Table of Contents
|Date | |Credits |3 credits |
|Course Title |Nursing Math and Pharmacology |Course Number |NUR 1141 |
|Pre-requisite (s) |MAT0002, DEP 1000, NUR 1889, 1822, 1045, 1025,|Co-requisite (s) |None |
| |1025C, 1025L | | |
|Hours |45 theory hours/45 clock hours |Total outside hours |90 hours |
|Note: A minimum of 2 hours of outside work is assigned per clock hour. |
|Place and Time of Class Meeting |
Institute of Healthcare Professions
2100 45th Street, Suite A2A
West Palm Beach, FL 33407
Hybrid
|Name and Contact Information of Instructor |
Instructor: Johnnetta Wider RN, MSN
Email: JWider@
Office Hours: By Appointment
Campus Telephone: (561) 202-6333
Method of Delivery: Online
|Book required |
[pic]
Lehne’s Pharmacology for Nursing Care, 9/e, Jacqueline Rosenjack Burchum & Laura D. Rosenthal
©2016 | Pearson | Published: 2/2015
ISBN-9780323322614
Classroom expectations for students
|Attendance Policy |
Students are expected to participate in all required instructional activities in their courses. Online courses are no different in this regard; however, participation must be defined in a different manner.
1. Student “attendance” in an online course is defined as active participation in the course as described in the course syllabus. Instructors are responsible for incorporating specific instructional activities within their course and will, at a minimum, have weekly mechanisms for documenting student participation. These mechanisms may include, but are not limited to, participating in a weekly discussion board, submitting/completing assignments in the online platform, or communicating with the instructor.
2. Students aware of necessary absences must inform the professor with as much advance notice as possible in order to make appropriate arrangements.
3. Any student absent 20 percent or more of the online course, i.e., non-participatory during 3 or more weeks of an 11 week term, may receive an F for that course.
4. Any student who has not actively participated in an online class prior to the census date for any given term is considered a "no-show" and will be administratively withdrawn from the class without record. To be counted as actively participating, it is not sufficient to log in and view the course. The student must be submitting work as described in the course syllabus.
5. Additional attendance and participation policies for each course, as defined by the instructor in the course syllabus, are considered a part of the attendance policy
Termination may occur for any of the following attendance situations:
1. Eight (8) consecutive absences per semester.
2. Absence in excess of 20 percent (20%) of available course hours.
3. Absence in excess of 20 percent (20%) of externship hours.
|Student Tardiness Policy |
Tardiness for didactic or clinical education will not be tolerated. Anytime beyond the scheduled reporting time will be considered late or tardy. When attending clinical externship, if a student is to be late, he or she must notify the clinical instructor at the facility and the program clinical coordinator. If a student must miss class, he or she must contact the program director or instructor at least 30 minutes prior to the class beginning for didactic education five episodes of tardiness or leaving IHP early per semester will result in an absence.
NOTE: Plagiarism is defined as the use, without proper acknowledgment, of the ideas, phrases, sentences, or larger units of discourse from another writer or speaker. Plagiarism includes the unauthorized copying of software and the violation of copyright laws. Students who commit plagiarism will obtain a grade of “Failure” on their exam or assignment.
|Course Description (must correspond exactly to Catalog description) |
This course combines theory and laboratory experiences to allow for mastery of the basic principles of pharmacotherapeutics and the role of the nurse in safe effective administration of medications with emphasis places on dosage calculations.
|Learning Objectives |
The primary goal is to establish knowledge and skills for the safety administration of drug therapy within the role of the registered professional nurse.
STUDENT LEARNING OUTCOMES (SLO)
All students successfully completing this course will be able to:
1.1.Collect, analyze, and prioritize relevant physical, developmental, psychosocial, cultural, spiritual, and functional assessment data to provide individualized patient care.
2 2. Utilize the nursing process, critical thinking, evidence-based information, and knowledge from the arts and sciences to support sound clinical decisions.
3 3. Communicate effectively through verbal, nonverbal, written, and technological means with individuals, families, and health care team members.
4 4. Plan and implement nursing care in a safe, compassionate, culturally sensitive manner that preserves human dignity and promotes growth of individuals and families.
5 5. Manage the efficient, effective use of human, physical, financial, and technological resources in providing continuity of care within and across healthcare settings.
6 6. Collaborate with individuals, families, and healthcare team members in providing comprehensive, individualized patient care.
7 7. Demonstrate accountability in adhering to standards of professional practice within legal and ethical frameworks.
8.8. Participate in activities that promote professional development and personal growth.
COURSE OBJECTIVES (CO)
All students successfully completing this course will be able to:
1. Describe the mechanism of action, therapeutic uses, side effects, and adverse reactions for
each major drug class. (SLO – 1, 2)
2. Discuss basic physiological and pathophysiological mechanisms involved in the rationale for
drug therapy. (SLO – 1, 2)
3. Examine recent research findings and developments related to drug therapy. (SLO-2)
4. Demonstrate the ability to accurately calculate drug dosages. (SLO- 3,4, 5)
5. Identify physical, developmental, psychosocial, religious, and cultural factors that impact
drug therapy. (SLO-1, 3, 4, 6)
6. Describe the nursing interventions and patient education necessary for safe administration of
the major drug classes. (SLO– 2, 3, 5, 7)
7. Explain the nurse’s role in teaching patients receiving drug therapy. (SLO – 3, 5)
8. Identify the legal and ethical standards related to the nurse’s role in drug therapy. (SLO – 3, 7)
9. Recognize the responsibility for continued learning regarding drug therapy. (SLO –3, 8)
|Topical Outline and Schedule |
|DATE |WEEK 1 |
|SPECIFIC OBJECTIVES |Describe the course. |
| |Discuss the library and library resources. |
| |Define these four basic terms: drug, pharmacology, clinical pharmacology, and therapeutics. |
| |List the three most important properties of an ideal drug as well as several other important properties, and |
| |explain why many drugs do not have these traits. |
| |Differentiate between therapeutic effect and maximum benefit with minimum harm. |
| |Identify factors in determining the intensity of drug responses. |
| |Utilize mobile applications to access information about medications. |
| |Relate the five steps of the nursing process to the administration of medications. List the Five Rights of Drug |
| |Administration and the patient’s rights regarding medications administered by healthcare providers. |
| |Discuss the purpose of preadministration assessment. |
| |Discuss the analysis of the data and development of nursing diagnoses to (1) judge the appropriateness of the |
| |prescribed regimen, (2) identify health problems the drug might cause, and (3) determine the patient’s capacity for|
| |self-care. |
| |Develop a plan of care that does the following: (1) defines the goal of drug therapy; (2) is prioritized based on |
| |the drug under consideration and the patient’s unique characteristics; (3) identifies nursing interventions based |
| |on [a] drug administration, [b] interventions to enhance therapeutic effects, [c] interventions to minimize adverse|
| |effects and interactions, and [d] patient education; and (4) establishes objective criteria for evaluation. |
| |Discuss implementation of the care plan in drug therapy. |
| |Understand how to record nursing interventions and observations of the patient’s responses to drug therapy. |
| |Describe the five diverse and important topics in pharmacology: (1) landmark drug legislation in the United States |
| |that reflects the evolution in our national viewpoint on regulation of the pharmaceutical industry; (2) new drug |
| |development (e.g., the cost of more than $800 million to develop a new drug); (3) the nuances of formulating drug |
| |names; (4) over-the-counter drugs; and (5) sources of drug information. All of these topics have significant |
| |implications for pharmacology and nursing care. Such information requires the profession of nursing and individual |
| |nurses to participate in continuing education in pharmacology and its administration. |
| |Discuss Phases I, II, III, and IV of the clinical testing of new drugs. Discuss the ethical and legal implications |
| |for the different phases of clinical testing. Phase I studies involve the use of healthy human volunteers to test |
| |the drugs. In Phases II and III, drugs are tested in patients. Upon completion of Phase III, the drug manufacturer |
| |applies to the FDA for conditional approval. |
| |Explain the purpose of Phase IV clinical studies after regulatory (i.e., FDA) approval. Discuss the important |
| |information that can be gained from Phase IV (postmarketing surveillance) of clinical drug testing and explain the |
| |roles and responsibilities of the nurse, nurse practitioner, and physician in gathering and reporting new data. |
| |Discuss chemical, generic, and proprietary (trade or brand) names of drugs and explain the benefits, if any, of |
| |generic drugs over brand-name drugs. |
| |Identify appropriate resources for pharmacology information and patient care and discuss why, in particular, some |
| |may be more suitable than others for a specific purpose (e.g., a specific type of information that is sought). |
| |Perform basic arithmetic calculations, including addition, subtraction, multiplication, and division with positive |
| |and negative numbers. |
| |Perform calculations incorporating rules for rounding numbers to achieve the correct result. |
| |Convert among fractions, decimal form, and percentage form. |
| |Convert between metric units. |
| |Convert between metric and nonmetric units. |
| |Perform ration and proportion calculations. |
|TOPIC (S) |Syllabus |
| |Introduction |
| |Orientation to pharmacology |
| |Application of Pharmacology in Nursing Practice |
| |Drug Regulation, Development, Names, and Information |
|LEARNING ACTIVITIES |READING ASSIGNMENTS |
| |Chapter 1: Orientation to Pharmacology – pp 1 - 4 |
| |Chapter 2: Application of Pharmacology in Nursing Practice – pp 5 – 13 |
| |Chapter 3: Drug Regulation, Development, Names, and Information – pp 14 - |
| |21 |
| | |
|OUTSIDE WORK & ASSIGNED |DISCUSSION |
|READINGS |Differentiate between therapeutic effect and maximum benefit with minimum harm. |
| |Discuss chemical, generic, and proprietary (trade or brand) names of drugs and explain the benefits, if any, of |
| |generic drugs over brand-name drugs. |
| | |
| |SUBMISSION |
| |Math worksheet |
| | |
| |ASSIGNMENT |
| |Review the syllabus |
| |Read assignments |
| |Post discussion topic by Wednesday at 11:55 pm EST |
| |Respond to at least one classmate by Friday at 11:55 pm EST |
| |Complete math worksheet & submit by Friday at 11:55 pm EST |
| |Complete Case Study |
| | |
| |ASSESSMENT |
| |Discussion & response |
| |Math worksheet |
| |Case study |
| |Quiz Chapter 1, 2, & 3 |
| | |
| |Homework: Chapter readings: Chapters 4, 5, 6, 7, 8 |
|DATE |Week 2 |
|SPECIFIC OBJECTIVES |At the end of this lesson, you will be able to: |
| |Discuss the four main processes that make up pharmacokinetics (absorption, distribution, metabolism, and excretion)|
| |and appropriately apply these processes to clinical usefulness. |
| |Discuss the advantages and disadvantages of the various techniques of drug administration as they relate to |
| |pharmacokinetics, noting especially any barriers to absorption associated with intravenous, intramuscular, and oral|
| |administration. Also compare oral administration with parenteral administration. |
| |Describe blood flow to tissues, the ability of a drug to exit the vascular system, and the ability of a drug to |
| |enter cells, and then discuss the characteristics of drug molecules that can alter these processes. |
| |Describe the ultimate “goal” of drug metabolism, also known as biotransformation. Discuss the general processes |
| |involved in drug metabolism and identify the major or vital organs in which most drug metabolism occurs. Discuss |
| |special considerations in drug metabolism. |
| |Discuss the importance of excretion of a drug from the body and some of the routes by which the drug may be |
| |excreted. |
| |Discuss the importance of understanding the time course of drug responses (plasma drug levels, single-dose time |
| |course, drug half-life, and drug levels produced with repeated doses). Explain why clinicians often monitor plasma |
| |drug levels, and describe how these levels are regulated to prevent drug toxicity. Identify the two factors that |
| |largely determine the duration of a single-dose time course, and compare drugs with short half-lives versus those |
| |with long half-lives. Discuss the negative effects of repeated drug doses. |
| |Discuss the consequences of drug blood levels that fluctuate considerably or erratically between doses, and |
| |describe how nurses identify such fluctuations. Discuss measures that traditionally have been taken to minimize |
| |fluctuation. |
| |Define pharmacodynamics and its relationship to the action of drugs on the body. |
| |Discuss dose-response relationships (e.g., basic features of the dose-response relationships, maximal efficacy, and|
| |relative potency), the effects drugs can produce, and the amount of drug needed to elicit an effect. |
| |Discuss properties of drug-receptor interactions (e.g., drug receptors, four primary receptor families, receptors |
| |and selectivity for drug action, theories of drug-receptor interaction, agonists, antagonists, partial agonists, |
| |and regulation of receptor sensitivity). |
| |Describe how receptors function in the responses to many drugs and physiologic processes, such as the activity of |
| |the respiratory and gastrointestinal systems. |
| |Differentiate drugs that are agonists, partial agonists, or antagonists. |
| |List the four primary families of receptors. |
| |Discuss “receptorless drugs” (e.g., antacids, antiseptics, saline laxatives, chelating agents, and so on). |
| |Discuss interpatient variability in drug responses and describe how to measure variability. |
| |Define the ED50 and the LD50. |
| |Discuss the concept of a drug’s therapeutic index and its application and benefits to clinical practice, such as |
| |the relationships between the doses of a drug and whether its effects are subtherapeutic (inadequate response), |
| |therapeutic (desired response), or toxic (adverse effects related to excessive dosage). |
| |Discuss the role of the nurse in achieving therapeutic responses of selected medications. |
| |Implement effective communication tools to advocate for patients in the clinical setting. |
| |Identify electronic resources available for determining action, side effects, therapeutic index, and anticipated |
| |effects of drugs. |
| |Discuss the consequences of drug-drug interactions, the basic mechanisms of drug-drug interactions, and the |
| |critical steps in minimizing adverse drug-drug interactions. |
| |Focus on the liver as an example of a drug-metabolizing system and explain why it is such a crucial organ in many |
| |drug-drug interactions. |
| |Discuss the effect of food on drug absorption, on drug metabolism (e.g., grapefruit juice), and on drug toxicity |
| |and action, as well as the timing of drug administration with respect to meals. |
| |Give examples of inhibitory interaction of drugs that can produce dangerous effects and those that are beneficial. |
| |Discuss the mechanisms and clinical consequences of drug-herb interactions and drug-food interactions. Focus on |
| |ways to minimize adverse drug-drug interactions and drug-food interactions. Include in the discussion the effect of|
| |food on drug absorption and metabolism, drug toxicity, drug action, and the timing of drug administration with |
| |respect to meals. |
| |Discuss the dilemma that increased consumption of herbal supplements has created in the pharmaceutical environment |
| |because of these supplements’ potential for common and significant interactions with prescription and |
| |over-the-counter drugs. |
| |Design a plan of care for patients who are prescribed medications that have known drug-drug or drug-food |
| |interactions. |
| |Identify electronic resources available for determining action, side effects, therapeutic index, and anticipated |
| |effects of drugs. |
| |Discuss the scope of the problem of adverse drug reactions. |
| |Discuss definitions for adverse drug reactions (e.g., side effect, toxicity, allergic reaction, idiosyncratic |
| |effect, iatrogenic disease, physical dependence, carcinogenic effect, and teratogenic effect). |
| |Discuss organ-specific toxicity. Focus on the liver as a drug-metabolizing system and explain why it is such a |
| |crucial participant in organ-specific toxicity with drugs. |
| |Discuss how and why adverse drug reactions occur, given that for a prescription drug to be approved for use, it |
| |must have demonstrated and been documented for safety, and also given the explicit printed information provided |
| |about such facts as doses, routes, interactions, and so on. |
| |Discuss adverse reactions to new drugs and the importance of being alert for unusual responses when giving new |
| |drugs. Also point out the importance of informing other nurses where to report unknown adverse effects of a new |
| |drug and of accessing a website where information on adverse effects can be reported. |
| |Discuss measures that can be used to minimize adverse drug events. |
| |Define medication errors and explain what constitutes an error, as well as who makes errors. |
| |Discuss types of medication errors, causes of medication errors, ways to reduce medication errors, and ways to |
| |report medication errors. |
| |Discuss the significance of body weight and composition, focusing on the effect of weight and the requirement for |
| |larger doses of a drug to obtain a therapeutic effect because of an increase in tissues to perfuse (percentage of |
| |body fat) and an increase in receptor sites in some reactive tissue. |
| |Discuss age as a factor in medication administration, noting that drug sensitivity varies with age and that infants|
| |are especially sensitive to drugs, as are the elderly. |
| |Discuss the effects of kidney disease, liver disease, acid-base imbalance, and altered electrolyte status on drug |
| |responses. |
| |Discuss the three categories of drug tolerance: pharmacodynamic tolerance, metabolic tolerance, and tachyphylaxis. |
| |Define placebo effects and explain the beneficial and negative effects. |
| |Discuss bioavailability and other causes of variable absorption. Explain why differences in bioavailability are a |
| |significant concern with drugs that have a narrow therapeutic index. |
| |Discuss common mechanisms by which genetic differences modify drug responses (for example, altered |
| |drug-metabolizing enzymes, altered drug targets). |
| |Discuss three gender-related differences that can occur in response to administration of the same drug. |
| |Discuss two primary determinants of race-related drug responses. |
| |Discuss factors that may result in the patient’s failure to take medications as prescribed. |
| |Discuss drug interaction as a source of variability. |
| |Discuss the effects of diet on drug responses. |
|TOPIC (S) |Unit 2: Basic Principles of Pharmacology |
| |Pharmacokinetics |
| |Pharmacodynamics |
| |Drug Interactions |
| |Adverse Drug Reactions and Medication Errors |
| |Individual Variation in Drug Responses |
|LEARNING ACTIVITIES |READING ASSIGNMENT |
| |Chapter 4: Pharmacokinetics – pp 22 – 43 |
| |Chapter 5: Pharmacodynamics – pp 44 – 54 |
| |Chapter 6: Drug Interactions – pp 55 – 61 |
| |Chapter 7: Adverse Drug Reactions and Medication Errors – pp 62 -72 |
| |Chapter 8: Individual Variation in Drug Responses – pp 73 - 80 |
| | |
| |DISCUSSION |
| |Discuss the effects of diet on drug responses. |
| |Define placebo effects and explain the beneficial and negative effects. |
| |Discuss measures that can be used to minimize adverse drug events. |
| |Discuss the role of the nurse in achieving therapeutic responses of selected medications. |
| | |
| |SUBMISSION |
| |Math Worksheet |
| | |
| |ASSIGNMENT |
