CardioPulmonary and Renal II –
MED 237 Syllabus
Kansas City University of Medicine and Biosciences
College of Osteopathic Medicine
COURSE DIRECTOR:
G. Michael Johnston, DO, MACOI
KC Office SEP 458
816-654-7338
GJohnston@kcumb.edu
CREDIT HOURS: 6.5
COURSE DESCRIPTION
The CardioPulmonary and Renal II (CPR II) course focuses on the pathophysiology, pathologic
entities, clinical features, diagnosis, and pharmacology/treatment/management of major disorders
of the cardiovascular, respiratory, and genitourinary systems. General principles of pharmacology
(i.e., pharmacodynamics, pharmacokinetics, drug biotransformation, and clinical trials) will be
discussed. Upon completion of the course, the student will be able to recognize presenting
signs and symptoms of various cardiovascular, pulmonary, and genitourinary
diseases and develop appropriate differential diagnoses and treatments. Emphasis on
interpretation of electrocardiograms (ECG’s), relationships between multisystem
diseases, and key aspects of clinical laboratory/diagnostic test ordering and data utilization in the
diagnosis, monitoring, and treatment of these systems will be presented. Some broad topics areas
that will be discussed will include: Ischemic Heart Disease, Hypertension, Atherosclerosis,
Congestive Heart Failure, Congenital Heart Disease, Arrhythmias, Pericardial and Myocardial
disease, Thromboembolic disorders, Valvular Heart Disease, Conduction abnormalities, Acute
Coronary Syndrome, Shock, a wide spectrum of physiologic functions of the human kidney,
including Acut e Kidney I nj ur y, Chr onic K id ney D isease, tubulointerstitial disorders, acidbase disturbances, f l u i d s a n d e l e c t r o l y t e s , s y s t e m r e l a t e d infections, toxic and
ischemic system insults, fundamentals of obstructive and restrictive lung disorders,
Pleural/Mediastinal Disease, system specific emergencies, and primary and secondary
malignancies.
Course Goals
Core
Competency
EPA
Year 2
Programmatic
Goals
II, III
1, 2
2.5
2. Diagnose and explain the manifestations (including
presenting signs and symptoms, in particular of
common clinical concerns) of diseases presented in
the course.
I, II, III, IV, VI,
VII, VIII, IX, X,
XI, XIII, XIV
1, 2, 3, 4,
5, 7, 8, 9,
10, 12
3. Compare and contrast through explanation the underlying
pathologic features of the various types of
II, III
1, 2
1. Explain the pathophysiology involved in clinical case
presentations and laboratory evaluations.
Date modified: 07/05/2019
2.4, 2.5
2.4, 2.5
c ar diovasc ular, pulm onar y,
g e n i t o u r i n a r y / r e n a l disease.
4. Explain normal vs pathologic characteristics findings on
electrocardiograms and provide an accurate clinical
interpretation leading to appropriate diagnosis.
II
3
2.4, 2.5
II, III
1, 2, 3,10
2.5
I, II, III, IV, V,
VI, VII, VIII, IX,
X, XI, XII, XIII,
XIV
1, 2, 3, 5,
6, 7, 8, 9,
10, 12
II, III
1, 2, 3,10
I, II, III, IV
1, 2, 3, 4,
7, 10
2.4
II, III
1, 2, 3, 10
2.5
II, III
1, 2, 4, 7,
10
2.5
II, III
1, 2, 4, 7,
10
2.5
II, III
1, 2, 4, 7,
10
2.5
I, II, III, IV, V,
VI, VII, VIII, IX,
X, XI, XII, XIII,
XIV, XV
1, 2, 3, 4,
5, 6, 7, 8,
9, 10, 11,
12, 13
14. Recognize basic risk factors associated with
cardiovascular disease and the importance of
d i s e a s e preventative health measures (exercise,
diet, compliance with medications, smoking
cessation).
II, VIII
1
15. Compare and contrast the various classes of antibiotics
used to treat infections associated with these systems.
I, II, III, VI, VII,
X
1, 2, 3, 4,
5, 7, 8, 9,
10, 12, 13
16. Explain pharmacologic general principles including drug
biotransformation, pharmacokinetics, and
pharmacodynamics. Additionally, discuss routes of
administration, clinical trials, and basics of prescription
writing.
I, III, IV, VII, X,
XIV
4, 9
5. Explain the types of glomerular injury.
6. Explain the pathophysiology and clinical evaluation of
patients with obstructive lung disease, interstitial lung
disease, and infectious lung disease.
7. Explain congenital and acquired cardiovascular,
pulmonary, and genitourinary disorders.
8. Generate a differential diagnosis, based on the patient’s
clinical presentation and history and physical, determine a
diagnostic approach and interpret these results.
9. Explain acute vs chronic and primary vs secondary
disease kidney disease.
10. Explain possible management and treatment interventions.
11. Explain advantages and disadvantages of antihypertensives agents on the Cardiovascular and
Renovascular systems.
12. Explain advantages and disadvantages of drugs for male
genitourinary disorders.
13. Explain the various neoplastic processes that occur within
these systems.
Date modified: 07/05/2019
2.4, 2.5
2.4, 2.5
2.5
2.4, 2.5, 2.6
2.5
2.5
INSTRUMENT(S) OF STUDENT EVALUATION AND ASSESSMENT

