1 ▪ Effect of exertion on the balance between oxygen supply and oxygen demand in the healthy heart and the heart with CAD. In the healthy heart, O2 supply and O2 demand are always in balance; during exertion, coronary arteries dilate, producing an increase in blood flow to meet the increase in O2 demand. In the heart with CAD, O2 supply and O2 demand are in balance only during rest. During exertion, dilation of coronary arteries cannot compensate for the increase in O2 demand, and an imbalance results.
Treatment strategy.
Overview of therapeutic agents.
Nondrug therapy.
TABLE 51–1 ▪ Mechanisms of Antianginal Action
Variant angina (prinzmetal’s angina, vasospastic angina)
Pathophysiology.
Treatment strategy.
Overview of therapeutic agents.
Unstable angina
Pathophysiology.
Treatment.
Organic nitrates
Nitroglycerin
Vasodilator actions
Mechanism of antianginal effects
Stable angina.
Variant angina.
Pharmacokinetics
Absorption.
Figure 51–2 ▪ Biochemistry of nitrate-induced vasodilation. Note that sulfhydryl groups are needed to catalyze the conversion of nitrate to its active form, nitric oxide. If sulfhydryl groups are depleted from VSM, tolerance to nitrates will occur.
Metabolism.
Adverse effects
Headache.
Orthostatic hypotension.
TABLE 51–2 ▪ Organic Nitrates: Time Course of Action
Reflex tachycardia.
Drug interactions
Hypotensive drugs.
Phosphodiesterase type 5 inhibitors.
Beta blockers, verapamil, and diltiazem.
Tolerance
Preparations and routes of administration
Sublingual tablets.
TABLE 51–3 ▪ Organic Nitrates: Trade Names and Dosages
Sustained-release oral capsules.
Transdermal delivery systems.
Translingual spray.
Topical ointment.
Intravenous infusion.
Discontinuing nitroglycerin
Summary of therapeutic uses
Acute therapy of angina.
Sustained therapy of angina.
Intravenous therapy.
Isosorbide mononitrate and isosorbide dinitrate
Amyl nitrite
Beta blockers
Calcium channel blockers
Ranolazine
Actions and therapeutic use
Pharmacokinetics
Adverse effects
QT prolongation.
Elevation of blood pressure.
Other adverse effects.
Drug interactions
CYP3A4 inhibitors.
QT drugs.
Calcium channel blockers.
Preparations, dosage, and administration
Revascularization therapy: CABG and PCI
Coronary artery bypass graft surgery
Percutaneous coronary intervention
Comparison of CABG surgery with PCI
Summary of treatment measures
Guidelines for management of chronic stable angina
Drugs used to prevent myocardial infarction and death
Figure 51–3 ▪ Flow plan for antianginal drug selection in patients with chronic stable angina. 1Avoid short-acting dihydropyridines. 2At any point in this process, based on coronary anatomy, severity of angina symptoms, and patient preference, it is reasonable to consider evaluation for coronary revascularization (PCI or CABG). Unless a patient is documented to have left main, three-vessel, or two-vessel CAD with significant stenosis of the proximal left anterior descending coronary artery, there is no demonstrated survival advantage associated with CABG or PCI in low-risk patients with chronic stable angina. Accordingly, medical therapy should be attempted in most patients before considering PCI or CABG.
Antiplatelet drugs.
Cholesterol-lowering drugs.
Angiotensin-converting enzyme (ACE) inhibitors.
Antianginal agents: drugs used to reduce anginal pain
TABLE 51–4 ▪ Choosing Between Beta Blockers and Calcium Channel Blockers for Treating Angina in Patients Who Have a Coexisting Condition
Reduction of risk factors
Smoking.
High cholesterol.
Hypertension.
Diabetes.
Obesity.
Physical inactivity.
Management of variant angina
Key points
Acute Myocardial Infarction (read text)
Summary of Major Nursing Implications*
Nitroglycerin
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Routes and administration
Sublingual tablets.
Use.
Technique of administration.
Sustained-release oral capsules.
Use.
Technique of administration.
Transdermal delivery systems.
Use.
Technique of administration.
Translingual spray.
Use.
Technique of administration.
Topical ointment.
Use.
Technique of administration.
Intravenous.
Uses.
Technique of administration.
Terminating therapy
Implementation: measures to enhance therapeutic effects
Reducing risk factors
Precipitating factors.
Weight reduction.
Exercise.
Smoking cessation.
Contributing disease states.
Ongoing evaluation and interventions
Evaluating therapeutic effects
Minimizing adverse effects
Headache.
Orthostatic hypotension.
Reflex tachycardia.
Minimizing adverse interactions
Hypotensive agents, including PDE5 inhibitors.
Isosorbide mononitrate and isosorbide dinitrate
CHAPTER 52 Anticoagulant, antiplatelet, and thrombolytic drugs
Coagulation: physiology and pathophysiology
Hemostasis
Stage one: formation of a platelet plug.
Stage two: coagulation.
Figure 52–1 ▪ Mechanism of platelet aggregation and actions of antiplatelet drugs. A, Multiple factors—TXA2, thrombin, collagen, PAF, and ADP—promote activation of the GP IIb/IIIa receptor. Each platelet has 50,000 to 80,000 GP IIb/IIIa receptors, although only one is shown. B, Activation of the GP IIb/IIIa receptor permits binding of fibrinogen, which then causes aggregation by forming cross-links between platelets. After aggregation occurs, the platelet plug is reinforced with fibrin (not shown).
Figure 52–2 ▪ Outline of coagulation pathways showing factors affected by warfarin and heparin. TF = tissue factor. Common names for factors shown in roman numerals: V = proaccelerin, VII = proconvertin, VIII = antihemophilic factor, IX = Christmas factor, X = Stuart factor, XI = plasma thromboplastin antecedent, and XII = Hageman factor. The letter “a” after a factor’s name (eg, factor VIIIa) indicates the active form of the factor.
Keeping hemostasis under control.
Physiologic removal of clots.
Thrombosis
Arterial thrombosis.
TABLE 52–1 ▪ Overview of Drugs for Thromboembolic Disorders
Venous thrombosis.
TABLE 52–2 ▪ Comparison of Drugs That Activate Antithrombin
Overview of drugs for thromboembolic disorders
Anticoagulants
Heparin and its derivatives: drugs that activate antithrombin
Heparin (unfractionated)
Source
Chemistry
Mechanism of anticoagulant action
Pharmacokinetics
Absorption and distribution.
Protein and tissue binding.
Metabolism and excretion.
Time course.
Therapeutic uses
Adverse effects
Hemorrhage.
Spinal/epidural hematoma.
Heparin-induced thrombocytopenia.
Figure 52–3 ▪ Mechanism of action of heparin, LMW heparins, and fondaparinux. All three drugs share a pentasaccharide sequence that allows them to bind with—and thereby activate—antithrombin, a protein that inactivates two major clotting factors: thrombin and factor Xa. All three drugs enable antithrombin to inactivate factor Xa, but only heparin also facilitates inactivation of thrombin. Upper Panel: Unfractionated heparin binds with antithrombin, thereby causing a conformational change in antithrombin that greatly increases its ability to interact with factor Xa and thrombin. As shown, when the heparin-antithrombin complex binds with thrombin, heparin changes its conformation such that both heparin and antithrombin come in contact with thrombin. Formation of this ternary complex is necessary for thrombin inactivation. Inactivation of factor Xa is different: It only requires contact between activated antithrombin and factor Xa; contact between heparin and factor Xa is unnecessary. Middle Panel: Low-molecular-weight (LMW) heparins have the same pentasaccharide sequence as unfractionated heparin, and hence can bind with and thereby activate antithrombin. However, in contrast to unfractionated heparin, which promotes inactivation of both thrombin and factor Xa, most molecules of LMW heparin can only inactivate factor Xa; they are unable to inactivate thrombin. Why? Because most molecules of LMW heparin are too small to form a ternary complex with thrombin and antithrombin. Lower Panel: Fondaparinux is a synthetic pentasaccharide identical in structure to the antithrombin binding sequence found in unfractionated heparin and LMW heparins. Being even smaller than LMW heparins, fondaparinux is too small to form a ternary complex with thrombin, and hence can only inactivate factor Xa.
Hypersensitivity reactions.
Other adverse effects.
Warnings and contraindications
Warnings.
Contraindications.
Drug interactions
Protamine sulfate for heparin overdose
Laboratory monitoring
Unitage and preparations
Unitage.
Preparations.
Dosage and administration
General considerations.
Intermittent IV therapy.
Continuous IV infusion.
Deep subq injection.
Low-dose therapy.
Low-molecular-weight heparins
Group properties
Production.
Mechanism of action.
Therapeutic use.
Pharmacokinetics.
Administration, dosing, and monitoring.
Adverse effects and interactions.
Cost.
Individual preparations
Enoxaparin.
Administration and dosage.
Dalteparin.
Tinzaparin.
Fondaparinux
Actions.
Therapeutic use.
Pharmacokinetics.
Adverse effects.
Preparations, dosage, and administration.
Warfarin, a Vitamin K antagonist
History
Mechanism of action
Pharmacokinetics
Absorption, distribution, and elimination.
Time course.
Therapeutic uses
Overview of uses.
Atrial fibrillation.
Monitoring treatment
TABLE 52–3 ▪ Monitoring Warfarin Therapy: Recommended Ranges of Prothrombin Time–Derived Values
Adverse effects
Hemorrhage.
Fetal hemorrhage and teratogenesis from use during pregnancy.
Use during lactation.
Other adverse effects.
Drug interactions
General considerations.
TABLE 52–4 ▪ Interactions Between Warfarin and Other Drugs
Specific interacting drugs.
Heparin.
Aspirin.
Nonaspirin antiplatelet drugs.
Acetaminophen.
Other notable interactions.
Warnings and contraindications
Vitamin K1 for warfarin overdose
What about dietary Vitamin K?
Contrasts between warfarin and heparin
Dosage
Basic considerations.
TABLE 52–5 ▪ Summary of Contrasts Between Heparin and Warfarin
Genetics and dosage adjustment.
Preparations
Direct thrombin inhibitors
Dabigatran etexilate
Mechanism of action
Therapeutic use
Atrial fibrillation.
TABLE 52–6 ▪ Properties of the Oral Anticoagulants
Knee or hip replacement.
Pharmacokinetics
Adverse effects
Bleeding.
Gastrointestinal disturbances.
Drug interactions
Preparations, dosage, administration, and storage
Preparations.
Administration.
Dosage for atrial fibrillation.
Switching from warfarin to dabigatran.
Switching from dabigatran to warfarin.
Storage.
Hirudin analogs
Bivalirudin
Actions and use.
Adverse effects.
Pharmacokinetics.
Comparison with heparin.
Preparations, dosage, and administration.
Lepirudin
Desirudin
Argatroban
Rivaroxaban, a direct factor xa inhibitor
Actions and uses
Clinical trials
Knee and hip replacement patients.
Nonvalvular atrial fibrillation patients.
Pharmacokinetics
Adverse effects
Bleeding.
Spinal/epidural hematoma.
Drug interactions
Precautions
Renal impairment.
Hepatic impairment.
Pregnancy.
Preparations, dosage, and administration
Antithrombin
Recombinant human antithrombin
Production.
Therapeutic use.
Adverse effects.
Interaction with heparin.
Comparison with plasma-derived at.
Preparations, dosage, and administration.
Plasma-derived antithrombin
Antiplatelet drugs
Aspirin
Mechanism of antiplatelet action.
TABLE 52–7 ▪ Properties of the Major Classes of Antiplatelet Drugs
Indications for antiplatelet therapy.
Primary prevention of MI.
Adverse effects.
Dosing.
P2y12 adenosine diphosphate receptor antagonists
Clopidogrel
Antiplatelet actions.
Pharmacokinetics.
Therapeutic use.
Adverse effects.
Bleeding.
Thrombotic thrombocytopenic purpura (ttp).
Drug interactions.
Drugs that promote bleeding.
Proton pump inhibitors (ppis).
Cyp2c19 inhibitors (other than ppis).
Preparations, dosage, and administration.
Prasugrel
Actions and uses.
Clinical trial.
Pharmacokinetics.
Adverse effects.
Drug interactions.
Preparations, dosage, and administration.
Ticagrelor
Actions and uses.
Clinical trial.
Pharmacokinetics.
Adverse effects.
Bleeding.
Dyspnea.
Ventricular pauses.
Drug interactions.
Aspirin.
Drugs that promote bleeding.
Inhibitors and inducers of CYP3A4.
Statins.
Digoxin.
Contraindications and precautions.
TABLE 52–8 ▪ Dosages for Glycoprotein IIb/IIIa Receptor Antagonists
Preparations, dosage, and administration.
Ticlopidine
Actions.
Uses.
Pharmacokinetics.
Adverse effects.
Hematologic effects.
Other adverse effects.
Preparations, dosage, and administration.
Glycoprotein IIb/IIIa receptor antagonists
Group properties
Actions.
Therapeutic use.
Acute coronary syndromes.
Percutaneous coronary intervention.
Properties of individual GP IIb/IIIa antagonists
Abciximab.
Description and use.
Adverse effects and interactions.
Eptifibatide.
Tirofiban.
Other antiplatelet drugs
Dipyridamole
Dipyridamole plus aspirin
Actions and use.
Clinical trial.
Adverse effects.
Preparations, dosage, and administration.
Cilostazol
Actions and therapeutic use.
Adverse effects.
Drug and food interactions.
Preparations, dosage, and administration.
Thrombolytic (fibrinolytic) drugs
Alteplase (TPA)
Description and mechanism.
TABLE 52–9 ▪ Properties of Thrombolytic (Fibrinolytic) Drugs
Therapeutic uses.
Pharmacokinetics.
Adverse effect: bleeding.
Preparations.
Dosage and administration.
Acute myocardial infarction (activase only).
Acute ischemic stroke (activase only).
Pulmonary embolism (activase only).
Clearing a central venous catheter (cathflo activase only).
TABLE 52–10 ▪ Contraindications and Cautions Regarding Thrombolytic Use for Myocardial Infarction
Tenecteplase
Reteplase
Key points
Heparin for Atrial Fibrillation (read text)
Acute Myocardial Infarction (read text)
Heparin for Acute Coronary Syndrome (read text)
Acute Myocardial Infarction(read text)
Thrombolytic Drugs; Clot Dissolving Drugs (read text)
Summary of Major Nursing Implications*
Heparin
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Routes
Administration
General considerations.
Intermittent IV administration.
Continuous IV infusion.
Deep subq injection.
Ongoing evaluation and interventions
Evaluating treatment
Minimizing adverse effects
Hemorrhage.
Heparin-induced thrombocytopenia.
Spinal/epidural hematoma.
Hypersensitivity reactions.
Minimizing adverse interactions
Antiplatelet drugs.
Warfarin, a Vitamin K antagonist
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Route
Administration
Implementation: measures to enhance therapeutic effects
Promoting adherence
Nondrug measures
Ongoing evaluation and interventions
Monitoring treatment
Minimizing adverse effects
Hemorrhage.
Use in pregnancy and lactation.
Minimizing adverse interactions
Clopidogrel, a p2y12 adenosine diphosphate receptor antagonist
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Route
Administration
Ongoing evaluation and interventions
Promoting beneficial effects
Minimizing adverse effects
Bleeding.
Thrombotic thrombocytopenic purpura (ttp).
Minimizing adverse interactions
Drugs that promote bleeding.
Proton pump inhibitors (ppis).
Cyp2c19 inhibitors (other than ppis).
Thrombolytic (fibrinolytic) drugs
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Route
Administration (for acute MI)
Alteplase.
Tenecteplase.
Reteplase.
Ongoing evaluation and interventions
Minimizing adverse effects
Hemorrhage.
Minimizing adverse interactions
Anticoagulants and antiplatelet drugs.
CHAPTER 53 Management of ST-elevation myocardial infarction
Pathophysiology of STEMI
Diagnosis of STEMI
Chest pain.
ECG changes.
Figure 53–1 ▪ ECG changes associated with ST-elevation myocardial infarction.
Biochemical markers for MI.
Management of STEMI
Routine drug therapy
Oxygen
TABLE 53–1 ▪ Comparison of Fibrinolytic Therapy with Primary PCI
Aspirin
Nonaspirin NSAIDs
Morphine
Beta blockers
Nitroglycerin
Reperfusion therapy
TABLE 53–2 ▪ Contraindications and Cautions Regarding Fibrinolytic Use for Myocardial Infarction
Primary percutaneous coronary intervention
Fibrinolytic therapy
Adjuncts to reperfusion therapy
Heparin
Antiplatelet drugs
Thienopyridines: clopidogrel and prasugrel.
Glycoprotein (GP) IIb/IIIa inhibitors.
Aspirin.
Angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers
Calcium channel blockers
Complications of STEMI
Ventricular dysrhythmias.
Cardiogenic shock.
Heart failure.
Cardiac rupture.
Secondary prevention of STEMI
Key points
CHAPTER 54 Drugs for hemophilia
Basic considerations
Pathophysiology
Figure 54–1 ▪ Outline of the coagulation cascade showing clotting factors used to treat hemophilia. TF = tissue factor. Common names for factors shown in roman numerals: II = prothrombin, IIa = thrombin, VII = proconvertin, VIII = antihemophilic factor, IX = Christmas factor, X = Stuart factor, XI = plasma thromboplastin antecedent, and XII = Hageman factor. The letter “a” after a factor’s name (eg, factor VIIIa) indicates the active form of the factor. Note that factors VIII and IX, which are deficient in hemophilia A and B, respectively, are part of the contact activation (intrinsic) coagulation pathway. The symbol indicates acceleration of the reaction.
TABLE 54–1 ▪ Clinical Classification of Hemophilia Severity
Inheritance pattern
Clinical features
Severe hemophilia.
Moderate hemophilia.
Mild hemophilia.
Overview of therapy
TABLE 54–2 ▪ Some Factor VIII and Factor IX Concentrates
Pain management
Immunization
Preparations used to treat hemophilia
Factor VIII concentrates
Production methods and product safety
Plasma-derived factor VIII.
Recombinant factor VIII.
Adverse effects: allergic reactions
Dosage and administration
On-demand therapy.
Prophylactic therapy.
Factor IX concentrates
Therapeutic use, production, and safety
Dosage and administration
On-demand therapy.
TABLE 54–3 ▪ Estimated Dosages for Factor VIII and Factor IX
Prophylactic therapy.
Desmopressin
Therapeutic use.
Preparations, dosage, and administration.
Antifibrinolytic agents
Aminocaproic acid.
Tranexamic acid.
Managing patients who develop inhibitors
Drugs for patients with factor VIII inhibitors
Activated factor VII (factor VIIa).
Anti-inhibitor coagulant complex (AICC).
Factor VIII concentrate.
Porcine factor VIII.
Drugs for patients with factor IX inhibitors
Key points
Summary of Major Nursing Implications*
Factor VIII and factor IX concentrates
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Route
Administration
Ongoing evaluation and interventions
Evaluating therapeutic effects
Minimizing adverse effects
Allergic reactions.
Minimizing adverse interactions
Aspirin.
NSAIDs other than aspirin.
CHAPTER 55 Drugs for deficiency anemias
Red blood cell development
Iron deficiency
Biochemistry and physiology of iron
Figure 55–1 ▪ Stages of red blood cell development.
Figure 55–2 ▪ Fate of iron in the body. Pathways labeled with circled numbers are explained in the text. Values in parentheses indicate percentage of total body stores. Elimination of iron is not shown, because most iron is rigidly conserved. (Fe = iron, RBC = red blood cell.)
Metabolic functions
Fate in the body
Uptake and distribution.
Utilization and storage.
Recycling.
TABLE 55–1 ▪ Recommended Dietary Allowances (RDAs) for Iron
Elimination.
Regulation of body iron content.
Daily requirements
Dietary sources
Iron deficiency: causes, consequences, and diagnosis
Causes
Consequences
Diagnosis
TABLE 55–2 ▪ Iron Preparations Available for Oral Therapy
TABLE 55–3 ▪ Commonly Used Oral Iron Preparations
Oral iron preparations
Ferrous iron salts
Ferrous sulfate
Indications.
Adverse effects.
GI disturbances.
Staining of teeth.
Toxicity.
Symptoms.
Diagnosis and treatment.
Drug interactions.
Preparations.
Dosage and administration.
General considerations.
Use in iron deficiency anemia.
Prophylactic use.
Ferrous gluconate, ferrous fumarate, and ferrous aspartate
Carbonyl iron
Figure 55–3 ▪ Formula for estimating total dosage of parenteral iron dextran.
Parenteral iron preparations
Iron dextran
Indications
Adverse effects
Anaphylactic reactions.
Other adverse effects.
Preparations, dosage, and administration
Preparations.
Dosage.
Administration.
Intravenous.
Intramuscular.
Sodium–ferric gluconate complex, iron sucrose, and ferumoxytol
Sodium–ferric gluconate complex
Iron sucrose
Ferumoxytol
Guidelines for treating iron deficiency
Assessment.
Routes of administration.
Duration of therapy.
Therapeutic combinations.
Vitamin B12 deficiency
Biochemistry and physiology of vitamin B12
Metabolic function
Fate in the body
Absorption.
Figure 55–4 ▪ Relationship of folic acid and vitamin B12 to DNA synthesis and cell maturation. Folic acid requires activation to be of use. Normally, activation occurs via a vitamin B12–dependent pathway. However, when folic acid is present in large amounts, activation can occur via an alternate pathway, thereby bypassing the need for B12.
Distribution and storage.
Elimination.
Daily requirements
Dietary sources
Vitamin B12 deficiency: causes, consequences, and diagnosis
Causes
Consequences
Megaloblastic anemia.
Neurologic damage.
Other effects.
Diagnosis
Vitamin B12 preparations: cyanocobalamin
Adverse effects
Preparations, dosage, and administration
Oral.
Parenteral.
Intranasal.
Guidelines for treating vitamin B12 deficiency
Route of b12 administration.
Treatment of moderate b12 deficiency.
Treatment of severe b12 deficiency.
Long-term treatment.
TABLE 55–4 ▪ Vitamin B12 Deficiency Versus Folic Acid Deficiency
Potential hazard of folic acid.
Folic acid deficiency
Physiology and biochemistry of folic acid
Metabolic function
Fate in the body
Daily requirements
Dietary sources
Folic acid deficiency: causes, consequences, and diagnosis
Causes
Alcoholism.
Sprue.
Consequences
All people.
The developing fetus.
Other consequences.
Diagnosis
Folic acid preparations
Nomenclature
Folic acid (pteroylglutamic acid)
Chemistry.
Indications.
Adverse effects.
Warning.
Formulations and routes of administration.
Dosage.
Leucovorin calcium (folinic acid)
Guidelines for treating folic acid deficiency
Choice of treatment modality.
Route of administration.
Prophylactic use of folic acid.
Treatment of severe deficiency.
Key points
Summary of Major Nursing Implications*
Iron preparations
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Routes
Oral.
Parenteral.
Oral administration
Parenteral administration: iron dextran
Intravenous.
Intramuscular.
Parenteral administration: sfgc
Parenteral administration: iron sucrose
Hemodialysis-dependent patients.
Peritoneal dialysis–dependent patients.
Non–dialysis-dependent patients.
Parenteral administration: ferumoxytol
Implementation: measures to enhance therapeutic effects
Ongoing evaluation and interventions
Evaluating therapeutic responses
Minimizing adverse effects
GI disturbances.
Anaphylactic reactions.
Managing acute toxicity.
Cyanocobalamin (vitamin B12)
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Routes and administration
Implementation: measures to enhance therapeutic effects
Promoting adherence
Improving diet
Ongoing evaluation and interventions
Evaluating therapeutic effects
Minimizing adverse effects
Minimizing adverse interactions
Folic acid (folacin, folate, pteroylglutamic acid)
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: dosage and administration
Routes
Oral, subq, IV, and IM.
Dosage
Prevention of neural tube defects.
Treatment of folate-deficient megaloblastic anemia.
Implementation: measures to enhance therapeutic effects
Improving diet
Ongoing evaluation and interventions
Evaluating therapeutic effects
CHAPTER 56 Hematopoietic agents
Hematopoietic growth factors
Erythropoietic growth factors
TABLE 56–1 ▪ Nomenclature for Hematopoietic Growth Factors
Epoetin alfa (erythropoietin)
Physiology
Therapeutic uses
Anemia of chronic renal failure.
Chemotherapy-induced anemia.
HIV-infected patients taking zidovudine.
Anemia in patients facing surgery.
Pharmacokinetics
Adverse effects and interactions
Hypertension.
Cardiovascular events.
Autoimmune pure red-cell aplasia.
Warnings
Excessive dosage.
Cancer patients.
Renal failure patients.
Preoperative patients.
Risk evaluation and mitigation strategy
All patients.
Cancer patients.
Monitoring
Preparations, dosage, and administration
Preparations.
General dosing guidelines.
Dosing in patients with chronic renal failure.
Route.
Dosage.
Dosing in patients receiving cancer chemotherapy.
Once-weekly dosing.
Thrice-weekly dosing.
Dosing in HIV-infected patients taking zidovudine.
Dosing in anemic patients scheduled for surgery.
Darbepoetin alfa (erythropoietin, long acting)
Actions and therapeutic use
Adverse effects and warnings
Monitoring
Preparations, dosage, administration, and monitoring
Preparations and storage.
General dosing guidelines.
Dosing in patients with chronic renal failure.
Dosing in patients undergoing cancer chemotherapy.
Methoxy polyethylene glycol–epoetin beta (erythropoietin, very long acting)
Description and therapeutic use
Adverse effects and warnings
Monitoring
Preparations, dosage, administration, and monitoring
Preparations and storage.
Administration.
Dosage.
Patients not currently using an esa.
Patients already stabilized on epoetin alfa or darbepoetin alfa.
Leukopoietic growth factors
Filgrastim (granulocyte colony-stimulating factor)
Physiology
Therapeutic uses
Cancer.
Patients undergoing myelosuppressive chemotherapy.
Patients undergoing bone marrow transplantation.
Harvesting of hematopoietic stem cells.
Severe chronic neutropenia.
Investigational uses.
Pharmacokinetics
Adverse effects and interactions
Bone pain.
Leukocytosis.
Other adverse effects.
Preparations, dosage, and administration
Preparations and storage.
Dosage and administration.
General considerations.
Cancer chemotherapy.
Bone marrow transplant.
Harvesting of hematopoietic stem cells.
Severe chronic neutropenia.
Pegfilgrastim (granulocyte colony-stimulating factor, long acting)
Preparations, dosage, and administration.
Sargramostim (granulocyte-macrophage colony-stimulating factor)
Physiology
Therapeutic uses
Adjunct to autologous bone marrow transplantation.
Treatment of failed bone marrow transplants.
Patients with acute myelogenous leukemia (aml).
Investigational uses.
Pharmacokinetics
Adverse effects and interactions
Leukocytosis and thrombocytosis.
Preparations, dosage, and administration
Preparations.
Dilution.
Storage.
Dosage and administration.
Thrombopoietic growth factor
Oprelvekin (interleukin-11)
Actions
Therapeutic use
Pharmacokinetics
Adverse effects
Fluid retention.
Cardiac dysrhythmias.
Severe allergic reactions.
Effects on the eye.
Sudden death.
Preparations, dosage, and administration
Preparation.
Dosage and administration.
Drugs that mimic hematopoietic growth factors or enhance their actions
Thrombopoietin receptor agonists
Romiplostim
Therapeutic use: idiopathic thrombocytopenic purpura.
Mechanism of action.
Pharmacokinetics.
Adverse effects.
Preparations, dosage, and administration.
Eltrombopag
Actions and therapeutic use.
Pharmacokinetics.
Adverse effects.
Drug interactions.
Preparations, dosage, and administration.
Plerixafor
Key points
Summary of Major Nursing Implications*
Epoetin alfa (erythropoietin)
Preadministration assessment
Therapeutic goal
Baseline data
All patients.
HIV-infected patients.
Identifying high-risk patients
Implementation: administration
Routes
Handling and storage
Administration
Chronic renal failure.
Chemotherapy-induced anemia.
Zidovudine-induced anemia.
Surgery patients.
Ongoing evaluation and interventions
Monitoring summary
Minimizing adverse effects
Hypertension.
Cardiovascular events.
Cancer patients: tumor progression and shortened survival.
Autoimmune pure red-cell aplasia.
Patient education.
Filgrastim (granulocyte colony-stimulating factor)
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Routes
Handling and storage
Administration
Cancer chemotherapy.
Bone marrow transplantation.
Chronic severe neutropenia.
Ongoing evaluation and interventions
Evaluating therapeutic effects
Minimizing adverse effects
Bone pain.