| |Review the syllabus |
| |Read assignments |
| |Post discussion topic by Wednesday at 11:55 pm EST |
| |Respond to at least one classmate by Friday at 11:55 pm EST |
| |Complete math worksheet & submit by Friday at 11:55 pm EST |
| |Complete case study |
| | |
| |ASSESSMENT |
| |Discussion & response |
| |Math worksheet |
| |Case study |
| |Quiz Chapters 4, 5, 6, 7, 8 |
| | |
| | |
| |Homework: Chapter readings: Chapters 9, 10, 11 |
| |WEEK 3 |
|SPECIFIC OBJECTIVES |At the end of this lesson, you will be able to: |
| |Identify four basic considerations of drug therapy during pregnancy. |
| |Discuss the physiologic changes that occur during pregnancy and their effect on drug disposition and dosing. |
| |Discuss placental drug transfer, focusing on the importance of clinicians assuming that any drug taken during |
| |pregnancy will reach the fetus. |
| |Discuss adverse reactions during pregnancy, focusing on the effects of drugs on the fetus and neonate. |
| |Discuss the term teratogenesis as it relates to drug therapy during pregnancy and the stages of fetal development. |
| |Identify teratogens and measures that can be taken to minimize their risks. |
| |Discuss the appropriate steps in determining exposure to teratogens. |
| |Discuss drug therapy during breast-feeding and the potential risks to the breast-feeding neonate or infant of a |
| |mother who is taking drugs. Consider the health and well-being of both the mother and the fetus. |
| |Distinguish among the categories established by the U.S. Food and Drug Administration (FDA) to classify potential |
| |drug risks to the fetus (A, B, C, D, X). Comment on the meaning of each category with regard to potential fetal |
| |risks, the reasons medications are categorized as they are, and the evidence upon which each drug is assigned to a |
| |classification. |
| |Provide an overview of the pharmacokinetics of neonates and infants. |
| |Discuss drug absorption in neonates and infants, focusing on a drug’s physicochemical properties and its effects on|
| |absorption. |
| |Discuss drug absorption as it relates to the route of administration in pediatric patients. |
| |Discuss factors directly related to drug distribution in neonates and infants (e.g., protein binding and the |
| |blood-brain barrier). |
| |Discuss hepatic metabolism and compare the drug-metabolizing capacity of a newborn with that of a 1-year-old |
| |infant. |
| |Discuss renal excretion and compare the drug-excreting capacity of a newborn with that of a 1-year-old infant. |
| |Discuss the pharmacokinetics of children 1 year old or older. |
| |Discuss reasons pediatric patients are subject to adverse drug reactions when drug levels rise too high. |
| |Discuss dosage determination, noting that pediatric doses have been established for some drugs but not for others |
| |and, therefore, for drugs that do not have established pediatric doses, the doses can be extrapolated from adult |
| |doses. |
| |Discuss methods that are effective at and critical to promoting parent and guardian adherence to pediatric drug |
| |regimens. |
| |Summarize some of the main reasons a very young patient may be considered “highly” sensitive to drugs, considering |
| |both pharmacokinetic factors (absorption, distribution, and elimination) and pharmacodynamic factors that affect |
| |this apparent sensitivity. |
| |Identify the main age-related physiologic, pathophysiologic, and pharmacologic factors that influence how older |
| |adults respond differently to drugs and state how those differences could (or likely would) affect drug responses. |
| |Identify the most important factors that predispose older patients to adverse drug reactions. |
| |Describe common reasons for noncompliance and nonadherence that are particularly relevant to older adults and list |
| |some approaches for minimizing those problems and improving compliance. |
| | |
|TOPIC (S) |Unit 3: Drug Therapy Across the Life Span |
| |Drug Therapy During Pregnancy and Breast-Feeding |
| |Drug Therapy in Pediatric Patients |
| |Drug Therapy in Geriatric Patients |
|LEARNING ACTIVITIES |READING ASSIGNMENT |
| |Chapter 9: Drug Therapy During Pregnancy and Breast-Feeding – pp 81 - 87 |
| |Chapter 10: Drug Therapy in Pediatric Patients – pp 88 - 91 |
| |Chapter 11: Drug Therapy in Geriatric Patients – pp 92 – 95 |
| | |
| | |
| |DISCUSSION (Choose 1) |
| |Discuss adverse reactions during pregnancy, focusing on the effects of drugs on the fetus and neonate. |
| |Discuss the pharmacokinetics of children 1 year old or older. |
| |Describe common reasons for noncompliance and nonadherence that are particularly relevant to older adults and list |
| |some approaches for minimizing those problems and improving compliance. |
| | |
| | |
| |SUBMISSION |
| |• Math Worksheet |
| | |
| |ASSIGNMENT |
| |Review the syllabus |
| |Read assignments |
| |Post discussion topic by Wednesday at 11:55 pm EST |
| |Respond to at least one classmate by Friday at 11:55 pm EST |
| |Complete math worksheet & submit by Friday at 11:55 pm EST |
| |Complete case study |
| | |
| |ASSESSMENT |
| |Discussion & response |
| |Math worksheet |
| |Case study |
| |Quiz Chapters 9, 10, 11 |
| | |
| | |
| |Homework: Chapter readings: Chapters 12, 13, 14, 15, 16, 17, 18, & 19 |
|DATE |WEEK 4 |
|SPECIFIC OBJECTIVES |At the end of this lesson, you will be able to: |
| |Discuss the reason most neuropharmacologic agents act by altering synaptic transmission instead of altering axonal |
| |conduction. |
| |Describe the general steps involved in neurotransmission (synaptic transmission) and axonal conduction. State the |
| |elements or processes that need to occur, regardless of the site in the nervous system, for synaptic transmission |
| |to work. |
| |Discuss specific ways in which drugs can alter the steps of synaptic transmission. |
| |Discuss the relationship between multiple receptor types and selective drug action. |
| |Identify the two major divisions of the peripheral nervous system. |
| |Differentiate between the somatic (motor) nervous system and the sympathetic and parasympathetic branches of the |
| |autonomic nervous system in terms of (1) overall anatomic organization (numbers, types of nerves); (2) |
| |neurotransmitters made and released by the nerves; and (3) the targets (effectors) of the neurotransmitters’ |
| |actions, whether those structures are innervated by one or both branches of the autonomic nervous system, and the |
| |effects of activating those structures. |
| |Describe the differences distinguishing the four main subtypes of adrenergic receptors – alpha1, alpha2, beta1, and|
| |beta2 – in terms of where (on what structures) they are found and the responses their activation causes. |
| |Describe the differences between the two main subtypes of cholinergic receptors – nicotinic (both nicotinicN and |
| |nicotinicM) and muscarinic – in terms of where (on what structures) they are found and the responses their |
| |activation causes. |
| |Identify the basic processes by which the main autonomic nervous system neurotransmitters are terminated |
| |physiologically. |
| |State the responses that a muscarinic agonist would be expected to cause through direct activation of muscarinic |
| |cholinergic receptors (consider bethanechol). The student should focus on the main “targets” of parasympathetic |
| |nervous system activity: eyes, respiratory system, heart and blood vessels, gastrointestinal (GI) and urinary |
| |tracts, and the secretory activity of exocrine glands (for example, lacrimal, mucous, and so on). |
| |List cholinergic responses not normally caused when the usual therapeutic doses of a muscarinic agonist are |
| |administered and explain why these effects do not occur. |
| |State the main side effects of a muscarinic agonist (for example, bethanechol) and related precautions or |
| |contraindications to its use. |
| |Give several reasons why acetylcholine itself is not used to produce selective muscarinic-activating effects and |
| |why other drugs generally are chosen. |
| |Describe the signs and symptoms of muscarinic antagonist (for example, atropine) “poisoning,” how it is managed, |
| |and how and where such a syndrome can occur without the patient receiving any therapeutic product. |
| |Describe the main effects of cholinesterase inhibitors on structures controlled by the autonomic nervous system and|
| |on skeletal muscle, and state the general mechanism by which these effects occur. |
| |Compare and contrast the effects of the cholinesterase inhibitors with those of bethanechol, which was described as|
| |the most representative muscarinic agonist (see Chapter 14). |
| |State the main clinical uses of cholinesterase inhibitors and precautions for and contraindications to their use. |
| |Recognize the meaning and importance of the term quaternary when applied to the structure of a drug; compare and |
| |contrast the actions of neostigmine and physostigmine in the context of whether they are quaternary compounds. |
| |Compare and contrast the cholinergic crisis and the myasthenic crisis in a hypothetical patient with myasthenia |
| |gravis; describe simple assessments that would help distinguish the two conditions; and state the rationale for |
| |using cholinesterase inhibitors to help confirm the diagnosis. |
| |Describe the signs and symptoms associated with cholinesterase inhibitor overdose and the general approaches to |
| |managing it. |
| |State the rationales for administering a cholinesterase inhibitor to a patient who has been intentionally paralyzed|
| |(such as, for surgery) with a neuromuscular blocking drug. State which class of neuromuscular blockers causes |
| |effects that can be reversed by the cholinesterase inhibitor. State the other main drug that is given as part of |
| |the postoperative reversal procedure and explain when and why it is given. |
| |Describe the signs and symptoms associated with “irreversible” cholinesterase inhibitors and the general approaches|
| |used to manage poisoning caused by these substances. |
| |Describe the anatomy of the somatic nervous system, the key transmitter and receptor type involved in skeletal |
| |muscle activation, and the physiologic consequences of activating those cell receptors. |
| |Compare and contrast the mechanisms of action of nondepolarizing and depolarizing neuromuscular blocking agents and|
| |state how these actions influence the use of one class rather than the other in specified clinical situations. |
| |Identify three specific uses for neuromuscular blocking agents and describe the monitoring and other measures |
| |necessary with their use. |
| |Discuss the main risks and main cause of death with neuromuscular blocking agents and describe steps to manage |
| |potentially fatal responses. |
| |Identify the class of drugs used to reverse the effects of nondepolarizing neuromuscular blockers and describe the |
| |mechanism by which they cause that reversal. Also explain why pharmacologic reversal is not used when |
| |succinylcholine is the neuromuscular blocker. |
| |Describe the etiology, signs, and symptoms of malignant hyperthermia; the drugs associated with a high risk for |
| |that condition; and interventions to be implemented should it develop. |
| |Discuss the rationale for the limited applications of mecamylamine. |
| |Recall (for example, from Chapter 13) the sites (effectors) of alpha1-, beta1-, and beta2-adrenergic receptors and |
| |state the expected responses from their activation by a suitable agonist. |
| |Classify the following agonists in terms of the adrenergic receptors they activate and the responses they cause as |
| |a result of direct receptor activation: (1) epinephrine, (2) norepinephrine, (3) phenylephrine, (4) isoproterenol, |
| |(5) terbutaline, (6) dobutamine. |
| |Explain the difference between direct cardiac (beta1) effects of adrenergic agonists and reflex (baroreceptor |
| |reflex–mediated) effects of those same drugs, using norepinephrine, phenylephrine, and isoproterenol as examples. |
| |Explain how each of the following affects structures controlled by the sympathetic nervous system, comparing how |
| |they work with how a direct-acting agonist such as epinephrine works, and state one or more clinical uses for each:|
| |(1) ephedrine, (2) amphetamines, (3) cocaine, (4) monoamine oxidase (MAO) inhibitors |
| |Identify the desired effects when a therapeutic dose of epinephrine is given for anaphylaxis and explain the |
| |actions of the drug that earn it the label “drug of choice” for anaphylaxis. |
| |Identify individuals who should carry an EpiPen, when they should use it, how dosage should be calculated, and how |
| |it should be stored and replaced. |
| |Explain the self-injection procedure for the EpiPen. |
| |Summarize the main adrenergic receptor subtypes that mediate the ocular, cardiovascular, pulmonary, and uterine |
| |responses to sympathetic nervous system activation. |
| |Describe the main direct and indirect effects of alpha- and beta-adrenergic blockers (antagonists) on the |
| |structures listed in the preceding objective and on stated sympathetic/adrenergic responses. For each effect, the |
| |student should be able to state any applicable precautions or contraindications to the use of such antagonists and |
| |explain the potential outcome if a stated blocker is administered to a patient for whom the antagonist ought not to|
| |be used. |
| |Describe the adverse effects of alpha blockade and compare them with the adverse effects of beta blockade. |
| |Describe the physiologic changes that affect blood pressure and other aspects of cardiovascular function as the |
| |patient goes from the supine to the standing position; also, explain the impact of alpha- and beta-adrenergic |
| |blockers on those compensatory processes. |
| |Explain the practical clinical implications of classifying some adrenergic blockers as “cardioselective” and others|
| |as having intrinsic sympathomimetic activity. Describe when and why they may be suitable (or potentially better) |
| |alternatives to nonselective beta blockers (for example, propranolol) overall, particularly for patients who may |
| |experience adverse responses to the nonselective blockers. |
| |Summarize the main mechanisms of action of reserpine, guanethidine, and methyldopa (or clonidine). |
| |Compare and contrast the general sites and mechanisms of action of reserpine, clonidine, and methyldopa with those |
| |of drugs that block adrenergic receptors (for example, propranolol and phentolamine). |
| |Explain the factors that lead to and the characteristics of the “rebound” phenomenon associated with sudden |
| |discontinuation of clonidine. |
| |Use the effects of the drugs described in this chapter to predict how responses to the main classes of adrenergic |
| |agonists (see Chapter 17) would be affected. |
|TOPIC (S) |Unit 4: Peripheral Nervous System Drugs |
| |Basic Principles of Neuropharmacology |
| |Physiology of the Peripheral Nervous System |
| |Muscarinic Agonists and Antagonists |
| |Cholinesterase Inhibitors and Their Use in Myasthenia Gravis |
| |Drugs that Block Nicotinic Cholinergic Transmission: Neuromuscular Blocking Agents |
| |Adrenergic agonists |
| |Adrenergic Antagonists |
| |Indirect-Acting Antiadrenergic Agents |
|LEARNING ACTIVITIES |READING ASSIGNMENT |
| |Chapter 12: Basic Principles of Neuropharmacology – pp 96 - 101 |
| |Chapter 13: Physiology of the Peripheral Nervous System – pp 102 – |
| |114 |
| |Chapter 14: Muscarinic Agonists and Antagonists – pp 115 - 126 |
| |Chapter 15: Cholinesterase Inhibitors and Their Use in Myasthenia |
| |Gravis – pp 127 - 133 |
| |Chapter 16: Drugs that Block Nicotinic Cholinergic Transmission: |
| |Neuromuscular Blocking Agents – pp 134 - 142 |
| |Chapter 17: Adrenergic agonists – pp – 143 - 155 |
| |Chapter 18: Adrenergic Antagonists – pp 156 - 167 |
| |Chapter 19: Indirect-Acting Antiadrenergic Agents – pp 168 - 172 |
| | |
| |DISCUSSION (Choose 1) |
| |Discuss specific ways in which drugs can alter the steps of synaptic transmission. |
| |Identify the basic processes by which the main autonomic nervous system neurotransmitters are terminated |
| |physiologically. |
| |Identify three specific uses for neuromuscular blocking agents and describe the monitoring and other measures |
| |necessary with their use. |
| | |
| | |
| |SUBMISSION |
| |Math Worksheet |
| | |
| |ASSIGNMENT |
| |Review the syllabus |
| |Read assignments |
| |Post discussion topic by Wednesday at 11:55 pm EST |
| |Respond to at least one classmate by Friday at 11:55 pm EST |
| |Complete math worksheet & submit by Friday at 11:55 pm EST |
| |Complete case study |
| | |
| |ASSESSMENT |
| |Discussion & response |
| |Math worksheet |
| |Case study |
| |Quiz Chapters 12, 13, 14, 15, 16, 17, 18, & 19 |
| | |
| |Homework: Chapter readings: Chapters 20, 221, 22, 23, 24, 25, 26, 27, 28, 29, & 30 |
|DATE |WEEK 5 |
|SPECIFIC OBJECTIVES |At the end of this lesson, you will be able to: |
| |Identify the main neurotransmitters of the central nervous system (CNS) and summarize some of their main |
| |physiologic effects. |
| |Discuss the significance of the blood-brain barrier in allowing or preventing the effects of drugs in general. |
| |Describe how, in many cases, control of key activities in the CNS involves more than one neural pathway, each with |
| |its own neurotransmitter and set of receptors. This is generally important for understanding much of the specific |
| |information presented in later chapters in this unit. |
| |Explain the interrelationships between the central nervous system (CNS) activities of dopamine and acetylcholine as|
| |they affect the signs and symptoms of Parkinsonism and as they relate to the general biochemical approach to |
| |correcting neurotransmitter imbalances with anti-Parkinsonian drugs. |
| |Discuss the drug treatment for Parkinson’s disease (PD), and discuss the current consensus on which agent or agents|
| |are recommended for initiating therapy in most patients with PD. |
| |Succinctly summarize the main anti-Parkinsonian mechanisms of action of levodopa, carbidopa, pramipexole, |
| |ropinirole, apomorphine, bromocriptine, amantadine, entacapone, tolcapone, and selegiline. Also, summarize the main|
| |adverse responses elicited by each of these drugs. |
| |Summarize the main neural pathologic changes involved in the etiology of Alzheimer’s disease (AD) (for example, |
| |define neuritic plaques and neurofibrillary tangles and explain how they form) and describe the main |
| |neurotransmitter “deficiency” that seems to account for most of the signs and symptoms. |
| |Summarize the main signs and symptoms of AD and the main risk factors for its development. |
| |Identify acetylcholinesterase inhibitors as the current main class of drugs for managing AD. State the main |
| |mechanism by which these drugs seem to confer some symptom relief in AD and summarize whether they seem to have |
| |short- or long-term benefit, providing symptomatic relief or a true cure. Donepezil should be used as the example |
| |drug. |
| |State the main properties of donepezil that make it a good first-choice agent for AD in most cases. Also, summarize|
| |one or two key reasons tacrine is not a preferred agent. |
| |Describe the therapeutic effects and mechanism of action of memantine [Namenda]. |
| |Comment on the status of vitamin E and selegiline, nonsteroidal antiinflammatory drugs (NSAIDs), estrogen, and |
| |ginkgo biloba as agents that might relieve, delay the progression of, or protect against AD. |
| |Identify the primary pathology of multiple sclerosis (MS), including how inflammation occurs, what initiates the |
| |autoimmune process, what happens when an acute attack is over, and whether MS injures the myelin sheath of |
| |peripheral neurons. |
| |Describe the signs and symptoms of MS, including a description of the diagnostic criteria and the diagnostic tools |
| |that can help confirm a suspected diagnosis of MS. |
| |Describe the four subtypes of MS (relapsing-remitting, secondary progressive, primary progressive, and |
| |progressive-relapsing) and comment on the symptom patterns that characterize each subtype. |
| |Describe the mechanism of action, therapeutic use, and adverse effects of immunomodulators and immunosuppressants. |
| |Discuss medications available for symptom management of bladder and bowel dysfunction, depression, fatigue, |
| |spasticity, sexual dysfunction, neuropathic pain, ataxia and tremor, and cognitive dysfunction. |
| |Differentiate between seizure and convulsion and between partial (focal) and generalized seizures. |
| |Describe how seizures are initiated and generated. |
| |State and describe three cellular mechanisms by which antiepileptic drugs act. |
| |Describe the general goals of the treatment of epilepsy and some of the problems commonly encountered in reaching |
| |them. While considering the problems, articulate social and occupational factors, not just the pharmacologic |