Students will be evaluated through a combination of one or more of the following
assessment modalities
o Written Examinations
o Formative ECG Module
COURSE SCHEDULE, LECTURE OBJECTIVES, AND ASSIGNMENTS
Please refer to the posted Outlook Student Calendar to view the course schedule. Syllabus,
learning objectives, reading assignments, and required materials are posted within course in
Canvas, and may also be attached to each scheduled activity in the calendar. Communication
of important course information may occur through KCU email and/or Canvas.
It is the student’s responsibility to check both email and Canvas daily.
COURSE MATERIALS
See the below required textbook list. Many of the required text books are available free online
through the library.
POLICIES
Please refer to student handbook and catalog for KCU-COM academic and course policies.
ATTENDANCE
Attendance of lectures and laboratories is based on the university’s stated attendance policy.
Refer to the student handbook for more information.
CLASSROOM BEHAVIOR AND ATTIRE
If a student is determined to demonstrate unprofessional behavior or wear unprofessional or
inappropriate attire, he/she may be subject to disciplinary action per Kansas City University of
Medicine and Biosciences policy.
EVALUATION
The student will receive a numerical grade in the form of a percent and letter grade at the end of
the course. The student must achieve a cumulative grade of 70% or higher on graded
assessments to pass the course.
An ECG module will be provided to enhance formative self-assessment skills of
interpretation. Student is required to attain a minimum competency of 70% or greater
upon completion of the module. There is no limitation in the number of attempts to attain
the competency goal.
Date modified: 07/05/2019
POINT ALLOTMENT
The following table is a breakdown of the allotment of points. These values are subject to
change with notice.
Activity
Point Value
128 pts
90 pts
48 pts
Quiz
5
Total points
271
Required Textbooks and Other Resource Material  this is AY1819
CLINICAL MEDICINE

Kasper, Dennis L.; et al., Harrison’s Manual of Medicine, 19th ed., 2016.
o ISBN: 978-0071828529 (paperback)
o ISBN: 978-0071828543

Dubin, Dale, Rapid Interpretation of EKGs: An Interactive Course, 6th ed., 2001.
o ISBN: 978-0912912066

Optional/Recommended Resource
o Hampton, John R Churchill Livingston, 150 ECG Problems, 4th ed., 2013.
 ISBN: 978-0702046452

Optional/Recommended Resource
o Jameson, J Larry: et al., Harrison’s Principles of Internal Medicine, 20th ed.,
2018
 ISBN: 978-1259644030
PATHOLOGY

Kumar, Vinay; Robbins and Cotran Pathologic Basis of Disease, 9th ed., 2014.
o ISBN: 978-1455726134 (hardcover)
o EISBN: 978-1437720150

Gladwin, Mark; et al., Clinical Microbiology Made Ridiculously Simple, 6th ed., 2014.
o ISBN: 978-1935660156 (paperback)

Optional/Recommended Resource
o McPherson, Richard A.; et al., Henry’s Clinical Diagnosis and Management by
Laboratory Methods, 23rd ed., 2017.
 ISBN: 978-0323295680
Date modified: 07/05/2019
PHYSIOLOGY

Costanzo, Linda, Physiology, 6th ed., 2018.
o ISBN: 978-0323478816
PHARMACOLOGY

Katzung, Bertram G., et al., Basic and Clinical Pharmacology, 14th ed., 2018.
o ISBN: 978-1259641152
PEDIATRICS

Kliegman, Robert M., et al., Nelson Textbook of Pediatrics, 20th ed., 2015.
o ISBN: 978-1455775668
AUDIENCE RESPONSE SYSTEM