Leukocytosis.
Sargramostim (granulocyte-macrophage colony-stimulating factor)
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Route
Handling and storage
Administration
Ongoing evaluation and interventions
Minimizing adverse effects
Leukocytosis and thrombocytosis.
Oprelvekin (interleukin-11)
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Route
Handling and storage
Administration
Ongoing evaluation and interventions
Monitoring summary
Minimizing adverse effects
Fluid retention.
Cardiac dysrhythmias.
VIII Drugs for Endocrine Disorders
Interactive Review – VIII: Drugs for Endocrine Disorders
CHAPTER 57 Drugs for diabetes mellitus
Diabetes mellitus: basic considerations
TABLE 57–1 ▪ Characteristics of Type 1 and Type 2 Diabetes Mellitus
Types of diabetes mellitus
Type 1 diabetes
Type 2 diabetes
Short-term complications of diabetes
Long-term complications of diabetes
Macrovascular damage
Microvascular damage
Retinopathy.
Nephropathy.
Sensory and motor neuropathy.
TABLE 57–2 ▪ Criteria for the Diagnosis of Diabetes Mellitus
Autonomic neuropathy: gastroparesis.
Amputations secondary to infection.
Erectile dysfunction.
Diabetes and pregnancy
Diagnosis
TABLE 57–3 ▪ General Treatment Targets for Patients with Diabetes*
Tests based on blood levels of glucose
Fasting plasma glucose test.
Casual plasma glucose test.
Oral glucose tolerance test.
Test based on blood levels of hemoglobin A1C
Prediabetes
Overview of treatment
Type 1 diabetes
Dietary measures.
Exercise.
Insulin replacement.
Managing hypertension and dyslipidemia.
Type 2 diabetes
Tight glycemic control
Type 1 diabetes
Benefits.
Drawbacks.
Type 2 diabetes
Monitoring treatment
TABLE 57–4 ▪ Hemoglobin A1c Levels and Their Corresponding eAG Levels*
Self-monitoring of blood glucose
Monitoring of hemoglobin A1C
Insulin
Physiology
Structure
Biosynthesis
Figure 57–1 ▪ Conversion of proinsulin to insulin. Proinsulin is the immediate precursor of the insulin secreted by our pancreas. Enzymes clip off connecting peptide (C-peptide) to release active insulin, composed of two peptide chains (A and B) connected by two disulfide (S–S) bonds. Since C-peptide arises only from endogenous insulin, its presence in blood indicates that at least some pancreatic insulin is being made.
TABLE 57–5 ▪ Metabolic Actions of Insulin
Secretion
Metabolic actions
TABLE 57–6 ▪ Amino Acids Substitutions in Human Insulin Analogs*
Metabolic consequences of insulin deficiency
Preparations and administration
Sources of insulin
Types of insulin
Short duration: rapid acting
Figure 57–2 ▪ Time-effect relationship for different types of insulin following subcutaneous injection.
TABLE 57–7 ▪ Types of Insulin: Time Course of Action After Subcutaneous Injection
Insulin lispro.
Insulin aspart.
TABLE 57–8 ▪ Properties of Insulin Types
Insulin glulisine.
Short duration: slower acting
Regular insulin injection.
Intermediate duration
Neutral protamine hagedorn (NPH) insulin suspension.
Insulin detemir.
Long duration
Insulin glargine.
Appearance
Concentration
Mixing insulins
TABLE 57–9 ▪ Premixed Insulin Combinations
Administration
Subcutaneous injection
Preparing for injection.
Injection sites.
Injection devices.
Syringe and needle.
Pen injectors.
Jet injectors.
Subcutaneous infusion
Portable insulin pumps.
Implantable insulin pumps.
Intravenous infusion
Inhalation
Storage
Therapeutic use
Indications
TABLE 57–10 ▪ Insulin Therapy of Diabetes Mellitus: Conventional Versus Intensive Conventional Therapy
Insulin therapy of diabetes
Dosage
Dosing schedules
Conventional therapy.
Intensive conventional therapy (ICT).
Continuous subcutaneous insulin infusion.
Achieving tight glucose control
Complications of insulin treatment
Hypoglycemia
Other complications
Hypokalemia.
Lipohypertrophy.
Allergic reactions.
Drug interactions
Hypoglycemic agents.
Hyperglycemic agents.
Beta-adrenergic blocking agents.
Drugs for type 2 diabetes
TABLE 57–11 ▪ Drugs for Type 2 Diabetes
Oral drugs
Biguanides: metformin
Mechanism of action.
Pharmacokinetics.
Therapeutic uses.
Glycemic control.
Prevention of type 2 diabetes.
Gestational diabetes.
Polycystic ovary syndrome (pcos).
Side effects.
Toxicity: lactic acidosis.
Drug interactions.
Alcohol.
Cimetidine.
Iodinated radiocontrast media.
Preparations, dosage, and administration.
Sulfonylureas
Mechanism of action.
Therapeutic use.
TABLE 57–12 ▪ Sulfonylureas: Time Course and Dosage
Adverse effects.
Hypoglycemia.
Cardiovascular toxicity.
Use in pregnancy and lactation.
Drug interactions.
Alcohol.
Drugs that can intensify hypoglycemia.
Beta-adrenergic blocking agents.
Preparations, dosage, and administration.
Thiazolidinediones (glitazones)
Pioglitazone
Actions and use.
Pharmacokinetics.
Adverse effects.
Drug interactions.
Preparations, dosage, and administration.
Rosiglitazone
Meglitinides (glinides)
Repaglinide
Actions and uses.
Pharmacokinetics.
Adverse effects.
Drug interactions.
Preparations, dosage, and administration.
Nateglinide
Basic pharmacology and therapeutic use.
Preparations, dosage, and administration.
Alpha-glucosidase inhibitors
Acarbose
Mechanism of action.
Therapeutic use.
Pharmacokinetics.
Adverse effects and interactions.
Preparations, dosage, and administration.
Miglitol
Gliptins (DPP-4 inhibitors)
Sitagliptin
Mechanism of action.
Therapeutic use.
Pharmacokinetics.
Adverse effects and interactions.
Preparations, dosage, and administration.
Saxagliptin
Actions and therapeutic use.
Pharmacokinetics.
Adverse effects.
Preparations, dosage, and administration.
Linagliptin
Actions and therapeutic use.
Pharmacokinetics.
Adverse effects.
Drug interactions.
Preparations, dosage, and administration.
Colesevelam
Bromocriptine
Dapagliflozin
Combination products
Metformin/glyburide [glucovance]
Metformin/glipizide [metaglip]
Metformin/pioglitazone [actoplus met, actoplus met xr]
Metformin/repaglinide [prandimet]
Metformin/saxagliptin [kombiglyze xr]
Metformin/sitagliptin [janumet]
Pioglitazone/glimepiride [duetact]
Rosiglitazone/glimepiride [avandaryl]
Rosiglitazone/metformin [avandamet]
Sitagliptin/simvastatin [juvisync]
Injected drugs (other than insulin)
Exenatide
Description and actions.
Therapeutic use.
Pharmacokinetics.
Adverse effects.
Drug interactions.
Preparations, dosage, and administration.
Liraglutide
Actions and uses.
Pharmacokinetics.
Adverse effects.
TABLE 57–13 ▪ Contrasts Between Diabetic Ketoacidosis and Hyperglycemic Hyperosmolar Nonketotic Syndrome
Drug interactions.
Preparations, dosage, and administration.
Pramlintide
Description and actions.
Therapeutic use.
Pharmacokinetics.
Adverse effects.
Drug interactions.
Preparations, dosage, and administration.
Acute complications of poor glycemic control
Figure 57–3 ▪ Pathogenesis of diabetic ketoacidosis. The syndrome of diabetic ketoacidosis (DKA) is caused by severe derangements of glucose metabolism and fat metabolism that occur in response to lack of insulin (see text for details). (FFA = free fatty acids.)
Diabetic ketoacidosis
Pathogenesis
Altered fat metabolism.
Altered glucose metabolism.
Treatment
Insulin replacement.
Bicarbonate for acidosis.
Water and sodium replacement.
Potassium replacement.
Normalization of glucose levels.
Hyperglycemic hyperosmolar nonketotic syndrome
Glucagon for insulin overdose
Key points
Type 1 Diabetes (read text)
Type 2 Diabetes (read text)
Insulin Function (read text)
Summary of Major Nursing Implications*
Insulin
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Routes
Preparing for subcutaneous injection
Sites of injection
Insulin storage
Dosage adjustment
Patient and family education
Ongoing evaluation and interventions
Measures to evaluate and enhance therapeutic effects
Minimizing adverse effects
Hypoglycemia.
Lipohypertrophy.
Allergic reactions.
Minimizing adverse interactions
Hypoglycemic agents.
Hyperglycemic agents.
Beta blockers.
Metformin
Preadministration assessment
Therapeutic goal
Identifying high-risk patients
Implementation: administration
Route
Administration
Ongoing evaluation and interventions
Minimizing adverse effects
Lactic acidosis.
Gastrointestinal effects.
Vitamin deficiency.
Minimizing adverse interactions
Alcohol.
Sulfonylureas
First-generation agents (rarely used)
Second-generation agents
Preadministration assessment
Therapeutic goal
Identifying high-risk patients
Implementation: administration
Route
Administration
Ongoing evaluation and interventions
Minimizing adverse effects
Hypoglycemia.
Minimizing adverse interactions
Alcohol.
Use in pregnancy and lactation
Pregnancy.
Lactation.
Pioglitazone
Preadministration assessment
Therapeutic goal
Identifying high-risk patients
Baseline data
Implementation: administration
Route
Administration
Ongoing evaluation and interventions
Minimizing adverse effects
Heart failure.
Liver injury.
Bladder cancer.
Fractures.
Hypoglycemia.
Ovulation.
Minimizing adverse interactions
Insulin.
Inhibitors and inducers of cyp2c8.
Glinides (meglitinides)
Preadministration assessment
Therapeutic goal
Identifying high-risk patients
Implementation: administration
Route
Administration
Ongoing evaluation and interventions
Minimizing adverse effects
Hypoglycemia.
Minimizing adverse interactions
Gemfibrozil.
CHAPTER 58 Drugs for thyroid disorders
Thyroid physiology
Chemistry and nomenclature
Synthesis and fate of thyroid hormones
Synthesis.
Fate.
Figure 58–1 ▪ Structural formulas of the thyroid hormones.
Figure 58–2 ▪ Steps in thyroid hormone synthesis. The reactions at each step (circled numbers) are explained in the text. (DIT = diiodotyrosine, MIT = monoiodotyrosine, T3 = triiodothyronine, T4 = thyroxine, Tyr = tyrosine.)
Thyroid hormone actions
Regulation of thyroid function by the hypothalamus and anterior pituitary
TABLE 58–1 ▪ Serum Values for Thyroid Function Tests
Figure 58–3 ▪ Regulation of thyroid function. TRH from the hypothalamus stimulates release of TSH from the pituitary. TSH stimulates all aspects of thyroid function, including release of T3 and T4. T3 and T4 act on the pituitary to suppress further TSH release. (T3 = triiodothyronine, T4 = thyroxine, TRH = thyrotropin-releasing hormone, TSH = thyrotropin [thyroid-stimulating hormone].)
Effect of iodine deficiency on thyroid function
Thyroid function tests
Serum TSH.
Serum T4 test.
Serum T3 test.
Thyroid pathophysiology
Hypothyroidism
Hypothyroidism in adults
Clinical presentation.
Causes.
Therapeutic strategy.
Hypothyroidism during pregnancy
Hypothyroidism in infants
Clinical presentation.
Causes.
Therapeutic strategy.
Hyperthyroidism
Graves’ disease
Clinical presentation.
Cause.
Treatment.
TABLE 58–2 ▪ Thyroid Hormone Preparations
Toxic nodular goiter (Plummer’s disease)
Thyrotoxic crisis (thyroid storm)
Thyroid hormone preparations for hypothyroidism
Levothyroxine (t4)
Pharmacokinetics
Absorption.
Conversion to t3.
Half-life and plasma levels.
Therapeutic uses
Adverse effects
Drug interactions
Drugs that reduce levothyroxine absorption.
Drugs that accelerate levothyroxine metabolism.
Warfarin.
Catecholamines.
Other interactions.
Are levothyroxine preparations interchangeable?
Dosage and administration I: general considerations
Routes of administration.
Evaluation.
TABLE 58–3 ▪ Pharmacokinetics of Methimazole and Propylthiouracil
Duration of therapy.
Dosage and administration II: specific applications
Hypothyroidism in adults.
Myxedema coma.
Cretinism.
Simple goiter.
Liothyronine (t3)
Contrasts with levothyroxine.
Evaluation.
Dosage and administration.
Other thyroid preparations
Liotrix
Thyroid (desiccated)
Drugs for hyperthyroidism
Antithyroid drugs: thionamides
Methimazole
Mechanism of action.
Pharmacokinetics.
Therapeutic uses
Adverse effects.
Agranulocytosis.
Hypothyroidism.
Effects in pregnancy.
Effects in lactation.
Preparations, dosage, and administration.
Propylthiouracil
Contrasts with methimazole.
Current role in treating hyperthyroidism.
Pharmacokinetics.
Adverse effects.
Adverse effects shared with methimazole.
Liver injury.
Preparations, dosage, and administration.
Treatment of Graves’ disease.
Radioactive iodine (131i)
Physical properties
Use in Graves’ disease
Effect on the thyroid.
Advantages and disadvantages of 131i therapy.
Who should be treated and who should not.
Dosage.
Use in thyroid cancer
Diagnostic use
Preparations
Nonradioactive iodine: lugol’s solution
Description.
Mechanism of action.
Therapeutic use.
Adverse effects.
Overdose.
Dosage and administration.
Beta blockers
Key points
Thyroid Release (read text)
Summary of Major Nursing Implications*
Levothyroxine (t4)
Preadministration assessment
Therapeutic goal
Baseline data
Implementation: administration
Routes
Administration
Oral.
Intravenous.
Ongoing evaluation and interventions
Evaluating therapeutic effects
Adults.
Infants.
Minimizing adverse effects
Thyrotoxicosis.
Atrial fibrillation and bone loss.
Minimizing adverse interactions
Drugs that reduce levothyroxine absorption.
Drugs that accelerate levothyroxine metabolism.
Warfarin.
Catecholamines.
Liothyronine (t3)
Evaluating therapeutic effects
Methimazole
Preadministration assessment
Therapeutic goals
Baseline data
Identifying high-risk patients
Implementation: administration
Route
Administration
Ongoing evaluation and interventions
Summary of monitoring
Minimizing adverse effects
Agranulocytosis.
Hypothyroidism.
Effects in pregnancy.
Effects in lactation.
Radioactive iodine (131i)
Use in Graves’ disease
Therapeutic goal.
Identifying high-risk patients.
Dosage and administration.
Promoting therapeutic effects.
Minimizing adverse effects.
Use in thyroid cancer
Diagnostic use
Strong iodine solution (lugol’s solution)
Preadministration assessment
Therapeutic goal
Baseline data
Implementation: administration
Route
Administration
Ongoing evaluation and interventions
Minimizing adverse effects
Mild toxicity.
Severe toxicity.
CHAPTER 59 Drugs related to hypothalamic and pituitary function
Overview of hypothalamic and pituitary endocrinology
Anatomic considerations
Hormones of the anterior pituitary
Hormones of the posterior pituitary
Hypothalamic release-regulating factors
Figure 59–1 ▪ Hormones and releasing factors of the hypothalamus and pituitary. Hypothalamic releasing factors: GnRH = gonadotropin-releasing hormone, GH-RH = growth hormone–releasing hormone, PRF = prolactin-releasing factor, CRH = corticotropin-releasing hormone, TRH = thyrotropin-releasing hormone. Anterior pituitary hormones: GH = growth hormone, ACTH = adrenocorticotropic hormone (corticotropin), TSH = thyroid-stimulating hormone, FSH = follicle-stimulating hormone, LH = luteinizing hormone.
Feedback regulation of the hypothalamus and anterior pituitary
Growth hormone
Physiology
Regulation of release
Biologic effects
Promotion of growth.
Figure 59–2 ▪ Negative feedback regulation of the hypothalamus and anterior pituitary. The feedback loop works as follows: Factor X stimulates the pituitary to release hormone A, which stimulates its target organ, causing release of hormone B. Hormone B then acts on the hypothalamus and pituitary to suppress further release of factor X and hormone A, thereby suppressing further release of hormone B itself.
Figure 59–3 ▪ Regulation of growth hormone release.
Promotion of protein synthesis.
Effect on carbohydrate metabolism.
Pathophysiology
Growth hormone deficiency
Pediatric.
Adult.
Growth hormone excess
Consequences.
Treatment overview.
Clinical pharmacology
Therapeutic uses
Pediatric growth hormone deficiency.
Pediatric non–growth-hormone-deficient (nghd) short stature.
Pediatric short stature associated with Prader-Willi syndrome.
Growth hormone deficiency in adults.
Other uses.
Adverse effects and interactions
Hyperglycemia.
Neutralizing antibodies.
Fatality in PWS patients.
Interaction with glucocorticoids.
Preparations, dosage, and administration
Preparations: somatropin.
Administration.
Mecasermin (insulin-like growth factor-1)
TABLE 59–1 ▪ Somatropin (Human Growth Hormone): Preparations, Indications, and Dosages
Prolactin
Regulation of release
Prolactin hypersecretion
Suppressing prolactin release with dopamine agonists
Thyrotropin
Adrenocorticotropic hormone
Gonadotropins
Antidiuretic hormone (vasopressin)
Physiology
Actions.
Production, storage, and release.
Pathophysiology: hypothalamic diabetes insipidus
Antidiuretic hormone preparations
Adverse effects
Water intoxication.
Excessive vasoconstriction.
TABLE 59–2 ▪ ADH Preparations
Therapeutic uses
Diabetes insipidus.
Cardiac arrest.
Other uses.
Antidiuretic hormone (vasopressin) antagonists
Conivaptan
Tolvaptan
Oxytocin
Drugs for acromegaly
Somatostatin analogs.
Pegvisomant, a growth hormone receptor antagonist.
Drugs related to hypothalamic function
Gonadotropin-releasing hormone agonists
Key points
Summary of Major Nursing Implications*
Somatropin (human growth hormone)
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Routes
Administration
Ongoing evaluation and interventions
Evaluating treatment
Minimizing adverse effects and interactions
Hyperglycemia.
Hypothyroidism.
Fatality in PWS patients.
Interaction with glucocorticoids.
Neutralizing antibodies.
Antidiuretic hormone
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Routes
Desmopressin.
Vasopressin.
Administration
Ongoing evaluation and interventions
Evaluating therapeutic effects
Minimizing adverse effects
Water intoxication.
Cardiovascular effects.
CHAPTER 60 Drugs for disorders of the adrenal cortex
Physiology of the adrenocortical hormones
Glucocorticoids
Physiologic effects
Carbohydrate metabolism.
Protein metabolism.
Fat metabolism.
Cardiovascular system.
Figure 60–1 ▪ Structural formulas of representative adrenocortical hormones.
Figure 60–2 ▪ Negative feedback regulation of glucocorticoid synthesis and secretion. (ACTH = adrenocorticotropic hormone, CRH = corticotropin-releasing hormone.)
Skeletal muscle.
Central nervous system.
Stress.
Respiratory system in neonates.
Regulation of synthesis and secretion
Mineralocorticoids
Physiologic effects.
Renal actions.
Cardiovascular actions.
Control of secretion.
Adrenal androgens
Pathophysiology of the adrenocortical hormones
Adrenal hormone excess
Cushing’s syndrome
Causes.
Clinical presentation.
Treatment.
Primary hyperaldosteronism
Clinical presentation, causes, and diagnosis.
Treatment.
Adrenal hormone insufficiency
General therapeutic considerations
Primary adrenocortical insufficiency (Addison’s disease)
Causes.
Clinical presentation.
Treatment.
Secondary and tertiary adrenocortical insufficiency
TABLE 60–1 ▪ Guidelines for Giving Supplemental Doses of Glucocorticoids at Times of Stress Related to Medical Conditions and Surgical Procedures
Acute adrenal insufficiency (adrenal crisis)
Clinical presentation.
Causes.
Treatment.
Congenital adrenal hyperplasia
Clinical presentation and causes.
Treatment.
Screening.
Agents for replacement therapy in adrenocortical insufficiency
Hydrocortisone
Therapeutic uses
Replacement therapy.
Nonendocrine applications.
Adverse effects
Preparations, dosage, and administration
Oral therapy.
Parenteral therapy.
Dexamethasone, prednisone, and cortisone
Fludrocortisone
Therapeutic uses.
Adverse effects.
Preparations, dosage, and administration.
Agents for diagnosing adrenocortical disorders
Cosyntropin
Dexamethasone
Overnight dexamethasone suppression test
Prolonged dexamethasone suppression test
Key points
Summary of Major Nursing Implications*
Glucocorticoids: hydrocortisone and cortisone
Use in addison’s disease
Administration.
Emergency preparedness.
Monitoring.
Use in congenital adrenal hyperplasia
Minimizing adverse effects
Fludrocortisone (a mineralocorticoid)
Route
Minimizing adverse effects
IX Women’s Health
Interactive Review – IX: Women’s Health
CHAPTER 61 Estrogens and progestins: basic pharmacology and noncontraceptive applications
The menstrual cycle
Ovarian and uterine events.
The roles of estrogens and progesterone.
The role of pituitary hormones.
Figure 61–1 ▪ The menstrual cycle: anatomic and hormonal changes. (FSH = follicle-stimulating hormone, LH = luteinizing hormone.)
Estrogens
Biosynthesis and elimination
Females.
Males.
Mechanism of action
Physiologic and pharmacologic effects
Effects on primary and secondary sex characteristics of females
Metabolic actions
Bone.
Cholesterol.
Blood coagulation.
Clinical pharmacology
Adverse effects
Endometrial hyperplasia and carcinoma.
Breast cancer.
Ovarian cancer.
Cardiovascular events.
Nausea.
Adverse effects from use during pregnancy.
Other adverse effects.
Therapeutic uses
Menopausal hormone therapy.
Female hypogonadism.
Acne.
Routes of administration
Oral.
Transdermal.
Intravaginal.
Parenteral.
Selective estrogen receptor modulators (SERMs)
Progestins
Biosynthesis
Mechanism of action
Physiologic and pharmacologic effects
Effects during the menstrual cycle.
Effects during pregnancy.
Other effects.
Clinical pharmacology
Adverse effects
Teratogenic effects.
Gynecologic effects.
Breast cancer.
Other adverse effects.
Therapeutic uses
Menopausal hormone therapy.
Dysfunctional uterine bleeding.
Amenorrhea.
Infertility.
Prematurity prevention.
Endometrial carcinoma and hyperplasia.
BOX 61–1 ▪ SPECIAL INTEREST TOPIC
PREMENSTRUAL SYNDROME (PMS)
Common Symptoms of PMS
Etiology
Diagnosis
Treatment guidelines
Selective serotonin reuptake inhibitors
Ovulation suppressants
Other remedies
Preparations and routes
Menopausal hormone therapy
Landmark studies: WHI and HERS
TABLE 61–1 ▪ Results of the Women’s Health Initiative: Impact of Hormone Therapy on the Incidence of Major Adverse Clinical Events
Benefits and risks of hormone therapy
Benefits of hormone therapy
Relief of vasomotor symptoms.
Management of urogenital atrophy.
Prevention of osteoporosis and related fractures.
TABLE 61–2 ▪ Benefits and Risks of Menopausal Hormone Therapy
Cardioprotection.
Improved quality of life?
Prevention of colorectal cancer?
Other benefits.
Adverse effects of hormone therapy
Cardiovascular events.
Endometrial cancer.
Breast cancer.
Ovarian cancer.
Lung cancer.
Gallbladder disease.
Dementia.
Urinary incontinence.
Minor adverse effects.
Warnings
Recommendations on hormone therapy use
General recommendations
Use for approved indications
TABLE 61–3 ▪ Intravaginal Estrogens for Menopausal Hormone Therapy*
Treatment of vasomotor symptoms.
Treatment of symptoms of vulvar and vaginal atrophy.
Prevention of osteoporosis.
Inappropriate uses: attempted prevention of heart disease and dementia
Heart disease.
TABLE 61–4 ▪ Oral Drugs for Menopausal Hormone Therapy
Alzheimer’s disease.
Safety in younger women who don’t have a uterus
Discontinuing hormone therapy
TABLE 61–5 ▪ Transdermal Drugs for Menopausal Hormone Therapy
Open questions
Drug products for hormone therapy
Preparations
Dosing schedules
Key points
Summary of Major Nursing Implications*
Estrogens
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Routes
Administration
Transdermal patch.
Transdermal emulsion.
Transdermal gel.
Transdermal spray.
Intravaginal cream.
Intravaginal ring.
Intravaginal tablet.
Dosing schedules for hormone therapy
Ongoing evaluation and interventions
Monitoring summary
Minimizing adverse effects
Nausea.
Endometrial hyperplasia and cancer.
Breast cancer.
Ovarian cancer.
Lung cancer.
Cardiovascular events.
Effects resembling those caused by oral contraceptives.
Minimizing adverse interactions
Progestins
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Routes
Administration
Ongoing evaluation and interventions
Minimizing adverse effects
Gynecologic effects.
Teratogenic effects.
CHAPTER 62 Birth control
Effectiveness of birth control methods
Figure 62–1 ▪ Percentage use for birth control methods, United States, 2006–2008. Note: The segment labeled “other methods” refers to Nexplanon, contraceptive patches, contraceptive ring, spermicides, cervical caps, female condoms, and other techniques.
TABLE 62–1 ▪ Effectiveness of Birth Control Methods
Selecting a birth control method
TABLE 62–2 ▪ Progestins Used in Combination Oral Contraceptives
Oral contraceptives
Combination oral contraceptives
Mechanism of action
Components
Estrogens.
Progestins.
Effectiveness
TABLE 62–3 ▪ Absolute and Relative Contraindications to the Use of Combination OCs
Overall safety
Adverse effects
Thromboembolic disorders.
Cancer.
Hypertension.
Abnormal uterine bleeding.
Use in pregnancy and lactation.
Stroke in women with migraine.
Benign hepatic adenoma.
Effects related to estrogen or progestin imbalance.
TABLE 62–4 ▪ Side Effects Caused by an Excess or Deficiency in the Estrogen or Progestin Content of an Oral Contraceptive Regimen
Hyperkalemia.
Glucose intolerance.
Other adverse effects.
Noncontraceptive benefits of OCs
Drug interactions
Drugs and herbs that reduce the effects of OCs.
Drugs whose effects are reduced by OCs.
Drugs whose effects are increased by OCs.
Preparations
Beyaz and safyral.
Natazia.
TABLE 62–5 ▪ Composition of Combination Oral Contraceptives
Dosing schedules
28-day-cycle schedules.
Extended-cycle and continuous schedules.
What to do in the event of missed doses
Progestin-only oral contraceptives
Combination contraceptives with novel delivery systems
Transdermal contraceptive patch
Vaginal contraceptive ring
Long-acting contraceptives
Subdermal etonogestrel implant
Description.
Mechanism of action.
Pharmacokinetics.
Drug interactions.
Adverse effect: irregular bleeding.
Use during breast-feeding.
Depot medroxyprogesterone acetate
Intrauterine devices
Spermicides
BOX 62–1 ▪ SPECIAL INTEREST TOPIC
EMERGENCY CONTRACEPTION
Progestin-only ecps
Plan b one-step
Plan b and next choice
Ulipristal acetate ecp
Estrogen/progestin ecps (yuzpe regimen)
EMERGENCY CONTRACEPTIVE PILLS*
Mifepristone as an ecp
The copper IUD
TABLE 62–6 ▪ Spermicides
Barrier devices
Condoms for men.
Condom for women.
Diaphragm.
Cervical cap.
Drugs for medical abortion
Mifepristone (ru 486) with misoprostol
Mechanism of action.
Clinical trials.
Adverse effects.
Contraindications.
Preparations, dosage, and administration.
Fda-approved protocol for abortion.
Day 1.
Day 3.
Day 14.
Methotrexate with misoprostol
Prostaglandins: misoprostol, carboprost, and dinoprostone
Nomenclature
Physiologic and pharmacologic effects
Uterine stimulation.
Cervical softening.
Therapeutic uses
Abortion.
Control of postpartum hemorrhage.
Induction of labor.
Cervical ripening.
Adverse effects
Precautions and contraindications
Preparations, dosage, and administration
Dinoprostone.
Carboprost tromethamine.
Misoprostol.