| |factors. |
| |Discuss important considerations related to selecting an antiepileptic drug, monitoring its effectiveness (or lack |
| |thereof), and recognizing side effects and how to deal with them. |
| |State the most common reason for “therapeutic failure” of anticonvulsant drugs and describe steps that might be |
| |taken to reduce the problem. |
| |Summarize the likely problems for which the patient must be assessed and treated when the decision is made to |
| |discontinue one anticonvulsant drug and switch to another. |
| |Summarize the likely problems for which the patient must be assessed and treated when a second agent must be added |
| |to a treatment plan that already includes one anticonvulsant drug. |
| |State why, in general, most anticonvulsants interact in important ways with many other drugs, regardless of their |
| |therapeutic classification. |
| |Discuss the risks and benefits of administering anticonvulsants during pregnancy (as they affect the mother and the|
| |fetus and newborn), and describe any special assessments or interventions indicated for a pregnant woman with |
| |epilepsy. |
| |Summarize a generally accepted drug plan for intervening in status epilepticus (generalized convulsive) and state |
| |why prompt suppression of seizures is essential but insufficient as the only goal. |
| |Discuss some basic differences between localized skeletal muscle spasm and spasticity (etiology, manifestations, |
| |and primary and adjunctive treatments). |
| |Explain the basic differences, in terms of sites and mechanisms of action, among centrally acting muscle relaxants,|
| |baclofen, diazepam, and dantrolene. State how these different mechanisms and sites of action relate to the drugs’ |
| |clinical uses. |
| |Describe the etiologies, signs and symptoms, and management of malignant hyperthermia (see Chapter 16). Likewise, |
| |demonstrate a good grasp of the overall pharmacology of the benzodiazepines as a class (see Chapter 34). |
| |Describe the physiologic manner by which local anesthetics work. |
| |Differentiate between ester and amide types of local anesthetics in terms of mechanism of action, mechanisms by |
| |which they are eliminated from the body, and adverse effects (particularly with respect to allergic reactions). |
| |Describe signs and symptoms of systemic local anesthetic toxicity, how to recognize them, and how to manage them. |
| |State reasons and rationales for including a vasoconstrictor (for example, epinephrine) in a parenteral formulation|
| |of local anesthetic. Focus on the time course and intensity of local anesthetic action, toxicity, and allergenicity|
| |as affected by the vasoconstrictor. |
| |Describe the properties of individual local anesthetics and discuss their clinical uses. |
| |Discuss the concept of balanced anesthesia (i.e., the overall goals of general anesthesia and the fact that no |
| |single drug has all the properties that might be considered “ideal” for inducing surgical anesthesia) |
| |Give a reasonable definition of minimum alveolar concentration (MAC) and state how it relates to inhaled general |
| |anesthetic potency and the concentrations that must be administered to induce general anesthesia. |
| |Using halothane or isoflurane as a representative inhaled general anesthetic, describe the elements of balanced |
| |anesthesia that can be expected with usually effective doses of the drug given alone; desired elements of balanced |
| |anesthesia that cannot be achieved by halothane alone; elements for which supplemental agents are needed; and the |
| |major toxicities that can occur with respect to the cardiovascular system. |
| |Describe the uses, benefits, and limitations of nitrous oxide in general anesthesia. |
| |State the roles for the following as adjuncts to general anesthesia: (a) barbiturates, especially short-acting |
| |ones; (b) benzodiazepines; (c) opioids; and (d) neuromuscular blockers. Use other chapters to review the general |
| |actions, uses, and toxicities of these drug groups, and integrate that information in the context of general |
| |anesthesia. |
| |Describe the basic sequence of drug administration for the reversal of postanesthesia skeletal neuromuscular |
| |blockade (paralysis), the rationale for each medication that is administered, and the expected effects of each |
| |medication. |
| |Describe the signs and symptoms, etiology (including the main pharmacologic causes), and management of malignant |
| |hyperthermia. |
| |State the roles of the mu, kappa, and delta opioid receptors in causing analgesia, respiratory depression, and |
| |euphoria. |
| |Give the precise definition of narcotic (as applied legally to classes of drugs) and compare it with the way the |
| |typical layperson uses the term. |
| |Distinguish among pure opioid agonists, agonist-antagonists, and antagonists in terms of their mechanism of action;|
| |also, place various named drugs in the appropriate category. |
| |Discuss the therapeutic uses for opioid agonists, agonist-antagonists, and antagonists. |
| |Discuss the adverse effects of opioids and both their pharmacologic and nondrug management. The discussion should |
| |include a typical opioid agonist such as morphine, mixed opioid agonist-antagonists, and pure opioid antagonists. |
| |State how meperidine differs from morphine in terms of adverse effects and proper clinical use. |
| |Describe opioid drug–related factors that contribute to the development of physical and psychologic dependence. |
| |Identify drug- and administration-related factors that affect the severity of physical dependence and the severity |
| |and duration of withdrawal signs and symptoms when administration of that drug is stopped suddenly. |
| |Compare and contrast acute withdrawal from an opioid (assume physical dependency has occurred) with the withdrawal |
| |signs, symptoms, and likely outcomes of unsupervised withdrawal from barbiturates, alcohol, and benzodiazepines. |
| |Compare and contrast neuropathic and nociceptive pain in terms of the causes and the drug classes that typically |
| |are (or are not) effective for managing them. |
| |Describe the various assessment tools used to evaluate the severity of and discomfort from a patient’s pain, and |
| |help plan optimal analgesic therapy. |
| |Comment on the statement that the various nonsurgical interventions used to treat cancer – chemotherapy and |
| |radiation therapy – can cause pain that needs to be managed every bit as much as the pain arising from the cancer |
| |itself. |
| |List and describe some of the main barriers or impediments to providing optimal pain control, particularly with |
| |opioids. Consider attitudes, beliefs, and even what might be described as fears involving healthcare providers |
| |responsible for prescribing and administering these drugs as well as the patients (and their families) who are |
| |recipients of these medications. |
| |Articulate the questions that a nurse would ask a patient to assess each of the following characteristics of the |
| |person’s pain: Onset and temporal pattern of pain; location of the pain; quality of the pain; pain intensity; |
| |modulating or modifying factors; previous treatment; and impact on function and overall quality of life |
| |Develop a prioritized list of “preferred,” rational, and effective drugs for a patient, given the type or types and|
| |severities of the person’s pain. The list should include traditional analgesics and drugs identified as adjuvant |
| |(adjunctive) drug therapies. |
| |Compare and contrast the benefits and limitations (or risks) of PRN pain control with those of around-the-clock |
| |administration of analgesics. Include in the summary the benefits of patient-controlled analgesia. Assume the |
| |patient has long-term pain that must be controlled. |
| |Summarize some general ways in which the elderly, very young children, and patients who are physically dependent on|
| |and abusers of opioids differ from an otherwise healthy young adult. Focus on problems with assessment of pain and |
| |its response to treatment, drug selection and dosing, and monitoring for adverse responses (caused by the analgesic|
| |itself or related to other drugs the patient may be taking). |
| |Explain the purpose of The Joint Commission (TJC), focusing on its new standards on pain assessment and treatment |
| |and patients’ rights in these important issues. |
| |Identify the various nondrug physical and psychosocial pain management interventions, and discuss the effectiveness|
| |of each option. |
| |Compare and contrast migraine headaches, cluster headaches, and tension-type headaches in terms of triggering |
| |factors, clinical presentations, and management. |
| |State the common underlying neurovascular causes of migraine, including the roles of calcitonin gene–related |
| |peptide (CGRP) and serotonin (5-hydroxytryptamine [5-HT]). |
| |Identify therapies that are usually effective for abortive and prophylactic therapy of migraine, and state which |
| |drugs are suitable for prophylaxis but not for acute intervention (abortive therapy). |
| |Describe the signs, symptoms, and potential consequences of ergotism and the main elements of its management. |
|TOPIC (S) |Unit 5: Central Nervous System Drugs |
| |Introduction to Central Nervous System Pharmacology |
| |Drugs for Parkinson’s Disease |
| |Drugs for Alzheimer’s Disease |
| |Drugs for Multiple Sclerosis |
| |Drugs for Epilepsy |
| |Drugs for Muscle Spasm and Spasticity |
| |Local Anesthetics |
| |General Anesthetics |
| |Opioid analgesics, Opioid Antagonist, and Nonopioid Centrally Acting Analgesics |
| |Pain management in Patients with Cancer |
| |Drugs for Headache |
|LEARNING ACTIVITIES |READING ASSIGNMENT |
| |Chapter 20: Introduction to Central Nervous System Pharmacology – pp 173 – 175 |
| |Chapter 21: Drugs for Parkinson’s Disease – pp 176 – 190 |
| |Chapter 22: Drugs for Alzheimer’s Disease – pp 191 – 198 |
| |Chapter 23: Drugs for Multiple Sclerosis – pp 199 – 215 |
| |Chapter 24: Drugs for Epilepsy – pp 216 – 239 |
| |Chapter 25: Drugs for Muscle Spasm and Spasticity – pp 240 – 244 |
| |Chapter 26: Local Anesthetics – pp 245 – 250 |
| |Chapter 27: General Anesthetics – pp 251 – 259 |
| |Chapter 28: Opioid Analgesics, Opioid Antagonists, and Nonopioid Centrally Acting Analgesics – pp 260 – 287 |
| |Chapter 29: Pain Management in Patients with Cancer – pp 286 – 304 |
| |Chapter 30: Drugs for Headache – pp 305 – 316 |
| | |
| |DISCUSSION (Choose 1) |
| |Describe the physiologic manner by which local anesthetics work. |
| |Explain the purpose of The Joint Commission (TJC), focusing on its new standards on pain assessment and treatment |
| |and patients’ rights in these important issues. |
| |Explain the basic differences, in terms of sites and mechanisms of action, among centrally acting muscle relaxants,|
| |baclofen, diazepam, and dantrolene. State how these different mechanisms and sites of action relate to the drugs’ |
| |clinical uses. |
| | |
| | |
| |SUBMISSION |
| |Math Worksheet |
| | |
| |ASSIGNMENT |
| |Review the syllabus |
| |Read assignments |
| |Post discussion topic by Wednesday at 11:55 pm EST |
| |Respond to at least one classmate by Friday at 11:55 pm EST |
| |Complete math worksheet & submit by Friday at 11:55 pm EST |
| |Complete case study |
| | |
| |ASSESSMENT |
| |Discussion & response |
| |Math worksheet |
| |Case study |
| |Quiz Chapters 20, 221, 22, 23, 24, 25, 26, 27, 28, 29, & 30 |
| | |
| |Homework: Chapter readings: Chapters 31, 32, 33, 34, 35, 36, 37, 38, 39, & 40 |
|DATE |WEEK 6 |
|SPECIFIC OBJECTIVES |At the end of this lesson, you will be able to: |
| |Describe the principal indications for antipsychotic drugs. |
| |Describe the clinical presentation of schizophrenia and diagnosis based on the criteria in the Diagnostic and |
| |Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (DSM-IV-TR). Compare and contrast the three |
| |groups of symptoms: positive, negative, and cognitive. |
| |Compare and contrast chlorpromazine and haloperidol with respect to their mechanisms and onsets of antipsychotic |
| |action, their uses, and the relative incidence of CNS and peripheral autonomic side effects. |
| |Explain why antipsychotic drugs may cause side effects or adverse responses that mimic many of the signs and |
| |symptoms of Parkinson’s disease. (Related to this, explain why excessive doses of dopaminergic drugs used for |
| |parkinsonism may trigger some signs and symptoms of schizophrenia.) |
| |Summarize the main signs and symptoms of extrapyramidal side effects caused by antipsychotic drugs and acceptable |
| |therapeutic approaches to minimize or reverse them. |
| |Associate the neuroleptic malignant syndrome as a relatively rare but serious adverse reaction to antipsychotic |
| |drugs, describe its signs and symptoms and time of onset after starting antipsychotic drug therapy, and state |
| |interventions that should be implemented if or when neuroleptic syndrome is suspected or confirmed. |
| |Highlight the key differences between and similarities of antipsychotics that are called high potency and those |
| |called low potency. |
| |State why clozapine, which is considered the prototype of the atypical antipsychotics, is not a first-line drug for|
| |managing schizophrenia but does seem to be preferred to phenothiazines for managing levodopa-induced psychosis. |
| |Discuss special monitoring that must be implemented, as well as special instructions that should be given to the |
| |patient who is receiving clozapine, regardless of the use. |
| |Describe the diagnostic criteria for major depression and the four treatment modalities available. |
| |Identify signs and symptoms that might indicate an increased risk of suicide in individuals taking antidepressants |
| |and explain ways the risk for suicide may be reduced. |
| |Compare and contrast the mechanisms of action and main adverse effects of TCAs, SSRIs, SNRIs, and MAOIs. Also, |
| |state the role or roles of each class in a stepwise approach to the management of depression pharmacologically; |
| |that is, explain which drug or drugs generally are chosen for first-line treatment and which generally are used |
| |only as a last resort and the reasons. |
| |Explain the mechanism of action that results in hypertensive crisis from dietary tyramine in individuals taking |
| |MAOIs. Also, describe the educational information that needs to be given to patients. In addition, explain how |
| |hypertensive crisis is treated. |
| |Identify the typical manifestations and clinical course of bipolar disorder (BPD) and the drugs used to manage |
| |them. |
| |Describe the best way to determine therapeutic lithium levels. |
| |Describe how and why the body’s sodium balance is important in maintaining steady blood lithium levels and |
| |responses to the drug. Also, identify drug- and diet-related aspects that affect those lithium levels and effects. |
| |State the main elements of patient assessment and patient education with respect to determining therapeutic |
| |response or adverse response to drug therapy. |
| |Explain why benzodiazepines are drugs of first choice for anxiety and insomnia. |
| |Identify the drug used for diagnosis and treatment of benzodiazepine overdosage and explain its basic mechanism of |
| |action. |
| |Describe the important considerations involved when using sedative-hypnotic drugs. |
| |Compare and contrast the withdrawal syndrome associated with abrupt discontinuation of benzodiazepines with that of|
| |barbiturates. |
| |Summarize the main points of sleep fitness – that is, approaches people can use to help themselves fall asleep, |
| |stay asleep, and sleep restfully without the need for medications. |
| |Compare and contrast the effects of buspirone (BuSpar), benzodiazepines, and antidepressants that might be |
| |prescribed for generalized anxiety disorder, focusing on the adverse reactions; interactions with other |
| |medications; and pharmacokinetics, particularly with respect to onset of action. |
| |Compare and contrast characteristics of generalized anxiety disorder, panic disorder, obsessive-compulsive |
| |disorder, social anxiety disorder, and post-traumatic stress disorder and identify treatment options for each |
| |disorder. |
| |Discuss the central nervous system (CNS) and peripheral autonomic effects of amphetamines and the general mechanism|
| |by which they occur. |
| |Describe the most common adverse and toxic effects of amphetamines and their management, and discuss the issues of |
| |tolerance, physical dependence, and abuse. |
| |Describe the various generally accepted drug treatments for attention-deficit/hyperactivity disorder (ADHD). |
| |Explain why CNS stimulation, such as with amphetamines or methylphenidate, is beneficial for managing the |
| |manifestations of hyperactivity disorder. |
| |Explain why it can be said that drug abuse is culturally defined. Also, discuss whether a single medical or social |
| |norm can be applied to determine whether a particular pattern of drug use (or misuse) or the use or misuse of a |
| |particular drug (or class of drugs) constitutes drug abuse. |
| |Discuss psychological and drug-related factors that in a broad sense contribute to substance abuse. |
| |Describe several of the common mechanisms by which tolerance to a drug’s effects can develop, and state whether the|
| |process of tolerance development depends on the properties of the drug or on processes inherent in the body. |
| |Differentiate between physical and psychological dependence. |
| |Describe the alleged roles or purposes of the Controlled Substances Act. |
| |State the prescribing requirements and restrictions on Schedule II, III, IV, and V medications. |
| |Differentiate between the beneficial and detrimental effects of alcohol. |
| |Discuss the metabolism of ethanol with respect to the following: The roles of alcohol and aldehyde dehydrogenases, |
| |the rate of alcohol metabolism as a function of blood alcohol levels, and the general mechanism or mechanisms by |
| |which acute high-dose and chronic “moderate” alcohol consumption affect elimination of many other drugs that |
| |undergo hepatic metabolism. |
| |Identify the major nonhepatic route of elimination of alcohol and its medicolegal implications. |
| |Identify several drugs – and nondrug measures – that have some hope of stopping or reducing the problems of chronic|
| |alcohol intake. |
| |Compare and contrast the typical signs, symptoms, and outcomes of acute “unsupervised” withdrawal from alcohol with|
| |those of acute withdrawal from barbiturates and opioids. |
| |Comment on the common use of aspirin to manage some of the common signs and symptoms of alcohol-induced “hangover.”|
| |Describe whether other over-the-counter analgesics might be preferred for managing hangovers. |
| |Identify the overall risks of cigarette smoking. |
| |Discuss endeavors to prevent tobacco use. Describe the mechanism of action and pharmacokinetics of nicotine. |
| |Describe the pharmacologic effects of nicotine on the cardiovascular system, the gastrointestinal (GI) system, and |
| |the central nervous system (CNS). |
| |Differentiate between tolerance and dependence with regard to cigarette smoking. |
| |Discuss the treatment options to aid smoking cessation. |
| |Recognize the seven main pharmacologic groups of commonly abused substances: (1) opioids, (2) psychostimulants, (3)|
| |depressants, (4) psychedelics, (5) dissociative drugs, (6) anabolic steroids, and (7) miscellaneous drugs of abuse.|
| |State whether any specific antidotes exist for the substances of abuse. Also, identify those groups and their |
| |antagonists. |
| |Compare and contrast the patterns of abuse for the seven major categories of abused drugs and summarize their main |
| |behavioral and systemic effects. |
| |Describe the signs, symptoms, and treatment for acute or long-term use or overdose for the seven major categories |
| |of abused drugs. |
| |Describe the key signs and symptoms of opioid withdrawal, its clinical management, and the likely clinical outcome |
| |of unsupervised or untreated opioid withdrawal. |
| |Discuss the issues of tolerance and cross-tolerance to drugs, focusing on the opioids and barbiturates. |
| |Cite at least two examples for which signs and symptoms of abuse (or overuse) of a particular substance cause |
| |radically different acute effects that are dose dependent. |
|TOPIC (S) |Unit 5: Central Nervous System Drugs |
| |Antipsychotic Agents and Their Use in Schizophrenia |
| |Antidepressants |
| |Drugs for Bipolar Drugs |
| |Sedative-Hypnotic Drugs |
| |Management of Anxiety Disorders |
| |Central Nervous System Stimulants and Attention-Deficit/Hyperactive Disorder |
| |Drug Abuse I: Basic Considerations |
| |Drug Abuse II: Alcohol |
| |Drug Abuse III: Nicotine and Smoking |
| |Drug Abuse IV: Major Drugs of Abuse Other Than Alcohol and Nicotine |
|LEARNING ACTIVITIES |READING ASSIGNMENT |