Mobile devices
o iClicker Reef polling
Contact Information
Mike Johnston, DO, MACOI (Course Director)
KC Office SEP 458
816-654-7338
GJohnston@kcumb.edu
Kansas City
Joplin
Pratima Singh, MD
Office SEP 222
816-654-7642
PSingh@kcumb.edu
Mary Jo Martin, MD
Office 2605
417-208-0652
MJMartin@kcumb.edu
Ramon Newman, MD
Office SEP 437
816-654-7403
RNewman@kcumb.edu
Marcus Iszard, PhD
Office 2613
417-208-0660
MIszard@kcumb.edu
Stephen Putthoff, DO
Office SEP 235
816-654-7553
SPutthoff@kcumb.edu
Rizwan Muhammad Khalid, MD
Office: J-Faculty Wing
417-208-0630
MKhalid@kcumb.edu
Ryan Sheehy, PhD
Office SEP 226
816-654-7613
RSheehy@kcumb.edu
Dennis Wolff, PhD
Office 2617
417-208-0701
DWolff@kcumb.edu
Kevin Hubbard, DO, HMDC, MACOI
Office SEP 433
816-654-7392
KHubbard@kcumb.edu
Bob Tyler, DO, MSc
Office
417-208-0740
RTyler@kcumb.edu
Date modified: 07/05/2019
Mike Johnston, DO, MACOI (Course Director)
KC Office SEP 458
816-654-7338
GJohnston@kcumb.edu
Kansas City
Joplin
Carol Kirila, DO
Office SEP 435
816-654-7395
CKirila@kcumb.edu
Michael Selby, MD
Office 2611
417-208-0630
MSelby@kcumb.edu
Eugene Konorev, MD, PhD
Office DCR 207
816-654-7639
EKonorev@kcumb.edu
Schoen Kruse, PhD, NAOME
Office SEP 456
816-654-7641
SKruse@kcumb.edu
JR Dobson, MD
Office SEP 236
816-654-7554
JDobson@kcumb.edu
Diane Karius, PhD, NAOME
Office KCCC 116
816-654-7802
DKarius@kcumb.edu
Date modified: 07/05/2019
MED 237: CardioPulmonary and Renal II (CPR)
AY 2019-20
Exam 1
LEARNING OBJECTIVES
CPR II- PATH- LECT/CIS/Path Quiz- Blood Vessels (Martin)
Chapter 11 Vascular Pathology
1. Describe the histologic structure of arteries, veins and capillaries; as well as describe variations in these
structures in different segments of the vascular system.
2. Describe the following vascular anomalies, and relate the potential clinical significance of each: berry
aneurysm, arteriovenous fistula, fibromuscular dysplasia.
3. List specific stimuli by which endothelial cells become activated, and the effects of the activated state.
4. Describe the processes of vascular response to injury, and any related morphologic changes.
5. Know the difference between primary (essential) hypertension and secondary hypertension (give specific
examples of secondary hypertension).
6. Describe the basic epidemiologic features of hypertension, and know disease states in which hypertensive
patients are at elevated risk.
7. Define and understand the determinants of blood pressure: cardiac output and peripheral resistance.
8. List specific factors influencing cardiac output and peripheral resistance, and the effects of these factors on
these determinants.
9. Describe in detail the renin-angiotensin-aldosterone system, and the ways this system influences blood
pressure.
10. Explain the effect that changes in renal perfusion has on blood pressure.
11. List several environmental factors and health conditions implicated in causing hypertension.
12. Describe vascular morphologic changes associated with hypertension.
13. Define atherosclerosis, and describe its epidemiology.
14. Detail the risk factors known to be related to atherosclerosis, and understand the effect of multiple risk
factors occurring concurrently in the same patient.
15. Relate the pathogenesis of atherosclerosis, using the “response to injury” model.
16. Be able to describe the morphologic changes seen in the initiation and development of an atherosclerotic
lesion; know the most common vascular locations where these lesions develop.
17. Describe the major clinically important pathologic changes of atherosclerotic lesions, and the major clinical
consequences of atherosclerotic disease.
18. Understand the pathogenesis and clinical importance of the following: atherosclerotic stenosis, acute
atherosclerotic plaque change, atherosclerotic plaque-induced thrombosis, and vasoconstriction.
19. Define aneurysm and vascular dissection, and describe their causes, pathogenesis, morphologic features,
and clinical significance.
20. Describe the most common locations of arterial aneurysms and their clinical manifestations.
21. Understand the relationship between aneurysm size and its risk of rupture.
22. List and describe causes of noninfectious vasculitis.
23. Describe anti-neutrophil cytoplasmic antibodies (ANCAs), their classification, and putative pathogenic role
in vasculitis.
24. Describe the following forms of vasculitis, including site(s) of involvement, clinical features, and
morphologic changes: giant cell arteritis, Takayasu arteritis, polyarteritis nodosa, Kawasaki disease,
microscopic polyangiitis (leukocytoclastic vasculitis), Churg-Strauss syndrome, Behçet disease,