Key points
Summary of Major Nursing Implications*
Combination oral contraceptives
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Dosing schedule
Responding to missed doses
Postpartum use
Promoting adherence
Ongoing evaluation and interventions
Minimizing adverse effects
Thrombotic disorders.
Hypertension.
Abnormal uterine bleeding.
Use in pregnancy and lactation
Glucose intolerance.
Stroke in women with migraine.
Hyperkalemia.
Minimizing adverse interactions
Agents that reduce oc levels.
Drugs whose effects are reduced by OCs.
Drugs whose effects are increased by OCs.
Drugs that elevate potassium.
Progestin-only oral contraceptives
Preadministration assessment
Therapeutic goal
Implementation: administration
Dosing schedule
Responding to missed doses
Ongoing evaluation and interventions
Minimizing adverse effects
Menstrual irregularities.
CHAPTER 63 Drug therapy of infertility
Infertility: causes and treatment strategies
Female infertility
Anovulation and failure of follicular maturation
Unfavorable cervical mucus
Hyperprolactinemia
Endometriosis
Polycystic ovary syndrome
Male infertility
Hypogonadotropic hypogonadism
Erectile dysfunction
Idiopathic male infertility
Drugs used to treat female infertility
Drugs for controlled ovarian stimulation
Clomiphene
Therapeutic use.
Mechanism of fertility promotion.
TABLE 63–1 ▪ Drugs for Controlled Ovarian Stimulation
Monitoring.
Adverse effects.
Preparations, dosage, and administration.
Menotropins
Therapeutic actions and uses.
Anovulatory women.
Ovulatory women.
Men.
Adverse effects.
Monitoring therapy.
Preparations, dosage, and administration.
Follitropins
Description.
Use in women.
Use in men.
Lutropin alfa
Human chorionic gonadotropin
Therapeutic use.
Adverse effects.
Preparations, dosage, and administration.
Choriogonadotropin alfa
Gonadotropin-releasing hormone antagonists
Dopamine agonists for hyperprolactinemia
Cabergoline
Therapeutic use.
Mechanism of fertility promotion.
Pharmacokinetics.
Adverse effects.
Preparations, dosage, and administration.
Bromocriptine
Actions and therapeutic uses.
Adverse effects.
Preparations, dosage, and administration.
Drugs for endometriosis
Gnrh agonists
Leuprolide.
Therapeutic uses.
Mechanism of action.
Adverse effects.
Preparations, dosage, and administration.
Nafarelin.
Danazol
Therapeutic use.
Mechanism of action.
Adverse effects and interactions.
Preparations, dosage, and administration.
Key points
Summary of Major Nursing Implications*
Clomiphene
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Route
Administration schedule
Implementation: measures to enhance therapeutic effects
Timing of coitus
Adjunctive use of hCG
Ongoing evaluation and interventions
Evaluating therapeutic effects
Minimizing adverse effects
Ovarian enlargement.
Reduced fertility.
Multiple births.
Visual disturbances.
Other adverse effects.
Menotropins
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Route
Administration
Implementation: measures to enhance therapeutic effects
Timing of coitus
Ongoing evaluation and interventions
Minimizing adverse effects
Ovarian hyperstimulation syndrome.
Other adverse effects.
Human chorionic gonadotropin
Preadministration assessment
Therapeutic goal
Implementation: administration
Route
Administration
Ongoing evaluation and interventions
Minimizing adverse effects
Ovarian hyperstimulation syndrome.
Cabergoline
Preadministration assessment
Therapeutic goal
Identifying high-risk patients
Implementation: administration
Route
Administration
Ongoing evaluation and interventions
Minimizing adverse effects
Nausea, headache, and dizziness.
CHAPTER 64 Drugs that affect uterine function
Drugs for preterm labor
Drugs used to suppress preterm labor
Control of myometrial contraction and mechanisms of tocolytic drug action
TABLE 64–1 ▪ Applications of Selected Tocolytic and Oxytocic Drugs
Specific tocolytic drugs
Terbutaline, a beta2-adrenergic agonist
Nifedipine, a calcium channel blocker
Figure 64–1 ▪ Control of myometrial contraction and the actions of tocolytic drugs. The figure shows five pathways that regulate availability of myosin LC phosphate (myosin LC PO4), the form of myosin needed for contractile interaction with actin. Note that two enzymes—myosin LC kinase and myosin LC phosphatase—play central roles. Four classes of tocolytic drugs (numbers 1, 2, 3, and 4 in the figure) work to reduce the activity of myosin LC kinase, and thereby reduce production of myosin LC phosphate. A fifth class—the nitric oxide donors—increases the activity of myosin LC phosphatase, and thereby stimulates conversion of myosin LC phosphate to its inactive (dephosphorylated) form. Note also the important role played by calcium in controlling the activity of myosin LC kinase.
Indomethacin, a cyclooxygenase inhibitor
TABLE 64–2 ▪ Adverse Effects of Tocolytic Drugs
Nitroglycerin, a nitric oxide donor
Atosiban, an oxytocin receptor antagonist
Magnesium sulfate
Drugs used to prevent preterm labor
Hydroxyprogesterone caproate
Therapeutic use.
Adverse effects and contraindications.
Preparations, dosage, and administration.
Antibiotics
Drugs for cervical ripening and induction of labor
Prostaglandins: dinoprostone and misoprostol
Dinoprostone
Dinoprostone gel.
Dinoprostone vaginal inserts.
Misoprostol
Oxytocin
Physiologic and pharmacologic effects
Uterine stimulation.
Milk ejection.
Water retention.
Pharmacokinetics
Use for induction of labor
Preinduction preparation.
Precautions and contraindications.
Adverse effect: water intoxication.
Dosage and administration.
Additional therapeutic uses
Augmentation of labor.
Postpartum use.
Abortion.
Drugs for postpartum hemorrhage
Oxytocin and misoprostol
Carboprost tromethamine
Therapeutic use
Adverse effects
Precautions and contraindications
Ergot alkaloids: ergonovine and methylergonovine
Pharmacologic effects
Effects on the uterus.
Vascular effects.
Pharmacokinetics
Therapeutic uses
Postpartum use.
Augmentation of labor.
Migraine.
Adverse effects
Contraindications
Preparations, dosage, and administration
Preparations.
Dosage and administration.
Parenteral.
Oral.
Drugs for menorrhagia
Tranexamic acid
Therapeutic uses
Menorrhagia.
Trauma patients.
Hemophilia.
Mechanism of action
Pharmacokinetics
Adverse effects and interactions
Preparations, dosage, and administration
Other drugs for menorrhagia
Nonsteroidal anti-inflammatory drugs.
Combination oral contraceptives.
Levonorgestrel-releasing intrauterine system.
Key points
Summary of Major Nursing Implications
Dinoprostone
Preadministration assessment
Therapeutic goal
Identifying high-risk patients
Implementation: administration
Route
Ongoing evaluation and interventions
Evaluating therapeutic effects
Minimizing adverse effects
GI disturbances.
Fever.
Oxytocin
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Route
Administration
Ongoing evaluation and interventions
Minimizing adverse effects
Ergot alkaloids: ergonovine and methylergonovine
Preadministration assessment
Therapeutic goal
Identifying high-risk patients
Implementation: administration
Routes
Oral and IM.
Intravenous.
Administration
Ongoing evaluation and interventions
Evaluating therapeutic effects
Minimizing adverse effects
X Men’s Health
Interactive Review – X: Men’s Health
CHAPTER 65 Androgens
Testosterone
Biosynthesis and secretion
Males.
Figure 65–1 ▪ Structural formulas of representative androgens.
Females.
Mechanism of action
Physiologic and pharmacologic effects
Effects on sex characteristics in males
Pubertal transformation.
Spermatogenesis.
Effects on sex characteristics in females
Anabolic effects
Erythropoietic effects
Clinical pharmacology of the androgens
Classification
Therapeutic uses
TABLE 65–1 ▪ Approved Uses of Individual Androgens
Male hypogonadism.
Replacement therapy.
Delayed puberty.
Replacement therapy in menopausal women.
Wasting in patients with AIDS.
Anemias.
Adverse effects
Virilization in women, girls, and boys.
Premature epiphyseal closure.
Hepatotoxicity.
TABLE 65–2 ▪ Products for Androgen Replacement Therapy in Hypogonadal Males
Effects on cholesterol levels.
Use in pregnancy.
Prostate cancer.
BOX 65–1 ▪ SPECIAL INTEREST TOPIC
TESTOSTERONE REPLACEMENT: CAN IT ENHANCE SEXUALITY IN MEN? OR WOMEN?
In men
In women
Edema.
Gynecomastia.
Abuse potential.
Androgen preparations for male hypogonadism
Oral androgens
Transdermal testosterone
Patches.
Gels.
Underarm liquid.
Implantable testosterone pellets
Testosterone buccal tablets
Intramuscular testosterone esters
Androgen (anabolic steroid) abuse by athletes
TABLE 65–3 ▪ Impact of Testosterone on Muscle Mass and Strength in Normal Men
Key points
Summary of Major Nursing Implications*
Androgens
Preadministration assessment
Therapeutic goals
Males.
Females.
Males and females.
Identifying high-risk patients
Implementation: administration
Routes
Administration
Oral.
Transdermal gel and underarm liquid.
Buccal.
Implantable pellets.
Ongoing evaluation and interventions
Minimizing adverse effects
Virilization.
Premature epiphyseal closure.
Hepatotoxicity.
Edema.
Teratogenesis.
Prostate cancer.
Injury from skin-to-skin transfer of topical testosterone.
CHAPTER 66 Drugs for erectile dysfunction and benign prostatic hyperplasia
Erectile dysfunction ExemplarErectile dysfunction
Physiology of erection
Oral drugs for ED: PDE5 inhibitors
Sildenafil
TABLE 66–1 ▪ Some Drugs That Can Cause Sexual/Erectile Dysfunction
Mechanism of action
Pharmacokinetics
Sexual benefits
In men with ED.
In men without ED.
In women.
Adverse effects
Hypotension.
Figure 66–1 ▪ Physiology of penile erection.In the flaccid state, there is free outflow of venous blood and restricted inflow of arterial blood. During sexual arousal, cGMP relaxes arterial and trabecular smooth muscle, thereby permitting free inflow of arterial blood and subsequent engorgement of sinusoidal spaces, whose expansion compresses penile veins, thereby restricting blood outflow. The resultant accumulation of blood at elevated pressure increases penile size and rigidity. Removal of cGMP by PDE5 restores penile smooth muscle to the nonaroused state, and hence detumescence ensues. (cGMP = cyclic guanosine monophosphate, GMP = guanosine monophosphate, GTP = guanosine triphosphate, PDE5 = phosphodiesterase type 5.)
Priapism.
Nonarteritic ischemic optic neuropathy (naion).
Sudden hearing loss.
Other adverse effects.
Drug interactions
Nitrates.
Alpha blockers.
Inhibitors of CYP3A4.
Is sildenafil safe for men with CHD?
Preparations, dosage, and administration
Vardenafil and tadalafil
Vardenafil
Actions and use.
Pharmacokinetics.
TABLE 66–2 ▪ Comparison of PDE5 Inhibitors
Adverse effects.
Drug interactions.
Preparations, dosage, and administration.
Tadalafil
Actions and uses.
Pharmacokinetics.
Adverse effects.
Drug interactions.
Preparation and dosage.
PRN dosing.
Daily dosing.
Nonoral drugs for ED
Papaverine plus phentolamine
Therapeutic use.
Mechanism of action.
Adverse effects.
Dosage and administration.
Alprostadil (prostaglandin e1)
Intracavernous.
Transurethral.
Benign prostatic hyperplasia
Pathophysiology and overview of treatment
Pathophysiology
Treatment modalities
Drug therapy of BPH
TABLE 66–3 ▪ Drugs for Benign Prostatic Hypertrophy
5-alpha-reductase inhibitors
Finasteride.
Dutasteride.
Alpha1-adrenergic antagonists
Mechanism of action.
Receptor specificity and impact on blood pressure.
Adverse effects.
Drug interactions.
Use in women.
Dosage and administration.
Alpha1 blocker/5-alpha-reductase inhibitor combination
Tadalafil, a PDE5 inhibitor
Other drugs for BPH
Saw palmetto.
Tolterodine.
Botulinum toxin.
Key points
Summary of Major Nursing Implications*
PDE5 inhibitors
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Route
Administration
Dosing with food.
PRN dosing.
Daily dosing.
Ongoing evaluation and interventions
Minimizing adverse effects
Cardiac risk.
Priapism.
Nonarteritic ischemic optic neuropathy.
Sudden hearing loss.
Minimizing adverse interactions
Nitrates.
Alpha-adrenergic blockers.
Inhibitors of CYP3A4.
Antidysrhythmic drugs.
XI Anti-inflammatory, Antiallergic, and Immunologic Drugs
Interactive Review – XI: Anti-inflammatory, Antiallergic, and Immunologic Drugs
CHAPTER 67 Review of the immune system
Introduction to the immune system
Natural immunity versus specific acquired immunity
Cell-mediated immunity versus antibody-mediated (humoral) immunity
Introduction to cells of the immune system
B lymphocytes (B cells).
Cytolytic T lymphocytes (cytolytic T cells, CD8 cells).
Figure 67–1 ▪ Maturation of blood cells. With the exception of platelets and erythrocytes, all of the mature blood cells shown participate in immune responses. However, only cells of lymphoid origin (cytolytic T cells, helper T cells, B cells) possess receptors that can recognize specific antigens. (CFU = colony-forming unit.) 1Monocytes that have moved into tissues are called macrophages. 2Basophils that have moved into tissues are called mast cells.
Helper T lymphocytes (helper T cells, CD4 cells).
Macrophages.
TABLE 67–1 ▪ Cells of the Immune System
Dendritic cells.
Mast cells and basophils.
Neutrophils.
Eosinophils.
Antibodies
Figure 67–2 ▪ Antibody structure. The basic antibody structure depicting heavy and light chains is shown on the left. Variable regions of the heavy and light chains, which form the antigen-binding site, appear in green. As shown on the right, papain digestion of antibodies produces two types of fragments: Fab fragments, which retain the ability to bind antigen, and Fc fragments, which do not bind antigen and tend to crystallize in the test tube.
TABLE 67–2 ▪ Functions of Antibody Classes
Antigens
Figure 67–3 ▪ Memory and time limitation of immune responses. After the initial exposure to antigen X, antibody levels rise slowly, peak at a low level, and then decline rapidly. After the second exposure to antigen X, antibody levels rise more rapidly, reach a higher peak, persist longer, and then slowly decline.
Characteristic features of immune responses
Specificity.
Diversity.
Memory.
Time limitation.
Selectivity for antigens of nonself origin.
Phases of the immune response
Recognition phase.
Activation phase.
Effector phase.
Major histocompatibility complex molecules
TABLE 67–3 ▪ Functions of Selected Cytokines
Cytokines, lymphokines, and monokines
Antibody-mediated (humoral) immunity
Production of antibodies
Overview of antibody production
Specific cellular events in antibody production
B cells.
Figure 67–4 ▪ Major events in antibody-mediated (humoral) immunity. Humoral immunity requires three types of cells: B cells, APCs, and helper T cells (CD4 cells). Binding of a CD4 cell with an APC activates the CD4 cell, which then binds with a B cell and releases cytokines, which then stimulate the B cell. (Ag = antigen, APC = antigen-presenting cell [macrophage or dendritic cell], Ig = immunoglobulin [antibody], MHC II = class II MHC molecule.)
Antigen-presenting cells.
Helper T cells (CD4 cells).
Antibody effector mechanisms
Opsonization of bacteria
Activation of the complement system
Neutralization of viruses and bacterial toxins
Cell-mediated immunity
Delayed-type hypersensitivity
Activation of helper T cells.
Activation of macrophages.
Figure 67–5 ▪ Cell-mediated immunity: delayed-type hypersensitivity. DTH requires two cells: an infected macrophage and a CD4 cell. Binding of the CD4 cell to the macrophage activates the CD4 cell, which then releases interferon gamma and several cytokines. Interferon gamma activates the macrophage. The cytokines cause the CD4 cell to proliferate and differentiate into memory cells. (Ag = antigen, MHC II = class II MHC molecule.)
Cytolytic T lymphocytes
Activation of cytolytic T cells.
Recognition of virally infected target cells.
Mechanisms of cell kill.
Figure 67–6 ▪ Cell-mediated immunity: cytolytic T cells. This branch of cell-mediated immunity requires three types of cells: CTLs, APCs, and CD4 cells. Binding of the pre-CTL with the APC begins the activation of the CTL. Stimulation of the CTL by cytokines from the CD4 cell completes the activation of the CTL, which then binds with and kills its target. Activation of the CD4 cells, which is not shown, takes place essentially as depicted in Figures 67–4 and 67–5. (Ag = antigen, APC = antigen-presenting cell, CTL = cytolytic T lymphocyte, MHC I = class I MHC molecule.)
Key points
CHAPTER 68 Childhood immunization
General considerations
Definitions
Vaccine.
Killed vaccines versus live vaccines.
Toxoid.
Vaccination.
Immunization: active versus passive.
TABLE 68–1 ▪ Impact of Vaccination on the Incidence of Some Vaccine-Preventable Diseases in the United States
Specific immune globulins.
Public health impact of immunization
Reporting vaccine-preventable diseases
TABLE 68–2 ▪ Contraindications That Apply to All Vaccines and Conditions Often Incorrectly Regarded as Contraindications
Immunization records
Adverse effects of immunization
Vaccine information statements
Childhood immunization schedule
Target diseases
Measles, mumps, and rubella
Measles.
Mumps.
Rubella.
Diphtheria, tetanus, and pertussis
Diphtheria.
Tetanus (lockjaw).
Pertussis (whooping cough).
Poliomyelitis
Haemophilus influenzae type b
Varicella (chickenpox)
Hepatitis B
Hepatitis A
Pneumococcal infection
Meningococcal infection
Influenza
Rotavirus gastroenteritis
Genital human papillomavirus infection
Specific vaccines and toxoids
Measles, mumps, and rubella virus vaccine (MMR)
Description.
Efficacy.
Adverse effects.
Mild.
Severe.
TABLE 68–3 ▪ Some Vaccines and Toxoids Available in the United States
Precautions and contraindications.
Route, site, and immunization schedule.
TABLE 68–4 ▪ Adverse Effects of Some Vaccines and Toxoids
Diphtheria and tetanus toxoids and acellular pertussis vaccine
Preparations.
Efficacy.
Adverse effects.
Mild.
Moderate.
Severe: encephalopathy.
Precautions and contraindications.
TABLE 68–5 ▪ Products for Immunization Against Diphtheria, Tetanus, and Pertussis
Route, site, and immunization schedule.
Poliovirus vaccine
Preparations.
Efficacy.
Adverse effects of ipv.
Adverse effects of opv.
Route, site, and immunization schedule.
Haemophilus influenzae type b conjugate vaccine
Preparations.
Efficacy.
Adverse effects.
Route, site, and immunization schedule.
Varicella virus vaccine
Description.
Efficacy.
Adverse effects.
Precautions and contraindications.
Route, site, and immunization schedule.
We need to vaccinate more children.
Hepatitis B vaccine
Preparations.
Efficacy.
Adverse effects and contraindications.
Route, site, and immunization schedule.
Hepatitis A vaccine
Preparations.
Efficacy.
Who should be vaccinated?
Adverse effects.
Route, site, and immunization schedule.
Pneumococcal conjugate vaccine
Description.
Efficacy.
Adverse effects.
Who should be vaccinated?
Route, site, and immunization schedule.
Children under 2 years of age.
Children between their second and fifth birthdays.
Children who have completed the 4-dose series with pcv7.
Meningococcal conjugate vaccine
Description.
Efficacy.
Adverse effects.
Who should be vaccinated?
How many doses?
Route and site.
Influenza vaccine
Rotavirus vaccine
Preparations and efficacy.
Safety.
Who should be vaccinated?
Who should not be vaccinated?
Preparations, route, and immunization schedule.
Human papillomavirus vaccine
Quadrivalent HPV vaccine: gardasil
Composition.
Indications.
Cancers and precancerous lesions in females.
Genital warts in females and males.
Anal cancer in females and males.
Efficacy.
Is a pap test still needed?
Safety.
Who should be vaccinated?
Females: routine vaccination.
Males: routine vaccination.
Females and males: catch-up vaccination.
Who should not be vaccinated?
Route, site, and immunization schedule.
Bivalent HPV vaccine: cervarix
Composition and indications.
Efficacy.
Duration of protection.
Safety.
Who should be vaccinated? and how?
Who should not be vaccinated?
Figure 68–1 ▪ Recommended Immunization Schedule for Children from Birth Through 6 Years—United States, 2011. This schedule indicates the recommended ages for routine administration of currently licensed vaccines, as of December 21, 2010, for children from birth through age 6 years. These recommendations are approved by the Advisory Committee on Immunization Practices (ACIP) of the Centers for Disease Control and Prevention, the American Academy of Pediatrics (AAP), and the American Academy of Family Physicians (AAFP). Gold-colored bars indicate recommended ages for each dose; a bar that spans more than one age bracket indicates an acceptable range of ages for that dose. Any dose not administered at the recommended age should be administered at any subsequent visit, when indicated and feasible. Licensed combination vaccines may be used whenever any components of the combination are both indicated and approved by the FDA for that dose of the series, provided other components of the combination are not contraindicated. Purple bars indicate certain high-risk groups.
Figure 68–2 ▪ Recommended Immunization Schedule for Children 7 Through 18 Years of Age—United States, 2011. This schedule indicates the recommended ages for routine administration of currently licensed vaccines, as of December 21, 2010, for children from 7 through 18 years of age. These recommendations are approved by the Advisory Committee on Immunization Practices (ACIP) of the Centers for Disease Control and Prevention, the American Academy of Pediatrics (AAP), and the American Academy of Family Physicians (AAFP). Gold-colored bars indicate recommended ages for each dose; a bar that spans more than one age bracket indicates an acceptable range of ages for that dose. Any dose not administered at the recommended age should be administered at any subsequent visit, when indicated and feasible. Licensed combination vaccines may be used whenever any components of the combination are both indicated and approved by the FDA for that dose of the series, provided other components of the combination are not contraindicated. Purple bars indicate certain high-risk groups. Green bars indicate times for catch-up immunization.
Key points
Vaccination (read text)
CHAPTER 69 Immunosuppressants
Figure 69–1 ▪ Sites of action of immunosuppressant drugs.
Calcineurin inhibitors
Cyclosporine
Mechanism of action
Therapeutic uses
Pharmacokinetics
Adverse effects
Nephrotoxicity.
Infection.
Hepatotoxicity.
Lymphomas.
Other common adverse effects.
Anaphylactic reactions.
Use in pregnancy and lactation.
Drug and food interactions
Drugs that can decrease cyclosporine levels.
Drugs that can increase cyclosporine levels.
Nephrotoxic drugs.
Grapefruit juice.
Repaglinide.
Preparations, dosage, and administration
Preparations.
Dosage and monitoring for allograft recipients.
Sandimmune.
Neoral and gengraf.
Monitoring.
Dosage for rheumatoid arthritis.
Dosage for psoriasis.
Tacrolimus
Therapeutic use.
Mechanism of action.
Pharmacokinetics.
Adverse effects.
Drug and food interactions.
Preparations, dosage, and administration.
Mtor inhibitors
Sirolimus
Actions and therapeutic use.
Pharmacokinetics.
Adverse effects.
Use in pregnancy and lactation.
Drug and food interactions.
Monitoring.
Preparations, dosage, and administration.
Everolimus
Therapeutic use.
Mechanism of action.
Pharmacokinetics.
Adverse effects.
Effects in pregnancy and lactation.
Drug and food interactions.
Preparations, dosage, and administration.
Glucocorticoids
Cytotoxic drugs
Azathioprine
Mechanism of action.
Therapeutic uses.
Adverse effects and drug interactions.
Preparations, dosage, and administration.
Cyclophosphamide
Methotrexate
Mitoxantrone
Mycophenolate mofetil
Therapeutic use.
Mechanism of action.
Pharmacokinetics.
Adverse effects.
Drug interactions.
Use in pregnancy.
Preparations, dosage, and administration.
Antibodies
Muromonab-cd3
Actions and uses.
Adverse effects.
Preparations, dosage, and administration.
Basiliximab
Actions and uses.
Adverse effects.
Preparations, dosage, and administration.
Lymphocyte immune globulin, antithymocyte globulin (equine)
Basic pharmacology.
Preparations, dosage, and administration.
Key points
Summary of Major Nursing Implications*
Cyclosporine
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Routes
Preparations
Patient education for oral administration
Intravenous dosage and administration
Dosage adjustment
Ongoing evaluation and interventions
Evaluating therapeutic effects
Minimizing adverse effects
Nephrotoxicity.
Infection.
Hepatotoxicity.
Hirsutism.
Use in pregnancy and lactation.
Anaphylactic reactions.
Minimizing adverse interactions
Drugs that can decrease cyclosporine levels.
Drugs that can increase cyclosporine levels.
Nephrotoxic drugs.
Grapefruit juice.
Repaglinide.
CHAPTER 70 Antihistamines
Histamine
Distribution, synthesis, storage, and release
Distribution.
Synthesis and storage.
Release.
Allergic release.
Nonallergic release.
Physiologic and pharmacologic effects
Effects of H1 stimulation
Vasodilation.
Increased capillary permeability.
Bronchoconstriction.
Figure 70–1 ▪ Release of histamine by allergen-antibody interaction. (IgE = immunoglobulin E.)
CNS effects.
Other effects.
Effects of H2 stimulation
Role of histamine in allergic responses
Mild allergy.
Severe allergic reactions (anaphylaxis).
The two types of antihistamines: h1 antagonists and h2 antagonists
H1 antagonists i: basic pharmacology
Classification of h1 antagonists
Mechanism of action
Pharmacologic effects
Peripheral effects.
Effects on the CNS.
Other pharmacologic effects.
Therapeutic uses
Mild allergy.
Severe allergy.
Motion sickness.
Insomnia.
Common cold.
Adverse effects
Sedation.
TABLE 70–1 ▪ Pharmacologic Effects of H1 Antagonists Used for Parenteral Therapy
Nonsedative CNS effects.
Gastrointestinal effects.
Anticholinergic effects.
Severe respiratory depression.
Severe local tissue injury.
Cardiac dysrhythmias.
TABLE 70–2 ▪ Some H1 Antagonists Used for Systemic Therapy: Trade Names, Routes, and Dosage
Drug interactions: CNS depressants
Use in pregnancy and lactation
Pregnancy.
Lactation.
Acute toxicity
Symptoms.
Treatment.
H1 antagonists ii: preparations
First-generation h1 antagonists
Second-generation (nonsedating) h1 antagonists
Fexofenadine.
Cetirizine.
Levocetirizine.
Loratadine.
Desloratadine.
Key points
Summary of Major Nursing Implications*
H1 receptor antagonists
First-generation antihistamines
Second-generation antihistamines
Preadministration assessment
Therapeutic goal
Oral therapy.
Parenteral therapy.
Identifying high-risk patients
Implementation: administration
Routes
Administration
Ongoing evaluation and interventions
Minimizing adverse effects
Sedation.
Anticholinergic effects.
Gastrointestinal distress.
Effects in the elderly.
Severe respiratory depression.
Severe tissue injury.
Minimizing adverse interactions
CNS depressants.
Fruit juice.
Managing toxicity
CHAPTER 71 Cyclooxygenase inhibitors: nonsteroidal anti-inflammatory drugs and acetaminophen
Mechanism of action
TABLE 71–1 ▪ Cyclooxygenase-1 and Cyclooxygenase-2: Functions and Effect of Inhibition
Classification of cyclooxygenase inhibitors
First-generation NSAIDs
Aspirin
Chemistry
TABLE 71–2 ▪ Principal Indications and Adverse Effects of the Four Major Types of Cyclooxygenase Inhibitors
Figure 71–1 ▪ Structural formulas of aspirin and related salicylates.
Mechanism of action
Pharmacokinetics
Absorption.
Metabolism.
Distribution.
Excretion.
Plasma drug levels.
Therapeutic uses
Suppression of inflammation.
Analgesia.
Reduction of fever.
Dysmenorrhea.
Suppression of platelet aggregation.
TABLE 71–3 ▪ Risk Level at Which CVD Events Prevented Exceed GI Harms
Cancer prevention.
Colorectal cancer.
Other cancers.
Adverse effects
Gastrointestinal effects.
Bleeding.
Renal impairment.
Salicylism.
Reye’s syndrome.
Adverse effects associated with use during pregnancy.
Hypersensitivity reactions.
Cardiovascular events.
Erectile dysfunction.
Summary of precautions and contraindications
Drug interactions
Anticoagulants: warfarin, heparin, and others.
Glucocorticoids.
Alcohol.