| |Chapter 31: Antipsychotic Agents and Their Use in Schizophrenia– pp 317 - 338 |
| |Chapter 32: Antidepressants – pp 338 - 363 |
| |Chapter 33: Drugs for Bipolar Drugs – pp 364 – 372 |
| |Chapter 34: Sedative-Hypnotic Drugs – pp 373 – 387 |
| |Chapter 35:Management of Anxiety Disorders – pp 388 – 394 |
| |Chapter 36: Central Nervous System Stimulants and Attention-Deficit/Hyperactive Disorder – pp |
| |Chapter 37: Drug Abuse I: Basic Considerations |
| |Chapter 38: Drug Abuse II: Alcohol |
| |Chapter 39: Drug Abuse III: Nicotine and Smoking |
| |Chapter 40: Drug Abuse IV: Major Drugs of Abuse Other Than Alcohol and Nicotine |
| | |
| |DISCUSSION (Choose 1) |
| |Discuss the treatment options to aid smoking cessation. |
| |Differentiate between physical and psychological dependence. |
| |Describe the best way to determine therapeutic lithium levels. |
| | |
| |SUBMISSION |
| |Math Worksheet |
| | |
| |ASSIGNMENT |
| |Review the syllabus |
| |Read assignments |
| |Post discussion topic by Wednesday at 11:55 pm EST |
| |Respond to at least one classmate by Friday at 11:55 pm EST |
| |Complete math worksheet & submit by Friday at 11:55 pm EST |
| |Complete case study |
| | |
| |ASSESSMENT |
| |Discussion & response |
| |Math worksheet |
| |Case study |
| |Quiz Chapters 31, 32, 33, 34, 35, 36, 37, 38, 39, & 40 |
| | |
| | |
| | |
| |Homework: Chapter readings: Chapters 41, 42, 43, 44, 45, 46, & 47 |
|DATE |WEEK 7 |
|SPECIFIC OBJECTIVES |At the end of this week, the students will be able to: |
| |State the common mechanism or mechanisms by which all diuretics increase urine production. |
| |Classify the following as potassium sparing or potassium wasting: thiazides, loop diuretics, spironolactone, and |
| |triamterene; also, state why a knowledge of the effects of diuretics on renal potassium excretion is important |
| |clinically. |
| |State factors that should be considered when selecting a diuretic, focusing on the efficacy of the various agents, |
| |dose-response relationships, and the potential for adverse effects in patients with other disorders. Also, discuss |
| |for which pathologies the various diuretics are suitable. |
| |Describe the adverse effects, contraindications, or precautions for the various diuretics. |
| |State the expected effects of thiazides and loop diuretics on blood levels of glucose, lipids, uric acid, calcium, |
| |and magnesium and identify the preexisting conditions that might require extra caution if use of these diuretics is|
| |anticipated. |
| |State how changes in the serum potassium level influence the effects of digoxin and the likely impact of |
| |hypokalemia or hyperkalemia on therapy with a cardiac glycoside. |
| |State whether combinations of named diuretics are rational and give a reason why. For example, is it reasonable and|
| |rational to administer two thiazides or two loop diuretics to the same patient? |
| |Compare and contrast the mechanisms of action, clinical uses, and typical adverse effects of mannitol with those of|
| |a thiazide or loop diuretic. |
| |Identify and describe the common etiologies and treatments for isotonic, hypertonic, and hypotonic volume |
| |contractions. |
| |Identify and describe the common etiologies and treatments for respiratory and metabolic acidosis and respiratory |
| |and metabolic alkalosis. |
| |Identify the main hormone responsible for regulating renal potassium excretion (or retention), and state the |
| |simultaneous effects of that hormone on renal handling of sodium and water. |
| |Describe the link between serum insulin and potassium levels, explaining why hyperinsulinism leads to hypokalemia. |
| |Identify the main potassium salt that is preferred (in most situations) for preventing or managing hypokalemia, and|
| |state why it is generally the preferred salt. |
| |Summarize the main physiologic roles of the pulmonary and systemic circulatory systems, particularly as they affect|
| |blood pressure and venous return to the heart. |
| |Describe the process that contributes to venous return. |
| |Write the equation used to calculate cardiac output, and state the main physiologic and pathophysiologic factors |
| |that can affect (increase or decrease) each of the two elements that determine cardiac output. |
| |State the main neural and hormonal controls over blood pressure. State the endogenous chemicals that help regulate |
| |arterial blood pressure. |
| |Compare and contrast the roles and mechanisms of the renin-angiotensin-aldosterone system (RAAS) and the autonomic |
| |nervous system (ANS) with respect to regulating hemodynamics. |
| |Explain how increases in the arterial pressure (AP) can affect overall hemodynamics and ultimately lead to |
| |congestive heart failure. |
| |Describe the main components of the renin-angiotensin-aldosterone system (RAAS) and explain how the overall system |
| |is regulated physiologically. |
| |State the main effects of aldosterone on renal handling of sodium, potassium, and water. Also, identify the main |
| |physiologic stimulus for aldosterone release and describe the likely effects of increased aldosterone release on |
| |hemodynamics (blood volume, pressure, cardiac function) and the blood electrolyte composition. |
| |Name the classes of drugs (and a prototype for each) that can affect blood pressure by altering the RAAS or targets|
| |of its activity, and state how the drugs cause those effects. |
| |Describe the effects of angiotensin-converting enzyme (ACE) inhibitors on blood pressure and on renal regulation of|
| |sodium, potassium, and water excretion. |
| |Compare and contrast the actions of angiotensin II receptor blockers (antagonists/receptor blockers, such as |
| |losartan) with those of an ACE inhibitor or direct renin inhibitors. |
| |State the two main contraindications to administration of ACE inhibitors, angiotensin II receptor blockers (ARBs), |
| |and direct renin inhibitors. |
| |Discuss the major adverse effect of aldosterone antagonists (hyperkalemia) and the implications that this effect |
| |has with regard to combination therapy with ACE inhibitors or ARBs. |
| |Briefly describe the calcium channel and the relationships between intracellular and extracellular calcium |
| |concentrations as they affect smooth and cardiac muscle contractile function. |
| |Describe the functional linkage between beta-adrenergic receptors and calcium channels in the heart. |
| |Compare and contrast the sites of action of nifedipine with those of diltiazem or verapamil. Also, explain how the |
| |differences between the dihydropyridines and verapamil or diltiazem affect their clinical use and name the most |
| |common side effects. |
| |Identify other drugs, noted and described in the cardiovascular unit, which should not be administered with calcium|
| |channel blockers (CCBs) because of the risk of excessive depression of cardiac contractility, rate, and electrical |
| |activity. Also, specify whether these precautions apply to dihydropyridine-type CCBs, just to verapamil or |
| |diltiazem, or to all CCBs, and explain why. |
| |Identify the main pharmacologic causes of vasodilation. Also, state the drugs (or drug classes) that have |
| |vasodilator action and describe how they cause blood vessels to dilate. |
| |Explain how reducing afterload and preload can help a patient with hypertension or heart failure. |
| |Describe how excessive vasodilation can cause adverse effects that can actually worsen many of the conditions for |
| |which vasodilators are given. |
| |State the expected compensatory cardiac and renal responses that occur when a drug that does nothing but dilate |
| |arterioles is given and identify adjunctive drugs that might be used to control those responses. |
| |Describe the metabolism of nitroprusside. Also, state precautions that need to be taken to ensure it is |
| |administered as safely as possible and explain the process of monitoring for its desired and adverse effects. |
| |Describe clinical settings in which diazoxide might be indicated (parenteral administration) and the likely adverse|
| |responses to it (cardiovascular and otherwise). |
| |State how the following systems contribute to the regulation of blood pressure and name the classes of |
| |antihypertensive drugs that target one or more of these processes or structures when given to lower elevated blood |
| |pressure: (1) heart (via the contractile force developed by the left ventricle); (2) peripheral vasculature; (3) |
| |parasympathetic nervous system; (4) sympathetic nervous system; (5) renin-angiotensin-aldosterone system (including|
| |the kidneys themselves). |
| |State the criteria used to classify hypertension as essential hypertension. |
| |State the factors that, beyond blood pressure per se, are used to classify the severity of hypertension according |
| |to Joint National Committee 7 (JNC 7). |
| |Explain how most pathophysiologic processes that occur during long-term hypertension simultaneously contribute to |
| |heart failure. |
| |State the major factors that influence the choice of antihypertensive drug (or drug combination) for a patient with|
| |a stated severity of essential hypertension. State how specified comorbidity (for example, heart failure, diabetes,|
| |asthma) would influence the drug choice for or against a particular drug class. |
| |State the blood pressure control gains to be expected by progressively increasing the dosage of one |
| |antihypertensive drug rather than adding drugs in other classes to the initial agent. |
| |State the blood pressure benefits to be gained by switching from one drug in a particular class to another agent in|
| |the same class (for example, switching from one beta blocker to another). |
| |List and describe several nondrug (for example, lifestyle) factors that should be encouraged to manage essential |
| |hypertension, regardless of the drug used. |
| |Describe general goals for the safe management of a hypertensive emergency and list drugs that would be suitable |
| |for such a situation. |
| |Discuss the etiology of hypertension during pregnancy, also addressing preeclampsia and eclampsia and the roles of |
| |antihypertensive drugs and magnesium sulfate. In addition, state the “definitive cure” for hypertension in |
| |eclampsia. |
|TOPIC (S) |Unit 6: Drugs that Affect Fluid and Electrolyte Balance |
| |Diuretics |
| |Agents affecting the Volume and Ion Content of Body fluids |
| |Unit 7: drugs that Affect the Heart, Blood Vessels and Blood |
| |Review of Hemodynamics |
| |Drugs Acting on the Renin-Angiotensin-Aldosterone System |
| |Calcium Channel Blockers |
| |Vasodilators |
| |Drugs for Hypertension |
|LEARNING ACTIVITIES |READING ASSIGNMENT |
| |Chapter 41: Diuretics – pp 447 - 458 |
| |Chapter 42: Agents affecting the Volume and Ion Content of Body fluids – pp 459 - 463 |
| |Chapter 43: Review of Hemodynamics – pp 464 - 469 |
| |Chapter 44: Drugs Acting on the Renin-Angiotensin-Aldosterone System - -pp 470 - 484 |
| |Chapter 45: Calcium Channel Blockers – pp 485 - 493 |
| |Chapter 46: Vasodilators – pp 494 - 498 |
| |Chapter 47: Drugs for Hypertension – pp 499 - 516 |
| | |
| |DISCUSSION (Choose 1) |
| |Describe the adverse effects, contraindications, or precautions for the various diuretics. |
| |Describe general goals for the safe management of a hypertensive emergency and list drugs that would be suitable |
| |for such a situation. |
| |Describe the effects of angiotensin-converting enzyme (ACE) inhibitors on blood pressure and on renal regulation of|
| |sodium, potassium, and water excretion. |
| | |
| |SUBMISSION |
| |Math Worksheet |
| | |
| |ASSIGNMENT |
| |Review the syllabus |
| |Read assignments |
| |Post discussion topic by Wednesday at 11:55 pm EST |
| |Respond to at least one classmate by Friday at 11:55 pm EST |
| |Complete math worksheet & submit by Friday at 11:55 pm EST |
| |Complete case study |
| | |
| |ASSESSMENT |
| |Discussion & response |
| |Math worksheet |
| |Case study |
| |Quiz Chapters 41, 42, 43, 44, 45, 46, & 47 |
| | |
| | |
| | |
| |Homework: Chapter readings: Chapters 48, 49, 50, 51, 52, 53, 54, 55, & 56 |
|DATE |WEEK 8 |
|SPECIFIC OBJECTIVES |At the end of this lesson, you will be able to: |
| |Summarize the essence of Starling’s law of the heart and translate it into factors that relate to ventricular |
| |end-diastolic volume. Also, describe how an alteration in ventricular end-diastolic volume relates to heart |
| |failure. |
| |Describe the characteristic signs and symptoms of heart failure, including those that could be called congestive. |
| |Summarize the characteristics or measures that are used to assign a patient with heart failure to the four American|
| |College of Cardiology/American Heart Association stages and those that make up the New York Heart Association |
| |classes. |
| |Discuss the goals for the treatment of chronic and acute heart failure. |
| |Recognize and describe the roles, benefits, and limitations of the following drugs (or drug groups) in the |
| |long-term management of heart failure: (1) drugs that inhibit the RAAS; (2) diuretics; (3) vasodilators (other than|
| |angiotensin-converting enzyme [ACE] inhibitors and angiotensin II receptor blockers [ARBs]); (4) beta-adrenergic |
| |blockers; (5) cardiac glycosides; (6) inotropic agents (other than cardiac glycosides). |
| |Describe what the terms afterload and afterload reduction mean and explain why afterload reduction is beneficial in|
| |the management of heart failure. |
| |State the main direct and indirect cardiac contractile and electrophysiologic effects of digoxin and explain the |
| |relationship between them and the serum potassium level. |
| |Explain how digoxin’s desired effects lead to beneficial systemic hemodynamic and metabolic/ endocrinologic |
| |effects. |
| |Explain why digoxin is a mixed blessing for the management of chronic heart failure, particularly with respect to |
| |problems related to the frequency and severity of toxicity. |
| |Describe how the use of diuretics (for example, furosemide) as an adjunct to digoxin can be considered both |
| |beneficial and dangerous. |
| |State the cardiac and other (noncardiac/extracardiac) signs and symptoms consistent with digoxin toxicity, |
| |especially those that would lead to suspicion of drug intoxication even before electrocardiographic and blood test |
| |results are available. Also, state the first thing that should be done or given as an instruction to the patient |
| |when digoxin toxicity is suspected. |
| |State the normal electrophysiologic roles of the following specialized portions of the heart: sinoatrial node, |
| |atrial myocardium, atrioventricular node, and His-Purkinje system. |
| |State what each of the following parts of a normal electrocardiogram (ECG) represent in terms of contractile or |
| |electrophysiologic activities of the heart: P wave, QRS complex, T wave, PR interval, and ST segment. |
| |Explain the pathophysiology of the development of dysrhythmias, focusing on the main electrophysiologic properties |
| |of heart cells and tissues: automaticity, conduction velocity, and refractoriness. |
| |Define the terms first-degree, second-degree, and third-degree heart block. Also, explain how the ECG signals that |
| |these heart blocks are occurring. In addition, identify the drugs that can cause heart block, including not only |
| |the antidysrhythmic drugs, but also other drugs that have been discussed in Unit VII. |
| |Explain how the type of dysrhythmia affects the selection of drugs used to manage it. |
| |Recognize the Vaughan Williams classification as one used for antidysrhythmic drugs and state the general |
| |principles that determine whether a particular drug “fits” in a particular category. State whether this |
| |classification scheme is clinically useful to the extent that it predicts adverse responses, side effects, or even |
| |clinical uses for every member of a given class. |
| |Summarize current trends and opinions about pharmacologic management of dysrhythmias (as opposed to nondrug |
| |interventions, such as catheter ablation or no treatment at all), based on the anatomic origin, severity, and |
| |acuity of the rhythm disorder. |
| |Describe the side effects or adverse responses that can be caused by virtually any antidysrhythmic drug and those |
| |that are unique to quinidine, amiodarone, procainamide, and disopyramide. |
| |Describe the general physiologic and biochemical processes involved in lipoprotein synthesis and the regulation of |
| |serum lipoprotein levels. |
| |Name the drug class generally regarded as the first choice for hypercholesterolemia and summarize its fundamental |
| |mechanism of action. |
| |Describe the signs and symptoms of rhabdomyolysis; identify the main class of drugs associated with it, its |
| |clinical consequences, and factors that increase the risk for this syndrome. |
| |Compare and contrast the lipid-lowering mechanisms of action, clinical indications, and side effects of (1) |
| |statins, (2) fibric acid derivatives, (3) niacin, and (4) bile-acid sequestrants. |
| |Develop a teaching plan that would maximize the therapeutic benefits of dyslipidemia therapy for patients taking |
| |one or several lipid-lowering drugs and describe adjustments needed when interactants that are clinically important|
| |are prescribed. |
| |Summarize the main factors that affect myocardial oxygen demand and oxygen supply and their relationships to angina|
| |pectoris. |
| |Describe, compare, and contrast chronic stable angina, variant angina, and unstable angina in terms of the |
| |etiology, clinical presentation, and drug therapy for each. |
| |Describe the mechanisms of action and therapeutic and adverse effects of organic nitrates, calcium channel |
| |blockers, and beta blockers in angina therapy. |
| |Identify drugs that can be used interchangeably in the management of angina. |
| |Compare and contrast cardioselective and nonselective beta blockers and calcium channel blockers. |
| |Summarize the pros and cons of using sustained-release oral capsules versus transdermal delivery systems of |
| |nitroglycerin for angina pectoris. |
| |Discuss the use of ranolazine, including adverse effects and drug interactions. |
| |Give a basic overview of the pathways involved in hemostasis, including platelet plug formation and reinforcement |
| |of platelet plugs, and the mechanisms by which the body protects against widespread coagulation. |
| |Explain the differences between anticoagulant, antiplatelet, and thrombolytic drugs in terms of what coagulation |
| |processes they affect and their main clinical uses. Likewise, state the main difference between a thrombus and an |
| |embolus. |
| |Describe the usual etiologies of arterial and venous thrombosis and discuss how prophylactic or interventional drug|
| |therapies for these two conditions are similar or different. |
| |Give a short summary of how and where heparins exert their desired anticoagulant effects and describe the |
| |mechanisms and risks of paradoxical increases in thrombotic events associated with heparin-induced |
| |thrombocytopenia. |
| |Compare and contrast unfractionated heparins and low-molecular-weight (LMW) heparins in terms of mechanisms of |
| |action, pharmacokinetics, dosing (schedules), suitability for outpatient therapy, and monitoring of responses. |
| |Summarize the key points that describe the differences between warfarin and heparin: mechanisms, onset, sites of |
| |action, and monitoring. |
| |Compare and contrast the actions and uses of aspirin with those of warfarin and heparin and state the typical |
| |“targets” for the laboratory test used to monitor the response to each. |
| |Summarize instructions on the use of aspirin to relieve common headache, pain, or fever for an outpatient who is |
| |taking warfarin; also, explain situations in which concomitantly taking warfarin and aspirin is acceptable and |
| |those in which doing so can be dangerous. |
| |Summarize general precautions and guidelines that apply when anticoagulation is indicated for a pregnant woman. In |
| |particular, state the required adjustment to the dosage of warfarin. |
| |Explain the purpose of the glycoprotein IIb/IIIa receptor and the clinical significance of blocking it. |
| |State how thrombolytic drugs differ in terms of mechanisms of action, pharmacokinetics, and relative safety, |
| |including in the discussion the need for repeat administration. |
| |State the main adverse response by anticoagulants, antiplatelet drugs, and thrombolytic drugs. |
| |Describe the pathophysiology involved in myocardial infarction. |
| |Discuss methods of reperfusion therapy. |
| |Describe the adverse effects of reperfusion therapy. |
| |Explain adjunctive drug therapy, including the use of anticoagulants. |
| |Discuss treatment methods for patients experiencing an acute myocardial infarction (MI). |
| |Discuss secondary treatment measures for those who have experienced an MI. |