granulomatosis with polyangiitis (Wegener granulomatosis), and thromboangiitis obliterans (Buerger
disease).
25. Understand and relate the importance of distinguishing between infectious and noninfectious vasculitis,
and the therapeutic implications of this distinction.
26. Distinguish primary from secondary Raynaud phenomenon.
27. Discuss the clinical features of varicose veins, including esophageal varices and hemorrhoids.
28. List the risk factors and clinical features of deep venous thrombosis (DVT), including potential
complications.
29. Define migratory thrombophlebitis, lymphangitis, and lymphedema.
30. Describe the clinical features of the following benign vascular tumors: ectasias, hemangiomas,
lymphangiomas, glomus tumor, and bacillary angiomatosis.
31. Discuss Kaposi sarcoma, including its epidemiologic features, pathogenesis, morphologic changes, and
clinical course.
32. Describe angiosarcoma, including its risk factors, morphology, and clinical course.
CPR II- PATH- LECT/CIS/Path Quiz - Heart 1: Heart failure, congenital & ischemic dz (Martin)
Chapter 12 Cardiac Pathology
33. Review normal cardiac structure and function.
34. List the effects of advancing age on the heart and aorta.
35. Understand and explain the basic mechanisms of cardiovascular dysfunction.
36. Define congestive heart failure, and list mechanisms by which the cardiovascular system adapts to
maintain pressure and perfusion.
37. Discuss cardiac hypertrophy, distinguishing pressure-overload hypertrophy from volume-overload
hypertrophy and the tissue and cellular adaptations to each.
38. Describe left-sided heart failure and its common clinical settings and clinical sequelae.
39. Distinguish systolic failure from diastolic failure, functionally and clinically.
40. Describe right-sided heart failure, and cor pulmonale.
41. Distinguish primary right heart failure from right-sided failure induced by left heart failure.
42. List the major left-to-right shunts, and describe their anatomical and clinical features.
43. List the major right-to-left shunts, and describe their anatomical and clinical features.
44. Describe the anatomy and clinical features of congenital obstructions to blood flow, including coarctation of
the aorta, pulmonary stenosis and atresia, and aortic stenosis and atresia.
45. Define ischemic heart disease, and relate its epidemiologic features, its most prominent causes, and its
consequences.
46. Define angina, and differentiate between stable, unstable, and Prinzmetal forms of angina.
47. Describe the incidence of and risk factors associated with myocardial infarction.
48. Relate the pathogenesis of myocardial infarction, and relate the geographic progression of ischemic
necrosis in the myocardium, and the approximate time evolution of the lesion.
49. Be able to anatomically describe the infarcts resulting from occlusion of the three major coronary vessels.
50. Describe the histologic findings associated with an evolving infarct, and the reparative process.
51. Relate the effects that reperfusion has on ischemic myocardium threatened by infarction.
52. Discuss the concept of reperfusion injury.
53. Describe the clinically useful biomarkers for myocardial infarction.
54. Describe complications of myocardial infarction.
CPR II- PATH- LECT/CIS/ Path Quiz - Heart 2: HTN, valves, cardiomyopathies, tumors, transplant
(Martin)
Chapter 12 Cardiac Pathology
55. List causes of cardiac arrhythmias and sudden cardiac death.
56. Compare the morphologic changes seen in the heart as a result of left-sided (systemic) hypertensive heart
disease and right-sided hypertensive heart disease.
57. Explain the different types of calcific valvular degeneration, including the clinical features of each, and the
significance of a congenitally bicuspid aortic valve.
58. Discuss the pathogenesis, morphology, and clinical features of mitral valve prolapse.
59. Explain rheumatic fever and rheumatic heart disease, including its pathogenesis, morphologic changes,
and clinical features.
60. Discuss the pathogenesis of infective endocarditis. Relate its clinical features and morphologic changes.
61. Discuss noninfective valve vegetations, including NBTE and endocarditis of SLE.
62. Describe carcinoid heart disease and compare how it affects the right and left sides of the heart differently.
63. List and briefly explain complications of prosthetic valves.
64. Describe the pathogenesis, morphologic changes and clinical features of dilated cardiomyopathy and
hypertrophic cardiomyopathy.
65. Discuss other forms of cardiomyopathy, including arrhythmogenic right ventricular cardiomyopathy, and