Nonaspirin NSAIDs.
ACE inhibitors and ARBs.
Vaccines.
Acute poisoning
Signs and symptoms.
Treatment.
Formulations
Aspirin tablets, plain.
Aspirin tablets, buffered.
TABLE 71–4 ▪ Aspirin Dosage
Buffered aspirin solution.
Enteric-coated preparations.
Timed-release tablets.
Rectal suppositories.
Dosage and administration
Nonaspirin first-generation NSAIDs
TABLE 71–5 ▪ Clinical Pharmacology of the Oral Nonsteroidal Anti-inflammatory Drugs
Nonacetylated salicylates: magnesium salicylate, sodium salicylate, and salsalate
Similarities to aspirin.
Contrasts with aspirin.
Preparations, dosage, and administration.
Ibuprofen
Basic pharmacology.
Oral preparations and dosages.
Intravenous preparations and dosages.
Fenoprofen
Flurbiprofen
Ketoprofen
Naproxen
Actions and uses.
Adverse effects.
Preparations, dosage, and administration.
Naproxen/esomeprazole [vimovo]
Oxaprozin
Diclofenac
Oral.
Topical.
Diclofenac/misoprostol [arthrotec]
Diflunisal
Etodolac
Indomethacin
Actions and uses.
Pharmacokinetics.
Adverse effects.
Precautions and contraindications.
Preparations, dosage, and administration.
Ketorolac
Actions and uses.
Pharmacokinetics.
Adverse effects and contraindications.
Preparations, dosage, and administration.
Parenteral and oral therapy.
Intranasal therapy.
Meclofenamate
Mefenamic acid
Nabumetone
Piroxicam
Sulindac
Tolmetin
Meloxicam
Second-generation NSAIDs (COX-2 inhibitors, coxibs)
Celecoxib
Therapeutic use
Mechanism of action
Pharmacokinetics
Adverse effects
Gastroduodenal ulceration.
Cardiovascular events.
Renal impairment.
Sulfonamide allergy.
Use in pregnancy.
Drug interactions
Warfarin.
Other interactions.
Preparations, dosage, and administration
Rofecoxib and valdecoxib
Figure 71–2 ▪ Metabolism of acetaminophen.
Acetaminophen
Mechanism of action
Pharmacokinetics
Adverse effects
Drug and vaccine interactions
Alcohol.
Warfarin.
Vaccines.
Therapeutic uses
Acute toxicity: liver damage
Signs and symptoms.
Treatment.
Minimizing risk.
Preparations, dosage, and administration
Preparations.
Dosage and administration.
Oral.
Rectal.
Intravenous.
AHA statement on COX inhibitors in chronic pain
Key points
Summary of Major Nursing Implications*
Nonsteroidal anti-inflammatory drugs
First-generation NSAIDs
Second-generation NSAIDs (coxibs)
Preadministration assessment
Therapeutic goal
Identifying high-risk patients
Implementation: administration
Routes
Oral.
Topical.
Intranasal.
Intramuscular.
Intravenous.
Rectal suppository.
Administration
Ongoing evaluation and interventions
Minimizing adverse effects
Gastrointestinal effects.
Bleeding.
Renal impairment.
Myocardial infarction and stroke.
Hypersensitivity reactions.
Salicylism.
Reye’s syndrome.
Use in pregnancy.
Liver injury.
Sulfonamide allergy.
Erectile dysfunction.
Minimizing adverse interactions
Anticoagulants.
Glucocorticoids.
Alcohol.
Aspirin-nsaid interactions.
ACE inhibitors and ARBs.
Vaccines.
Managing aspirin toxicity
Acetaminophen
Preadministration assessment
Therapeutic goal
Identifying high-risk patients
Implementation: administration
Routes
Administration
Ongoing evaluation and interventions
Minimizing adverse effects
Hypertension.
Asthma.
Anaphylaxis.
Liver damage.
Minimizing adverse interactions
Alcohol.
Warfarin.
Vaccines.
CHAPTER 72 Glucocorticoids in nonendocrine disorders
Review of glucocorticoid physiology
Physiologic effects
Metabolic effects.
Cardiovascular effects.
Effects during stress.
Effects on water and electrolytes.
TABLE 72–1 ▪ Systemic Glucocorticoids: Half-Lives, Relative Potencies, and Equivalent Doses
Respiratory system effects in neonates.
Control of synthesis and secretion
Pharmacology of the glucocorticoids
Molecular mechanism of action
Pharmacologic effects
Effects on metabolism and electrolytes
Figure 72–1 ▪ Feedback regulation of glucocorticoid synthesis and secretion. (ACTH = adrenocorticotropic hormone, CNS = central nervous system, CRH = corticotropin-releasing hormone.)
Anti-inflammatory and immunosuppressant effects
Pharmacokinetics
Absorption.
Duration of action.
Metabolism and excretion.
Therapeutic uses in nonendocrine disorders
Rheumatoid arthritis.
Systemic lupus erythematosus.
Inflammatory bowel disease.
Miscellaneous inflammatory disorders.
Allergic conditions.
Asthma.
Dermatologic disorders.
Neoplasms.
Suppression of allograft rejection.
Prevention of respiratory distress syndrome in preterm infants.
Adverse effects
Adrenal insufficiency.
Osteoporosis.
Development.
Management.
Infection.
Glucose intolerance.
Myopathy.
Fluid and electrolyte disturbance.
Growth retardation.
Psychologic disturbances.
Cataracts and glaucoma.
Peptic ulcer disease.
Iatrogenic cushing’s syndrome.
Use in pregnancy and lactation
Pregnancy.
Lactation.
Drug interactions
Interactions related to potassium loss.
Nonsteroidal anti-inflammatory drugs.
Insulin and oral hypoglycemics.
Vaccines.
Summary of precautions and contraindications
Contraindications.
Precautions.
Adrenal suppression
Development of adrenal suppression.
Adrenal suppression and physiologic stress.
Glucocorticoid withdrawal.
Preparations and routes of administration
Preparations
Routes of administration
Dosage
General guidelines for dosing
Alternate-day therapy
TABLE 72–2 ▪ Glucocorticoid Routes of Administration*
Key points
Corticosteroids (read text)
Summary of Major Nursing Implications*
Glucocorticoids
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration and dosage
Routes and administration
Dosage
Alternate-day therapy
Drug withdrawal
Ongoing evaluation and interventions
Evaluating therapeutic effects
Minimizing adverse effects
General measures.
Adrenal insufficiency.
Osteoporosis.
Infection.
Glucose intolerance.
Fluid and electrolyte disturbance.
Growth retardation.
Cataracts and glaucoma.
Peptic ulcer disease.
Psychologic disturbances.
Use in pregnancy and lactation.
Other adverse effects.
Minimizing adverse interactions
Interactions related to potassium loss.
Nonsteroidal anti-inflammatory drugs.
Insulin and other hypoglycemics.
Vaccines.
XII Drugs for Bone and Joint Disorders
Interactive Review – XII: Drugs for Bone and Joint Disorders
CHAPTER 73 Drug therapy of rheumatoid arthritis
Pathophysiology of rheumatoid arthritis
Overview of therapy
Nondrug measures
Figure 73–1 ▪ Progressive joint degeneration in rheumatoid arthritis. A, Healthy joint. B, Inflammation of synovial membrane. C, Onset of pannus formation and cartilage erosion. D, Pannus formation progresses and cartilage deteriorates further. E, Complete destruction of joint cavity together with fusion of articulating bones.
Drug therapy
Classes of antiarthritic drugs
Drug selection
TABLE 73–1 ▪ Nonsteroidal Anti-inflammatory Drugs: Oral Dosage for Rheumatoid Arthritis
Nonsteroidal anti-inflammatory drugs
Therapeutic role.
NSAID classification.
Drug selection.
Efficacy.
Safety and cost.
Dosage.
Glucocorticoids
Nonbiologic (traditional) DMARDs
Methotrexate
Sulfasalazine
Leflunomide
Actions and uses.
Pharmacokinetics.
Adverse effects.
Leflunomide and pregnancy.
Drug interactions.
Preparations, dosage, and administration.
Hydroxychloroquine
Minocycline
Other nonbiologic DMARDs
Penicillamine.
Gold salts.
Azathioprine.
Cyclosporine.
Protein a column [prosorba].
Biologic DMARDs
Tumor necrosis factor antagonists
TABLE 73–2 ▪ Disease-Modifying Antirheumatic Drugs (DMARDs)
TABLE 73–3 ▪ Approved Indications for TNF Antagonists
Etanercept
Mechanism of action.
Therapeutic uses.
Pharmacokinetics.
Adverse effects.
Mild effects.
Serious infections.
Severe allergic reactions.
Heart failure.
Cancer.
Hematologic disorders.
Liver injury.
Central nervous system (CNS) demyelinating disorders.
Drug interactions.
Preparations, dosage, and administration.
Infliximab
Actions and uses.
Adverse effects.
Preparations, dosage, and administration.
Adalimumab
Golimumab
Certolizumab pegol
Rituximab, a b-lymphocyte–depleting agent
Actions and uses
Adverse effects
Infusion reactions.
Mucocutaneous reactions.
Hepatitis B reactivation.
Progressive multifocal leukoencephalopathy (pml).
Other adverse effects.
Preparations, dosage, and administration
Abatacept, a T-cell activation inhibitor
Therapeutic uses.
Mechanism of action.
Adverse effects.
Drug interactions.
Preparations, dosage, and administration.
Intravenous.
Subcutaneous.
Tocilizumab, an interleukin-6 receptor antagonist
Actions and therapeutic use
Adverse effects
Serious infections.
GI perforation.
Liver injury.
Neutropenia and thrombocytopenia.
Drug interactions
Preparations, dosage, and administration
Anakinra, an interleukin-1 receptor antagonist
Key points
Summary of Major Nursing Implications*
Tumor necrosis factor antagonists
Preadministration assessment
Therapeutic goal
Identifying high-risk patients
Implementation: administration
Routes
Subcutaneous.
Intravenous.
Administration
Adalimumab, certolizumab, etanercept, golimumab.
Infliximab.
Ongoing evaluation and interventions
Minimizing adverse effects
Serious infections.
Allergic reactions.
Heart failure.
Cancer.
Hematologic disorders.
Liver injury.
CNS demyelinating disorders.
Injection-site reactions: adalimumab, certolizumab pegol, etanercept, and golimumab.
Infusion reactions: infliximab.
Minimizing adverse interactions
Immunosuppressants.
Live vaccines.
CHAPTER 74 Drug therapy of gout
Pathophysiology of gout
Overview of drug therapy
Drugs for acute gouty arthritis
Nonsteroidal anti-inflammatory drugs
Glucocorticoids
Colchicine
Therapeutic use
Acute gouty arthritis.
Prophylaxis of gouty attacks.
Mechanism of action
Pharmacokinetics
Adverse effects
Gastrointestinal effects.
Myelosuppression.
Myopathy.
Drug interactions
Statins.
Drugs that can increase colchicine levels.
Precautions and contraindications
Preparations, dosage, and administration
Preparations.
Dosage.
Drugs for hyperuricemia (urate-lowering therapy)
Xanthine oxidase inhibitors: allopurinol and febuxostat
Figure 74–1 ▪ Drugs that lower plasma levels of uric acid. These drugs lower plasma urate by three mechanisms: Allopurinol and febuxostat reduce uric acid formation, pegloticase catalyzes conversion of uric acid to allantoin, and probenecid facilitates uric acid excretion by the kidney.
Allopurinol
Therapeutic uses.
Mechanism of action.
Pharmacokinetics.
Adverse effects.
Drug interactions.
Preparations. dosage, and administration.
Febuxostat
Probenecid, a uricosuric agent
Actions and uses.
Adverse effects.
Drug interactions.
Preparations, dosage, and administration.
Pegloticase, a recombinant form of uric acid oxidase
Therapeutic use.
Mechanism of action.
Adverse effects.
Preparations, dosage, and administration.
Key points
CHAPTER 75 Drugs affecting calcium levels and bone mineralization
Calcium physiology
Functions, sources, and daily requirements
Functions.
Dietary sources.
Daily requirements.
Figure 75–1 ▪ Bone remodeling cycle. A, Quiescent bone with lining cells covering the surface. B, Resorption of old bone by multinucleated osteoclasts. C, Osteoblasts migrate to the absorption site. D, Osteoblasts deposit osteoid, a matrix of collagen and other proteins. E, Osteoid undergoes calcification.
TABLE 75–1 ▪ Daily Calcium Intake by Life-Stage Group
Body stores
Calcium in bone.
Calcium in blood.
Absorption and excretion
Absorption.
Excretion.
Physiologic regulation of calcium levels
TABLE 75–2 ▪ Effects of Parathyroid Hormone, Vitamin D, and Calcitonin on Calcium and Phosphate
Parathyroid hormone.
Vitamin D.
Calcitonin.
Calcium-related pathophysiology
Hypercalcemia
Clinical presentation.
Causes.
Treatment.
Hypocalcemia
Clinical presentation and cause.
Treatment.
Rickets
Osteomalacia
Osteoporosis
Paget’s disease of bone
Clinical presentation.
Treatment.
Hypoparathyroidism
Hyperparathyroidism
Primary hyperparathyroidism.
Secondary hyperparathyroidism.
Drugs for disorders involving calcium
Calcium salts
Oral calcium salts
Therapeutic uses.
TABLE 75–3 ▪ Oral Calcium Salts
Adverse effects.
Drug interactions.
Food interactions.
Preparations and dosage.
Parenteral calcium salts
Therapeutic use.
Adverse effects.
TABLE 75–4 ▪ Parenteral Calcium Salts
Drug interactions.
Dosage and administration.
Vitamin D
Physiologic actions
Health benefits
Sources and daily requirements
Sources.
Requirements.
Vitamin D deficiency
Figure 75–2 ▪ Vitamin D activation. Ergosterol is found in yeasts and fungi. 7-Dehydrocholesterol is present in the skin. Green boxes indicate forms of vitamin D used therapeutically.
Activation of vitamin D
Pharmacokinetics
Viewing vitamin D as a hormone
Toxicity (hypervitaminosis d)
Clinical presentation.
Treatment.
Therapeutic uses
Preparations, dosage, and administration
Ergocalciferol (vitamin D2).
Cholecalciferol (vitamin D3).
Calcifediol (25-hydroxy-d3).
Calcitriol (1,25-dihydroxy-d3).
Doxercalciferol.
Paricalcitol.
Calcitonin-salmon
Actions
Therapeutic uses
Osteoporosis.
Paget’s disease of bone.
Hypercalcemia.
Adverse effects
Preparations, dosage, and administration
Intranasal spray.
Parenteral.
Bisphosphonates
Figure 75–3 ▪ Structure of pyrophosphate and general structure of bisphosphonates.
TABLE 75–5 ▪ Bisphosphonates: Routes and Uses
Alendronate
Pharmacokinetics.
Mechanism of action.
Therapeutic use.
Osteoporosis in postmenopausal women.
Osteoporosis in men.
Glucocorticoid-induced osteoporosis.
Paget’s disease of bone.
Adverse effects.
Esophagitis.
Fracture ExemplarAtypical femoral fractures.
Esophageal cancer.
Musculoskeletal pain.
Ocular problems.
Osteonecrosis of the jaw.
Hyperparathyroidism.
Atrial fibrillation.
Administration.
Preparations and dosage.
Risedronate
Actions and uses.
Pharmacokinetics.
Adverse effects.
Preparations, dosage, and administration.
Ibandronate
Actions and uses.
Pharmacokinetics.
Adverse effects and interactions.
Preparations, dosage, and administration.
Oral.
Intravenous.
Tiludronate
Actions and uses.
Pharmacokinetics.
Adverse effects.
Preparations, dosage, and administration.
Etidronate
Actions, uses, and adverse effects.
Preparations, dosage, and administration.
Zoledronate
Actions and uses.
Adverse effects.
Drug interactions.
Preparations, dosage, and administration.
Pamidronate
Therapeutic use and dosage.
Hypercalcemia of malignancy.
Paget’s disease of bone.
Osteolytic bone metastases.
Adverse effects.
Raloxifene
Mechanism of action
Pharmacokinetics
Therapeutic uses
Postmenopausal osteoporosis.
Breast cancer.
Cardiovascular disease.
Adverse effects and interactions
Venous thromboembolism.
Fetal harm.
Hot flushes.
Comparison with estrogen
Preparations, dosage, and administration
Teriparatide
TABLE 75–6 ▪ Comparison of Estrogen and Raloxifene
Preparations, dosage, and administration.
Denosumab
Therapeutic uses
Clinical trials
Osteoporosis in postmenopausal women.
Prevention of skeletal-related events in patients with bone metastases.
Mechanism of action
Pharmacokinetics
Adverse effects
Hypocalcemia.
Serious infections.
Dermatologic reactions.
Osteonecrosis of the jaw.
Preparations, dosage, and administration
Prolia: dosage and administration.
Xgeva: dosage and administration.
Prolia and xgeva: storage, warming, and inspection.
Cinacalcet
Actions and therapeutic use.
Pharmacokinetics.
Adverse effects.
Drug interactions.
Monitoring.
Preparations, dosage, and administration.
Drugs for hypercalcemia
Furosemide.
Glucocorticoids.
Gallium nitrate.
Bisphosphonates.
Inorganic phosphates.
Edetate disodium.
Osteoporosis
General considerations
Bone mass
Primary prevention: calcium, vitamin D, and lifestyle
Diagnosing osteoporosis and assessing fracture risk
Who should be treated?
Treating osteoporosis in women
Antiresorptive therapy
Estrogen.
Raloxifene.
Bisphosphonates.
Alendronate.
Risedronate, ibandronate, and zoledronate.
Calcitonin-salmon.
Denosumab.
Bone-forming therapy: teriparatide
Treating osteoporosis in men
Key points
Summary of Major Nursing Implications*
Vitamin D
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Routes
Administration
Ongoing evaluation and interventions
Monitoring summary
Minimizing adverse interactions
Digoxin.
Management of toxicity
Oral calcium salts
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Route
Dosage
Administration
Ongoing evaluation and interventions
Minimizing adverse effects
Minimizing adverse interactions
Glucocorticoids.
Tetracyclines.
Thyroid hormone.
Thiazide diuretics.
Parenteral calcium salts
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Route
Administration
Ongoing evaluation and interventions
Evaluating therapeutic effects
Minimizing adverse effects
Hypercalcemia.
Minimizing adverse interactions
Digoxin.
Calcitonin-salmon
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Routes
Intranasal.
Parenteral (IM, subq).
Administration
Intranasal.
Subcutaneous.
Ongoing evaluation and interventions
Evaluating therapeutic effects
Postmenopausal osteoporosis.
Paget’s disease of bone.
Hypercalcemia.
Bisphosphonates used for osteoporosis
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Route
Oral.
Intravenous.
Dosing schedule
Alendronate.
Risedronate.
Ibandronate.
Zoledronate.
Administration
Oral.
Intravenous.
Ongoing evaluation and interventions
Evaluating therapeutic effects
Minimizing adverse effects
Esophagitis.
Atypical femoral fractures.
Esophageal cancer.
Musculoskeletal pain.
Ocular problems.
Osteonecrosis of the jaw.
Renal toxicity.
Minimizing adverse interactions
Interactions with zoledronate.
Raloxifene
Preadministration assessment
Therapeutic goals
Baseline data
Identifying high-risk patients
Implementation: administration
Route
Administration
Ongoing evaluation and interventions
Promoting therapeutic effects
Evaluating therapeutic effects
Minimizing adverse effects
Venous thromboembolism.
Fetal harm.
Estrogen
XIII Respiratory Tract Drugs
Interactive Review – XIII: Respiratory Tract Drugs
CHAPTER 76 Drugs for asthma
Basic considerations
Pathophysiology of asthma
Overview of drugs for asthma
Figure 76–1 ▪ Allergen-induced inflammation and bronchospasm in asthma.
Administering drugs by inhalation
Metered-dose inhalers
Dry-powder inhalers
TABLE 76–1 ▪ Overview of Major Drugs for Asthma
Nebulizers
Anti-inflammatory drugs
Glucocorticoids
Mechanism of antiasthma action
Use in asthma
Inhalation use.
BOX 76–1 ▪ SPECIAL INTEREST TOPIC
CHRONIC OBSTRUCTIVE PULMONARY DISEASE
Diagnosis based on symptoms and spirometry.
Initial monotherapy.
Combination therapy.
Use of oxygen.
Pulmonary rehabilitation.
Reducing exacerbations.
Oral use.
Adverse effects
Inhaled glucocorticoids.
Figure 76–2 ▪ Impact of a spacer device on the distribution of inhaled medication. Note that, when a spacer is used, more medication reaches its site of action in the lungs, and less is deposited in the mouth and throat.
Oral glucocorticoids.
Preparations, dosage, and administration
Inhaled glucocorticoids.
TABLE 76–2 ▪ Inhaled Glucocorticoids: Formulations and Dosages
Glucocorticoids in mdis.
Nebulized budesonide.
Oral glucocorticoids.
Leukotriene modifiers
Zileuton
Zafirlukast
Montelukast
Cromolyn
Effects on the lung.
Pharmacokinetics.
Therapeutic uses.
Chronic asthma.
Exercise-induced bronchospasm.
Allergic rhinitis.
Adverse effects.
Preparations, dosage, and administration.
Omalizumab
Mechanism of action.
Therapeutic use.
Pharmacokinetics.
Adverse effects.
Preparations, dosage, and administration.
Bronchodilators
Beta2-adrenergic agonists
Mechanism of antiasthma action
Classification by route and time course
Use in asthma
Short-acting inhaled beta2 agonists.
Long-acting inhaled beta2 agonists.
TABLE 76–3 ▪ Beta2-Adrenergic Agonists Used in Asthma
Oral beta2 agonists.
Adverse effects
Inhaled preparations: short acting.
Inhaled preparations: long acting.
Oral preparations.
Preparations, dosage, and administration
Inhaled preparations for quick relief.
Inhaled preparations for long-term control.
Oral preparations for long-term control.
Methylxanthines
Theophylline
Mechanism of action
Use in asthma
Pharmacokinetics
Absorption.
Metabolism.
Drug levels.
Toxicity
Symptoms.
Treatment.
Drug interactions
Caffeine.
Drugs that reduce theophylline levels.
Drugs that increase theophylline levels.
Oral formulations
Dosage and administration
Oral.
Intravenous.
Other methylxanthines
Aminophylline
Administration and dosage.
Intravenous.
Oral.
Dyphylline
Anticholinergic drugs
Ipratropium
Actions and use in asthma.
Adverse effects.
Preparations, dosage, and administration.
Tiotropium
Actions and therapeutic use.
Adverse effects.
Preparations, dosage, and administration.
Glucocorticoid/laba combinations
Fluticasone/salmeterol
Budesonide/formoterol
Mometasone/formoterol
Management of asthma
Measuring lung function
Classification of asthma severity
TABLE 76–4 ▪ Classification of Asthma Severity and Recommended Step for Initial Treatment
Treatment goals
Chronic drug therapy
TABLE 76–5 ▪ Drugs for Asthma: Agents for Long-Term Control Versus Quick Relief
TABLE 76–6 ▪ Stepwise Approach to Managing Asthma in Patients Age 12 Years and Older
Drugs for acute severe exacerbations
Drugs for exercise-induced bronchospasm
TABLE 76–7 ▪ Assessment of Asthma Control in Patients Age 12 and Older and Recommended Action for Treatment
Reducing exposure to allergens and triggers
Key points
Summary of Major Nursing Implications*
Glucocorticoids
Inhaled
Oral
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Inhaled glucocorticoids.
Oral glucocorticoids.
Implementation: administration
Routes
Administration
Inhalation.
Oral.
Ongoing evaluation and interventions
Evaluating therapeutic effects
Minimizing adverse effects
Inhaled glucocorticoids.
Oral glucocorticoids.
Beta2-adrenergic agonists
Inhaled, short acting
Inhaled, long acting
Oral
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Routes
Usual.
Occasional.
Administration
Inhalation.
Oral.
Ongoing evaluation and interventions
Evaluating therapeutic effects
Minimizing adverse effects
Inhaled short-acting beta2 agonists.
Inhaled long-acting beta2 agonists.
Oral beta2 agonists.
Cromolyn
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Route
Administration
Administration devices.
Acute prophylaxis.
Long-term prophylaxis.
Ongoing evaluation and interventions
Evaluating therapeutic effects
Minimizing adverse effects and interactions
Theophylline
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Routes
Administration
Oral.
Intravenous.
Ongoing evaluation and interventions
Evaluating therapeutic effects
Minimizing adverse effects
Minimizing adverse interactions
Caffeine.
Drugs that reduce theophylline levels.
Drugs that increase theophylline levels.
Managing toxicity.
CHAPTER 77 Drugs for allergic rhinitis, cough, and colds
Drugs for allergic rhinitis
Intranasal glucocorticoids
Actions and uses.
Adverse effects.
Preparations, dosage, and administration.
TABLE 77–1 ▪ Overview of Drugs for Allergic Rhinitis
TABLE 77–2 ▪ Some Glucocorticoid Nasal Sprays for Allergic Rhinitis
Antihistamines
Oral antihistamines
TABLE 77–3 ▪ Some Antihistamines for Allergic Rhinitis
Intranasal antihistamines
Intranasal cromolyn sodium
Actions and uses.
Preparations, dosage, and administration.
Sympathomimetics (decongestants)
Actions and uses
Adverse effects
Rebound congestion.
TABLE 77–4 ▪ Sympathomimetics Used for Nasal Decongestion
Central nervous system stimulation.
Cardiovascular effects.
Abuse.
TABLE 77–5 ▪ Some Antihistamine/Sympathomimetic Combinations
Hemorrhagic stroke.
Factors in topical administration
General considerations.
Drops.
Sprays.
Summary of contrasts between oral and topical agents
Comparison of phenylephrine, ephedrine, and pseudoephedrine
Antihistamine/sympathomimetic combinations
Ipratropium, an anticholinergic agent
Montelukast, a leukotriene antagonist
Omalizumab
Drugs for cough
Antitussives
Opioid antitussives
Codeine.
Nonopioid antitussives
Dextromethorphan.
Other nonopioid antitussives.
Expectorants and mucolytics
Expectorants.
Mucolytics.
BOX 77–1 ▪ SPECIAL INTEREST TOPIC
ZINC FOR KIDS WITH COLDS?
Cold remedies: combination preparations
Basic considerations
Use in young children
Key points
XIV Gastrointestinal Drugs
Interactive Review – XIV: Gastrointestinal Drugs
CHAPTER 78 Drugs for peptic ulcer disease
Pathogenesis of peptic ulcers
Defensive factors
Mucus.
Bicarbonate.
Figure 78–1 ▪ The relationship of mucosal defenses and aggressive factors to health and peptic ulcer disease. When aggressive factors outweigh mucosal defenses, gastritis and peptic ulcers result. (NSAIDs = nonsteroidal anti-inflammatory drugs.)
Blood flow.
Prostaglandins.
Aggressive factors
Helicobacter pylori.
Nonsteroidal anti-inflammatory drugs.
Gastric acid.
Pepsin.
Smoking.
Summary
Overview of treatment
Drug therapy
Classes of antiulcer drugs
TABLE 78–1 ▪ Classification of Antiulcer Drugs
Drug selection
Helicobacter pylori–associated ulcers.
NSAID-induced ulcers.
Prophylaxis.
Treatment.
Evaluation
A note about the effects of drugs on pepsin
Nondrug therapy
Diet.
Other nondrug measures.
Antibacterial drugs
Tests for helicobacter pylori
Antibiotics employed
Clarithromycin.
Amoxicillin.
Bismuth.
Tetracycline.
Metronidazole.
Tinidazole.
Antibiotic regimens
TABLE 78–2 ▪ First-Line Regimens for Eradicating H. pylori
Histamine2 receptor antagonists
Cimetidine
Mechanism of action
Pharmacokinetics
Figure 78–2 ▪ A model of the regulation of gastric acid secretion showing the actions of antisecretory drugs and antacids. Production of gastric acid is stimulated by three endogenous compounds: (1) acetylcholine (ACh) acting at muscarinic (M) receptors; (2) histamine (Hist) acting at histamine2 (H2) receptors; and (3) gastrin (Gast) acting at gastrin (G) receptors. As indicated, all three compounds act through intracellular messengers—either calcium (Ca++) or cyclic AMP (cAMP)—to increase the activity of H+,K+-ATPase, the enzyme that actually produces gastric acid. Prostaglandins (PG) decrease acid production, perhaps by suppressing production of intracellular cAMP. The actions of histamine2 receptor antagonists (H2RAs), proton pump inhibitors (PPIs), and other drugs are indicated. (P = prostaglandin receptor.)