| |Discuss the pathophysiology, inheritance pattern, and clinical features of hemophilia. |
| |Identify the cornerstone of treatment for hemophilia A and hemophilia B. |
| |Discuss pain management options and the reason aspirin should never be used in patients with hemophilia. |
| |Describe the variances, if any, in the immunization schedule for children with hemophilia. |
| |Discuss the various preparations used to treat hemophilia, and describe adverse effects and dosage calculations. |
| |Discuss treatment options for patients who have developed inhibitors to therapy. |
| |Summarize the roles of erythropoietin, iron, vitamin B12, and folic acid in erythropoiesis (red blood cell |
| |production). |
| |State the main factor that determines daily iron requirements, and explain how the body adjusts iron uptake from |
| |dietary sources to ensure adequate levels yet prevent iron overload. |
| |List several foods or food groups that are naturally rich sources of iron. |
| |State three common conditions that lead to iron deficiencies, and explain whether reduced iron delivery or |
| |increased iron demand usually contributes to the imbalance. |
| |Describe the physiologically essential interrelationship between vitamin B12 and folic acid and the major |
| |physiologic roles of active folate. Also, name the main physiologic roles of each and the signs and symptoms of |
| |deficiency. |
| |Describe the consequences of vitamin B12 deficiency for neural function, erythrocyte count and appearance, |
| |coagulation, and immune system function. Also, summarize the signs and symptoms likely to be seen in a patient with|
| |vitamin B12 deficiency, and discuss therapy for mild, moderate, and severe cases of the disorder. |
| |Summarize the likely consequences for the fetus of folate deficiency in the pregnant mother, as well as general |
| |guidelines on folate supplementation in women, especially during pregnancy. Also, state the trimester or trimesters|
| |in which an adequate maternal intake of folate is particularly critical. |
| |Discuss the need for epoetin alfa. |
| |Discuss the use of leukopoietic growth factors to reduce the risk of infection in patients with neutropenia. |
| |Describe the adverse effects of filgrastim. |
| |Discuss the medication used after failure of a bone marrow transplant. |
| |Discuss the therapeutic use and adverse effects of oprelvekin (interleukin-11) [Neumega]. |
|TOPIC (S) |Unit 7: Drugs that Affect Heart, Blood Vessels and Blood |
| |Drugs for heart Failure |
| |Antidysrhythmic Drugs |
| |Prophylaxis of atherosclerotic Cardiovascular Disease: Drugs that Help Normalize Cholesterol and Triglyceride |
| |levels |
| |Drugs for Angina Pectoris |
| |Anticoagulant, Antiplatelet, and Thrombolytic Drugs |
| |Management of ST-Elevation Myocardial Infarction |
| |Drugs for Hemophilia |
| |Drugs for Deficiency Anemias |
| |Hematopoietic Agents |
|LEARNING ACTIVITIES |READING ASSIGNMENT |
| |Chapter 48: Drugs for heart Failure – pp 517 - 533 |
| |Chapter 49: Antidysrhythmic Drugs – pp 534 - 555 |
| |Chapter 50: Prophylaxis of atherosclerotic Cardiovascular Disease: Drugs that Help Normalize Cholesterol and |
| |Triglyceride levels – pp 556 - 580 |
| |Chapter 51: Drugs for Angina Pectoris – pp 581 - 593 |
| |Chapter 52: Anticoagulant, Antiplatelet, and Thrombolytic Drugs |
| |– pp 594 - 624 |
| |Chapter 53: Management of ST-Elevation Myocardial Infarction |
| |– pp 625 - 631 |
| |Chapter 54: Drugs for Hemophilia – pp 632 – 639 |
| |Chapter 55: Drugs for Deficiency Anemias – pp 640 – 654 |
| |Chapter 56: Hematopoietic Agents – pp 655 - 666 |
| | |
| |DISCUSSION (Choose 1) |
| |Describe what the terms afterload and afterload reduction mean and explain why afterload reduction is beneficial in|
| |the management of heart failure. |
| |Discuss the pathophysiology, inheritance pattern, and clinical features of hemophilia. |
| |Describe the usual etiologies of arterial and venous thrombosis and discuss how prophylactic or interventional drug|
| |therapies for these two conditions are similar or different. |
| | |
| |SUBMISSION |
| |Math Worksheet |
| | |
| |ASSIGNMENT |
| |Review the syllabus |
| |Read assignments |
| |Post discussion topic by Wednesday at 11:55 pm EST |
| |Respond to at least one classmate by Friday at 11:55 pm EST |
| |Complete math worksheet & submit by Friday at 11:55 pm EST |
| |Complete case study |
| | |
| |ASSESSMENT |
| |Discussion & response |
| |Math worksheet |
| |Case study |
| |Quiz Chapters 48, 49, 50, 51, 52, 53, 54, 55, & 56 |
| | |
| | |
| | |
| |Homework: Chapter readings: Chapters 57, 58, 59, & 60 |
| |Week 9 |
|SPECIFIC OBJECTIVES |At the end of this lesson, you will be able to: |
| |Discuss the physiologic effects of insulin on carbohydrate, lipid, and protein metabolism, and identify the body |
| |cells and tissues that most depend on insulin to provide glucose as the main metabolic fuel. |
| |Differentiate between the two major types of diabetes based on etiology, demographics, and treatment. |
| |State three classic signs or symptoms of diabetes, and identify the main pathophysiologic risks from long-term, |
| |poorly controlled diabetes. |
| |Describe the values and limitations of monitoring diabetes therapy based on urine testing and blood testing for |
| |glucose and ketones. |
| |Explain the glycosylated hemoglobin (hemoglobin A1c), what it reflects (in terms of blood chemistry), and why it is|
| |an important adjunct to static (total) blood glucose levels in monitoring the response of diabetes to therapy. |
| |State the main goals of therapy for all patients with diabetes in terms of both symptom control and quantitative |
| |targets for fasting blood glucose levels and for the hemoglobin A1c. |
| |Differentiate among the different insulins for therapeutic use in terms of their mechanisms of action, |
| |pharmacokinetics, and administration routes. Also, identify the pharmaceutical formulations that can be given |
| |intravenously and those that cannot, and explain which pharmaceutical property governs whether intravenous (IV) |
| |administration is safe. |
| |Discuss insulin resistance in terms of what it means, factors that contribute to it, and things that can be done to|
| |reduce the problem. |
| |Identify the main groups of drugs that can interfere with diabetes therapy, whether by directly altering blood |
| |glucose levels, or by interacting with the current antidiabetic drug or drugs. |
| |Identify the main groups of oral antidiabetic drugs (and a prototype in each). Compare and contrast their main |
| |mechanisms of action, their main adverse responses, and drug-drug interactions. |
| |Describe appropriate interventions for managing acute or chronic hypoglycemia. |
| |Describe the potential maternal and fetal consequences of poorly controlled blood glucose levels during pregnancy. |
| |Also, in the case of a pregnant woman being treated for type 1 or type 2 diabetes, describe drug therapy changes |
| |that usually are indicated until parturition. |
| |Summarize the general cause, signs, symptoms, and clinical outcomes of diabetic ketoacidosis and hyperglycemic |
| |hyperosmolar nonketotic syndrome (HHNS). |
| |Summarize the biosynthesis of thyroid hormones, the processes for regulating synthesis and release, and the |
| |feedback regulation of both. |
| |Compare and contrast triiodothyronine (T3) and thyroxine (T4) in terms of relative abundance, biologic activity, |
| |and onset and duration of action. |
| |Describe the physiologic actions of thyroid hormones on basal metabolism, cell growth, and regulation of adrenergic|
| |receptor activity. |
| |Compare and contrast the effects of dietary iodine/iodide deficiency, normal dietary intake, and high-dose iodine |
| |supplementation on thyroid hormone status and thyroid gland function. |
| |Describe signs and symptoms typically associated with hypothyroidism and hyperthyroidism. |
| |Compare and contrast the biologic activities of thyroid hormone replacement products; also, state which are |
| |generally preferred for managing hypothyroidism and why. |
| |Describe the imminent dangers of the two extremes of thyroid hormone status – myxedema coma and |
| |thyrotoxicosis/thyroid storm – and summarize a reasonable treatment plan for each. |
| |Discuss drug treatments usually used in preparation for thyroidectomy and the rationales for their use. |
| |Describe the uses of and contraindications to radioactive iodine in terms of diagnosing or treating thyroid |
| |disorders. |
| |Discuss the general pathways and mechanisms by which the pituitary, hypothalamus, and many endocrine glands in the |
| |periphery work in concert to regulate blood hormone levels. |
| |Summarize the main consequences of growth hormone (GH) deficiency and excess, comparing and contrasting likely |
| |clinical presentations depending on whether the dysfunction occurs before or after puberty. Also, state the |
| |expected effects on protein and carbohydrate metabolism. |
| |State the main actions of prolactin and describe how its release is regulated. Also, summarize the main clinical |
| |findings in hyperprolactinemia and explain its management. |
| |Explain the main systemic effects of antidiuretic hormone (ADH), the expected effects of hypersecretion and |
| |hyposecretion, and their management. |
| |Demonstrate an understanding of the similarities and differences between vasopressin, ADH, and oxytocin in terms of|
| |composition and physiologic or pathophysiologic effects. |
| |State the three classes of steroid hormones produced by the adrenal cortex and generally describe how their |
| |physiologic effects differ. |
| |Compare and contrast glucocorticoids and mineralocorticoids in terms of which substance or substances and processes|
| |in the body they mainly regulate. Also, explain why labeling a corticosteroid drug as either a glucocorticoid or a |
| |mineralocorticoid is, to a degree, an oversimplification. |
| |Describe the physiologic processes and pathways that regulate cortisol production and release. Compare and contrast|
| |those with how aldosterone production and release are regulated physiologically. |
| |State three basic ways hormones or drugs with glucocorticoid activity promote carbohydrate availability to the |
| |brain and other essential tissues or organs. In addition, state the expected effects of these agents on protein and|
| |lipid metabolism. |
| |Describe the signs and symptoms of insufficiency and excess of cortisol and of aldosterone. State the main |
| |laboratory test alterations, applicable diagnostic tests, and reasonable treatment plans for these conditions. |
| |Describe how glucocorticoid administration at pharmacologic doses affects the hypothalamic-pituitary-adrenal (HPA) |
| |cortical axis; state the signs and symptoms and relative duration of withdrawal; and give some strategies for |
| |minimizing suppression of the HPA. |
|TOPIC (S) |Unit 8: Drugs for Endocrine Disorders |
| |Drugs for Diabetes mellitus |
| |Drugs for Thyroid Disease |
| |Drugs Related to Hypothalamic and Pituitary Function |
| |Drugs for Disorders of the Adrenal Cortex |
|LEARNING ACTIVITIES |READING ASSIGNMENT |
| |Chapter 57: Drugs for Diabetes Mellitus – pp 667 – 702 |
| |Chapter 58: Drugs for Thyroid Disease – pp 703 – 714 |
| |Chapter 59: Drugs Related to Hypothalamic and Pituitary Function – pp 715 – 724 |
| |Chapter 60: Drugs for Disorders of the Adrenal Cortex – pp 725 – 732 |
| | |
| |DISCUSSION (Choose 1) |
| |Discuss the physiologic effects of insulin on carbohydrate, lipid, and protein metabolism, and identify the body |
| |cells and tissues that most depend on insulin to provide glucose as the main metabolic fuel. |
| |Describe appropriate interventions for managing acute or chronic hypoglycemia. |
| |Describe the physiologic processes and pathways that regulate cortisol production and release. Compare and contrast|
| |those with how aldosterone production and release are regulated physiologically. |
| | |
| | |
| |SUBMISSION |
| |Math Worksheet |
| | |
| |ASSIGNMENT |
| |Review the syllabus |
| |Read assignments |
| |Post discussion topic by Wednesday at 11:55 pm EST |
| |Respond to at least one classmate by Friday at 11:55 pm EST |
| |Complete math worksheet & submit by Friday at 11:55 pm EST |
| |Complete case study |
| | |
| |ASSESSMENT |
| |Discussion & response |
| |Math worksheet |
| |Case study |
| |Quiz Chapters 57, 58, 59, & 60 |
| | |
| |Homework: Chapter readings: Chapters 61, 62, 63, 64, 65, & 66. |
|DATE |WEEK 10 |
|SPECIFIC OBJECTIVES |At the end of this lesson, you will be able to: |
| |Discuss the menstrual cycle, including phasic changes of hormone levels and their effects on other body systems, |
| |and identify the major regulatory stimuli for these changes. |
| |Summarize the main physiologic effects of estrogen and progestin. |
| |Compare and contrast the benefits and adverse effects of estrogen and progesterone hormones as replacement therapy |
| |compared with the risks and benefits of not replacing them. Consider such important outcomes as breast cancer, |
| |ovarian or endometrial cancer, and osteoporosis. |
| |Describe premenstrual syndrome (PMS) and summarize the effects and actions of drugs that are effective for it. |
| |Give a succinct but accurate description of the aims of the Heart and Estrogen/Progestin Replacement Study (HERS I |
| |and II), the Women’s Health Initiative (WHI) study, and the major findings of each. |
| |Describe the different methods of birth control and their main known benefits, adverse effects, and overall |
| |contraception rates. |
| |Describe the general meaning of the term minipill with regard to the active ingredient or ingredients in one of |
| |these birth control drugs. Also, explain what seems to be the main advantage of the minipill compared to a |
| |combination OC. |
| |Summarize the main features that distinguish monophasic, biphasic, and triphasic OCs, including each type’s |
| |ingredients, dosages, and cycle-related changes in the dosages of the ingredients. |
| |Summarize the main interactions involving oral contraceptives, including other drugs that may lower the |
| |contraceptive effects of OCs and drugs that are targets of interactions caused by OCs. Summarize the main |
| |pharmacokinetic mechanisms responsible for these interactions. Specifically, focus on the following: (1) warfarin; |
| |(2) anticonvulsants/antiepileptic drugs (for example, phenytoin); (3) tetracycline antibiotics and ampicillin; and |
| |(4) theophylline. |
| |Explain the Yuzpe regimen, including its purpose, the drugs used, the main way to optimize the desired outcome, and|
| |the most common side effects. |
| |Describe the causes of and treatment strategies for male and female infertility, including those for unfavorable |
| |cervical mucus, hyperprolactinemia, endometriosis, polycystic ovary syndrome (PCOS), erectile dysfunction, and |
| |idiopathic male infertility. |
| |Describe the therapeutic uses and adverse effects of clomiphene, menotropins, follitropins, human chorionic |
| |gonadotropin (hCG), dopamine agonists for hyperprolactinemia, and gonadotropin-releasing hormone (GnRH) agonists |
| |for endometriosis. |
| |Describe three major clinical settings in which use of an oxytocic is deemed acceptable. |
| |Discuss the factors that should be considered in selecting a particular oxytocic drug or drug class for use before |
| |versus after delivery. |
| |State the major risks of magnesium sulfate, used as a tocolytic drug, in terms of potential adverse effects on the |
| |mother, on the fetus, and on the infant shortly after delivery. |
| |Identify the three main groups of uterine stimulant drugs, compare and contrast their effects on uterine muscle |
| |tone and rhythmicity, and state why their different intensities of effects do (or do not) make them suitable for |
| |use before or after labor and delivery. |
| |Discuss the physiologic effects of androgens in males and females, including likely effects in utero, during |
| |childhood growth and development (e.g., through puberty), and in later life. |
| |Summarize the expected beneficial actions of androgens when used to manage hypogonadism in adult males. Also, |
| |discuss the key physiologic and psychologic signs and symptoms that might lead to a diagnosis of male hypogonadism |
| |and a decision to begin testosterone therapy. |
| |Summarize current knowledge about the use and abuse of androgens (anabolic steroids) in athletes, including key |
| |points about the desired (and sometimes clinically proven) physical, metabolic, and psychologic effects of these |
| |drugs. Also, describe adverse responses that pose risks with such use and explain basic legal or other regulatory |
| |points concerning use of anabolic steroids. |
| |Identify the main patient-related conditions and other applicable factors that contraindicate safe use of |
| |phosphodiesterase type 5 (PDE5) inhibitors. Also, in doing so, describe the main systemic hemodynamic effects of |
| |the drug. |
| |State the likely consequences of administering PDE5 inhibitors with drugs that inhibit the liver’s cytochrome P450 |
| |system (specifically the enzyme CYP3A4). Also, identify the main groups of these drugs. |
| |Discuss guidelines or recommendations for the use of PDE5 inhibitors by a patient who is taking nitroglycerin or |
| |any other nitrate vasodilator/antianginal drug; also, describe the likely outcome if these recommendations are |
| |ignored. |
| |Discuss the underlying pathophysiology of benign prostatic hyperplasia (BPH) and relate it to the mechanism of |
| |action of 5-alpha-reductase inhibitors and alpha blockers. |
|TOPIC (S) |Unit 9: Women’s Health |
| |Estrogens and Progestins: Basic Pharmacology and Noncontraceptive Application |
| |Birth Control |
| |Drug Therapy of Infertility |
| |Drugs that Affect Uterine Function |
| | |
| |Unit 10: Men's Health |
| |Androgens |
| |Drugs for Erectile Dysfunction and Benign Prostatic Hyperplasia |
|LEARNING ACTIVITIES |READING ASSIGNMENT |
| |Chapter 61: Estrogens and Progestins: Basic Pharmacology and Noncontraceptive Applications – pp 733 – 750 |
| |Chapter 62: Birth Control – pp 751 – 768 |
| |Chapter 63: Drug Therapy of Infertility – pp 769 – 776 |
| |Chapter 64: Drugs that Affect Uterine Function – pp 777 – 787 |
| |Chapter 65: Androgens – pp 788 – 795 |
| |Chapter 66: Drugs for Erectile Dysfunction and Benign Prostatic Hyperplasia – pp 796 – 805 |
| | |
| |DISCUSSION (Choose 1) |
| |Describe premenstrual syndrome (PMS) and summarize the effects and actions of drugs that are effective for it. |
| |Describe the different methods of birth control and their main known benefits, adverse effects, and overall |
| |contraception rates. |
| |Summarize current knowledge about the use and abuse of androgens (anabolic steroids) in athletes, including key |
| |points about the desired (and sometimes clinically proven) physical, metabolic, and psychologic effects of these |
| |drugs. Also, describe adverse responses that pose risks with such use and explain basic legal or other regulatory |
| |points concerning use of anabolic steroids. |
| | |
| |SUBMISSION |
| |Math Final |
| | |
| |ASSIGNMENT |
| |Review the syllabus |
| |Read assignments |
| |Post discussion topic by Wednesday at 11:55 pm EST |
| |Respond to at least one classmate by Friday at 11:55 pm EST |
| |Complete math final by Friday at 11:55 pm EST |
| |Complete case study |
| | |
| |ASSESSMENT |
| |Discussion & response |
| |Math final |
| |Case study |
| |Quiz Chapters 61, 62, 63, 64, 65, & 66. |
| | |
| | |
| |Homework: Chapter readings: Chapters 67, 68, 69, 70, 71, & 72 |
| | |
|DATE |WEEK 11 |
|SPECIFIC OBJECTIVES |At the end of this lesson, you will be able to: |
| |Compare and contrast antibody-mediated (humoral) immunity and cell-mediated immunity, including in the discussion |
| |the general mechanisms of antibody production on the host and how antibodies produce actions or defenses in the |
| |host. |
| |Identify the origins and roles of helper T lymphocytes (CD4 cells), macrophages, and cytolytic T lymphocytes (CD8 |
| |cells). |
| |State the main roles of the following cells, which are important in the immune response: B lymphocytes (B cells), |
| |cytolytic T lymphocytes (T cells, CD8 cells), helper T lymphocytes, macrophages/monocytes, and mast |
| |cells/basophils. |
| |Explain the general roles of the immunoglobulins and explain why they are divided into five major classes. |
| |Explain the MHC and its main functions, considering the functions in terms of preventing autoimmune diseases and |
| |aiding organ/tissue/cell transplantation. |
| |Compare and contrast the basic mechanisms and outcomes of delayed and immediate hypersensitivity reactions. In |
| |discussing delayed hypersensitivity, integrate general concepts about cell-mediated immunity. |
| |Summarize the main purpose of the classical complement pathway and how its activation eventually leads to cell |
| |death. |
| |Describe the role of vaccines in maintaining health. |