restrictive cardiomyopathy.
66. Describe myocarditis, and list the most common organisms associated with this entity.
67. Discuss the different forms of pericardial disease, including effusion, hemopericardium, and pericarditis.
68. Describe the different types of pericardial inflammatory reactions.
69. List the common primary cardiac tumors, and their clinical and morphologic features.
70. Briefly discuss the major complications of cardiac transplant.
CPR II- PHAR- LECT- Introduction to Pharmacology- Orientation and Scope (Iszard)
1.
2.
3.
4.
5.
6.
7.
8.
9.
Describe key aspects of each drug class and how drugs are developed.
Define and explain select terminology related to the discipline of Pharmacology.
Understand the history of pharmacology and the overall components of ADME.
Delineate the various electronic resources useful for drug information and medication identification.
Delineate drug equivalency ratings and pregnancy categories used by the FDA.
Describe the various medication designations used in medicine.
Detail the components of the prescription and how to read/write prescription medications.
Define select abbreviations utilized in medicine.
Perform basic drug dosing and flow-rate calculations.
CPR II- PHAR- LECT- Pharmacokinetics (Wolff)
1. Delineate the various factors relating to drug absorption and discuss examples of factors, which can
alter/modify drug absorption.
2. Describe the process of transmembrane distribution and excretion of drugs (both weak acids and weak
bases) as it relates to pH/ pKa.
3. Delineate the concept of drug distribution and the role protein binding has as well as its role in drugdrug interactions.
4. Describe the concepts of biotransformation and its physiological role as it relates to drug therapy.
5. Describe the major site(s) for biotransformation and the role the cytochrome P450 (CYP450) iso-enzymes
have in drug biotransformation.
6. Define substrate, induction, and inhibition and their role in drug-drug interactions, and
pharmacogenetics and polymorphism as it relates to the cytochrome P450 (CYP 450) system.
7. Define and explain the meanings of the various basic pharmacokinetic parameters (e.g., F, Vd, S, Ka, t½,
Cl, etc.)
8. Describe the basic pharmacokinetic equations used to determine loading dose, concentration in
plasma, half-life.
9. Delineate the difference between first-order and zero-order pharmacokinetics.
10. Describe the concepts of latency of onset, peak level, trough level, minimum effective concentration
(MEC), minimum toxic concentration (MTC), therapeutic window, maximum conc. (Cmax), and
minimum conc. (Cmin).
CPR II- PHAR- DSA/CIS- Pharmacodynamics (Konorev)
Drug-receptor interactions
1. Define the term pharmacodynamics and distinguish pharmacodynamics from pharmacokinetics.
2. Provide definitions of a receptor, ligand, and inert binding site.
3. Define how the formation of covalent vs. non-covalent bonds determines drug-receptor interactions, and
rank the types of bonds according to their strengths.
4. Define “affinity”, “KD”, and the relationship between these two parameters.
5. Define the term selectivity and describe its relationship to side effects of a drug.
6. Describe intrinsic activity and relate this concept to antagonist and various types of agonist drugs. Describe
the differences among the various classes of agonist drugs.
7. Classify drugs as full, partial, or inverse agonists according to their dose-response curves.
8. Define pharmacologic, chemical, and physiologic antagonism.
9. Define different types of pharmacologic antagonists.
10. Distinguish between competitive and non-competitive antagonism based on dose-response curves.
Dose-response curves
11. Define a dose-response curve and distinguish between arithmetically and logarithmically plotted doseresponse curves.
12. Describe the dose-response curve parameters, such as ED50 and Emax.
13. Distinguish between quantal and graded responses and recognize when a response is graded vs. quantal.
14. Recognize and interpret quantal dose-response curves when plotted cumulatively or non-cumulatively.
15. Define the terms median Effective, Toxic, and Lethal doses (ED50, TD50, and LD50), determine their values
from quantal dose-response curves and use them to calculate therapeutic index (TI).
16. Rank drugs in terms of safety based on TI.
17. Define therapeutic window, describe the relationship between wide or narrow therapeutic window and the
safety of the drug.
18. Describe pharmacological effects of drugs in terms of their potency and efficacy.
19. Rank drugs in terms of efficacy and potency based on their dose-response curves.