Therapeutic uses
Gastric and duodenal ulcers.
Gastroesophageal reflux disease (GERD).
Zollinger-Ellison syndrome.
Aspiration pneumonitis.
Heartburn, acid indigestion, and sour stomach.
Adverse effects
Antiandrogenic effects.
CNS effects.
Pneumonia.
Other adverse effects.
Drug interactions
Interactions related to inhibition of drug metabolism.
Antacids.
Preparations, dosage, and administration
Oral.
Parenteral.
Ranitidine
Actions.
Pharmacokinetics.
Adverse effects.
Drug interactions.
Therapeutic uses.
Preparations, dosage, and administration.
Preparations.
Oral dosage.
Parenteral dosage.
Famotidine
Basic and clinical pharmacology.
Preparations, dosage, and administration.
Nizatidine
Basic and clinical pharmacology.
Preparations, dosage, and administration.
Proton pump inhibitors
Omeprazole
Mechanism of action.
Pharmacokinetics.
Therapeutic use.
Adverse effects.
Minor effects.
Pneumonia.
Fractures.
Rebound acid hypersecretion.
Hypomagnesemia.
Clostridium difficile infection.
Gastric cancer.
BOX 78–1 ▪ SPECIAL INTEREST TOPIC
GASTROESOPHAGEAL REFLUX DISEASE
Drug interactions.
Clopidogrel.
Preparations, dosage, and administration.
Esomeprazole
Lansoprazole
Dexlansoprazole
Rabeprazole
Pantoprazole
Other antiulcer drugs
Sucralfate
Mechanism of antiulcer action.
Pharmacokinetics.
Therapeutic uses.
Adverse effects.
Drug interactions.
Preparations, dosage, and administration.
Misoprostol
Therapeutic use.
Mechanism of action.
Adverse effects.
Preparations, dosage, and administration.
Antacids
Beneficial actions
Therapeutic uses
Peptic ulcer disease.
Other uses.
Potency, dosage, and formulations
Potency.
Dosage.
Formulations.
Adverse effects
Constipation and diarrhea.
Sodium loading.
Drug interactions
Antacid families
Representative antacids
Magnesium hydroxide.
Aluminum hydroxide.
Calcium carbonate.
Sodium bicarbonate.
TABLE 78–3 ▪ Composition and Acid-Neutralizing Capacity of Commonly Used Over-the-Counter Antacid Suspensions
TABLE 78–4 ▪ Classification of Antacids
TABLE 78–5 ▪ Representative Antacids: Summary of Distinguishing Properties
Anticholinergics
Pirenzepine.
Combination packs
Helidac.
Pylera.
Prevpac.
Key points
Summary of Major Nursing Implications*
H2 receptor antagonists
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Routes
Cimetidine and ranitidine.
Famotidine.
Nizatidine.
Administration
Oral.
Intramuscular: cimetidine and ranitidine.
Intravenous: cimetidine, famotidine, and ranitidine.
Implementation: measures to enhance therapeutic effects
Ongoing evaluation and interventions
Evaluating therapeutic effects
Ulcer healing.
Helicobacter pylori.
Minimizing adverse effects
Antiandrogenic effects.
CNS effects.
Pneumonia.
Minimizing adverse interactions
Interactions secondary to inhibition of drug metabolism.
Antacids.
Proton pump inhibitors
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Routes
Dexlansoprazole, esomeprazole, omeprazole, and rabeprazole.
Pantoprazole and lansoprazole.
Administration
Oral.
Intravenous.
Implementation: measures to enhance therapeutic effects
Ongoing evaluation and interventions
Evaluating therapeutic effects
Minimizing adverse effects
In general.
Pneumonia.
Fractures.
Rebound acid hypersecretion.
Hypomagnesemia.
Minimizing adverse interactions
Atazanavir, delavirdine, and nelfinavir.
Clopidogrel.
CHAPTER 79 Laxatives
General considerations
Function of the colon
Dietary fiber
Constipation
TABLE 79–1 ▪ Rome II Criteria for Constipation
TABLE 79–2 ▪ Classification of Laxatives by Pharmacologic Category
Indications for laxative use
Precautions and contraindications to laxative use
TABLE 79–3 ▪ Classification of Laxatives by Therapeutic Response
Laxative classification schemes
Basic pharmacology of laxatives
Bulk-forming laxatives
Mechanism of action.
Indications.
Adverse effects.
Preparations, dosage, and administration.
Surfactant laxatives
Actions.
TABLE 79–4 ▪ Representative Laxatives: Trade Names, Dosage Forms, and Dosages
Preparations, dosage, and administration.
Stimulant laxatives
Bisacodyl.
Senna.
Castor oil.
Osmotic laxatives
Laxative salts
Actions and uses.
Preparations.
Adverse effects.
Polyethylene glycol
Lactulose
Other laxatives
Lubiprostone
TABLE 79–5 ▪ Oral Bowel Cleansing Products for Colonoscopy
Mineral oil
Glycerin suppository
Bowel cleansing products for colonoscopy
Polyethylene glycol–electrolyte solutions
Sodium phosphate products
Laxative abuse
Causes.
Consequences.
Treatment.
Key points
Summary of Major Nursing Implications*
Laxatives
Implications that apply to all laxatives
Identifying high-risk patients
Reducing laxative abuse
Implications that apply to specific laxatives
Bulk-forming laxatives: psyllium, methylcellulose, and polycarbophil
Surfactants: docusate salts
Stimulant laxatives
Bisacodyl.
Senna.
Castor oil.
Osmotic laxatives: magnesium salts and sodium salts
CHAPTER 80 Other gastrointestinal drugs
Antiemetics
The emetic response
Figure 80–1 ▪ The emetic response: stimuli, pathways, and receptors. (CTZ = chemoreceptor trigger zone.)
TABLE 80–1 ▪ Antiemetic Drugs: Classes, Trade Names, and Dosages
Antiemetic drugs
Serotonin receptor antagonists
Ondansetron.
TABLE 80–2 ▪ Antiemetic Drugs: Uses and Mechanism of Action
Granisetron.
Dolasetron.
Palonosetron.
Glucocorticoids
Substance p/neurokinin1 antagonists
Aprepitant.
Actions and use.
Pharmacokinetics.
Adverse effects.
Drug interactions.
Preparations, dosage, and administration.
Fosaprepitant.
Casopitant.
Benzodiazepines
Dopamine antagonists
Phenothiazines.
Butyrophenones.
Metoclopramide.
Cannabinoids
Therapeutic uses.
TABLE 80–3 ▪
Adverse effects and drug interactions.
Abuse potential.
Preparations, dosage, and administration.
Dronabinol.
Nabilone.
Chemotherapy-induced nausea and vomiting
Nausea and vomiting of pregnancy
Drugs for motion sickness
Scopolamine
Antihistamines
Antidiarrheal agents
TABLE 80–4 ▪ Opioids Used to Treat Diarrhea
Nonspecific antidiarrheal agents
Opioids
Diphenoxylate.
Loperamide.
Difenoxin.
Paregoric.
Opium tincture.
Other nonspecific antidiarrheals
Bismuth subsalicylate.
Bulk-forming agents.
Anticholinergic antispasmodics.
Management of infectious diarrhea
General considerations.
Traveler’s diarrhea.
Clostridium difficile–associated diarrhea.
Drugs for irritable bowel syndrome
Nonspecific drugs
IBS-specific drugs
Alosetron
Indications.
Mechanism of action and clinical effects.
Pharmacokinetics.
Drug interactions.
Adverse effects and contraindications.
Risk management program.
Preparations, dosage, and administration.
Lubiprostone
Tegaserod
Therapeutic use.
Regulatory history.
Actions.
Pharmacokinetics.
Adverse effects and drug interactions.
Contraindications.
Contrasts with alosetron.
Preparations, dosage, and administration.
TABLE 80–5 ▪ Therapeutic Options for Inflammatory Bowel Disease
Drugs for inflammatory bowel disease
5-aminosalicylates
Sulfasalazine.
Actions.
Therapeutic uses.
Adverse effects.
Preparations, dosage, and administration.
Mesalamine.
Olsalazine.
Balsalazide.
Glucocorticoids
Immunosuppressants
Thiopurines: azathioprine and mercaptopurine.
Cyclosporine.
Methotrexate.
Immunomodulators
Infliximab.
Certolizumab pegol.
Adalimumab.
Natalizumab.
Antibiotics
Metronidazole.
Ciprofloxacin.
Nicotine
Prokinetic agents
Metoclopramide
Actions.
Therapeutic uses.
Adverse effects.
Preparations, dosage, and administration.
Diabetic gastroparesis.
Symptomatic gastroesophageal reflux.
Chemotherapy-induced nausea and vomiting.
Cisapride
Therapeutic use.
Mechanism of action.
Pharmacokinetics.
Adverse effects: cardiac dysrhythmias.
Drug interactions.
TABLE 80–6 ▪ Drugs That Can Increase the Risk of Cisapride-Induced Dysrhythmias
Preparations, dosage, and administration.
Palifermin
Mechanism of action
Indications and clinical benefits
Pharmacokinetics
Adverse effects
Drug interactions
Preparations, dosage, and administration
Pancreatic enzymes
Drugs used to dissolve gallstones
Chenodiol (chenodeoxycholic acid)
Actions.
Therapeutic use.
Adverse effects.
Ursodiol (ursodeoxycholic acid)
Anorectal preparations
Nitroglycerin for anal fissures
Other anorectal preparations
Key points
XV Nutrition
Interactive Review – XV: Nutrition
CHAPTER 81 Vitamins
Basic considerations
Dietary reference intakes
Recommended dietary allowance.
Adequate intake.
Tolerable upper intake level.
Estimated average requirement.
Classification of vitamins
TABLE 81–1 ▪ Where to Find Food and Nutrition Board Updates for Specific Vitamins*
Should we take multivitamin supplements?
Fat-soluble vitamins
Vitamin A (retinol)
Actions.
Sources.
Units.
Requirements.
Pharmacokinetics.
Deficiency.
Toxicity.
Therapeutic uses.
Preparations, dosage, and administration.
Vitamin D
Vitamin E (alpha-tocopherol)
Forms of vitamin E.
Sources.
Requirements.
Deficiency.
Potential benefits.
Potential risks.
TABLE 81–2 ▪ Recommended Vitamin Intakes for Individuals
BOX 81–1 ▪ SPECIAL INTEREST TOPIC
THE INCREASINGLY STRONG CASE AGAINST ANTIOXIDANTS
Vitamin K
Action.
Forms and sources of Vitamin K.
Requirements.
Pharmacokinetics.
Deficiency.
Adverse effects.
Severe hypersensitivity reactions.
Hyperbilirubinemia.
Therapeutic uses and dosage.
Vitamin K deficiency.
Warfarin overdose.
Preparations and routes of administration.
Water-soluble vitamins
Vitamin C (ascorbic acid)
Actions.
Sources.
Requirements.
Deficiency.
Adverse effects.
Therapeutic use.
Preparations and routes of administration.
Niacin (nicotinic acid)
Physiologic actions.
Sources.
Requirements.
Deficiency.
Adverse effects.
Therapeutic uses.
Preparations, dosage, and administration.
Riboflavin (vitamin B2)
Actions.
Sources and requirements.
Toxicity.
Use in riboflavin deficiency.
Use in migraine headache.
Thiamin (vitamin B1)
Actions and requirements.
Sources.
Deficiency.
Adverse effects.
Therapeutic use.
Preparations, dosage, and administration.
Pyridoxine (vitamin B6)
Actions.
Requirements.
Sources.
Deficiency.
Adverse effects.
Drug interactions.
Therapeutic uses.
Preparations, dosage, and administration.
Cyanocobalamin (vitamin B12) and folic acid
Rdas and uls.
Food folate versus synthetic folate.
Folic acid deficiency and fetal development.
Folic acid and cancer risk.
Pantothenic acid
Biotin
Key points
CHAPTER 82 Drugs for weight loss
Assessment of weight-related health risk
Body mass index.
Figure 82–1 ▪ Adult weight classification based on body mass index (BMI).
TABLE 82–1 ▪ Disease Risk Based on BMI and WC
Waist circumference.
Risk status.
Overview of obesity treatment
Who should be treated?
Benefits of treatment
Treatment goal
Treatment modalities
Caloric restriction.
Exercise.
Behavior modification.
TABLE 82–2 ▪ Drugs Approved for Weight Loss in the United States
Drug therapy.
Bariatric surgery.
Weight-loss drugs for long-term use
Orlistat, a lipase inhibitor
Actions and use
Adverse effects
Gastrointestinal effects.
Possible liver damage.
Other adverse effects.
Contraindications.
Drug and nutrient interactions
Reduced absorption of vitamins.
Warfarin.
Levothyroxine.
Preparations, dosage, and administration
Investigational drugs for long-term use
Locaserin
Bupropion/naltrexone [contrave]
Phentermine/topiramate [qnexa]
Leptin
Other investigational long-term drugs
Cetilistat.
Tesofensine.
Exenatide and liraglutide.
Bupropion/zonisamide [empatic].
Pramlintide/metreleptin.
Weight-loss drugs for short-term use: sympathomimetic amines
Nonamphetamines: diethylpropion and phentermine
Amphetamines
Discontinued weight-loss drugs
TABLE 82–3 ▪ Sugar Substitutes
Sibutramine
Rimonabant
Dexfenfluramine and fenfluramine
Calorie-saving foods
Sugar substitutes
Calorie-free sweeteners
Reduced-calorie sweetener: tagatose
Olestra, a fat substitute
Key points
XVI Chemotherapy of Infectious Diseases
Interactive Review – XVI: Chemotherapy of Infectious Diseases
CHAPTER 83 Basic principles of antimicrobial therapy
Selective toxicity
What is selective toxicity?
TABLE 83–1 ▪ Classification of Antimicrobial Drugs by Susceptible Organisms
How is selective toxicity achieved?
Disruption of the bacterial cell wall.
Inhibition of an enzyme unique to bacteria.
Disruption of bacterial protein synthesis.
Classification of antimicrobial drugs
Classification by susceptible organism
Classification by mechanism of action
TABLE 83–2 ▪ Classification of Antimicrobial Drugs by Mechanism of Action
Acquired resistance to antimicrobial drugs
Microbial mechanisms of drug resistance
Reduction of drug concentration at its site of action.
TABLE 83–3 ▪ Drugs for Some Highly Resistant Bacteria
Alteration of drug target molecules.
Antagonist production.
Drug inactivation.
New delhi metallo-beta-lactamase 1 (ndm-1) gene.
Mechanisms by which resistance is acquired
Spontaneous mutation.
Conjugation.
Relationships between antibiotic use and emergence of drug-resistant microbes
How do antibiotics promote resistance?
Which antibiotics promote resistance?
Does the amount of antibiotic use influence the emergence of resistance?
Nosocomial infections.
Suprainfection (superinfection)
Figure 83–1 ▪ Pocket card from the CDC’s Campaign to Prevent Antimicrobial Resistance.
Delaying the emergence of resistance in hospitals
Step 1. vaccinate.
Step 2. get the catheters out.
Step 3. target the pathogen.
Step 4. access the experts.
Step 5. practice antimicrobial control.
Step 6. use local data.
Step 7. treat infection, not contamination.
Step 8. treat infection, not colonization.
BOX 83–1 ▪ SPECIAL INTEREST TOPIC
ANTIBIOTICS IN ANIMAL FEED: DYING FOR A BIG MAC AND CHICKEN McNUGGETS
Step 9. know when to say “no” to vanco.
Step 10. stop treatment when infection is cured or unlikely.
Step 11. isolate the pathogen.
Step 12. break the chain of contagion.
Selection of antibiotics
Empiric therapy prior to completion of laboratory tests
Identifying the infecting organism
Determining drug susceptibility
TABLE 83–4 ▪ Antibacterial Drugs of Choice
Disk diffusion.
Serial dilution.
Gradient diffusion.
Host factors that modify drug choice, route of administration, or dosage
Host defenses
Site of infection
Other host factors
Age.
Pregnancy and lactation.
Previous allergic reaction.
Genetic factors.
Dosage size and duration of treatment
Therapy with antibiotic combinations
Antimicrobial effects of antibiotic combinations
Indications for antibiotic combinations
Initial therapy of severe infection.
Mixed infections.
Preventing resistance.
Decreased toxicity.
Enhanced antibacterial action.
Disadvantages of antibiotic combinations
Prophylactic use of antimicrobial drugs
Surgery.
Bacterial endocarditis.
Neutropenia.
Other indications for antimicrobial prophylaxis.
TABLE 83–5 ▪ Examples of Inappropriate Antibiotic Prescriptions
Misuses of antimicrobial drugs
Attempted treatment of untreatable infection.
Treatment of fever of unknown origin.
Improper dosage.
Treatment in the absence of adequate bacteriologic information.
Omission of surgical drainage.
Monitoring antimicrobial therapy
Key points
CHAPTER 84 Drugs that weaken the bacterial cell wall I: penicillins
Introduction to the penicillins
Mechanism of action
Mechanisms of bacterial resistance
The gram-negative cell envelope
Figure 84–1 ▪ Structural formulas of representative penicillins. The unique structure of individual penicillins is determined by the side chain coupled to the penicillin nucleus at the position labeled R. This side chain influences acid stability, pharmacokinetic properties, penicillinase resistance, and ability to bind specific penicillin-binding proteins.
Figure 84–2 ▪ Inhibition of transpeptidase by penicillins. The bacterial cell wall is composed of long strands of a peptidoglycan polymer. As depicted, transpeptidase enzymes create cross-bridges between the peptidoglycan strands, giving the cell wall added strength. By inhibiting transpeptidases, penicillins prevent cross-bridge synthesis and thereby weaken the cell wall.
Penicillinases (beta-lactamases)
Altered penicillin-binding proteins
Chemistry
Figure 84–3 ▪ The bacterial cell envelope. Note that the gram-negative cell envelope has an outer membrane, whereas the gram-positive envelope does not. The outer membrane of the gram-negative cell envelope prevents certain penicillins from reaching their target molecules.
Figure 84–4 ▪ The effect of beta-lactamase on the penicillin nucleus.
Classification
Properties of individual penicillins
Penicillin G
Antimicrobial spectrum
TABLE 84–1 ▪ Classification of the Penicillins
Therapeutic uses
Pharmacokinetics
Absorption.
Oral.
Intramuscular.
Intravenous.
Distribution.
Metabolism and excretion.
Figure 84–5 ▪ Blood levels of penicillin G following IM injection of three different penicillin G salts.
Side effects and toxicities
Penicillin allergy
General considerations.
Types of allergic reactions.
Development of penicillin allergy.
Skin tests for penicillin allergy.
Management of patients with a history of penicillin allergy.
Drug interactions
Aminoglycosides.
Probenecid.
Bacteriostatic antibiotics.
Preparations, dosage, and administration
Preparations and routes of administration.
Dosage.
Administration.
Penicillin v
Penicillinase-resistant penicillins (antistaphylococcal penicillins)
TABLE 84–2 ▪ Dosages for Penicillins
Nafcillin
Oxacillin and dicloxacillin
Methicillin
Broad-spectrum penicillins (aminopenicillins)
Ampicillin
BOX 84–1 ▪ SPECIAL INTEREST TOPIC
METHICILLIN-RESISTANT STAPHYLOCOCCUS AUREUS
Hospital-associated MRSA
Community-associated MRSA
Amoxicillin
Extended-spectrum penicillins (antipseudomonal penicillins)
Ticarcillin
Piperacillin
Penicillins combined with a beta-lactamase inhibitor
Key points
Summary of Major Nursing Implications*
Penicillins
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Routes
Dosage
Administration
Ongoing evaluation and interventions
Evaluating therapeutic effects
Monitoring kidney function
Minimizing adverse effects
Allergic reactions.
Sodium loading.
Hyperkalemia.
Effects resulting from incorrect injection.
Minimizing adverse interactions
Aminoglycosides.
CHAPTER 85 Drugs that weaken the bacterial cell wall II: cephalosporins, carbapenems, vancomycin, telavancin, aztreonam, teicoplanin, and fosfomycin
Cephalosporins
Chemistry
Mechanism of action
Resistance
Classification and antimicrobial spectra
Figure 85–1 ▪ Structural formulas of representative cephalosporins. The unique structure and pharmacologic properties of individual cephalosporins are determined by additions made to the cephalosporin nucleus at the positions labeled R1 and R2.
TABLE 85–1 ▪ Major Differences Between Cephalosporin Generations
TABLE 85–2 ▪ Pharmacokinetic Properties of the Cephalosporins
First generation.
Second generation.
Third generation.
Fourth generation.
Pharmacokinetics
Absorption.
Distribution.
Elimination.
Adverse effects
Allergic reactions.
Bleeding.
Thrombophlebitis.
Hemolytic anemia.
Other adverse effects.
Drug interactions
Probenecid.
Alcohol.
Drugs that promote bleeding.
Calcium and ceftriaxone.
Therapeutic uses
First-generation cephalosporins.
Second-generation cephalosporins.
Third-generation cephalosporins.
Drug selection
TABLE 85–3 ▪ Cephalosporin Dosages
Antimicrobial spectrum.
Adverse effects.
Pharmacokinetics.
Route of administration.
Duration of action.
Distribution to CSF.
Route of elimination.
Dosage and administration
Routes.
Dosage.
Administration.
Oral.
Intramuscular.
Intravenous.
Carbapenems
Imipenem
Mechanism of action.
Figure 85–2 ▪ Miscellaneous beta-lactam antibiotics.
Antimicrobial spectrum.
Pharmacokinetics.
Adverse effects.
Interaction with valproate.
Therapeutic use.
Preparations, dosage, and administration.
Other carbapenems
Meropenem
Actions and uses.
Pharmacokinetics.
Adverse effect and interactions.
Preparations, dosage, and administration.
Ertapenem
Actions and uses.
Pharmacokinetics.
Adverse effects and interactions.
Preparations, dosage, and administration.
Doripenem
Actions and uses.
Pharmacokinetics.
Adverse effects and interactions.
Preparations, dosage, and administration.
Other inhibitors of cell wall synthesis
Vancomycin
Mechanism of action.
BOX 85–1 ▪ SPECIAL INTEREST TOPIC
Clostridium difficile INFECTION
Recommended Treatments for Clostridium difficile Infection
Antimicrobial spectrum.
Pharmacokinetics.
Therapeutic use.
Adverse effects.
Preparations, dosage, and administration.
Intravenous dosing.
Oral dosing.
Rectal dosing.
Telavancin
Actions and uses.
Pharmacokinetics.
Adverse effects.
Drug interactions.
Preparations, dosage, and administration.
Aztreonam
Chemistry.
Mechanism of action.
Antimicrobial spectrum and therapeutic use.
Pharmacokinetics.
Adverse effects.
Preparations, dosage, and administration.
Parenteral.
Inhalational.
Teicoplanin
Chemistry and actions.
Pharmacokinetics.
Therapeutic use.
Adverse effects.
Dosage and administration.
Fosfomycin
Key points
Summary of Major Nursing Implications*
Cephalosporins
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Routes
Dosage
Administration
Oral.
Intramuscular.
Intravenous.
Ongoing evaluation and interventions
Evaluating therapeutic effects
Minimizing adverse effects
Allergic reactions.
Bleeding.
Thrombophlebitis.
Hemolytic anemia.
Clostridium difficile infection (cdi).
Milk-protein hypersensitivity.
Carnitine deficiency.
Minimizing adverse interactions
Alcohol.
Drugs that promote bleeding.
Calcium and ceftriaxone.
Vancomycin
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high risk patients
Implementation: administration
Routes
Intravenous.
Oral.
Rectal.
Dosage
Intravenous.
Oral.
Rectal.
Administration
Intravenous.
Oral.
Rectal.
Ongoing evaluation and interventions
Evaluating therapeutic effects
Minimizing adverse effects and interactions
Renal failure.
Nephrotoxic drugs.
Red man syndrome.
Thrombophlebitis.
CHAPTER 86 Bacteriostatic inhibitors of protein synthesis: tetracyclines, macrolides, and others
Tetracyclines
Mechanism of action
Microbial resistance
Antimicrobial spectrum
Therapeutic uses
Treatment of infectious diseases.
Treatment of acne.
TABLE 86–1 ▪ Pharmacokinetic Properties of the Tetracyclines
Peptic ulcer disease.
Periodontal disease.
Oral therapy.
Topical therapy.
Rheumatoid arthritis.
Pharmacokinetics
Duration of action.
Absorption.
Distribution.
Elimination.
Adverse effects
Gastrointestinal irritation.
Effects on bones and teeth.
Suprainfection.
Hepatotoxicity.
Renal toxicity.
Photosensitivity.
Other adverse effects.
Drug and food interactions
Dosage and administration
Administration.
Dosage.
Summary of major precautions
TABLE 86–2 ▪ Tetracyclines: Routes of Administration, Dosing Interval, and Dosage
Summary of unique properties of individual tetracyclines
Tetracycline.
Demeclocycline.
Doxycycline.
Minocycline.
Macrolides
Erythromycin
Mechanism of action
Acquired resistance
Antimicrobial spectrum
Therapeutic uses
Pharmacokinetics
Absorption and bioavailability.
Distribution.
Elimination.
Adverse effects
Gastrointestinal effects.
QT prolongation and sudden cardiac death.
Other adverse effects.
Drug interactions
Preparations, dosage, and administration
Preparations.
Oral dosage and administration.
Intravenous dosage and administration.
Clarithromycin
Actions and therapeutic uses.
Pharmacokinetics.
Adverse effects and interactions.
Preparations, dosage, and administration.
Azithromycin
Actions and therapeutic uses.
Pharmacokinetics.
Adverse effects and interactions.
Preparations, dosage, and administration.
Oral, immediate release.
Oral, extended release.
Intravenous.
Other bacteriostatic inhibitors of protein synthesis
Clindamycin
Mechanism of action
Antimicrobial spectrum
Therapeutic use
Pharmacokinetics
Absorption and distribution.
Elimination.
Adverse effects
Clostridium difficile–associated diarrhea.
Other adverse effects.
Preparations, dosage, and administration
Preparations.
Oral dosage and administration.
Parenteral dosage and administration.
Intravaginal administration.
Linezolid
Mechanism, resistance, and antimicrobial spectrum
Therapeutic use
Pharmacokinetics
Adverse effects
Drug interactions
Preparations, dosage, and administration
Telithromycin
Therapeutic use.
Mechanism of action.
Pharmacokinetics.
Adverse effects.
Drug interactions.
Preparations, dosage, and administration.
Dalfopristin/quinupristin
Mechanism of action.
Therapeutic use.
Adverse effects.
Drug interactions.
Preparations, dosage, and administration.
Chloramphenicol
Mechanism of action
Antimicrobial spectrum
Resistance
Pharmacokinetics
Therapeutic use
Adverse effects
Gray syndrome.
Reversible bone marrow suppression.
Aplastic anemia.
Other adverse effects.
Drug interactions
Preparations, dosage, and administration
Tigecycline
Mechanism of action and resistance.
Antimicrobial spectrum.
Therapeutic use.
Pharmacokinetics.
Adverse effects.
Drug interactions.
Preparations, dosage, and administration.
Retapamulin and mupirocin
Retapamulin
Mupirocin
Key points
Summary of Major Nursing Implications*
Tetracyclines
Preadministration assessment
Therapeutic goal
Identifying high-risk patients
Implementation: administration
Routes
Systemic.
Topical.
Administration
Oral.
Parenteral.
Ongoing evaluation and interventions
Minimizing adverse effects
Gastrointestinal irritation.
Effects on teeth.
Suprainfection.
Hepatotoxicity.
Renal toxicity.
Photosensitivity.
Erythromycin
Preadministration assessment
Therapeutic goal
Identifying high-risk patients
Implementation: administration
Routes
Oral.
Intravenous.
Administration
Oral.
Intravenous.
Ongoing evaluation and interventions
Minimizing adverse effects
Gastrointestinal effects.
QT prolongation and sudden cardiac death.
Minimizing adverse interactions
Clindamycin
Preadministration assessment
Therapeutic goal
Implementation: administration
Routes
Administration
Ongoing evaluation and interventions
Minimizing adverse effects
Clostridium difficile–associated diarrhea.
CHAPTER 87 Aminoglycosides: bactericidal inhibitors of protein synthesis
Basic pharmacology of the aminoglycosides
Chemistry
Mechanism of action
Microbial resistance
Antimicrobial spectrum
Therapeutic use
Parenteral therapy.
Figure 87–1 ▪ Structural formulas of the major aminoglycosides.
Oral therapy.
Topical therapy.
Pharmacokinetics
Absorption.
Distribution.
Elimination.
Interpatient variation.