| |Differentiate between active and passive immunity and explain how vaccines work. |
| |Summarize the three main contraindications that apply to administration of any vaccine. |
| |State where to look for current information on required or recommended vaccinations for children, and explain when |
| |and how these vaccines should be given. |
| |Explain why multiple doses of a vaccine are given for a particular preventable infectious disease, rather than just|
| |a single dose. |
| |Identify the two most common clinical uses for immunosuppressive drugs. |
| |Explain why immunosuppressants can be considered both a blessing and a potential curse to the host. |
| |Summarize the main mechanism of action, pharmacokinetics, toxicity, and drug-drug interactions involving |
| |calcineurin inhibitors in the context of a holistic care plan that maximizes the drug’s desired effects while |
| |minimizing the risks of adverse responses or drug interactions. |
| |Name some of the common autoimmune disorders for which immunosuppressants are used. |
| |State the richest physiologic source of histamine and name the part or parts of the body where histamine is found |
| |in abundance. Also, describe the two main processes by which this chemical can be released from these structures. |
| |Summarize the main effects of histamine on airway smooth muscle tone, arteriolar and venular tone, gastric acid |
| |secretion, and the heart (e.g., rate), and identify the receptor or receptors involved in these effects. |
| |Identify the receptors that are blocked by a typical first-generation H1 antagonist, especially as they relate to |
| |clinical uses and precautions for their use. |
| |Compare and contrast the effects of first- and second-generation H1 antagonists on the central nervous system |
| |(CNS). |
| |Summarize the benefits or limitations of antihistamines for managing anaphylaxis, the signs and symptoms of the |
| |common cold, allergic rhinitis, and asthma. |
| |Describe the similarities or differences between the COX-1 and COX-2 pathways and state which (pathologic) |
| |physiologic process is mainly responsible for analgesia, antiinflammatory activity, antipyresis, bleeding |
| |tendencies, and gastric mucosal damage. |
| |Discuss the beneficial and adverse actions of NSAIDs and the basic mechanisms by which they occur. |
| |Identify situations in which aspirin should not be used, even for relief of mild or episodic headache or fever. |
| |Also, state which of the alternative over-the-counter (OTC) analgesic/antipyretic drugs would be a more acceptable |
| |alternative to aspirin and why. |
| |Compare and contrast the signs and symptoms of acute poisoning with aspirin and with acetaminophen; the time course|
| |of the signs and symptoms and underlying causes; and the management of these conditions. |
| |Describe the feedback loop and its components that regulate physiologic glucocorticoid secretion. |
| |Describe the general mechanism by which glucocorticoids cause their biologic effects. Also, compare the cellular |
| |site of glucocorticoid receptors with those of typical agonists, such as epinephrine or acetylcholine. |
| |State and describe the main therapeutic uses of glucocorticoids for nonendocrine disorders. |
| |In terms of mechanisms and targets of action, state why glucocorticoids have greater antiinflammatory activity than|
| |nonsteroidal antiinflammatory drugs (NSAIDs). |
| |State and describe the physiologic effects of glucose administration on the metabolism, the cardiovascular system, |
| |the stress response, fluid and electrolytes, and the respiratory system in neonates. |
| |Describe issues related to the timing of glucocorticoid administration, particularly with regard to maximizing |
| |therapeutic responses and minimizing adverse responses during corticosteroid administration and discontinuation. |
| |Describe the potential risks to and relative glucocorticoid requirements of patients who are under physiologic |
| |stress and during discontinuation of systemic glucocorticoids. |
| |Discuss issues and concerns related to administering pharmacologic doses of glucocorticoids to women who are |
| |pregnant or breast-feeding their infants. |
|TOPIC (S) |Unit 11: Anti-inflammatory, Antiallergic, and Immunologic Drugs |
| |Review of the Immune System |
| |Childhood Immunization |
| |Immunosuppressants |
| |Antihistamines |
| |Cyclooxygenase Inhibitors: Nonsteroidal Anti-inflammatory Drugs and acetaminophen |
| |Glucocorticoids in Nonedocrine Disorders |
|LEARNING ACTIVITIES |READING ASSIGNMENT |
| |Chapter 67: Review of the Immune System – pp 806 – 816 |
| |Chapter 68: Childhood Immunization – pp 817 – 833 |
| |Chapter 69: Immunosuppressants – pp 834 – 840 |
| |Chapter 70: Antihistamines – pp 841 – 848 |
| |Chapter 71: Cyclooxygenase Inhibitors: Nonsteroidal Anti-inflammatory Drugs and Acetaminophen – pp 849 – 868 |
| |Chapter 72: Glucocorticoids in Nonedocrine Disorders – pp 869 - 917 |
| | |
| |DISCUSSION (Choose 1) |
| |Summarize the three main contraindications that apply to administration of any vaccine. |
| |Explain why immunosuppressants can be considered both a blessing and a potential curse to the host. |
| |Discuss issues and concerns related to administering pharmacologic doses of glucocorticoids to women who are |
| |pregnant or breast-feeding their infants. |
| | |
| | |
| |ASSIGNMENT |
| |Review the syllabus |
| |Read assignments |
| |Post discussion topic by Wednesday at 11:55 pm EST |
| |Respond to at least one classmate by Friday at 11:55 pm EST |
| |Complete math quiz by Friday at 11:55 pm EST |
| |Complete case study |
| | |
| |ASSESSMENT |
| |Discussion & response |
| |Math quiz |
| |Case study |
| |Quiz Chapters 67, 68, 69, 70, 71, & 72 |
| | |
| | |
| |Homework: Chapter readings: Chapters 73, 74, 75, 76, & 77. |
|DATE |WEEK 12 |
|SPECIFIC OBJECTIVES |At the end of this lesson, you will be able to: |
| |Discuss the etiology, pathophysiology, clinical presentation, and long-term complications of rheumatoid arthritis |
| |(RA). |
| |Discuss the three classes of drugs used in the treatment of rheumatoid arthritis and identify the importance of |
| |early use of disease-modifying antirheumatic drugs (DMARDs). |
| |Compare and contrast the main adverse effects of the nonbiologic and biologic DMARDs used in the treatment of RA. |
| |Discuss the role of nonsteroidal antiinflammatory drugs (NSAIDs) and glucocorticoids in the treatment of RA based |
| |on current management guidelines. |
| |Discuss the etiology, pathophysiology, clinical presentation, and treatment of gouty arthritis. |
| |Discuss the first-line agents for relieving the pain of an acute gouty attack and explain when glucocorticoids and |
| |colchicine are acceptable alternatives. |
| |Give an overview of the metabolic pathway by which uric acid is formed, starting with the original source, |
| |adenosine triphosphate (ATP); name the enzyme involved in the conversion of hypoxanthine to xanthine and xanthine |
| |to uric acid; and compare and contrast the solubility of hypoxanthine, xanthine, and uric acid in body fluids |
| |(e.g., urine, synovial fluid). |
| |Summarize the mechanisms of action of allopurinol, probenecid, and colchicine in the context of hyperuricemia, |
| |gout, and gouty arthritis. In addition, state where each fits into a treatment plan for asymptomatic hyperuricemia,|
| |treatment of acute gout, and prophylaxis of recurrent attacks, and when and why each should not be used. |
| |Describe the dose-dependent effects of aspirin on renal handling of uric acid and discuss the roles of this |
| |nonsteroidal antiinflammatory drug (NSAID), which is the one most commonly used in the therapy of asymptomatic |
| |hyperuricemia and gout. |
| |Briefly describe the roles of parathyroid hormone and vitamin D as they affect absorption of dietary calcium and |
| |bone mineral metabolism. |
| |Briefly describe the roles of osteoblasts and osteoclasts in bone formation and resorption. |
| |Compare and contrast the benefits, limitations, and risks of estrogen replacement therapy with those of raloxifene |
| |in terms of their effects on bone metabolism and integrity; risks of breast and endometrial cancer; menstrual |
| |bleeding; other signs and symptoms of menopause; the incidence of thromboembolism; and fetal development, should |
| |the patient receiving the drug be pregnant. |
| |Describe the typical etiologies and characteristic signs, symptoms, and laboratory abnormalities associated with |
| |hypocalcemia and hypercalcemia. |
| |Describe drug therapies and nondrug interventions that are indicated for osteoporosis, making sure to distinguish |
| |between prophylaxis and treatment of the disease once it has been diagnosed. |
| |State a reasonably accurate definition of asthma that includes an understanding of the roles and involvement of |
| |airway smooth muscle hyper-responsiveness and inflammation in the disease. Also, describe the typical signs and |
| |symptoms that would lead to the diagnosis of a respiratory disorder as asthma. |
| |State the criteria used to classify the severity of asthma based on impairment and risk. |
| |Summarize the mechanisms of action, roles, and limitations of the following drugs in the therapy of asthma: |
| |beta-adrenergic agonists, glucocorticoids, methylxanthines, mast cell stabilizers, leukotriene modifiers, |
| |anticholinergic drugs, and glucocorticoid/LABA combinations. |
| |Describe the two basic goals in the treatment of chronic asthma. |
| |Compile a list of drugs or drug groups that are relatively or absolutely contraindicated in patients with asthma, |
| |and state the main reasons why. |
| |Discuss some nondrug interventions that might be used to reduce the frequency and severity of asthma attacks. |
| |Review the basic pharmacology of drugs for allergic rhinitis. |
| |Summarize the roles of antihistamines, glucocorticoids, and sympathomimetic decongestants in terms of managing the |
| |signs, symptoms, and underlying causes of the common cold. |
| |Discuss the use of zinc and vitamin C for colds in children and adults. |
|TOPIC (S) |Unit 12: Drugs for Bone and Joint Disorders |
| |Drug Therapy of Rheumatoid Arthritis |
| |Drug Therapy of Gout |
| |Drugs Affecting Calcium levels and Bone Mineralization |
| |Unit 13: Respiratory Tract Drugs |
| |Drugs for Asthma and Chronic Obstructive Pulmonary Disease |
| |Drugs for Allergic Rhinitis, Cough, and Colds |
|LEARNING ACTIVITIES |READING ASSIGNMENT |
| |Chapter 73: drug Therapy of Rheumatoid Arthritis – pp 879 – 890 |
| |Chapter 74: Drug Therapy of Gout – pp 891 – 895 |
| |Chapter 75: Drugs Affecting Calcium Levels and Bone Mineralization – pp 896 – 917 |
| |Chapter 76: Drugs for Asthma and Chronic Obstructive Pulmonary Disease – pp 918 – 938 |
| |Chapter 77: Drugs for Allergic Rhinitis, Cough, and Colds – pp 939 – 948 |
| |DISCUSSION (Choose 1) |
| |Discuss the use of zinc and vitamin C for colds in children and adults. |
| |Describe the two basic goals in the treatment of chronic asthma. |
| |Discuss the etiology, pathophysiology, clinical presentation, and treatment of gouty arthritis. |
| |ASSIGNMENT |
| |Read assignments |
| |Post discussion topic by Wednesday at 11:55 pm EST |
| |Respond to at least one classmate by Friday at 11:55 pm EST |
| |Complete math final by Friday at 11:55 pm EST |
| |Complete case study |
| |ASSESSMENT |
| |Discussion & response |
| |Math quiz |
| |Case study |
| |Quiz Chapters 73, 74, 75, 76, & 77 |
| | |
| |Homework: Chapter readings: Chapters 78, 79, 80,81,& 82 |
|DATE |WEEK 13 |
|SPECIFIC OBJECTIVES |At the end of this lesson, you will be able to: |
| |Describe peptic ulcer disease as an imbalance between protective and destructive factors on the gastrointestinal |
| |(GI) mucosa. Also, state the contributions of histamine, gastrin, and acetylcholine to overall gastric acid |
| |secretion and explain why gastric acid is a necessary (but not in itself sufficient) component of the development |
| |of peptic ulcers. |
| |Summarize the benefits and limitations of drug therapy targeted at the destructive factors on the GI mucosa and |
| |identify which drugs or drug groups truly alter the underlying disease processes rather than creating a local |
| |environment that is conducive to natural ulcer healing. |
| |Discuss short-term and long-term goals of therapy for peptic ulcer disease and identify one or more drugs or drug |
| |groups that can meet those goals quicker or better than others. |
| |State conditions for which a trial of over-the-counter (OTC) drug therapy might be indicated, either for peptic |
| |ulcer disease (PUD) or gastroesophageal reflux disease (GERD). In addition, recommend a treatment plan that |
| |involves OTC drugs; also, with regard to this plan, highlight the limitations and potential dangers of |
| |self-medication with OTCs and state findings that necessitate a visit to a physician. |
| |Identify the four main chemicals in single-ingredient antacid products and the major benefits or limitations of |
| |each. State the ingredients typically found in proprietary antacid combination products and give the rationale for |
| |using them rather than single-ingredient products. Include the main expected effects of single-ingredient antacids |
| |on gut motility. |
| |Compare and contrast the H2 blockers in terms of efficacy, side effects, and drug-drug interactions. Also, be able |
| |to argue for or against the selection of a particular H2 blocker over another. |
| |State the role of antihistamines (e.g., diphenhydramine) in the management of PUD. |
| |State the role of proton pump inhibitors in the management of PUD. |
| |Prepare a short list of drugs or drug groups (classes) that are ulcerogenic. |
| |Describe the principal functions of the colon and what constitutes a normal bowel movement. |
| |Define constipation and describe nondrug measures to correct it. |
| |Identify indications for the use of a laxative. |
| |Describe the basic pharmacology of laxatives and distinguish among surfactant laxatives, stimulant laxatives, and |
| |osmotic laxatives. |
| |Describe the causes, consequences, and treatment of laxative abuse. |
| |Discuss the mechanisms by which emesis is triggered and the main neurotransmitters that participate in the |
| |triggering of signs and symptoms. |
| |Describe the drugs used as antiemetics and summarize their mechanism of action, if known. |
| |Describe a care plan for managing chemotherapy-induced nausea and vomiting, including interventions and drugs that |
| |would be suitable for the three main types of emesis seen in this setting (anticipatory, acute, and delayed), as |
| |well as considerations for effective routes of administration. |
| |State the overall functional role of vitamins in maintaining good health. |
| |In general terms, compare and contrast the Recommended Dietary Allowance (RDA), Adequate Intake (AI), Tolerable |
| |Upper Intake Level (UL), and Estimated Average Requirement (EAR) with regard to vitamin intake. |
| |Identify the two major vitamin groups or classifications and the factor or factors that place a vitamin in either |
| |of those groups. |
| |Recognize the common synonyms or alternative terms (or common pharmaceutical products) for the following vitamins: |
| |1. Niacin ‒ nicotinic acid, nicotinamide; 2. Vitamin A ‒ retinol; 3. Vitamin B1 ‒ thiamine; 4. Vitamin B12 ‒ |
| |cyanocobalamin; 5. Vitamin B2 ‒ riboflavin; 6. Vitamin B6 ‒ pyridoxine; 7. Vitamin C ‒ ascorbic acid; 8. Vitamin E |
| |‒ alpha-tocopherol. |
| |State the main biochemical roles of the following vitamins and the clinical findings or consequences of inadequate |
| |or excessive levels: vitamins A, C, D, E, K, B1, B2, B6, B12, niacin, and folic acid. |
| |State the common comorbidities associated with obesity. |
| |Give a general overview of the importance of existing comorbidities in determining whether or how to initiate |
| |weight-loss therapy. |
| |Discuss the management of obesity, including the benefits, risks, and limitations of lifestyle changes, drug |
| |therapy, and surgery. |
| |Identify the main pharmacologic classes and mechanisms of appetite suppressants and the common medical or |
| |psychologic conditions they may aggravate. |
| |Describe serotonin syndrome and the weight-loss medication that is most likely to trigger it; also, identify drugs |
| |that increase the risk of this serious response. |
| |Summarize the main calorie-lowering actions of and indications for orlistat. Also, identify its main site of |
| |action, compare it with that of such drugs as sibutramine or the amphetamines, and explain the clinical |
| |consequences of orlistat’s different site of action. |
| |Identify the main drug used in many over-the-counter (OTC) weight-loss aids, the potential adverse peripheral |
| |autonomic effects, and common and important contraindications to its use. |
|TOPIC (S) |Unit 14: Gastrointestinal Drugs |
| |Drugs for Peptic Ulcer Disease |
| |Laxatives |
| |Other Gastrointestinal Drugs |
| |Unit 15: Nutrition |
| |Vitamins |
| |Drugs for Weight Loss |
|LEARNING ACTIVITIES |READING ASSIGNMENT |
| |Chapter 78: Drugs for Peptic Ulcer Disease – pp 947 – 962 |
| |Chapter 79: Laxatives – pp 963 – 970 |
| |Chapter 80: Other Gastrointestinal Drugs – pp 971 – 986 |
| |Chapter 81: Vitamins – pp 987 – 995 |
| |Chapter 82: Drugs for Weight Loss – pp 996 – 1000 |
| | |
| |DISCUSSION (Choose 1) |
| |Describe the basic pharmacology of laxatives and distinguish among surfactant laxatives, stimulant laxatives, and |
| |osmotic laxatives. |
| |Describe the overall functional role of vitamins in maintaining good health. |
| |Identify the main drug used in many over-the-counter (OTC) weight-loss aids, the potential adverse peripheral |
| |autonomic effects, and common and important contraindications to its use. |
| | |
| |ASSIGNMENT |
| |Read assignments |
| |Post discussion topic by Wednesday at 11:55 pm EST |
| |Respond to at least one classmate by Friday at 11:55 pm EST |
| |Complete math final by Friday at 11:55 pm EST |
| |Complete case study |
| | |
| |ASSESSMENT |
| |Discussion & response |
| |Math quiz |
| |Case study |
| |Quiz Chapters 78, 79, 80, 81, & 82. |
| | |
| |Homework: Chapter readings: 83, 84, 85, 86, 87, 88, & 89. |
|DATE |WEEK 14 |
|SPECIFIC OBJECTIVES |At the end of the week, the student will be able to: |
| |Define selective toxicity as it applies to the general mechanisms by which antibiotics work against invading |
| |pathogens but not against host cells. |
| |Give a working definition of narrow-spectrum antibiotics and broad-spectrum antibiotics and state when one or the |
| |other would be preferred as a therapeutic approach and why. |
| |Explain the fundamental difference between bactericidal and bacteriostatic drugs and state the host-related factors|
| |required for successful therapy with a bacteriostatic agent. |
| |State the main mechanisms by which microbes develop resistance to antimicrobial drugs. Also, address the important |
| |issues of spontaneous mutations and R factors. |
| |Understand the concept and purpose of the broth dilution procedure and the disk-diffusion test in determining the |
| |susceptibility of bacteria to antibiotics. |
| |Discuss the general rationale and need for using antibiotics in combination as well as situations in which |
| |antibiotic combinations should be avoided. |
| |Describe generally accepted indications for prophylactic antimicrobial therapy. |
| |Discuss the misuse of antibiotics, its general prevalence, why misuse persists as a major health problem, and the |
| |consequences. Give some examples of common situations in which iatrogenic antibiotic misuse occurs. |
| |Start preparing a table to be completed in the remaining chapters in this unit. Include (1) the names of each main |
| |drug class as well as prototypes and important related drugs; (2) whether and for what infections and infectious |
| |organisms the drugs are considered first-line treatment; (3) whether the drugs are bacteriostatic or bactericidal; |
| |(4) specific and important contraindications; (5) the relative degree to which resistance develops and a general |
| |mechanism by which resistance occurs; (6) the general risk for allergic reactions and whether antibiotics in other |
| |classes may cross-react to trigger allergic responses; and (7) any specific host toxicities. |
| |Describe the basic mechanism of action of the penicillins. |
| |Compare and contrast gram-positive and gram-negative bacteria; state which penicillins are able to penetrate the |
| |outer membrane of gram-negative bacteria. |
| |Describe the beta-lactam ring. Also, explain why penicillins are part of the family of antibiotics called the |
| |beta-lactam antibiotics, and state how that relates to the vulnerability of these antibiotic classes to |
| |inactivation by certain bacteria. |
| |State the four main classes of penicillins: (1) narrow-spectrum penicillins that are penicillinase sensitive, (2) |