Figure 87–2 ▪ Mechanism of action of aminoglycosides. A, Protein synthesis begins with binding of the 50S and 30S ribosomal subunits to messenger RNA (mRNA), followed by attachment of the first amino acid of the new protein to the 50S subunit. As the ribosome moves down the mRNA strand, additional amino acids are added to the growing peptide chain. When the new protein is complete, it separates from the ribosome, and then the ribosomal subunits separate from the mRNA. B, Aminoglycosides bind to the 30S ribosomal subunit and can thereby (1) block initiation, (2) terminate synthesis before the new protein is complete, and (3) cause misreading of the genetic code, which causes synthesis of faulty proteins.
Adverse effects
Ototoxicity.
TABLE 87–1 ▪ Dosages and Pharmacokinetics of Systemic Aminoglycosides
Nephrotoxicity.
Neuromuscular blockade.
Other adverse effects.
Beneficial drug interactions
Penicillins.
Cephalosporins and vancomycin.
Adverse drug interactions
Ototoxic drugs.
Nephrotoxic drugs.
Skeletal muscle relaxants.
Dosing schedules
Figure 87–3 ▪ Plasma gentamicin levels produced with once-daily doses versus divided doses. The curves depict plasma levels of gentamicin produced with (1) a single large dose administered once a day versus (2) the same daily total given as three smaller doses spaced 8 hours apart. Plasma levels with both regimens are high enough to produce good bactericidal effects. The shaded area indicates levels that are low enough to permit washout of the drug from vulnerable cells in the inner ear. Note that, with once-daily dosing, levels are in the washout range for over 12 hours, versus a total of only 6 hours when divided doses are used. As a result, ototoxicity and nephrotoxicity are lower with the once-a-day schedule.
Monitoring serum drug levels
Properties of individual aminoglycosides
Gentamicin
Therapeutic use
Adverse effects and interactions
Preparations, dosage, and administration
Treatment of gram-negative infections.
Intravenous and intramuscular.
Intrathecal.
Treatment of gram-positive infections.
Tobramycin
Uses, adverse effects, and interactions.
Preparations, dosage, and administration.
Intravenous and intramuscular.
Nebulization.
Amikacin
Uses, adverse effects, and interactions.
Preparations, dosage, and administration.
Other aminoglycosides
Neomycin
Kanamycin
Streptomycin
Paromomycin
Key points
Summary of Major Nursing Implications*
Aminoglycosides
Preadministration assessment
Therapeutic goal
Parenteral therapy.
Oral therapy.
Topical therapy.
Identifying high-risk patients
Implementation: administration
Routes
Intramuscular and intravenous.
Oral.
Topical.
Dosing schedule
Administration
Ongoing evaluation and interventions
Monitoring summary
Minimizing adverse effects
Ototoxicity.
Nephrotoxicity.
Neuromuscular blockade.
Minimizing adverse interactions
Penicillins.
Ototoxic and nephrotoxic drugs.
Skeletal muscle relaxants.
CHAPTER 88 Sulfonamides and trimethoprim
Sulfonamides
Basic pharmacology
Chemistry
Mechanism of action
Microbial resistance
Antimicrobial spectrum
Therapeutic uses
Urinary tract infections.
Figure 88–1 ▪ Structural relationships among sulfonamides, PABA, and folic acid.
Figure 88–2 ▪ Sites of action of sulfonamides and trimethoprim. Sulfonamides and trimethoprim inhibit sequential steps in the synthesis of tetrahydrofolic acid (FAH4). In the absence of FAH4, bacteria are unable to synthesize DNA, RNA, and proteins.
Other uses.
Pharmacokinetics
Absorption.
Distribution.
Metabolism.
Excretion.
Adverse effects
Hypersensitivity reactions.
Hematologic effects.
Kernicterus.
Renal damage from crystalluria.
Drug interactions
Metabolism-related interactions.
Cross-hypersensitivity.
Sulfonamide preparations
Systemic sulfonamides
Sulfamethoxazole.
Sulfisoxazole.
Sulfadiazine.
Topical sulfonamides
Sulfacetamide.
Silver sulfadiazine and mafenide.
Trimethoprim
Mechanism of action
Microbial resistance
Antimicrobial spectrum
Therapeutic uses
Pharmacokinetics
Adverse effects and interactions
Hematologic effects.
Hyperkalemia.
Effects in pregnancy and lactation.
Preparations, dosage, and administration
Trimethoprim/sulfamethoxazole
Mechanism of action
Microbial resistance
Antimicrobial spectrum
Therapeutic uses
Urinary tract infection ExemplarUrinary tract infection.
Pneumocystis pneumonia (PCP).
Gastrointestinal infections.
Other infections.
Pharmacokinetics
Absorption and distribution.
Plasma drug levels.
Elimination.
Adverse effects
Drug interactions
Preparations, dosage, and administration
Preparations.
Oral dosing.
Intravenous dosing.
Key points
Summary of Major Nursing Implications*
Sulfonamides (systemic)
Preadministration assessment
Therapeutic goal
Identifying high-risk patients
Implementation: administration
Routes
Administration
Ongoing evaluation and interventions
Minimizing adverse effects
Hypersensitivity reactions.
Photosensitivity.
Hematologic effects.
Kernicterus.
Renal damage.
Minimizing adverse interactions
Metabolism-related interactions.
Cross-hypersensitivity.
Trimethoprim
Preadministration assessment
Therapeutic goal
Identifying high-risk patients
Implementation: administration
Route
Dosage and administration
Ongoing evaluation and interventions
Minimizing adverse effects and interactions
Hematologic effects.
Hyperkalemia.
Use in pregnancy and lactation.
Trimethoprim/sulfamethoxazole
Preadministration assessment
Therapeutic goal
Identifying high-risk patients
Implementation: administration
Routes
Dosage adjustment
Administration
Ongoing evaluation and interventions
Minimizing adverse effects
Minimizing adverse interactions
CHAPTER 89 Drug therapy of urinary tract infections
Organisms that cause urinary tract infections
Specific urinary tract infections and their treatment
Acute cystitis
TABLE 89–1 ▪ Regimens for Oral Therapy of Urinary Tract Infections in Nonpregnant Women
Acute uncomplicated pyelonephritis
Complicated urinary tract infections
Recurrent urinary tract infection
Reinfection.
Relapse.
Acute bacterial prostatitis
Urinary tract antiseptics
Nitrofurantoin
Mechanism of action
Antimicrobial spectrum
Therapeutic use
Pharmacokinetics
Absorption and distribution.
Metabolism and excretion.
Adverse effects
Gastrointestinal effects.
Pulmonary reactions.
Hematologic effects.
Peripheral neuropathy.
Hepatotoxicity.
Birth defects.
CNS effects.
Preparations, dosage, and administration
Preparations.
Administration.
Dosage.
Methenamine
Mechanism of action
Antimicrobial spectrum
Therapeutic uses
Pharmacokinetics
Absorption and distribution.
Excretion.
Adverse effects and precautions
Drug interactions
Urinary alkalinizers.
Sulfonamides.
Preparations, dosage, and administration
Key points
CHAPTER 90 Antimycobacterial agents: drugs for tuberculosis, leprosy, and mycobacterium avium complex infection
Drugs for tuberculosis
Clinical considerations
Pathogenesis
Primary infection
Reactivation
Diagnosis and treatment of active tuberculosis
Diagnosis
Drug resistance
The prime directive: always treat tuberculosis with two or more drugs
TABLE 90–1 ▪ Representative Antituberculosis Regimens
Determining drug sensitivity
Treatment regimens
Drug-sensitive tuberculosis.
Isoniazid- or rifampin-resistant tuberculosis.
Multidrug-resistant TB and extensively drug-resistant TB.
Patients with TB plus HIV infection.
Duration of treatment
Promoting adherence: directly observed therapy combined with intermittent dosing
Evaluating treatment
Diagnosis and treatment of latent tuberculosis
Who should be tested for latent tuberculosis?
TABLE 90–2 ▪ Candidates for Targeted Tuberculosis Testing
TABLE 90–3 ▪ Tuberculin Skin Test Results That Are Considered Positive—and Hence Justify Treatment—in Patients at Low, Moderate, and High Risk of Latent Tuberculosis
How do we test for latent tuberculosis?
Tuberculin skin test.
Interferon gamma release assays.
How do we treat latent tuberculosis?
Isoniazid.
Isoniazid plus rifapentine.
Vaccination against tuberculosis
Pharmacology of individual antituberculosis drugs
Isoniazid
Antimicrobial spectrum and mechanism of action
TABLE 90–4 ▪ Antituberculosis Drugs: Routes and Major Adverse Effects
Resistance
Pharmacokinetics
Absorption and distribution.
Metabolism.
Excretion.
Therapeutic use
Adverse effects
Hepatotoxicity.
Peripheral neuropathy.
Other adverse effects.
Drug interactions
Interactions from inhibiting drug metabolism.
Alcohol, rifampin, rifapentine, rifabutin, and pyrazinamide.
Preparations, dosage, and administration
Preparations.
Oral dosage.
Intramuscular dosage.
Rifampin
Antimicrobial spectrum
Mechanism of action and bacterial resistance
Pharmacokinetics
Absorption and distribution.
Elimination.
Therapeutic use
Tuberculosis.
Leprosy.
Meningococcus carriers.
Adverse effects
Hepatotoxicity.
Discoloration of body fluids.
Other adverse effects.
Drug interactions
Accelerated metabolism of other drugs.
Isoniazid and pyrazinamide.
Preparations, dosage, and administration
Preparations.
Oral.
Intravenous.
Oral dosage and administration.
Intravenous administration.
Rifapentine
Actions and uses.
Pharmacokinetics.
Adverse effects.
Drug interactions.
Preparation, dosage, and administration.
Rifabutin
Actions and uses.
Pharmacokinetics.
Adverse effects.
Drug interactions.
Preparations, dosage, and administration.
Pyrazinamide
Antimicrobial activity and therapeutic use
Pharmacokinetics
Adverse effects and interactions
Hepatotoxicity.
Nongouty polyarthralgias.
Other adverse effects.
Preparations, dosage, and administration
Ethambutol
Antimicrobial action
Therapeutic use
Pharmacokinetics
Adverse effects
Optic neuritis.
Other adverse effects.
Preparations, dosage, and administration
Second-line antituberculosis drugs
Fluoroquinolones
Injectable drugs
Capreomycin.
Amikacin, kanamycin, and streptomycin.
Other second-line drugs
Para-aminosalicylic acid.
Actions and uses.
Pharmacokinetics.
Adverse effects.
Preparations, dosage, and administration.
Ethionamide.
Actions and uses.
Pharmacokinetics.
Adverse effects.
Preparations, dosage, and administration.
Cycloserine.
Actions and uses.
Pharmacokinetics.
Adverse effects.
Preparations, dosage, and administration.
Tmc207, a promising investigational drug
Drugs for leprosy (hansen’s disease)
Overview of treatment
Pharmacology of individual antileprosy drugs
Rifampin
Dapsone
Actions and uses.
Pharmacokinetics.
Adverse effects.
Preparations, dosage, and administration.
Clofazimine
Actions and uses.
Pharmacokinetics.
Adverse effects.
Preparations, dosage, and administration.
The rom regimen
TABLE 90–5 ▪ Adult Regimens for Leprosy, as Recommended by the World Health Organization
TABLE 90–6 ▪ Regimens for MAC Infection in Immunocompetent Adults
Drugs for mycobacterium avium complex infection
Key points
Summary of Major Nursing Implications*
Implications that apply to all antituberculosis drugs
Promoting adherence
Evaluating treatment
Isoniazid
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Routes
Administration
Ongoing evaluation and interventions
Minimizing adverse effects
Hepatotoxicity.
Peripheral neuropathy.
Minimizing adverse interactions
Phenytoin.
Rifampin
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Routes
Dosage
Administration
Ongoing evaluation and interventions
Minimizing adverse effects
Hepatotoxicity.
Discoloration of body fluids.
Minimizing adverse interactions
Accelerated metabolism of other drugs.
Pyrazinamide and isoniazid.
Pyrazinamide
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Route
Administration
Ongoing evaluation and interventions
Minimizing adverse effects
Hepatotoxicity.
Nongouty polyarthralgias.
Ethambutol
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Route
Administration
Ongoing evaluation and interventions
Minimizing adverse effects
Optic neuritis.
CHAPTER 91 Miscellaneous antibacterial drugs: fluoroquinolones, metronidazole, daptomycin, rifampin, rifaximin, bacitracin, and polymyxins
Fluoroquinolones
Ciprofloxacin
Mechanism of action
Antimicrobial spectrum
Bacterial resistance
Pharmacokinetics
Therapeutic uses
Adverse effects
Drug and food interactions
Cationic compounds.
Elevation of drug levels.
Preparations, dosage, and administration
Preparations.
Dosage and administration.
Oral.
Intravenous.
Inhalational anthrax.
Other systemic fluoroquinolones
Ofloxacin
Basic pharmacology.
Preparations, dosage, and administration.
Moxifloxacin
Basic pharmacology.
Preparations, dosage, and administration.
Norfloxacin
Pharmacokinetics.
Therapeutic uses.
Adverse effects.
Drug and food interactions.
Preparations, dosage, and administration.
Levofloxacin
Gemifloxacin
Therapeutic use.
Adverse effects.
Drug interactions.
Preparations, dosage, and administration.
Additional antibacterial drugs
Metronidazole
Mechanism of antibacterial action.
Antibacterial spectrum.
Therapeutic uses.
Preparations, dosage, and administration.
Intravenous formulations.
Preparation of powdered metronidazole for IV infusion.
Intravenous dosage and administration.
Oral preparations and dosage.
Daptomycin
Mechanism of action.
Antibacterial spectrum.
Therapeutic use.
Resistance.
Pharmacokinetics.
Adverse effects.
Drug interactions.
Preparations, dosage, and administration.
Rifampin
Rifaximin
Fidaxomicin
Bacitracin
Mechanism of action and antimicrobial spectrum.
Therapeutic uses.
Adverse effects.
Polymyxin b
Antibacterial spectrum and mechanism of action.
Therapeutic uses.
Adverse effects.
Key points
Summary of Major Nursing Implications*
Fluoroquinolones
Preadministration assessment
Therapeutic goal
Identifying high-risk patients
Implementation: administration
Routes
Oral.
Intravenous.
Inhalation.
Administration
Oral.
Intravenous.
Dosage
Ongoing evaluation and interventions
Minimizing adverse effects
Tendinitis and tendon rupture.
Phototoxicity.
QT prolongation.
Myasthenia gravis.
Minimizing adverse drug and food interactions
Cationic compounds.
Warfarin.
Theophylline.
CHAPTER 92 Antifungal agents
Drugs for systemic mycoses
Amphotericin B, a polyene antibiotic
TABLE 92–1 ▪ Drugs of Choice for Systemic Mycoses
TABLE 92–2 ▪ Classes of Systemic Antifungal Drugs
Mechanism of action
Microbial susceptibility and resistance
Therapeutic uses
Pharmacokinetics
Absorption and distribution.
Metabolism and excretion.
Adverse effects
Infusion reactions.
Nephrotoxicity.
Hypokalemia.
Hematologic effects.
Effects associated with intrathecal injection.
Other adverse effects.
Drug interactions
Nephrotoxic drugs.
Flucytosine.
Preparations, dosage, and administration
Preparations.
Routes.
Intravenous dosage and administration.
Fungal infections.
Leishmaniasis.
Azoles
Itraconazole
Mechanism of action.
Therapeutic use.
Pharmacokinetics.
Adverse effects.
Cardiac suppression.
Liver injury.
Drug interactions.
Inhibition of hepatic drug-metabolizing enzymes.
TABLE 92–3 ▪ Some Drugs Whose Levels Can Be Increased by Azole Antifungal Drugs
Drugs that raise gastric pH.
Preparations, dosage, and administration.
Fluconazole
Actions and uses.
Pharmacokinetics.
Adverse effects.
Use in pregnancy.
Drug interactions.
Preparations, dosage, and administration.
Voriconazole
Actions and uses.
Pharmacokinetics.
Adverse effects.
Hepatotoxicity.
Visual disturbances.
Hypersensitivity reactions.
Teratogenicity.
Drug interactions.
Preparations, dosage, and administration.
Ketoconazole
Actions and antifungal spectrum.
Therapeutic use.
Pharmacokinetics.
Absorption.
Distribution.
Elimination.
Adverse effects.
Hepatotoxicity.
Effects on sex hormones.
Other adverse effects.
Drug interactions.
Preparations, dosage, and administration.
Posaconazole
Actions and uses.
Pharmacokinetics.
Adverse effects.
Drug interactions.
Preparations, dosage, and administration.
Echinocandins
Caspofungin
Actions and uses.
Pharmacokinetics.
Adverse effects.
Use in pregnancy.
Drug interactions.
Preparations, dosage, and administration.
Micafungin
Actions and uses.
Pharmacokinetics.
Adverse effects.
Drug interactions.
Preparations, dosage, and administration.
Anidulafungin
Actions and uses.
Pharmacokinetics.
Adverse effects.
Drug interactions.
Preparations, dosage, and administration.
Flucytosine, a pyrimidine analog
Mechanism of action.
Fungal resistance.
Antifungal spectrum and therapeutic uses.
Pharmacokinetics.
Adverse effects.
Hematologic effects.
Hepatotoxicity.
Drug interactions.
Preparations, dosage, and administration.
Drugs for superficial mycoses
Overview of drug therapy
Dermatophytic infections (ringworm)
Tinea pedis.
Tinea corporis.
TABLE 92–4 ▪ Drugs for Superficial Fungal Infections*
Tinea cruris.
Tinea capitis.
Candidiasis
Vulvovaginal candidiasis.
Oral candidiasis.
Onychomycosis (fungal infection of the nails)
TABLE 92–5 ▪ Some Preferred Products for Uncomplicated Vulvovaginal Candidiasis
Oral therapy.
Topical therapy with ciclopirox.
Azoles
Clotrimazole
Therapeutic uses.
Adverse effects.
Preparations, dosage, and administration.
Ketoconazole
Miconazole
Therapeutic uses.
Adverse effects.
Drug interactions.
Preparations, dosage, and administration.
Itraconazole
Fluconazole
Newer azole drugs
Econazole.
Oxiconazole and sulconazole.
Butoconazole, terconazole, and tioconazole.
Sertaconazole.
Griseofulvin
Mechanism of action.
Pharmacokinetics.
Therapeutic uses.
Adverse effects.
Drug interactions.
Preparations, dosage, and administration.
Polyene antibiotics
Nystatin
Actions, uses, and adverse effects.
Preparations, dosage, and administration.
Allylamines
Naftifine
Terbinafine
Actions and uses.
Adverse effects.
Preparations, dosage, and administration.
Butenafine
Other drugs for superficial mycoses
Tolnaftate
Undecylenic acid
Ciclopirox
Key points
Summary of Major Nursing Implications*
Amphotericin B
Preadministration assessment
Therapeutic goal
Identifying high-risk patients
Implementation: administration
Routes
Intravenous administration
Ongoing evaluation and interventions
Minimizing adverse effects
General considerations.
Infusion reactions.
Nephrotoxicity.
Hypokalemia.
Hematologic effects.
Minimizing adverse interactions
Nephrotoxic drugs.
Itraconazole
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Route
Administration
Ongoing evaluation and interventions
Minimizing adverse effects
Liver injury.
Cardiac suppression.
Minimizing adverse interactions
Pimozide, quinidine, dofetilide, and cisapride.
Cyclosporine, digoxin, warfarin, and sulfonylureas.
Drugs that raise gastric pH.
Flucytosine
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Route
Dosage and administration
Ongoing evaluation and interventions
Monitoring summary
Minimizing adverse effects
Hematologic effects.
Hepatotoxicity.
Minimizing adverse interactions
Amphotericin B.
CHAPTER 93 Antiviral agents I: drugs for non-HIV viral infections
TABLE 93–1 ▪ Major Drugs for Non-HIV Viral Infections
TABLE 93–2 ▪ Treatment of Herpes Simplex Virus and Varicella-Zoster Virus Infections
Drugs for infection with herpes simplex viruses and varicella-zoster virus
Acyclovir
Antiviral spectrum
Mechanism of action
Resistance
Therapeutic uses
Mucocutaneous herpes simplex infections.
Varicella-zoster infections.
Herpes simplex genitalis.
Pharmacokinetics
Adverse effects
Intravenous therapy.
Oral and topical therapy.
Preparations, dosage, and administration
Topical ointment.
Topical cream.
Oral.
Intravenous.
Valacyclovir
Actions and uses.
Pharmacokinetics.
Adverse effects.
Preparations, dosage, and administration.
Famciclovir
Pharmacokinetics.
Mechanism of action and antiviral spectrum.
Therapeutic use.
Adverse effects.
Preparations, dosage, and administration.
Preparations.
Acute herpes zoster.
Herpes simplex genitalis.
Topical drugs for herpes labialis
Penciclovir cream
Docosanol cream
Topical drugs for ocular herpes infections
Trifluridine ophthalmic solution
Vidarabine ointment
Ganciclovir gel
Drugs for cytomegalovirus infection
Ganciclovir
Mechanism of action.
Pharmacokinetics.
Therapeutic use.
Adverse effects.
Granulocytopenia and thrombocytopenia.
Reproductive toxicity.
Other adverse effects.
Preparations, dosage, and administration.
Intravenous.
Oral.
Ocular implant.
Ocular gel.
Valganciclovir
Basic and clinical pharmacology.
Preparations, dosage, and administration.
Cidofovir
Mechanism of action.
Antiviral spectrum and therapeutic use.
Pharmacokinetics.
Adverse effects.
Nephrotoxicity.
Other adverse effects.
Preparations, dosage, and administration.
Foscarnet
Mechanism of action.
Therapeutic use.
Pharmacokinetics.
Adverse effects and interactions.
Nephrotoxicity.
Electrolyte and mineral imbalances.
Other adverse effects.
Preparations, dosage, and administration.
TABLE 93–3 ▪ Characteristics of Hepatitis A, Hepatitis B, and Hepatitis C
Drugs for hepatitis
Hepatitis C
Interferon alfa
TABLE 93–4 ▪ Interferon Alfa Preparations: Dosages for Chronic Hepatitis B and Hepatitis C
Mechanism of action.
Conventional versus long-acting interferons.
Effects in chronic hepatitis C.
Adverse effects.
Ribavirin (oral)
Actions and therapeutic use.
Pharmacokinetics.
Clinical trials.
Adverse effects.
Hemolytic anemia.
Fetal injury.
Other adverse effects.
Preparations, dosage, and administration.
Preparations.
Dosage for ribasphere capsules, rebetol oral solution, and rebetol capsules (combined with interferon alfa-2b).
Dosage for copegus tablets and ribasphere tablets (combined with peginterferon alfa-2a).
Dosage for interferon alfa used with ribavirin.
Protease inhibitors: boceprevir and telaprevir
Boceprevir
Therapeutic use.
Mechanism of action.
Pharmacokinetics.
Adverse effects.
Effect in pregnancy.
Drug interactions.
Preparations, dosage, and administration.
Telaprevir
Actions and therapeutic use.
Pharmacokinetics.
Adverse effects.
Effect in pregnancy.
Drug interactions.
TABLE 93–5 ▪ Drug Interactions for Boceprevir and Telaprevir
TABLE 93–6 ▪ Drugs for Chronic Hepatitis B
Preparations, dosage, and administration.
Hepatitis B
Interferon alfa
Nucleoside analogs
Lamivudine
Adefovir
Therapeutic use.
Mechanism of action.
Pharmacokinetics.
Adverse effects.
Drug interactions.
Precautions.
Preparations, dosage, and administration.
Entecavir
Therapeutic use.
Mechanism of action.
Pharmacokinetics.
Adverse effects and precautions.
Preparations, dosage, and administration.
Telbivudine
Therapeutic use.
Mechanism of action.
Adverse effects.
Drug interactions.
Preparations, dosage, and administration.
Tenofovir
Drugs for influenza
Influenza vaccines
TABLE 93–7 ▪ Influenza Vaccines
Types of influenza vaccines
Composition
Efficacy
Adverse effects
Inactivated influenza vaccine.
Live, attenuated influenza vaccine.
Precautions and contraindications
Who should be vaccinated?
Who should not be vaccinated?
When should vaccination be done?
Dosage and administration
Inactivated influenza vaccine: intramuscular.
Inactivated influenza vaccine: intradermal.
Live, attenuated influenza vaccine.
Avian influenza.
Neuraminidase inhibitors
Oseltamivir
Therapeutic effects.
Mechanism of action.
Pharmacokinetics.
Adverse effects.
Interaction with live influenza vaccine.
Preparations, dosage, and administration.
Treatment of influenza.
Prevention of influenza.
Zanamivir
Actions and uses.
Clinical trials.
Pharmacokinetics.
Adverse effects and interactions.
Preparations, dosage, and administration.
Influenza treatment.
Influenza prevention.
Adamantanes
Drugs for respiratory syncytial virus infection
Ribavirin (inhaled)
Antiviral actions.
Use in rsv infection.
Pharmacokinetics.
Adverse effects.
Use in pregnancy.
Preparations, dosage, and administration.
Palivizumab
Actions and uses.
Adverse effects.
Preparations, dosage, and administration.
Key points
Summary of Major Nursing Implications*
Acyclovir
Preadministration assessment
Therapeutic goal
Identifying high-risk patients
Implementation: administration
Routes
Dosage
Administration
Topical.
Oral.
Intravenous.
Implementation: measures to enhance therapeutic effects
Ongoing evaluation and interventions
Evaluating therapeutic effects
Minimizing adverse effects
Nephrotoxicity.
Ganciclovir
Preadministration assessment
Therapeutic goal
Baseline data
Identifying high-risk patients
Implementation: administration
Routes
Dosage
Administration
Intravenous.
Oral.
Intraocular implants.
Topical to the eye.
Ongoing evaluation and interventions
Minimizing adverse effects
Granulocytopenia and thrombocytopenia.
Reproductive toxicity.
CHAPTER 94 Antiviral agents II: drugs for HIV infection and related opportunistic infections
Pathophysiology
Characteristics of HIV
Target cells
Structure of HIV
Figure 94–1 ▪ Structure of the human immunodeficiency virus. Note that HIV has two single strands of RNA, and that each strand is associated with a molecule of reverse transcriptase.
Figure 94–2 ▪ Replication cycle of the human immunodeficiency virus. See text for description of events.
Replication cycle of HIV
TABLE 94–1 ▪ Acute Retroviral Syndrome: Associated Signs and Symptoms
Replication rate
Mutation and drug resistance
Transmission of HIV
Clinical course of HIV infection
Classification of antiretroviral drugs
Nucleoside/nucleotide reverse transcriptase inhibitors
Zidovudine
Mechanism of antiviral action
Therapeutic use
Pharmacokinetics
Adverse effects
Anemia and neutropenia from bone marrow suppression.
TABLE 94–2 ▪ Classification of Antiretroviral Drugs
Lactic acidosis with hepatic steatosis.
Other adverse effects.
TABLE 94–3 ▪ Properties of Nucleoside/Nucleotide Reverse Transcriptase Inhibitors
Drug interactions
Preparations, dosage, and administration
Preparations.
Oral therapy.
Intravenous therapy: adults with pneumocystis pneumonia.
Intravenous therapy: preventing mother-to-infant transmission.
Other nrtis
Didanosine
Actions and uses.
Pharmacokinetics.
Adverse effects.
Pancreatitis.
Lactic acidosis with hepatic steatosis.
Other adverse effects.
Drug interactions.
Preparations, dosage, and administration.
Both formulations.
Enteric-coated capsules.
Buffered powder for oral solution.
Stavudine
Actions and uses.
Pharmacokinetics.
Adverse effects.
Peripheral neuropathy.
Pancreatitis.
Lactic acidosis with hepatic steatosis.
Neuromuscular weakness.
Other adverse effects.
Drug interactions.
Preparations, dosage, and administration.
Lamivudine
Actions and uses.
Pharmacokinetics.
Adverse effects.
Preparations, dosage, and administration.
Abacavir
Actions and use.
Pharmacokinetics.
Adverse effects.
Hypersensitivity reactions.
Myocardial infarction.
Other adverse effects.
Drug interactions.
Preparations, dosage, and administration.
Preparations.
Dosage and administration.
Tenofovir disoproxil fumarate
Mechanism of action.
Therapeutic use.
Pharmacokinetics.
Adverse effects.
Drug interactions.
Preparations, dosage, and administration.
Preparations.
Dosage and administration.
Emtricitabine
Actions and uses.
Pharmacokinetics.
Adverse effects.
Drug interactions.
Preparations, dosage, and administration.
Preparations.
Dosage and administration.
Combination products
Abacavir/zidovudine/lamivudine.