| |narrow-spectrum penicillins that are penicillinase resistant, (3) broad-spectrum penicillins, and (4) |
| |extended-spectrum penicillins. Also, for each group, identify the prototype and indicate the bacterial types or |
| |strains that typically respond to them. |
| |Explain the clinical significance of various salts of penicillin G in terms of pharmacokinetics, spectrum of |
| |activity, susceptibility to penicillinases, unique side effects, and adverse reactions. |
| |Recognize penicillins as a main cause of drug-induced allergic reactions. Also, compare and contrast immediate, |
| |accelerated, and delayed hypersensitivity reactions in terms of time of onset and main signs and symptoms. |
| |Given a patient’s history of severe hypersensitivity reactions to penicillin, state at least one other group of |
| |antibiotics that should not be administered because of the risk of cross-reactivity. |
| |Recognize clavulanic acid, sulbactam, and tazobactam as penicillinase inhibitors that are combined with certain |
| |broad- or extended-spectrum penicillins and as drugs that lack intrinsic toxicity and antibiotic effects and do |
| |nothing to reduce the risk or severity of hypersensitivity reactions in susceptible patients. |
| |Describe the general rationale and indications for using both intravenous penicillin and an aminoglycoside. State |
| |the practical and correct reason for administering them together. |
| |Compare and contrast cephalosporins (as a single large drug class) and penicillins with respect to general |
| |mechanisms of action and mechanisms by which resistance develops. |
| |Identify a prototype or representative example for each of the four generations of cephalosporins. Differentiate |
| |the groups in terms of mechanism of action, spectrum of action, susceptibility to destruction/inactivation by |
| |beta-lactamases, and access to the cerebrospinal fluid. |
| |Focus on imipenem as the prototype for carbapenems; also, recognize its broad spectrum of activity and explain how |
| |it influences when the drug should or should not be used. |
| |State the characteristics of vancomycin that make it such a critically important drug, yet one that is not used |
| |unless an infection is very serious or other antibiotics fail or cannot be given to a particular patient. |
| |Recognize the drugs discussed in the chapter as mainly bacteriostatic inhibitors of bacterial protein synthesis and|
| |explain in general terms why they affect bacteria rather than host cells. |
| |State the antibacterial spectrums of the drugs discussed in this chapter and explain whether and why these drugs |
| |are first-line (first-choice) agents for the stated indications. |
| |Describe the mechanism and potential outcomes of interactions between oral tetracyclines and such minerals as |
| |calcium, aluminum, magnesium, iron, and zinc and describe common sources of these interactants. |
| |State the drugs (and drug groups) described in this chapter for which caution is warranted regarding use in people |
| |with liver and/or renal disease, children, and pregnant women; also, explain the basis for such caution and the |
| |potential consequences if the stated drugs are administered to those individuals. |
| |Recognize the macrolides as usually good alternatives to penicillin (e.g., penicillin G) for patients who are or |
| |may be allergic to penicillins. |
| |List the drugs that should not be combined with erythromycin and explain the basic mechanisms and outcomes of |
| |interactions caused by combined administration. |
| |State the unique adverse responses that apply to chloramphenicol and linezolid. |
| |Discuss the mechanism of action and main indications for aminoglycosides. |
| |Recognize that nephrotoxicity and ototoxicity are the two main toxicities of aminoglycosides and describe |
| |precautions that need to be taken to prevent them. |
| |Identify other drugs that increase the risk for aminoglycoside-induced nephrotoxicity and ototoxicity and describe |
| |the factors that should be considered when deciding whether to use them with aminoglycosides. |
| |State the antimicrobial mechanism of action of sulfonamides and of trimethoprim and explain why their effects on |
| |susceptible bacteria do not affect human cells at the same time. |
| |Describe the primary uses for sulfonamides, trimethoprim, and the combination of the two drugs. Explain the |
| |clinical and biochemical rationales for the common combination of sulfamethoxazole with trimethoprim. |
| |Recognize the link between sulfonamides and Stevens-Johnson syndrome, hemolytic anemia, and kernicterus. Describe |
| |the patient populations at highest risk for these potentially serious disorders. State how a nurse might recognize |
| |Stevens-Johnson syndrome or hemolytic anemia; list their major signs and symptoms in the context of how nurses |
| |should be monitoring for these untoward responses. |
| |Explain the general way that sulfonamide-induced crystalluria occurs and state two simple yet usually effective and|
| |appropriate ways to reduce the risks. |
| |Name two or three other groups of drugs that might cross-react and cause adverse responses in patients who have had|
| |hypersensitivity reactions to sulfonamide antibiotics. |
| |Compare and contrast the etiologies and symptoms of acute cystitis and acute pyelonephritis. |
| |Recognize Escherichia coli as the main cause of uncomplicated, community-acquired urinary tract infections (UTIs) |
| |and the cause of less than 50% of hospital-acquired UTIs. |
| |Compare and contrast what the text describes as short-course and conventional therapy for lower UTIs. Identify the |
| |major patient populations that generally are not candidates for short-course treatment. |
| |State which key aspect of therapy distinguishes pharmacologic approaches to uncomplicated lower UTIs versus acute |
| |pyelonephritis. |
| |Differentiate between relapse and reinfection as a cause of recurrent UTIs and identify the relative prevalence of |
| |each. Also, state the general clinical approaches for each and the general clinical presentations that would |
| |warrant consideration of long-term prophylaxis. |
|TOPIC (S) |Unit 16: Chemotherapy of Infectious Diseases |
| |Basic Principles of Antimicrobial Therapy |
| |Drugs that Weaken the Bacterial Cell Wall I: Penicillins |
| |Drugs that Weaken the Bacterial Cell Wall II: Cephalosporins, Carbapenems, Vancomycin, Telavancin, Aztreonam, and |
| |Fosfomycin |
| |Bacteriostatic Inhibitors of Protein Sybthesis: Tetracyclines, Macrolides, and Others |
| |Aminoglycosides: Bactericidal Inhibitors of Protein Synthesis |
| |Sulfonamides and Trimethoprim |
| |Drug Therapy of Urinary Tract Infections. |
|LEARNING ACTIVITIES |READING ASSIGNMENT |
| |Chapter 83: Basic Principles of Antimicrobial Therapy – pp 1001 = 1014 |
| |Chapter 84: Drugs that weaken the Bacterial Cell Wall I:Penicillins – 1015 – 1024 |
| |Chapter 85: Drugs th Drugs that Weaken the Bacterial Cell Wall II: Cephalosporins, Carbapenems, Vancomycin, |
| |Telavancin, Aztreonam, and Fosfomycin – pp 1025 – 1036 |
| |Chapter 86: Bacteriostatic Inhibitors of Protein Sybthesis: Tetracyclines, Macrolides, and Others – pp 1037 - 1049 |
| |Chapter 87: Aminoglycosides: Bactericidal Inhibitors of Protein Synthesis – pp 1050 - 1057 |
| |Chapter 88: Sulfonamides and Trimethoprim – pp 1058 - 1065 |
| |Chapter 89: Drug Therapy of Urinary Tract Infections – pp 1066 – 1070 |
| | |
| |DISCUSSION (Choose 1) |
| |Name two or three other groups of drugs that might cross-react and cause adverse responses in patients who have had|
| |hypersensitivity reactions to sulfonamide antibiotics. |
| |Describe the basic mechanism of action of the penicillin’s. |
| |Discuss the misuse of antibiotics, its general prevalence, why misuse persists as a major health problem, and the |
| |consequences. Give some examples of common situations in which iatrogenic antibiotic misuse occurs. |
| | |
| | |
| |ASSIGNMENT |
| |Read assignments |
| |Post discussion topic by Wednesday at 11:55 pm EST |
| |Respond to at least one classmate by Friday at 11:55 pm EST |
| |Complete math final by Friday at 11:55 pm EST |
| |Complete case study |
| | |
| |ASSESSMENT |
| |Discussion & response |
| |Math quiz |
| |Case study |
| |Quiz Chapters 83, 84, 85, 86, 87, 88, & 89. |
| | |
| |Homework: Chapter readings: 90, 91, 92, 93, 94, 95, & 96. |
|DATE |WEEK 15 |
|SPECIFIC OBJECTIVES |At the end of this lesson, the student will be able to: |
| |Discuss the concept of targeted tuberculin skin testing for Mycobacterium tuberculosis in the context of who should|
| |be targeted and who should be treated if a skin test result is positive. |
| |Describe the first-line drugs used for tuberculosis (TB): what they are, their individual and collective risks of |
| |toxicity to the host, and drug interactions likely to be encountered. |
| |Describe the additional issues involved when treating patients who have TB and also infection with the human |
| |immunodeficiency virus (HIV). |
| |Recognize that genetically based differences affect how quickly a person metabolizes isoniazid. Given that fact, |
| |compare and contrast the effect of slow and fast metabolization on the therapeutic response to this drug and |
| |toxicity that affects the liver and other structures or functions. |
| |Recognize that rifampin induces hepatic-metabolizing enzymes, including those responsible for its own inactivation.|
| |Discuss the other drugs rifampin affects by induction of cytochrome P450 enzymes. |
| |Summarize the main clinical uses for the fluoroquinolones, focusing on the organisms or infections for which one of|
| |these drugs is considered first-choice therapy. |
| |Describe the adverse effects of fluoroquinolones. |
| |Recognize that tendon rupture is a rather unusual adverse response associated with ciprofloxacin and other |
| |fluoroquinolones. Also, demonstrate understanding of how tendon rupture may occur; point out that the risk means |
| |certain patient populations should not use the drug; and explain how to monitor for tendon rupture when the drug is|
| |used. |
| |Recognize the potential for serious neurotoxicity and nephrotoxicity associated with parenteral use of polymyxin B |
| |and the impact of such concerns on the use of this medication. |
| |Compare and contrast opportunistic and nonopportunistic infections (the general terms), particularly the patient |
| |populations most likely to acquire them. |
| |Identify the drug that is the agent of choice for most systemic mycoses; describe its main mechanism of antifungal |
| |action; and state whether it is best used for minor or more serious fungal infections and why. |
| |Compare and contrast the basic biology, epidemiology, and treatment of fungi with that of bacteria, explaining why |
| |amphotericin B is effective against fungi but not against bacteria and why host-centered toxicity of amphotericin B|
| |is much greater and more prevalent than with most antibiotics. |
| |Discuss the main indications for intravenous amphotericin B; also, identify the drug’s three most common adverse |
| |responses and the precautions that should be taken to minimize their effects. |
| |Explain what azole antifungal drugs are and give examples; also, recognize that these drugs, when given |
| |systemically, can be a major cause of interactions with other drugs by inhibiting their hepatic metabolism. |
| |Summarize the main similarities and differences between how a typical antibiotic affects bacterial metabolism, |
| |having minimal or no effects on host-cell metabolism, and how antiviral drugs more often affect both the target |
| |organisms and the host. |
| |Recognize that acyclovir is the drug of choice for most herpes simplex and varicella-zoster virus infections and |
| |explain the drug’s main actions, uses, and other key clinical pharmacologic properties. |
| |Describe the adverse effects of acyclovir and ganciclovir and how the route of administration affects those |
| |responses. |
| |Compare and contrast hepatitis B and hepatitis C, the two most common strains of viral hepatitis, in terms of |
| |prevalence, mode of transmission, incidence of acute and chronic disease, lethality, and prevention and management |
| |(for example, vaccines, treatments for active disease). |
| |Summarize current guidelines or recommendations for prophylactic influenza vaccination and identify high-risk |
| |populations most likely to benefit from prophylaxis. Also, explain why the vaccines seem to keep changing from one |
| |flu season to the next. |
| |Define a retrovirus in terms of the transcription of information between viral deoxyribonucleic acid (DNA) and |
| |ribonucleic acid (RNA). Also, compare the sequence of the basic events in retroviruses with what goes on in a |
| |typical host cell. |
| |Recognize that helper T-lymphocyte (CD4) cells are the main target of HIV. Also, explain what CD4 cells do to/for |
| |the human immunodeficiency virus (HIV), why they are important to the host, and how these facts relate to the |
| |opportunistic infections that accompany acquired immunodeficiency syndrome (AIDS). |
| |Describe the three phases of HIV infection and the likely levels of CD4 cells and HIV in each. Also, explain why |
| |the CD4 and HIV levels change as they do. |
| |In simple terms, explain what the main classes of antiretroviral drugs do to impair viral replication or function |
| |biochemically. (Understanding what these drugs do ensures a good grasp of how retroviruses such as HIV cause |
| |infections and damage host cells.) |
| |Give a reasonable explanation of why HIV infection does not kill people directly, pointing out that infected |
| |individuals die of the consequences of other events that develop when the infection turns into AIDS. |
| |Briefly summarize the antiretroviral mechanism of action of the protease inhibitors and recognize hyperglycemia and|
| |its consequences, a pseudo-Cushing’s syndrome, and hyperlipidemias as key adverse responses to these drugs. Also, |
| |state the main monitoring methods or interventions for these adverse responses. |
| |Explain highly active antiretroviral therapy (HAART) and indicate why multidrug therapy for HIV/AIDS is important. |
| |Also, explain drug or drug class selection and the merits of combination therapy. |
| |Recognize that the blood levels, effects, and toxicity of saquinavir as the prototype protease inhibitor are very |
| |dependent on the level of activity of the liver’s P450 drug-metabolizing system. Recognize that the proteases, in |
| |general, inhibit the P450 system. Identify some of the key drugs that interact with protease inhibitors, either by |
| |inhibiting or inducing the P450 system, and predict the consequences of such interactions. |
| |Identify the three main reasons for changing antiretroviral therapy and summarize some reasonable guidelines for |
| |the process of changing treatment. |
| |Identify some of the common opportunistic infections in patients with HIV/AIDS. Also, identify and describe some of|
| |the common modalities for prophylaxis and treatment of these opportunistic infections. |
| |Explain some of the main impediments to proper, optimal therapy of HIV/AIDS, including not only pharmacologic |
| |considerations but also economic and compliance factors. |
| |Describe the special therapeutic and preventive approaches that must be taken for pregnant HIV/AIDS patients, for |
| |adolescents with active infection, and for infected neonates and infants. |
| |Give an accurate definition of sexually transmitted diseases (STDs) and explain how the term encompasses more than |
| |one clinical presentation. |
| |Make an accurate statement about the overall incidence of an individual STD in the context of diseases likely to be|
| |encountered in clinical practice. |
| |Describe the various treatments and prophylactic measures for STDs and explain how and why previously effective |
| |antibiotic therapies have become outmoded because of resistance. |
| |Describe the symptoms and time courses of the three main stages of syphilis, as well as the typically recommended |
| |therapies for syphilis in adults, during pregnancy, and in newborns with congenital exposure to Treponema pallidum.|
| |Summarize a general drug plan for a patient with syphilis who also has a history of severe hypersensitivity |
| |reaction to penicillin. |
| |State the most common route by which neonatal gonococcal infection occurs and the most common and handicapping |
| |consequence of that neonatal infection; also, describe the usual prophylactic measures taken with neonates and why |
| |they must be done. |
| |State the main criterion that differentiates an antiseptic from a disinfectant. |
| |Discuss how healthcare providers can use antiseptics and disinfectants to protect patients and themselves from |
| |infections. |
| |Describe the preferred treatments for established local cutaneous infections. |
|TOPIC (S) |Unit 16: Chemotherapy of Infectious Diseases |
| |Antimycobacterial Agents: Drugs for Tuberculosis, Leprosy, and Mycobacterium Avium Complex Infection |
| |Miscellaneious Antibacterial Drugs: Fluoroquinolones, Metronidazole, Daptomycin, Rifampin, Rifaximin, Bacitracin, |
| |and Polymyxins |
| |Antifungal Agents |
| |Antiviral Agents I: Drugs for Non-HIV Viral Infections |
| |Antiviral agents II: Drugs for HIV Infection and Related Opportunistic Infections |
| |Drug Therapy of Sexually Transmitted Diseases |
| |Antiseptics and Disinfectants |
|LEARNING ACTIVITIES |READING ASSIGNMENT |
| |Chapter 90: Antimycobacterial Agents: Drugs for Tuberculosis, Leprosy, and Mycobacterium Avium Complex Infection – |
| |pp 1071 – 1085 |
| |Chapter 91: Miscellaneious Antibacterial Drugs: Fluoroquinolones, Metronidazole, Daptomycin, Rifampin, Rifaximin, |
| |Bacitracin, and Polymyxins – pp 1086 - 1092 |
| |Chapter 92: Antifungal Agents – pp 1093 - 1105 |
| |Chapter 93: Antiviral Agents I: Drugs for Non-HIV Viral Infections – pp 1106 - 1123 |
| |Chapter 94: Antiviral agents II: Drugs for HIV Infection and Related Opportunistic Infections – pp 1124 - 1166 |
| |Chapter 95: Antifungal Agents – pp 1167 - 1174 |
| |Chapter 96: Antiseptics and Disinfectants – pp 1175 - 1181 |
| | |
| |DISCUSSION (Choose 1) |
| |Describe the various treatments and prophylactic measures for STDs and explain how and why previously effective |
| |antibiotic therapies have become outmoded because of resistance. |
| |Describe the three phases of HIV infection and the likely levels of CD4 cells and HIV in each. Also, explain why |
| |the CD4 and HIV levels change as they do. |
| |Describe the additional issues involved when treating patients who have TB and also infection with the human |
| |immunodeficiency virus (HIV). |
| | |
| | |
| | |
| |ASSIGNMENT |
| |Read assignments |
| |Post discussion topic by Wednesday at 11:55 pm EST |
| |Respond to at least one classmate by Friday at 11:55 pm EST |
| |Complete math quiz by Friday at 11:55 pm EST |
| |Complete case study |
| | |
| |ASSESSMENT |
| |Discussion & response |
| |Math quiz |
| |Case study |
| |Quiz Chapters 90, 91, 92, 93, 94, 95, & 96. |
| | |
| |Homework: Chapter readings: 97, 98, 99, & 100 |
|DATE |WEEK 16 |
|SPECIFIC OBJECTIVES |At the end of this lesson, the student will be able to: |
| |Summarize the main risk factor for helminthiasis, the main way to prevent such infestations, and the reasons |
| |certain types of helminthiasis are endemic in certain regions of the world rather than more globally prevalent. |
| |Recognize the three major classes of parasitic worms and their lay descriptions: nematodes (roundworms), cestodes |
| |(tapeworms), and trematodes (flukes). Also, state where these parasitic worms generally are found and explain the |
| |main way they infect human hosts. |
| |Recognize the main therapies for helminthiasis. Also, identify when drug therapy is definitely indicated, as well |
| |as factors that may preclude drug therapy. |
| |Recognize that discussions or comments about Plasmodium (P. falciparum, P. vivax) are focusing on common causes of |
| |malaria. |
| |Compare and contrast P. vivax malaria and P. falciparum malaria in terms of cause, prevalence, signs and symptoms, |
| |severity, and overall management. |
| |Summarize the usual appropriate drug and nondrug measures that should be implemented before a patient travels to an|
| |area where malaria is endemic. |
| |State why a student living in developed countries should be concerned and knowledgeable about diseases such as |
| |malaria, which rarely occur in the United States. Also comment on why the modern ability to travel to distant parts|
| |of the world has such a dramatic effect on what a healthcare provider needs to know. |
| |Summarize the main elements of drug therapy for malaria once it has developed, demonstrating understanding of the |
| |terms clinical cure, radical cure, and suppressive therapy as they apply to |
| |P. vivax malaria. |