Abacavir/lamivudine.
Emtricitabine/tenofovir.
Lamivudine/zidovudine.
Emtricitabine/tenofovir/efavirenz.
Emtricitabine/tenofovir/rilpivirine.
Non-nucleoside reverse transcriptase inhibitors
Efavirenz
Mechanism of action.
Therapeutic use.
Pharmacokinetics.
Adverse effects.
Drug interactions.
Preparations, dosage, and administration.
Other nnrtis
Nevirapine
Mechanism of action.
Pharmacokinetics.
Therapeutic use and resistance.
Adverse effects.
Drug interactions.
Preparations, dosage, and administration.
Delavirdine
Actions, resistance, and use.
Adverse effects.
Drug interactions.
Preparations, dosage, and administration.
Etravirine
Actions and use.
Pharmacokinetics.
TABLE 94–4 ▪ Properties of Non-nucleoside Reverse Transcriptase Inhibitors
Adverse effects.
Use in pregnancy and lactation.
Drug interactions.
Preparations, dosage, and administration.
Rilpivirine
Actions and use.
Pharmacokinetics.
Adverse effects.
Use in pregnancy and lactation.
Drug interactions.
Preparations, dosage, and administration.
Protease inhibitors
Group properties
Adverse effects
Hyperglycemia/diabetes.
Fat maldistribution.
Hyperlipidemia.
Increased bleeding in people with hemophilia.
Reduced bone mineral density.
Elevation of serum transaminases.
Drug interactions
P450 inhibitors.
P450 inducers.
P450 substrates.
Protease inhibitor combinations: ritonavir boosting.
Herb interactions
St. John’s wort.
Garlic.
Lopinavir/ritonavir
Description and use.
TABLE 94–5 ▪ Properties of Protease Inhibitors (PIs)
TABLE 94–6 ▪ Drug Interactions of Protease Inhibitors (PIs)
Mechanism of action.
Pharmacokinetics.
Adverse effects.
Cardiac effects.
Toxicity in newborns.
Drug interactions.
Preparations, dosage, and administration.
Other protease inhibitors
Ritonavir
Actions and uses.
Pharmacokinetics.
Adverse effects.
Drug interactions.
Preparations, dosage, and administration.
Preparations.
Dosage and administration.
Storage.
Indinavir
Actions and use.
Pharmacokinetics.
Adverse effects.
Drug interactions.
Preparations, dosage, administration, and storage.
Saquinavir
Formulations.
Actions and therapeutic use.
Pharmacokinetics.
Adverse effects.
Cardiac effects.
Drug and food interactions.
Preparations, dosage, and administration.
Nelfinavir
Actions and uses.
Pharmacokinetics.
Adverse effects.
Drug interactions.
Preparations, dosage, and administration.
Fosamprenavir
Actions and use.
Pharmacokinetics.
Adverse effects.
Drug interactions.
Preparations, dosage, and administration.
Atazanavir
Actions and uses.
Pharmacokinetics.
Adverse effects.
Drug interactions.
Preparations, dosage, and administration.
Tipranavir (plus ritonavir)
Therapeutic use.
Mechanism of action.
Pharmacokinetics.
Adverse effects.
Hepatotoxicity.
Intracranial hemorrhage.
Other adverse effects.
Drug interactions.
Preparations, dosage, administration, and storage.
Darunavir (plus ritonavir)
Raltegravir, an integrase strand transfer inhibitor
Actions and use.
Pharmacokinetics.
Adverse effects.
Use during pregnancy and lactation.
Drug interactions.
Preparations, dosage, and administration.
Enfuvirtide, an HIV fusion inhibitor
Chemistry
Mechanism of action
Resistance
Pharmacokinetics
Therapeutic use
Adverse effects
Injection-site reactions.
Pneumonia.
Hypersensitivity reactions.
Effects during pregnancy and lactation.
Drug interactions
Preparations, dosage, administration, and storage
Preparations and storage.
Dosage and administration.
Maraviroc, a CCR5 antagonist
Actions.
Therapeutic use.
Pharmacokinetics.
Adverse effects.
Effects during pregnancy and lactation.
Drug interactions.
Preparations, dosage, and administration.
Management of HIV infection
Screening and diagnosis
Initial screening.
Follow-up confirmation.
Laboratory tests
CD4 T-cell counts
Viral load (plasma HIV RNA)
TABLE 94–7 ▪ Times When Plasma HIV RNA Should Be Measured
HIV drug resistance
Hla-b 5701 screening
CCR5 tropism
Therapeutic drug monitoring
Treatment of adult and adolescent patients
Symptomatic HIV disease
TABLE 94–8 ▪ Preferred and Alternative Antiretroviral Regimens for Initial Therapy of Established HIV Infection
Chronic asymptomatic HIV disease
TABLE 94–9 ▪ Factors to Consider When Deciding to Initiate Antiretroviral Therapy During the Asymptomatic Phase of HIV Disease (with CD4 T-Cell Counts Above 350 cells/mm3)
Acute HIV disease
Changing the regimen
Treatment failure.
Drug toxicity.
Promoting patient adherence
Patient- and medication-related strategies
Clinician- and healthcare team–related strategies
Treatment of infants and young children
Treatment of pregnant patients
Basic principles
Mitochondrial toxicity from nrtis
Preconception counseling and care
Preventing HIV infection with drugs
Treatment as prevention
Pre-exposure prophylaxis
Oral pre-exposure prophylaxis.
Topical (vaginal) pre-exposure prophylaxis.
Postexposure prophylaxis
Nonoccupational postexposure prophylaxis
Occupational postexposure prophylaxis
Preventing perinatal HIV transmission
Prophylaxis and treatment of opportunistic infections
TABLE 94–10 ▪ Intrapartum Maternal and Neonatal Zidovudine for Prevention of Mother-to-Child HIV Transmission*
Pneumocystis pneumonia (pcp)
Treatment of active PCP.
Prophylaxis of PCP.
Cytomegalovirus retinitis
TABLE 94–11 ▪ Drugs for Pneumocystis Pneumonia
Ganciclovir.
Valganciclovir.
Foscarnet.
Cidofovir.
Mycobacterium tuberculosis and mycobacterium avium complex
Mycobacterium tuberculosis.
Mycobacterium avium complex.
Toxoplasma encephalitis
Cryptococcal meningitis
Varicella-zoster virus infection
Herpes simplex virus infection
Candidiasis
HIV vaccines
Obstacles to vaccine development
Current status of vaccine development
Keeping current
Key points
Summary of Major Nursing Implications*
Nucleoside/nucleotide reverse transcriptase inhibitors
Preadministration assessment
Therapeutic goals
Baseline data
All nrtis.
Zidovudine.
Abacavir.
Identifying high-risk patients
Didanosine.
Zidovudine.
Implementation: administration
Routes
All nrtis.
Zidovudine.
Administration
All nrtis.
Didanosine.
IV zidovudine.
Ongoing evaluation and interventions
Evaluating therapeutic effects
Plasma HIV RNA.
CD4 T-cell counts.
Minimizing adverse effects
Anemia and neutropenia.
Lactic acidosis with hepatic steatosis.
Pancreatitis.
Peripheral neuropathy.
Hypersensitivity reactions.
Exacerbation of hepatitis.
Myocardial infarction.
HIV transmission.
Minimizing adverse interactions
Zidovudine.
Ribavirin and allopurinol.
All nrtis.
Non-nucleoside reverse transcriptase inhibitors
Preadministration assessment
Therapeutic goals
Baseline data
Implementation: administration
Route
Administration
All nnrtis.
Delavirdine.
Efavirenz.
Etravirine.
Nevirapine.
Rilpivirine.
Ongoing evaluation and interventions
Evaluating therapeutic effects
Minimizing adverse effects
Rash and other hypersensitivity reactions.
Hepatotoxicity.
CNS symptoms.
Depression.
Birth defects.
HIV transmission.
Minimizing adverse interactions
Nevirapine.
Delavirdine.
Efavirenz.
Etravirine.
Rilpivirine.
Protease inhibitors
Preadministration assessment
Therapeutic goals
Baseline data
Identifying high-risk patients
Implementation: administration
Route
Administration and storage
All protease inhibitors.
Atazanavir.
Darunavir.
Fosamprenavir.
Indinavir.
Lopinavir/ritonavir.
Nelfinavir.
Ritonavir.
Saquinavir.
Tipranavir.
Ongoing evaluation and interventions
Evaluating therapeutic effects
Minimizing adverse effects
Hyperglycemia/diabetes.
Fat maldistribution.
Hyperlipidemia.
Increased bleeding in patients with hemophilia.
Increased transaminase levels.
Nephrolithiasis.
Bone loss.
Diarrhea.
Cardiac effects.
Toxicity in newborns.
Indirect hyperbilirubinemia.
HIV transmission.
Minimizing adverse interactions
Interactions resulting from inhibition of p450.
Ritonavir boosting.
Didanosine.
Rifampin.
Oral contraceptives.
St. John’s wort.
Enfuvirtide, an HIV fusion inhibitor
Preadministration assessment
Therapeutic goals
Baseline data
Identifying high-risk patients
Implementation: administration
Route
Preparation and storage
Administration
Ongoing evaluation and interventions
Evaluating therapeutic effects
Minimizing adverse effects
Injection-site reactions.
Pneumonia.
Hypersensitivity reactions.
HIV transmission.
Maraviroc, a CCR5 antagonist
Preadministration assessment
Therapeutic goals
Baseline data
Identifying high-risk patients
Implementation: administration
Route
Administration
Ongoing evaluation and interventions
Evaluating therapeutic effects
Minimizing adverse effects
Hepatotoxicity.
Cardiovascular events.
HIV transmission.
Raltegravir, an integrase strand transfer inhibitor
Preadministration assessment
Therapeutic goals
Baseline data
Implementation: administration
Route
Administration
Ongoing evaluation and interventions
Evaluating therapeutic effects
Minimizing adverse effects
Severe hypersensitivity reactions.
HIV transmission.
CHAPTER 95 Drug therapy of sexually transmitted diseases
Chlamydia trachomatis infections
Characteristics
Treatment
Adults and adolescents.
Infection in pregnancy.
Infants.
Preadolescent children.
Figure 95–1 ▪ Incidence of sexually transmitted diseases.
TABLE 95–1 ▪ Drug Therapy of Sexually Transmitted Diseases*
Lymphogranuloma venereum.
Gonococcal infections
Characteristics
Treatment
Urethral, cervical, and rectal infection.
Pharyngeal infection.
Conjunctivitis.
Disseminated gonococcal infection.
Neonatal infection.
Preadolescent children.
Nongonococcal urethritis
Pelvic inflammatory disease
Acute epididymitis
Syphilis
Characteristics.
Treatment.
Acquired immunodeficiency syndrome
Bacterial vaginosis
Nonpregnant women.
Pregnant women.
Trichomoniasis
Chancroid
Herpes simplex virus infections
Characteristics.
Neonatal infection.
Treatment.
Suppression of transmission.
Proctitis
Venereal warts
Key points
CHAPTER 96 Antiseptics and disinfectants
General considerations
Terminology
Properties of an ideal antiseptic
Time course of action
Using antiseptics to treat established local infection
Using antiseptics and disinfectants most effectively
TABLE 96–1 ▪ Antiseptics and Disinfectants: Chemical Category and Application
Properties of individual antiseptics and disinfectants
Alcohols
Ethanol
Isopropanol
Aldehydes
Glutaraldehyde
Formaldehyde
Iodine compounds: iodine solution and iodine tincture
Iodophors: povidone-iodine
Chlorine compounds
Oxychlorosene sodium
Sodium hypochlorite
Phenols
Hexachlorophene
Actions.
Uses.
Adverse effects.
TABLE 96–2 ▪ Selected Chlorhexidine Products
Preparations.
Miscellaneous agents
Chlorhexidine
Hydrogen peroxide
Thimerosal
Benzalkonium chloride
Actions.
Antiseptic uses.
Disinfectant use.
Preparations and dosage.
Hand hygiene for healthcare workers
Specific CDC hand-hygiene recommendations
Indications for hand washing and hand antisepsis
TABLE 96–3 ▪ Antimicrobial Spectrum and Characteristics of Hand-Hygiene Antiseptic Agents
Hand-hygiene technique
Surgical hand antisepsis
Other aspects of hand hygiene
Administrative measures regarding hand hygiene
Key points
XVII Chemotherapy of Parasitic Diseases
Interactive Review – XVII: Chemotherapy of Parasitic Diseases
CHAPTER 97 Anthelmintics
Classification of parasitic worms
Nematodes (roundworms)
Cestodes (tapeworms)
Trematodes (flukes)
Helminthic infestations
Nematode infestations (intestinal)
Ascariasis (giant roundworm infestation).
Enterobiasis (pinworm infestation).
Ancylostomiasis and necatoriasis (hookworm infestation).
Trichuriasis (whipworm infestation).
TABLE 97–1 ▪ Drugs of Choice for Parasitic Worms
Strongyloidiasis (threadworm infestation).
Nematode infestations (extraintestinal)
Trichinosis (pork roundworm infestation).
Wuchereriasis and brugiasis (lymphatic filarial infestation).
Onchocerciasis (river blindness).
Cestode infestations
Taeniasis (beef and pork tapeworm infestation).
Diphyllobothriasis (fish tapeworm infestation).
Trematode infestations
Schistosomiasis (blood fluke infestations).
TABLE 97–2 ▪ First-Choice Anthelmintic Drugs: Target Organisms and Dosages
Fascioliasis (liver fluke infestation).
Fasciolopsiasis (intestinal fluke infestation).
Drugs of choice for helminthiasis
Mebendazole
Target organisms.
Mechanism of action.
Pharmacokinetics.
Adverse effects.
Preparations, dosage, and administration.
Albendazole
Target organisms.
Mechanism of action.
Pharmacokinetics.
Adverse effects.
Preparations, dosage, and administration.
Pyrantel pamoate
Target organisms.
Mechanism of action.
Pharmacokinetics.
Adverse effects.
Preparations, dosage, and administration.
Praziquantel
Target organisms.
Mechanism of action.
Pharmacokinetics.
Adverse effects.
Preparations, dosage, and administration.
Diethylcarbamazine
Target organisms.
Mechanism of action.
Pharmacokinetics.
Adverse effects.
Preparations, dosage, and administration.
Ivermectin
Target organisms.
Mechanism of action.
Pharmacokinetics.
Adverse effect: mazotti reaction.
Use in pregnancy.
Preparations, dosage, and administration.
Key points
CHAPTER 98 Antiprotozoal drugs I: antimalarial agents
Life cycle of the malaria parasite
Types of malaria
Figure 98–1 ▪ Life cycle of the malaria parasite.
Vivax malaria
Falciparum malaria
TABLE 98–1 ▪ Comparison of Vivax Malaria and Falciparum Malaria
Principles of antimalarial therapy
Therapeutic objectives
Treatment of an acute attack.
Prevention of relapse.
Prophylaxis.
Drug selection
Treatment of acute attacks.
Prevention of relapse.
Prophylaxis.
TABLE 98–2 ▪ Drugs of Choice for Malaria*
Pharmacology of the major antimalarial drugs
Chloroquine
Actions and use.
Pharmacokinetics.
Adverse effects.
TABLE 98–3 ▪ Activity of Antimalarial Drugs Against Hepatic and Erythrocytic Stages of the Malaria Parasite
Routes of administration.
Preparations, dosage, and administration.
Primaquine
Actions and use.
Pharmacokinetics.
Adverse effect: hemolysis.
Preparations, dosage, and administration.
Quinine
Actions and use.
Pharmacokinetics.
Adverse effects.
Use in pregnancy.
Preparations, dosage, and administration.
Quinidine gluconate
Mefloquine
Actions and uses.
Pharmacokinetics.
Adverse effects.
Drug interactions.
Preparations, dosage, and administration.
Artemisinin derivatives
Artemether/lumefantrine
Indications and efficacy.
Mechanism of action.
Pharmacokinetics.
Why do we combine artemether with lumefantrine?
Adverse effects.
Drug interactions.
Preparations, dosage, and administration.
Adult dosage.
Pediatric dosage.
Artesunate
Atovaquone/proguanil
Activity and therapeutic use.
Mechanism of action.
Pharmacokinetics.
Adverse effects and interactions.
Preparations, dosage, and administration.
Pyrimethamine/sulfadoxine
Antibacterial drugs
Tetracyclines.
Clindamycin.
Key points
CHAPTER 99 Antiprotozoal drugs II: miscellaneous agents
Protozoal infections
TABLE 99–1 ▪ Drugs of Choice for Protozoal Infection
Amebiasis
Cryptosporidiosis
Giardiasis
Leishmaniasis
Toxoplasmosis
Trichomoniasis
Trypanosomiasis
American trypanosomiasis (chagas’ disease).
African trypanosomiasis (sleeping sickness).
Drugs of choice for protozoal infections
Iodoquinol
Metronidazole
Therapeutic uses.
Mechanism of action.
Pharmacokinetics.
Adverse effects.
Use in pregnancy and lactation.
Drug interactions.
Alcohol and disulfiram.
Warfarin.
Phenytoin, lithium, fluorouracil, cyclosporine, and tacrolimus.
Cholestyramine.
Drugs that affect CYP3A4.
Preparations, dosage, and administration.
Tinidazole
Therapeutic uses.
Mechanism of action.
Pharmacokinetics.
Adverse effects.
Use in pregnancy and lactation.
Drug interactions.
Preparations, dosage, and administration.
Benznidazole
Nitazoxanide
Therapeutic uses.
Actions.
Pharmacokinetics.
Adverse effects.
Drug interactions.
Preparations, dosage, and administration.
Oral suspension.
Tablets.
Pentamidine
Target diseases and actions.
Uses.
Pneumocystis pneumonia.
West African sleeping sickness.
Pharmacokinetics.
Adverse effects associated with parenteral pentamidine.
Adverse effects associated with aerosolized pentamidine.
Preparations, dosage, and administration.
Pneumocystis pneumonia.
West African sleeping sickness.
Suramin
Actions and uses.
Pharmacokinetics.
Adverse effects.
Preparations, dosage, and administration.
Melarsoprol
Therapeutic use.
Mechanism of action.
Adverse effects.
Preparations, dosage, and administration.
East African trypanosomiasis.
West African trypanosomiasis.
Eflornithine
Actions and uses.
Pharmacokinetics.
Adverse effects.
Preparations, dosage, and administration.
Nifurtimox
Therapeutic use.
Pharmacokinetics.
Adverse effects.
Preparations, dosage, and administration.
Pyrimethamine
Sodium stibogluconate
Miltefosine
Amphotericin B
Key points
CHAPTER 100 Ectoparasiticides
Ectoparasitic infestations
Pediculosis (infestation with lice)
Head lice
Body lice
Pubic lice
TABLE 100–1 ▪ Preferred Drugs for Mites and Lice
Scabies (infestation with mites)
Pharmacology of ectoparasiticides
Permethrin
Basic pharmacology
Actions and uses.
Resistance.
Pharmacokinetics.
Adverse effects.
Preparations and administration
Preparations.
Administration.
Head lice.
Scabies.
Pyrethrins plus piperonyl butoxide
Malathion
Actions and uses.
Adverse effects and interactions.
Preparations and administration.
Benzyl alcohol
Spinosad
Crotamiton
Lindane
Actions and uses
Adverse effects
Irritation.
Convulsions.
Preparations and administration
Preparations.
Administration.
Scabies.
Head lice.
Pubic lice.
Body lice.
Ivermectin
Key points
XVIII Cancer Chemotherapy
Interactive Review – XVIII: Cancer Chemotherapy
CHAPTER 101 Basic principles of cancer chemotherapy
What is cancer?
TABLE 101–1 ▪ Estimated New Cancer Cases and Deaths, United States, 2011
Characteristics of neoplastic cells
Persistent proliferation.
Invasive growth.
Formation of metastases.
Immortality.
Etiology of cancer
Figure 101–1 ▪ The cell cycle.
TABLE 101–2 ▪ Some Cancers for Which Drugs May Be Curative*
The growth fraction and its relationship to chemotherapy
The cell cycle
The growth fraction
Impact of tissue growth fraction on responsiveness to chemotherapy
Obstacles to successful chemotherapy
Toxicity to normal cells
Cure requires 100% cell kill
Kinetics of drug-induced cell kill.
Host defenses contribute little to cell kill.
Figure 101–2 ▪ Gompertzian tumor growth curve showing the relationship between tumor size and clinical status.
When should treatment stop?
Absence of truly early detection
TABLE 101–3 ▪ American Cancer Society Recommendations for the Early Detection of Breast, Colorectal, Prostate, and Cervical Cancers, 2011
Solid tumors respond poorly
Figure 101–3 ▪ Recovery of critical normal cells during intermittent chemotherapy. Cancer cells and normal cells (eg, cells of the bone marrow) are killed each time cytotoxic drugs are given. In the interval between doses, both types of cells proliferate. Because, in this example, normal cells repopulate faster than the cancer cells, normal cells are able to recover entirely between doses, whereas regrowth of the cancer cells is only partial. As a result, with each succeeding round of treatment, the total number of cancer cells becomes smaller, whereas the number of normal cells remains within a tolerable range. Note that differential loss of malignant cells is possible only if these cells repopulate more slowly than the normal cells. If cancer cells grow back as fast as normal cells do, intermittent chemotherapy will fail.
Drug resistance
Heterogeneity of tumor cells
Limited drug access to tumor cells
Strategies for achieving maximum benefits from chemotherapy
Intermittent chemotherapy
TABLE 101–4 ▪ Single-Drug Treatment Versus Combination Chemotherapy
TABLE 101–5 ▪ Effects of Cyclophosphamide and Vincristine Alone and in Combination
Combination chemotherapy
Benefits of drug combinations
Suppression of drug resistance.
Increased cancer cell kill.
Reduced injury to normal cells.
TABLE 101–6 ▪ Effect of Dosing Schedule on Therapeutic Response
Guidelines for drug selection
Optimizing dosing schedules
Regional drug delivery
Intra-arterial delivery.
Intrathecal delivery.
Other specialized routes.
Major toxicities of chemotherapeutic drugs
Bone marrow suppression
Neutropenia
Thrombocytopenia
Anemia
Digestive tract injury
Stomatitis.
TABLE 101–7 ▪ Emetogenic Potential of Selected Intravenous Anticancer Drugs
Diarrhea.
Nausea and vomiting
Other important toxicities
Alopecia.
Reproductive toxicity.
Hyperuricemia.
TABLE 101–8 ▪ Karnofsky Performance Scale
Local injury from extravasation of vesicants.
Unique toxicities.
Carcinogenesis.
Making the decision to treat
Looking ahead
Key points
CHAPTER 102 Anticancer drugs I: cytotoxic agents
Introduction to the cytotoxic anticancer drugs
Mechanisms of cytotoxic action
Cell-cycle phase specificity
Cell-cycle phase–specific drugs.
Cell-cycle phase–nonspecific drugs.
TABLE 102–1 ▪ Cytotoxic Anticancer Drugs
TABLE 102–2 ▪ Actions of Representative Cytotoxic Anticancer Drugs
Toxicity
Dosage, handling, and administration
Handling cytotoxic drugs.
Administering vesicants.
Alkylating agents
Shared properties
Mechanism of action.
Figure 102–1 ▪ Cross-linking of DNA by an alkylating agent. A, Reactions leading to cross-linkage between guanine moieties in DNA. B, Schematic representation of interstrand cross-linking within the DNA double helix.
Resistance.
Toxicities.
Properties of individual alkylating agents
Nitrogen mustards
Cyclophosphamide.
Mechlorethamine.
Bendamustine.
Chlorambucil.
Melphalan.
Ifosfamide.
Nitrosoureas
Carmustine (BCNU).
Lomustine (ccnu).
Streptozocin.
Other alkylating agents
Busulfan.
Temozolomide.
Therapeutic uses.
Pharmacokinetics and mechanism of action.
Adverse effects.
Platinum compounds
Cisplatin
Carboplatin
Oxaliplatin
Actions and uses.
Toxicity.
Peripheral sensory neuropathy.
Other toxicities.
Antimetabolites
Folic acid analogs
Figure 102–2 ▪ Actions of methotrexate, leucovorin, and fluorouracil. (FdUMP = 5-fluoro-2′-deoxyuridine-5′-monophosphate, = blockade of reaction.)
Methotrexate
Mechanism of action.
Pharmacokinetics.
Resistance.
Therapeutic uses.
Toxicity.
Pemetrexed
Mechanism of action.
Therapeutic uses.
Pharmacokinetics.
Toxicity.
Pralatrexate
Mechanism of action.
Therapeutic use.
Pharmacokinetics.
Toxicity.
Pyrimidine analogs
Cytarabine
Mechanism of action.
Resistance.
Pharmacokinetics.
Therapeutic uses.
Toxicity.
Fluorouracil
Mechanism of action.
Resistance.
Therapeutic uses.
Pharmacokinetics.
Toxicity.
Capecitabine
Floxuridine
Gemcitabine
Mechanism of action.
Therapeutic uses.
Toxicity.
Purine analogs
Mercaptopurine
Mechanisms of action and resistance.
Pharmacokinetics.
Therapeutic uses.
Toxicity.
Thioguanine
Actions and uses.
Pharmacokinetics.
Toxicity.
Pentostatin
Fludarabine
Cladribine
Nelarabine
Clofarabine
Hypomethylating agents
Azacitidine
Decitabine
Antitumor antibiotics
Anthracyclines
Doxorubicin, conventional
Mechanism of action.
Pharmacokinetics.
Therapeutic uses.
Cardiotoxicity.
Other toxicities.
Doxorubicin, liposomal
Daunorubicin
Epirubicin
Mechanism of action and therapeutic use.
Pharmacokinetics.
Adverse effects.
Idarubicin
Mitoxantrone
Nonanthracyclines
Dactinomycin (actinomycin d)
Actions and uses.
Pharmacokinetics.
Toxicity.
Bleomycin
Mitomycin
Mitotic inhibitors
Vinca alkaloids
Vincristine
Mechanism of action.
Pharmacokinetics.
Therapeutic uses.
Toxicity.
VinBLAStine
Vinorelbine
Taxanes
Paclitaxel
Actions and uses.
Pharmacokinetics.
Formulations.
Toxicity.
Docetaxel
Actions, uses, and source.
Toxicity.
Cabazitaxel
Actions and use.
Toxicity.
Other mitotic inhibitors
Ixabepilone
Eribulin mesylate
Estramustine
Topoisomerase inhibitors
Topotecan
Mechanism of action.
Therapeutic uses.
Toxicity.
Irinotecan
Actions and uses.
Metabolic activation and inactivation.
Adverse effects.
Etoposide
Teniposide
Miscellaneous cytotoxic drugs
Asparaginase
Pegaspargase
Hydroxyurea
Mitotane
Procarbazine
Mechanism of action.
Pharmacokinetics.
Therapeutic uses.
Toxicity.
Drug interactions.
Dacarbazine
Actions and uses.
Pharmacokinetics.
Toxicity.
Altretamine (hexamethylmelamine)
Key points
CHAPTER 103 Anticancer drugs II: hormonal agents, targeted drugs, and other noncytotoxic anticancer drugs
Drugs for breast cancer
Antiestrogens
Tamoxifen
Overview of actions.
Mechanism of action in breast cancer.
Use for treatment of breast cancer.
Use for prevention of breast cancer.
TABLE 103–1 ▪ Drugs for Adjuvant Therapy of Breast Cancer
Pharmacokinetics.
Adverse effects.
Interaction with CYP2D6 inhibitors.
Dosage and administration.
Toremifene
Actions and use.
Pharmacokinetics.
Adverse effects.
Fulvestrant
Actions and use.
Clinical trials.
Pharmacokinetics.
Adverse effects and drug interactions.
Preparations, dosage, and administration.
Aromatase inhibitors
Anastrozole
Mechanism, use, and dosage.
Adverse effects.
Comparison with tamoxifen.
Letrozole
Exemestane
Trastuzumab
Actions and use.
Clinical trials.
Adverse effects.
Dosage and administration.
Lapatinib
Actions and use.
Adverse effects.
Drug interactions.
Preparations, dosage, and administration.
Cytotoxic drugs (chemotherapy)
Denosumab and bisphosphonates for skeletal-related events
Zoledronate and other bisphosphonates
Denosumab
Drugs for prostate cancer
Androgen deprivation therapy
Gonadotropin-releasing hormone agonists
TABLE 103–2 ▪ Drugs for Prostate Cancer
Leuprolide
Therapeutic use.
Mechanism of action.
Co-treatment with an androgen receptor blocker.
Adverse effects.
Preparations, dosage, and administration.