| |Discuss the adverse effects of the various drug therapies used for the different forms and stages of malaria. |
| |Describe the principal protozoal infections endemic to the United States and those seen in the United States |
| |because of world travel. |
| |Discuss drug therapies for the various protozoal infections. |
| |Discuss precautions that patients should take with the drug therapies for protozoal infections. |
| |Discuss the fungal infection Pneumocystis pneumonia (PCP). |
| |Discuss the drug therapies for PCP. |
| |Summarize the differences between scabies and the three main types of pediculosis so as to clarify them to a |
| |layperson. |
| |Identify the common modes of acquiring and transmitting pediculosis and scabies, the characteristic signs or |
| |symptoms of these ectoparasitic infestations, and generally effective first-line approaches, both pharmacologic and|
| |nondrug, to managing them. |
|TOPIC (S) |Unit 17: Chemotherapy of Parasitic Diseases |
| |Anthelmintics |
| |Antiprotozoal Drugs I: Antimalarial Agents |
| |Antiprotozoal Drugs II: Miscellaneous Agents |
| |Ectoparasiticides |
|LEARNING ACTIVITIES |READING ASSIGNMENT |
| |Chapter 97: Anthelmintics – pp 1182 - 1186 |
| |Chapter 98: Antiprotozoal Drugs I: Antimalarial Agents – pp 1187 - 1194 |
| |Chapter 99: Antiprotozoal Drugs II: Miscellaneous Agents – pp 1195 - 1200 |
| |Chapter 100: Ectoparasiticides – pp 1201 – 1205 |
| | |
| |DISCUSSION (Choose 1) |
| |• |
| | |
| |ASSIGNMENT |
| |Review the syllabus |
| |Read assignments |
| |Post discussion topic by Wednesday at 11:55 pm EST |
| |Respond to at least one classmate by Friday at 11:55 pm EST |
| |Complete math quiz by Friday at 11:55 pm EST |
| |Complete case study |
| | |
| |ASSESSMENT |
| |Discussion & response |
| |Math quiz |
| |Case study |
| |Quiz Chapters 97, 98, 99, & 100 |
| | |
| | |
| |Homework: Chapter readings: Chapters 101, 102, & 103 |
|DATE |WEEK 17 |
|SPECIFIC OBJECTIVES |At the end of this lesson, the student will be able to: |
| |Describe why the three main treatment approaches to cancer (drugs, surgery, and radiation) can be considered and |
| |often are used as adjuvants to one another. Also, state the general types of cancers for which surgery and |
| |radiation therapy generally are not the primary approaches and for which pharmacologic treatment therefore is |
| |mainly used. |
| |Summarize the main states of the cell cycle (G0, G1, S, G2, M) and briefly describe what occurs in each stage. |
| |Also, explain the following: whether or why the cell cycle state is in affects a cell’s response to anticancer |
| |drugs; how this relates to the concept of growth fraction; and how, in general, solid tumors differ from |
| |disseminated cancers in terms of their responsiveness to cancer chemotherapy. |
| |In general terms, compare and contrast the typical cancer chemotherapeutic drug with the typical antibiotic with |
| |respect to the concept of selective toxicity. |
| |Recognize that cancer cells tend to develop resistance to anticancer drugs through random mutation and that these |
| |mutations can have the following consequences in terms of the cancer cells’ response to a specific drug. The cells |
| |may do any of the following: become less able to take up the drug, improve their ability to pump the drug out of |
| |the cells, lose their ability to transform the drug into an active and cytotoxic metabolite, or develop better or |
| |faster ways to repair the damage caused by the chemotherapeutic agent. |
| |Summarize the basic principles and concepts that apply to how and why multidrug therapy is preferred for treating |
| |cancers. |
| |Give a succinct but accurate explanation of why drug therapy of disseminated cancers usually is more successful |
| |than drug treatment of solid tumors. |
| |Identify and describe the main classes of anticancer drugs in terms of their main mechanisms of action. |
| |Differentiate between cell-cycle phase–specific and cell-cycle phase–nonspecific anticancer drugs in terms of their|
| |mechanisms of action on cell growth and replication. Also, state the main advantages or limitations of drugs in |
| |these two groups in terms of general efficacy against cancer cells. |
| |Summarize the main roles of deoxyribonucleic acid (DNA) replication, transfer of DNA’s genetic message to |
| |ribonucleic acid (RNA) and onto protein synthesis, and the role of mitosis and microtubular formation as they |
| |affect cancer cell growth and reproduction. |
| |Identify the side effects and adverse responses that are generally common to all anticancer drugs and explain why |
| |they occur. |
| |Identify the anticancer drugs that exert selective toxicities that are not shared by many or any other anticancer |
| |agents, focusing on pulmonary, cardiac, renal, and hepatic toxicity and neurotoxicity. |
| |Compare and contrast the basic mechanisms of action, clinical indications, and general toxicities of anticancer |
| |drugs discussed in this chapter. |
| |Summarize the likely benefits of glucocorticoids, not merely as anticancer drugs per se, but also as useful |
| |adjuncts in management of cancers with other drugs or nondrug modalities. Consider the main systemic adverse |
| |responses that almost always occur, along with the beneficial effects. |
| |State the precautions and related risk factors that should go into a decision about whether to administer tamoxifen|
| |either to prevent or treat estrogen-sensitive breast cancers in women. |
| |Summarize the desired and unwanted effects of antiestrogens and selective estrogen receptor modifiers (SERMs) when |
| |used for cancer. |
| |Describe the paradoxic effects of leuprolide on androgen-dependent advanced prostatic cancer, and name the |
| |adjunctive intervention that might prevent the drug’s unwanted effects on the cancer. |
|TOPIC (S) |Unit 18: Cancer Chemotherapy |
| |Basic Principles of Cancer Chemotherapy |
| |Anticancer Drugs I: Cytotoxic Agents |
| |Anticancer Drugs II: hormonal Agents, Targeted Drugs, and Other Noncytotoxic Anticancer Drugs |
|LEARNING ACTIVITIES |READING ASSIGNMENT |
| |Chapter 101: Basic Principles of Cancer Chemotherapy – pp 1206 – 1219 |
| |Chapter 102: Anticancer Drugs I: Cytotoxic Agents – pp 1220 – 1237 |
| |Chapter 103: • Anticancer Drugs II: hormonal Agents, Targeted Drugs, and Other Noncytotoxic Anticancer Drugs – pp |
| |1238 - 1266 |
| | |
| |DISCUSSION (Choose 1) |
| |Describe why the three main treatment approaches to cancer (drugs, surgery, and radiation) can be considered and |
| |often are used as adjuvants to one another. |
| |Identify and describe the main classes of anticancer drugs in terms of their main mechanisms of action. |
| | |
| | |
| |ASSIGNMENT |
| |Review the syllabus |
| |Read assignments |
| |Post discussion topic by Wednesday at 11:55 pm EST |
| |Respond to at least one classmate by Friday at 11:55 pm EST |
| |Complete math quiz by Friday at 11:55 pm EST |
| |Complete case study |
| | |
| |ASSESSMENT |
| |Discussion & response |
| |Math quiz |
| |Case study |
| |Quiz Chapters 101, 102, 103 |
| | |
| | |
| |Homework: Chapter readings: Chapters 104, 105, 106, 107, 108, 109, 110; Call Michelle, order your Pharm HESI exam |
| |and schedule your testing date. |
|DATE |WEEK 18 |
|SPECIFIC OBJECTIVES |At the end of this lesson, the student will be able to: |
| |Compare and contrast open-angle glaucoma and angle-closure glaucoma in terms of etiology, prevalence, and |
| |management. |
| |Summarize how the sympathetic and parasympathetic branches of the autonomic nervous system control pupil size, and |
| |explain why pupil size is important for narrow-angle glaucoma. Also state the classes of autonomic drugs that cause|
| |miosis and mydriasis, and explain whether the effects of these drugs are beneficial or harmful in glaucoma and why.|
| |State the fundamental mechanism of all drugs that have been shown to be effective for managing glaucoma, regardless|
| |of their particular mechanism of action or class. |
| |Give a description of how the following may help lessen IOP: adrenergic agonists, muscarinic agonists, |
| |acetylcholinesterase inhibitors, carbonic anhydrase inhibitors, and prostaglandin F2 alpha or its analogs. |
| |State comorbidities that might be aggravated by stated drugs or drug groups that are suitable for managing |
| |glaucoma. Conversely, name the drugs or drug classes (and the main indications for their use) that might raise the |
| |IOP and aggravate glaucoma. |
| |Summarize the basic etiology and pathophysiology of common acne. Also, explain the benefits and limitations of and |
| |indications for the main drugs used for acne. |
| |Identify the main drugs or other factors that can increase the risk for local or systemic toxicity of topical |
| |retinoic acid derivatives. |
| |Summarize the main adverse responses associated with isotretinoin therapy and the precautions that should be taken |
| |to prevent them or to deal with adverse responses that may occur. Include comments on the drug’s common adverse |
| |effects, the potential for psychiatric depression, concerns related to pregnancy and breast-feeding, and |
| |interactions with other drugs and vitamins. |
| |Compare and contrast acute otitis media (AOM), otitis media with effusion (OME), and antibiotic-resistant otitis |
| |media (OM) in terms of the most common pathogenic causes, typical signs and symptoms, and treatment. |
| |Comment on the pros and cons of routinely treating all causes of acute otitis media with antibiotics, rather than |
| |waiting for a short time and seeing whether the signs and symptoms of the condition resolve spontaneously before |
| |treating with antibiotics. |
| |Comment on the use of antibiotic prophylaxis for recurrent otitis media in children. For example, demonstrate |
| |talking with a mother who has brought her daughter to the pediatrics office three times in the past year with an |
| |ear infection and who wants a prescription for antibiotics to prevent another infection. |
| |Describe pulmonary arterial hypertension (PAH) and identify the drugs used to treat the condition, their mechanism |
| |of action, and significant side effects. |
| |State the likely consequences of administering bosentan or sildenafil with drugs that inhibit the liver’s |
| |cytochrome P450 system. Also, identify the main groups of these drugs. |
| |Discuss the drugs used for neonatal respiratory distress syndrome (RDS) and include time frames for their |
| |administration. |
| |Describe the pathophysiologic process of cystic fibrosis and explain the effect of the disorder on the pancreas, |
| |lungs, and reproductive organs. |
| |Discuss the pathophysiologic process of amyotrophic lateral sclerosis (ALS) and describe the only medication |
| |approved for its treatment. |
| |Define the terms dietary supplement and complementary and alternative medicine. |
| |Recognize that herbal products usually do contain active ingredients, some of which can cause desired effects and |
| |some that can cause serious adverse effects or interact beneficially or not with prescribed FDA-approved drugs. |
| |List and describe some of the main reasons patients may turn to herbal products, either as supplements or as |
| |alternatives to traditional medicines and medical practice. |
| |Recognize what the German Commission E is as it applies to herbal products. |
| |Summarize what the Dietary Supplement Health and Education Act (DSHEA-1994) permits (and does not permit) in the |
| |way of manufacturing, advertising, and labeling herbal products. Compare and contrast this with the general |
| |criteria that a potential manufacturer of a prescription medication must prove before the drug can be marketed. |
| |Explain how calling products dietary supplements, rather than drugs, may allow the manufacturers of these products |
| |to circumvent standards of purity, efficacy, and safety that apply to FDA-approved drugs, and describe how that |
| |ability to skirt more stringent regulations and requirements can be harmful. |
| |Recognize that an array of ostensibly equal herbal products, prepared and sold by various individuals or companies,|
| |are likely to have very large differences in the amounts of active substance, impurities, and adulterants, thus |
| |providing little uniformity. |
| |State the main reasons that some practitioners of traditional Western medicine are skeptical of herbal products and|
| |nutritional supplements. |
| |Combine knowledge and personal beliefs to summarize the major benefits and risks of using herbal products instead |
| |of or in addition to prescription drugs, and then translate those ideas into advice that would be given to a |
| |friend, family member, or patient who wants to use an herbal product. |
| |Describe the five basic elements of managing poisonings. |
| |Identify five mechanisms for reducing the absorption of toxicants, commenting on the pros and cons, benefits and |
| |limitations, and settings for appropriate use of each. |
| |Describe methods (including drugs) that can be used to accelerate the removal of absorbed poisons. |
| |Discuss the general mechanism of action by which chelating agents work, why no single chelator is effective for all|
| |heavy metal poisonings, and other properties that chelators should have to cause their desired effects. |
| |Identify the main biotoxins, as discussed in this chapter, and the common properties that make this diverse group |
| |of agents suitable for their malevolent uses. |
| |Discuss the controversies surrounding the prophylactic use of antibiotics for anthrax by the general population, |
| |which is not likely to be exposed to the causative bacterium. |
| |Describe the signs, symptoms, and typical times to onset (after exposure) of cutaneous and inhalational anthrax. |
| |Summarize the general approaches to treating the infection and preventing the spread to others. |
| |Identify agents for which toxicity can be transmitted from person to person via exposure to body fluids, thereby |
| |constituting an infectious disease. |
| |Discuss the controversies surrounding the issue of vaccinating healthcare workers and first responders against |
| |smallpox, including some concept of the estimated risks from the vaccination itself. Also, compare and contrast |
| |these risks with the potential risks of being exposed (or of caring for an exposed patient) without being |
| |vaccinated beforehand. |
| |Discuss chemical weapons and describe the signs and symptoms of exposure and of treatment after exposure to these |
| |weapons. |
| |Discuss treatments used after radiation exposure, including how soon treatment must be implemented and the factors |
| |that determine the choice of treatment. |
|TOPIC (S) |Unit 19: Miscellaneous Drugs and Therapies |
| |Drugs for the eye |
| |Drugs for the skin |
| |Drugs for the ear |
| |Additional noteworthy drugs |
| |Complementary and alternative therapy |
| |Unit 20: Toxicology |
| |Management of Poisoning |
| |Potential Weapons of Biologic, Radiologic, and chemical Terrorism |
|LEARNING ACTIVITIES |READING ASSIGNMENT |
| |Chapter 104: Drugs for the Eye – pp 1267 – 1277 |
| |Chapter 105: Drugs for the Skin – pp 1278 – 1295 |
| |Chapter 106: Drugs for the Ear – pp 1296 – 1301 |
| |Chapter 107: Additional Noteworthy Drugs – pp 1302 – 1317 |
| |Chapter 108: Complementary and Alternative Therapy – pp 1318 – 1329 |
| |Chapter 109: Management of Poisoning – pp 1330 – 1335 |
| |Chapter 110: Potential weapons of Biologic, Radiologic, and Chemical Terrorism – pp 1336 - 1345 |
| | |
| |DISCUSSION (Choose 1) |
| |Discuss chemical weapons and describe the signs and symptoms of exposure and of treatment after exposure to these |
| |weapons. |
| |Compare and contrast open-angle glaucoma and angle-closure glaucoma in terms of etiology, prevalence, and |
| |management. |
| |Compare and contrast acute otitis media (AOM), otitis media with effusion (OME), and antibiotic-resistant otitis |
| |media (OM) in terms of the most common pathogenic causes, typical signs and symptoms, and treatment. |
| | |
| | |
| |ASSIGNMENT |
| |Review the syllabus |
| |Read assignments |
| |Post discussion topic by Wednesday at 11:55 pm EST |
| |Respond to at least one classmate by Friday at 11:55 pm EST |
| |Complete math quiz by Friday at 11:55 pm EST |
| |Complete case study |
| | |
| |ASSESSMENT |
| |Discussion & response |
| |Math quiz |
| |Case study |
| |Quiz Chapters 104, 105, 106, 107, 108, 109, & 110 |
| |Math Final |
| | |
| |Homework: Take your HESI Pharm exam. |
|DATE |WEEK 19 |
|SPECIFIC OBJECTIVES |At the end of this lesson, the student will be able to: |
| |Pass your HESI Pharm exam with an 850. |
|TOPIC (S) |HESI Pharm Review |
|LEARNING ACTIVITIES |HESI Review |
|DATE |WEEK 20 |
|SPECIFIC OBJECTIVES |At the end of this lesson, the student will be able to: |
| |Pass your HESI Pharm retest exam with a 900. |
|TOPIC (S) |HESI Pharm Review |
|LEARNING ACTIVITIES |HESI Remediation review |
| |
The following strategies may be used in this class:
1. Threaded Discussions
2. Case studies
3. Quizzes
4. Readings
5. Exams
Academic Honesty: When learners fail to complete their own work, they are cheating themselves out of their education and are committing plagiarism. Plagiarism, or failing to meet the academic honesty policy, will result in disciplinary actions by the institution.
Plagiarism is dishonest behavior that will not be tolerated. A student will not receive credit if found to have plagiarized his/her work and may result in suspension or dismissal from the school. Follow the link for examples of plagiarism:
APA Format: All of your writing must be done following APA format. For more information regarding this format, go to Purdue Owl or follow this link:
Late work & Educational Responsibility: All assignments must be completed by the last day of the schedule unless an alternate due date has been previously approved by your instructor or documentation has been provided regarding extreme circumstances. It is the learner's responsibility to communicate with the instructor about extreme circumstances or ask questions concerning the assignment and their due dates.
Threaded discussions: Students are to respond to the instructor’s weekly discussion post by Wednesday at 1159 PM (EST). The responses must be substantial (at least 125 words in length using correct grammar).
These are intended to stimulate discussion and re-enforce course content. The student must also respond to two other student posts by Friday at 11:59 PM (EST). Please refer to the assignment calendar for assignment due dates.
ASSESSMENT TESTING FOR NURSING PROGRAM REQUIREMENT:
As part of certain nursing courses, students are required to take third-party computerized assessments, These assessments are intended to provide students with the tools they need to be successful in the Nursing program and on the NCLEX; as well as. Increase confidence and familiarity with computerized testing, The assessments typically include various types of formats, including multiple choice items, multiple response items, fill-in-the-blank items, drag-and drop items, hot spots items, chart/exhibit items, and other items,. The assessments help identify deficit areas and provide students opportunities to practice and learn. Each assessment can represent up to the percent (10%) of a student’s course grade. Failure to achieve the minimum assessment score may result in a loss of points on an examination, or required remediation or retesting (as outlined in the course syllabus). Students who do not successfully complete the remediation or retest associated with an assessment examination (as outlined in the course syllabus) may receive an incomplete in a course and may be required to repeat the course in its entirety. An incomplete due to failure to successfully complete the assessment testing remediation or successfully retest is considered a failure for the course.
|Additional Resources |
Web sites
|Assessment Criteria and Methods of Evaluating Students |
90 – 100% ( A
80 – 89% ( B
75 – 79% ( C
< 75% ( F
Do not count on a curve!
Generally, the grades “A” through “C-” are considered passing grades. Grades "W" and "I" indicate that no grades were earned for the course. A "W" grade indicates that the student withdrew from the course. An "I" grade indicates that the student was passing the course, but failed to complete all the required course work. The instructor, in his/her discretion may grant an "I" grade instead of an "F", pending completion of the course work by the student within a specified time arranged by the instructor and told to the student. It is the student's responsibility to follow-up with the instructor to complete the course work. If the course work is not completed by the arranged time, the “I” grade becomes an “F".
|Distribution of Grade Elements |
Discussions 10%
Case Studies: 15%
Math worksheets: 15%
Math Final: 30%
HESI Final: 30%
Total: 100 %
Revised: June 9, 2015
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