Triptorelin, goserelin, histrelin
Gonadotropin-releasing hormone antagonists
Degarelix
Androgen receptor blockers
Flutamide
Bicalutamide
Nilutamide
Abiraterone, a cyp17 inhibitor
Actions and use.
Adverse effects.
Drug interactions.
Preparations, dosage, and administration.
Ketoconazole
Other drugs for prostate cancer
Sipuleucel-t
Therapeutic use.
Production.
Adverse effects.
Dosage, administration, and cost.
Cytotoxic drugs
Docetaxel and cabazitaxel
Estramustine
Targeted anticancer drugs
Kinase inhibitors
Egfr tyrosine kinase inhibitors
Cetuximab
Mechanism of action.
Therapeutic uses.
Colorectal cancer.
Head and neck cancer.
Adverse effects.
Dosage, administration, and cost.
TABLE 103–3 ▪ Targeted Anticancer Drugs
Panitumumab
Gefitinib
Therapeutic use.
Mechanism of action.
Responding populations.
Pharmacokinetics.
Adverse effects.
Drug and herb interactions.
Use in pregnancy and lactation.
Dosage and administration.
Erlotinib
Actions and use.
Responding populations.
Pharmacokinetics.
Adverse effects.
Drug interactions.
Preparations, dosage, and administration.
Lapatinib
Bcr-abl tyrosine kinase inhibitors
Imatinib
Indications.
CML and its treatment.
Mechanism of action and clinical effects.
Pharmacokinetics.
Adverse effects.
Effects in pregnancy and breast-feeding.
Drug interactions.
Preparations, dosage, and administration.
Dasatinib
Nilotinib
Multi–tyrosine kinase inhibitors
Sorafenib
Sunitinib
Pazopanib
Vandetanib
Mtor kinase inhibitors
Temsirolimus
Everolimus
Vemurafenib, a braf v600e kinase inhibitor
Actions and use.
Clinical trial.
Adverse effects.
Drug interactions.
Preparations, dosage, and administration.
Crizotinib, an alk inhibitor
Other targeted drugs
Cd20-directed antibodies
Rituximab
Actions, use, and dosage.
Adverse effects.
Infusion reactions.
Tumor lysis syndrome (TLS).
Mucocutaneous reactions.
Hepatitis B reactivation.
Progressive multifocal leukoencephalopathy (pml).
Other adverse effects.
Ofatumumab
Actions and use.
Adverse effects.
Dosage and administration.
Ibritumomab tiuxetan linked with yttrium-90
Description, actions, and use.
Adverse effects.
Bexxar (tositumomab with 131i-tositumomab)
Description, actions, and use.
Adverse effects.
Use in pregnancy and lactation.
Elimination of iodine-131.
Radiation precautions.
Brentuximab vedotin, an antibody-drug conjugate
Angiogenesis inhibitors
Bevacizumab
Mechanism of action.
Therapeutic use.
BOX 103–1 ▪ SPECIAL INTEREST TOPIC
ANGIOGENESIS INHIBITORS: KEEPING CANCER IN CHECK
Angiogenesis in normal tissues and tumors
Comparison with cytotoxic anticancer drugs
A new treatment paradigm
Clinical status
Pharmacokinetics.
Adverse effects.
Effect in pregnancy.
Dosage, administration, and cost.
Proteasome inhibitors
Bortezomib
Actions.
Therapeutic use.
Adverse effects.
Drug interactions.
Dosage and administration.
Multiple myeloma.
Mantle cell lymphoma.
Histone deacetylase inhibitors
Vorinostat
Romidepsin
Ipilimumab
TABLE 103–4 ▪ Immunostimulants
Immunostimulants
Interferon alfa-2b
Aldesleukin (interleukin-2)
Description and actions.
Therapeutic use.
Pharmacokinetics.
Adverse effects.
Bcg vaccine
Description and therapeutic use.
Mechanism of action.
Adverse effects.
Other noncytotoxic anticancer drugs
Glucocorticoids
Retinoids
Alitretinoin
Bexarotene
Mechanism and use.
Pharmacokinetics.
Adverse effects and interactions.
Tretinoin
Arsenic trioxide
Denileukin diftitox
Therapeutic use.
Description and mechanism of action.
Adverse effects.
BOX 103–2 ▪ SPECIAL INTEREST TOPIC
THALIDOMIDE REDEEMED—AND STRICTLY CONTROLLED
Thalidomide
Lenalidomide
Progestins
Key points
XIX Additional Important Drugs
Interactive Review – XIX: Additional Important Drugs
CHAPTER 104 Drugs for the eye
Drugs for glaucoma
Pathophysiology and treatment overview
Primary open-angle glaucoma
Characteristics.
Figure 104–1 ▪ Anatomy of the normal eye.
TABLE 104–1 ▪ Topical Drugs for Open-Angle Glaucoma
Risk factors.
Screening.
Management.
Angle-closure glaucoma
Figure 104–2 ▪ Comparative anatomy of the eye in open-angle and angle-closure glaucoma. A, Note that the angle between the iris and cornea is open in open-angle glaucoma, permitting unimpeded outflow of aqueous humor through the canal of Schlemm and trabecular meshwork. B, Note that the angle between the iris and cornea is constricted in angle-closure glaucoma, thereby blocking outflow of aqueous humor through the canal of Schlemm and trabecular meshwork.
Drugs used to treat glaucoma
Beta-adrenergic blocking agents
Actions and use in glaucoma.
Adverse effects.
Local.
Systemic.
TABLE 104–2 ▪ Beta Blockers Used in Glaucoma
Prostaglandin analogs
Latanoprost.
Other prostaglandin analogs.
Alpha2-adrenergic agonists
Brimonidine.
Apraclonidine.
Alpha2 agonist/beta blocker combination
Pilocarpine, a direct-acting muscarinic agonist
Effects on the eye.
Therapeutic uses.
Adverse effects.
Preparations, dosage, and administration.
Pilocarpine solutions.
Pilocarpine gel.
Echothiophate, a cholinesterase inhibitor
Effects on the eye.
Use in glaucoma.
Adverse effects.
Preparations, dosage, and administration.
Carbonic anhydrase inhibitors: topical
Dorzolamide.
Brinzolamide.
Carbonic anhydrase inhibitors: systemic
Actions and uses in glaucoma.
Adverse effects.
Preparations, dosage, and administration.
Osmotic agents
TABLE 104–3 ▪ Prostaglandin Analogs Used in Glaucoma
TABLE 104–4 ▪ Muscarinic Antagonists Used for Mydriasis and Cycloplegia
Cycloplegics and mydriatics
Anticholinergic agents
Effects on the eye
Ophthalmic applications
Adjunct to measurement of refraction.
Intraocular examination.
Intraocular surgery.
Treatment of anterior uveitis.
Adverse effects
Blurred vision and photophobia.
Precipitation of angle-closure glaucoma.
Systemic effects.
Phenylephrine (an adrenergic agonist)
Therapeutic and diagnostic applications
Adverse effects
Effects on the eye.
Systemic effects.
Drugs for allergic conjunctivitis
Pathophysiology
Drug therapy
Drugs for age-related macular degeneration
Pathophysiology of ARMD
TABLE 104–5 ▪ Topical Drugs for Allergic Conjunctivitis
Management of dry ARMD
Management of wet (neovascular) ARMD
TABLE 104–6 ▪ Intravitreal Angiogenesis Inhibitors for Neovascular (Wet) ARMD
Angiogenesis inhibitors
Actions and benefits.
Adverse effects.
Pegaptanib, ranibizumab, aflibercept, and bevacizumab: comparisons and contrasts.
Molecular structure.
Approved usage and cost.
Efficacy.
Laser therapy
Photodynamic therapy
Additional ophthalmic drugs
Demulcents (artificial tears)
Ocular decongestants
Glucocorticoids
Dyes
Topical drugs for ocular infections
TABLE 104–7 ▪ Some Topical Ophthalmic Antibacterial Agents
Key points
CHAPTER 105 Drugs for the skin
Anatomy of the skin
Epidermis.
Dermis.
Subcutaneous tissue.
Topical glucocorticoids
Actions and uses.
Figure 105–1 ▪ Anatomy of the skin. A, Major structures of the skin. B, Growth layers of the epidermis.
Relative potency.
Absorption.
Adverse effects.
Local reactions.
Systemic toxicity.
Administration.
Keratolytic agents
Salicylic acid.
Sulfur.
TABLE 105–1 ▪ Relative Potency of Topical Glucocorticoids
Acne
Pathophysiology
Overview of treatment
Nondrug therapy
Drug therapy
Topical drugs for acne
Antibiotics
Benzoyl peroxide.
TABLE 105–2 ▪ Drugs for Acne
Clindamycin and erythromycin.
Dapsone.
Retinoids
Tretinoin.
Use for acne.
Use for fine wrinkles.
Adverse effects.
Preparations, dosage, and administration.
Adapalene.
Tazarotene.
Azelaic acid
Oral drugs for acne
Antibiotics
Isotretinoin
Actions and use.
Pharmacokinetics.
Adverse effects.
Common effects.
Rare effect: depression.
Drug interactions.
Contraindication: pregnancy.
IPLEDGE program.
Requirements for female patients.
Requirements for prescribers.
TABLE 105–3 ▪ Properties of UVB and UVA Radiation
Preparations, dosage, and administration.
Hormonal agents
Oral contraceptives.
Spironolactone.
Sunscreens
Types of ultraviolet radiation: uvb and uva
Benefits of sunscreens
Compounds employed as sunscreens
Figure 105–2 ▪ Range of UVB and UVA protection conferred by FDA-approved sunscreens.
Organic (chemical) screens.
Inorganic (physical) screens.
Sun protection factor
Adverse effects of sunscreens
New rules for sunscreen labeling
Range of uv protection and spf.
Water/sweat resistance.
Safe sunning
Using a sunscreen effectively.
Other protection measures.
TABLE 105–4 ▪ Treatments for Psoriasis
Psoriasis
Pathophysiology
Overview of treatment
Topical drugs for psoriasis
Glucocorticoids
Vitamin D3 analogs
Tazarotene
Anthralin
Tars
Systemic drugs for psoriasis: conventional agents
Methotrexate
Actions and use in psoriasis.
Adverse effects.
Dosage and administration.
Acitretin
Mechanism of action.
Therapeutic use.
Pharmacokinetics.
Adverse effects.
Drug interactions.
Contraindication: pregnancy.
Preparations, dosage, and administration.
Cyclosporine
Systemic drugs for psoriasis: biologic agents
Alefacept, a T-cell antagonist
Actions and therapeutic use.
Adverse effects.
Drug interactions.
Monitoring.
Preparations, dosage, and administration.
Tumor necrosis factor antagonists
Ustekinumab, an interleukin antagonist
Actions and uses.
Adverse effects.
Preparations, dosage, and administration.
Phototherapy
Coal tar plus ultraviolet b irradiation
Photochemotherapy (puva therapy)
Drugs for actinic keratoses
Fluorouracil
Actions and uses in dermatology.
Adverse effects.
Preparations and administration.
Diclofenac sodium
Imiquimod
Aminolevulinic acid plus blue light
Drugs for atopic dermatitis (eczema)
Topical immunosuppressants
Tacrolimus ointment.
TABLE 105–5 ▪ Treatment and Prevention of Venereal Warts
Pimecrolimus cream.
Agents used to remove warts
Venereal warts
Provider-applied drugs
Podophyllin.
Bichloroacetic acid (bca) and trichloroacetic acid (tca).
Patient-applied drugs
Imiquimod.
Podofilox.
Kunecatechins (sinecatechins) ointment.
Common warts
Antiperspirants and deodorants
Antiperspirants.
Deodorants.
Drugs for seborrheic dermatitis and dandruff
Drugs for hair loss
Topical minoxidil
Finasteride
Approved Uses of Botulinum Toxin Products
Eflornithine for unwanted facial hair
TABLE 105–6 ▪ Some Antibiotics for Impetigo
Drugs for impetigo
Local anesthetics
BOX 105–1 ▪ SPECIAL INTEREST TOPIC
FACE TIME WITH BOTOX
Not just a pretty face
Key points
Corticosteroids (read text)
CHAPTER 106 Drugs for the ear
Anatomy of the ear
Otitis media and its management
Acute otitis media
Characteristics, pathogenesis, and microbiology
Diagnosis
Figure 106–1 ▪ Anatomy of the ear. The purple arrows indicate flow of the mucociliary system, which can transport bacteria out of the middle ear.
TABLE 106–1 ▪ Primary Pathogens Found in Fluid from the Middle Ear of Children with Acute Otitis Media
Standard treatment
TABLE 106–2 ▪ Criteria for Choosing Initial Antibacterial Therapy Versus Observation in Children with AOM
Treatment of antibiotic-resistant AOM
TABLE 106–3 ▪ Recommended Antibacterial Drugs for Acute Otitis Media
Prevention
Prevention and treatment of influenza.
Vaccination against streptococcus pneumoniae.
Recurrent otitis media
Short-term antibacterial therapy.
Prophylactic antibacterial therapy.
Prevention and treatment of influenza.
Tympanostomy tubes.
Otitis media with effusion
Otitis externa and its management
Acute otitis externa
Characteristics, pathogenesis, and microbiology
Treatment
Topical medications.
Oral medications.
Prevention
Necrotizing otitis externa
Fungal otitis externa (otomycosis)
Key points
CHAPTER 107 Miscellaneous noteworthy drugs
Drugs for pulmonary arterial hypertension
Prostacyclin analogs
Epoprostenol
TABLE 107–1 ▪ Drugs for Pulmonary Arterial Hypertension
Treprostinil
Iloprost
Endothelin-1 receptor antagonists
Bosentan
Actions and use.
Pharmacokinetics.
Adverse effects.
Hepatotoxicity.
Fetal injury.
Anemia.
Drug interactions.
Preparations, dosage, and administration.
Ambrisentan
Phosphodiesterase type 5 inhibitors
Sildenafil
Tadalafil
Drugs for neonatal respiratory distress syndrome
Prenatal and postnatal glucocorticoids
Lung surfactant
Drugs for cystic fibrosis
Pathophysiology of cystic fibrosis
Pancreas.
Lungs.
Reproductive organs.
Drug therapy
Nutritional drugs
Pancreatic enzymes.
Fat-soluble vitamins.
Pulmonary drugs
Inhaled antibiotics for chronic suppressive therapy.
Oral and intravenous antibiotics for acute therapy.
Inhaled dornase alfa.
Oral ibuprofen.
Inhaled beta2-adrenergic agonists.
Drugs for sickle cell anemia
Analgesics and glucocorticoids
Hydroxyurea
Mechanism of action.
Clinical trials.
Adverse effects.
Hematologic monitoring.
Preparations, dosage, and administration.
Drugs for hyperuricemia caused by cancer chemotherapy
Rasburicase
Action and use.
Adverse effects.
Preparations, dosage, and administration.
Allopurinol
Phosphate binders for patients on dialysis
TABLE 107–2 ▪ Phosphate Binders for Patients on Renal Dialysis
Gamma-hydroxybutyrate for cataplexy in patients with narcolepsy
History.
Therapeutic use.
Adverse effects and abuse.
Availability.
Preparations, dosage, and administration.
Riluzole for amyotrophic lateral sclerosis
Riluzole.
Tetrabenazine for chorea of Huntington’s disease
Huntington’s disease
TABLE 107–3 ▪ Drugs for Chorea of Huntington’s Disease
Tetrabenazine
Drugs for fibromyalgia syndrome
TABLE 107–4 ▪ Drugs for Fibromyalgia Syndrome
Antidepressants and related drugs
Tricyclic antidepressants and cyclobenzaprine
Selective serotonin reuptake inhibitors (SSRIs)
Serotonin/norepinephrine reuptake inhibitors
Duloxetine.
Milnacipran.
Anticonvulsants
Analgesics
Tramadol.
Opioid analgesics.
Nonsteroidal anti-inflammatory agents (NSAIDs).
Drugs for sleep disturbances
Drugs for heriditary angioedema
Old drugs for HAE
New drugs for HAE
C1-inhibitor
Figure 107–1 ▪ Drug actions in hereditary angioedema. Two drugs—C1-inhibitor and ecallantide—suppress production of kallikrein, and thereby suppress production of bradykinin. Icatibant blocks bradykinin B2 receptors, and thereby prevents bradykinin-mediated increases in vessel permeability, the immediate cause of edema.
TABLE 107–5 ▪ Drugs for Hereditary Angioedema
Ecallantide
Icatibant
Belimumab for systemic lupus erythematosus
Belimumab
Mechanism of action.
Clinical trials.
Adverse effects.
Infusion/hypersensitivity reactions.
Depression.
Infection.
Mortality.
Drug interactions.
Vaccine interactions.
Preparations, dosage, and administration.
Key points
XX Alternative Therapy
Interactive Review – XX: Alternative Therapy
CHAPTER 108 Dietary supplements
TABLE 108–1 ▪ Why People Use Dietary Supplements
Regulation of dietary supplements
Dietary supplement health and education ACT of 1994
Core provisions
Package labeling
Adverse effects
Impurities, adulterants, and variability
Other provisions
Current good manufacturing practices ruling
Dietary supplement and nonprescription drug consumer protection ACT
A comment on the regulatory status of dietary supplements
Private quality certification programs
Standardization of herbal products
TABLE 108–2 ▪ Concentrations of Active Agents in Some Standardized Herbal Preparations
Adverse interactions with conventional drugs
Some commonly used dietary supplements
Black cohosh
Uses.
Actions.
Effectiveness.
Adverse effects.
Interactions with conventional drugs.
Comments.
Coenzyme Q-10
Uses.
Actions.
Effectiveness.
Adverse effects.
Interactions with conventional drugs.
Cranberry juice
Uses.
Actions.
Effectiveness.
Adverse effects.
Interactions with conventional drugs.
Echinacea
Uses.
Actions.
Effectiveness.
Adverse effects.
Interactions with conventional drugs.
Feverfew
Uses.
Actions.
Effectiveness.
Adverse effects.
Interactions with conventional drugs.
Comments.
Flaxseed
Uses.
Actions.
Effectiveness.
Adverse effects.
Interactions with conventional drugs.
Garlic
Uses.
Actions.
Effectiveness.
Adverse effects.
Interactions with conventional drugs.
Ginger root
Uses.
Actions.
Effectiveness.
Adverse effects.
Interactions with conventional drugs.
Ginkgo biloba
Uses.
Preparations.
Actions.
Effectiveness.
Adverse effects.
Interactions with conventional drugs.
Glucosamine
Uses.
Actions.
Effectiveness.
Adverse effects.
Interactions with conventional drugs.
Green tea
Uses.
Actions.
Effectiveness.
Adverse effects.
Interactions with conventional drugs.
Probiotics
Uses.
Actions.
Effectiveness.
Adverse effects.
Interactions with conventional drugs.
Resveratrol
Uses and sources.
Actions.
Effectiveness.
Adverse effects and interactions with conventional drugs.
Saw palmetto
Uses.
Actions.
Effectiveness.
Adverse effects.
Interactions with conventional drugs.
Soy
Uses.
Actions.
Effectiveness.
Adverse effects.
Interactions with conventional drugs.
St. John’s wort
Uses.
Actions.
Effectiveness.
Adverse effects.
Interactions with conventional drugs.
Valerian
Uses.
Actions.
Effectiveness.
Adverse effects.
Interactions with conventional drugs.
Comments.
Harmful supplements to avoid
Comfrey
Kava
Ma huang (ephedra)
Key points
XXI Toxicology
Interactive Review – XXI: Toxicology
CHAPTER 109 Management of poisoning
Fundamentals of treatment
Supportive care
Poison identification
Prevention of further absorption
Promotion of poison removal
Use of specific antidotes
Drugs and procedures used to minimize poison absorption
Reducing absorption of ingested poisons
Activated charcoal
Gastric lavage and aspiration
Whole-bowel irrigation
Surface decontamination
Drugs and procedures used for poison removal
Drugs that enhance renal excretion
Nondrug methods of poison removal
Figure 109–1 ▪ Chelation of mercury by dimercaprol.
Specific antidotes
Heavy metal antagonists
Chelators for iron toxicity
Deferoxamine.
Actions and uses.
Pharmacokinetics.
Adverse effects.
Contraindications.
Preparations, dosage, and administration.
Deferasirox.
Actions and uses.
Pharmacokinetics.
Adverse effects.
Drug interactions.
Preparations, dosage, and administration.
Deferiprone.
Dimercaprol
Actions and uses.
Pharmacokinetics.
Adverse effects.
Preparations, dosage, and administration.
Edetate calcium disodium (calcium edta)
Actions and uses.
Pharmacokinetics.
Adverse effects.
Preparations, dosage, and administration.
Penicillamine
Actions.
Therapeutic uses.
Pharmacokinetics.
Adverse effects.
Contraindications.
Preparations, dosage, and administration.
Succimer
Actions and uses.
Pharmacokinetics.
Adverse effects.
Preparations, dosage, and administration.
TABLE 109–1 ▪ Specific Antidotes Discussed in Other Chapters
Fomepizole
Actions and uses.
Pharmacokinetics.
Adverse effects.
Preparations, dosage, and administration.
Other important antidotes
Poison control centers
Key points
CHAPTER 110 Potential weapons of biologic, radiologic, and chemical terrorism
Bacteria and viruses
Bacillus anthracis (anthrax)
Microbiology
TABLE 110–1 ▪ Online Resources for Information on Biologic, Radiologic, and Chemical Terrorism
TABLE 110–2 ▪ Therapy of Inhalational Anthrax in the Limited Casualty Setting
Clinical manifestations
Inhalational anthrax.
Cutaneous anthrax.
Treatment of established infection
Inhalational anthrax.
TABLE 110–3 ▪ Therapy of Inhalational Anthrax in the Mass Casualty Setting
Cutaneous anthrax.
Pre-exposure vaccination
Postexposure prophylaxis: antibiotics plus vaccination
Francisella tularensis (tularemia)
Clinical manifestations.
Treatment.
Yersinia pestis (pneumonic plague)
Clinical manifestations.
Treatment.
Variola virus (smallpox)
Pathogenesis and clinical manifestations
Transmission
Treatment
Smallpox vaccine
Description.
Efficacy.
Duration of protection.
Administration.
Interpreting the response.
Adverse effects.
Mild effects.
Moderate to severe effects.
Possible cardiac effects.
Management of adverse effects.
TABLE 110–4 ▪ Medical Conditions and Other Factors That Contraindicate Routine Smallpox Vaccination*
Who should not be vaccinated?
Biotoxins
Botulinum toxin
Mechanism of action.
Clinical manifestations.
Treatment.
Ricin
Mechanism of action.
Clinical manifestations.
Treatment.
Chemical weapons
Nerve agents
Sulfur mustard (mustard gas)
Properties.
Clinical manifestations.
Treatment.
Radiologic weapons
Weapon types
Nuclear bombs
Attacks on nuclear power plants
Dirty bombs (radiologic dispersion devices)
Drugs for radiation emergencies
Potassium iodide
Penetrate zinc trisodium and penetrate calcium trisodium
Prussian blue
Key points
Appendixes
Appendix A Adult immunization, United States, 2011
Immunization schedule notes
1. Influenza vaccination
2. Tetanus, diphtheria, and acellular pertussis (Td/Tdap) vaccination
Figure A–1 ▪ Recommended adult immunization schedule by age group, United States, 2011.
Figure A–2 ▪ Vaccines that might be indicated for adults based on medical and other conditions, United States, 2011.
3. Varicella vaccination (“shingles”)
4. Human papillomavirus (HPV) vaccination
5. Herpes zoster vaccination
6. Measles, mumps, rubella (MMR) vaccination
Measles component.
Mumps component.
Rubella component.
Healthcare personnel born before 1957.
7. Pneumococcal polysaccharide (PPSV) vaccination
Medical indications.
Other indications.
8. Revaccination with PPSV
9. Meningococcal vaccination
Medical indications.
Other indications.
10. Hepatitis A vaccination
Medical indications.
Behavioral indications.
Occupational indications.
Other indications.
11. Hepatitis B vaccination
Behavioral indications.
Occupational indications.
Medical indications.
Other indications.
Dosing schedules.
12. Selected conditions for which haemophilus influenzae type b (hib) vaccine may be used
13. Immunocompromised persons
Appendix B Guide to gender-related drugs
Drugs used in pregnancy
Drugs related to labor and delivery
Drugs used in perinatal therapy
Drugs and breast-feeding
Drugs for women’s health disorders
Drugs used to prevent or terminate pregnancy
Drugs for male health disorders
Drugs for sexually transmitted diseases (STDs)
Appendix C Commonly used abbreviations
Appendix D Canadian drug information
International system of units
Drug serum concentrations
Canadian drug legislation
Prescription drugs (schedule F)
Table D–1 ▪ Therapeutic Serum Drug Concentrations
Nonprescription medications
National drug schedules
New drug development in Canada
Patent laws
References
Appendix E Prototype drugs and their major uses
Peripheral nervous system drugs
Muscarinic agonists
Muscarinic antagonists
Cholinesterase inhibitors
Neuromuscular blockers
Adrenergic agonists
Alpha-adrenergic blockers
Beta-adrenergic blockers
Indirect-acting antiadrenergics
Central nervous system drugs
Drugs for Parkinson’s disease
Drugs for Alzheimer’s disease
Drugs for multiple sclerosis
Drugs for epilepsy
Drugs for migraine
Local anesthetics
General anesthetics
Opioid (narcotic) analgesics and antagonists
Antipsychotic agents
Antidepressants
Drugs for bipolar disorder (manic-depressive illness)
Drugs for anxiety and insomnia
Central nervous system stimulants
Drugs for attention-deficit/hyperactivity disorder
Pharmacologic aids to smoking cessation
Diuretics
Drugs that affect the heart, blood vessels, and blood
Drugs that affect the Renin-Angiotensin-Aldosterone system
Calcium channel blockers
Drugs for hypertension
Drugs for angina pectoris
Drugs for heart failure
Antidysrhythmic drugs
Drugs used to lower blood cholesterol
Anticoagulants
Antiplatelet and thrombolytic drugs
Hematopoietic and thrombopoietic growth factors
Drugs for hemophilia
Drugs for endocrine disorders
Drugs for diabetes
Drugs for thyroid disorders
Drugs for adrenal insufficiency
Women’s health
Estrogens
Progestins
Contraceptive agents
Drugs for infertility
Drugs that affect uterine function
Men’s health
Androgens
Drugs for erectile dysfunction
Drugs for benign prostatic hyperplasia
Anti-inflammatory, antiallergic, and immunologic drugs
Immunosuppressants
Antihistamines (h1 antagonists)
COX inhibitors (aspirin-like drugs)
Glucocorticoids
Drugs for bone and joint disorders
Drugs for rheumatoid arthritis
Drugs for hyperuricemia of gout
Drugs for osteoporosis
Respiratory tract drugs
Drugs for asthma
Drugs for allergic rhinitis
Drugs for cough
Gastrointestinal drugs
Drugs for peptic ulcer disease
Laxatives
Antiemetics
Drugs for irritable bowel syndrome (IBS)
Drugs for inflammatory bowel disease
Drugs for weight loss
Drugs for bacterial infections
Penicillins, cephalosporins, and other drugs that weaken the bacterial cell wall
Bacteriostatic inhibitors of protein synthesis
Aminoglycosides (bactericidal inhibitors of protein synthesis)
Fluoroquinolones
Cyclic lipopeptides
Sulfonamides and trimethoprim
Drugs for tuberculosis
Drugs for fungal infections
Drugs for viral infections
Drugs for cytomegalovirus infection
Drugs for herpes simplex virus infection
Drugs for hepatitis
Drugs for influenza
Drugs for respiratory syncytial virus infection
Drugs for HIV infection
Drugs for parasitic diseases
Drugs for malaria
Drugs for ectoparasitic infestation
Anticancer drugs: cytoxic agents
Anticancer drugs: hormonal agents, targeted drugs, and other noncytotoxic anticancer drugs
Drugs for breast cancer
Drugs for prostate cancer
Glucocorticoids
Biologic response modifiers: immunostimulants
Targeted drugs
Other important drugs
Drugs for acne
Drugs for open-angle glaucoma
Drugs for age-related macular degeneration
Drugs for pulmonary arterial hypertension
Drugs for neonatal respiratory distress syndrome
Drugs for fibromyalgia syndrome
Drugs for hereditary angioedema
Index
Index
0-9, and symbols
A
B
C
D
E
F
G
H
I
J
K
L
M
N
O
P
Q
R
S
T
U
V
W
X
Y
Z
Special interest topics
Special interest topics
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Free Sample Test bank for Pharmacology for Nursing Care 8th Edition by Richard A. Lehne

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Test bank for Pharmacology for Nursing Care 8th Edition by Richard A. Lehne