Common signal transduction pathways as drug targets
20. List major categories of drug targets.
21. Define cell signaling process and list components of the signaling process.
22. Describe protein phosphorylation-dephosphorylation cycle as part of cellular signal transduction, and types
of protein kinases.
23. Define a transcription factor; describe a general mechanism of action of transcription factors.
24. Describe general structure of a G-protein-coupled receptor and heterotrimeric G-protein cycle.
25. Describe G-protein families and their targets.
26. Describe mechanisms of desensitization/downregulation of GPCRs.
27. Describe signaling involving cyclic AMP system and the role phosphodiesterase in regulating the
intracellular concentration of this signaling intermediate.
28. Describe signal transduction involving IP3 (inositol 3-phosphate) and DAG (diacylglycerol).
29. Describe receptor tyrosine kinase signaling, ligands activating this type of receptors, and mechanism of
their activation.
30. Provide examples of receptors that are coupled to Janus kinase (JAK), describe JAK-STAT pathway.
31. Describe signaling involving intracellular (nuclear) receptors and provide examples of ligands that utilize
such signaling.
CPR II- PHAR- DSA/LECT/CIS- Adrenergic Drugs (Konorev)
1. Provide definitions of adrenergic drugs, adrenomimetics, and antiadrenergic drugs.
2. Distinguish between adrenergic drugs that are direct-acting and indirect-acting. Identify targets for directacting and indirect-acting adrenomimetic drugs.
3. List types and subtypes of adrenergic receptors and characterize the signal transduction pathways
associated with them.
4. Describe the types and subtypes of adrenoceptors that are expressed in different organs and tissues, and
effects of their activation.
5. List direct-acting adrenomimetic drugs and their selectivity at adrenergic receptor subtypes.
6. Describe pharmacodynamic effects of mixed alpha/beta and dopamine agonists (endogenous
catecholamines).
7. Identify the receptor selectivity of epinephrine vs. norepinephrine and describe how differences in
selectivity affect their effects on blood pressure and heart rate.
8. Describe important pharmacodynamic effects of alpha agonist drugs. Explain the regulation of adrenergic
transmission by presynaptic adrenoceptors.
9. Describe important pharmacodynamic effects of selective and non-selective beta agonist drugs.
10. List indirect acting sympathomimetic drugs. Describe mechanisms of activation of adrenergic transmission
by indirect acting drugs.
11. Describe indications for using adrenomimetic drugs, list drugs that may be used in these conditions.
12. List general cardiovascular and central nervous system adverse effects of adrenergic agonist drugs.
13. Identify mechanisms of direct-acting and indirect-acting antiadrenergic drugs.
14. List selective and non-selective alpha-adrenoceptor antagonist drugs.
15. Compare irreversible inhibitor of alpha-AR phenoxybenzamine with reversible antagonist phentolamine.
16. Describe organ system effects of alpha-antagonists.
17. Describe clinical uses and side effects of alpha adrenergic antagonist drugs.
18. List beta-antagonist and mixed antagonist drugs and their selectivity at adrenergic receptor subtypes.
19. List beta-blocker drugs that are antagonists, partial agonists, and inverse agonists at beta-AR.
20. Define what is meant by a beta blocker with ISA and why such agent may be useful.
21. Describe effects of beta-blockers on organs and tissues.
22. Describe clinical uses of beta-blockers.
23. Describe adverse effects of beta-blockers. Distinguish between beta-1-selective and non-selective beta
blockers and describe when non-selective beta-blockers should be avoided.
CPR II- PHAR- DSA/CIS- Biotransformation, Pharmacogenomics, and Clinical Trials (Kruse)
Drug Biotransformation
In order to prescribe safe and appropriate treatment for patients, you should be able to
1.
explain the general strategy of drug elimination.
2.
explain how biotransformation can cause activation and inactivation of drugs.
3.
compare and contrast the two major categories of biotransformation reactions (phase I and
phase II).
4.
explain the concepts of a prodrug and first-pass effect.
5.
compare and contrast genetic and non-genetic effects on biotransformation; provide
examples.
6.
explain how biotransformation can lead to toxicity (provide examples).
7.
compare and contrast the effects of disease and age on biotransformation.
Pharmacogenomics
In order to explain how genetic variation within the population affects drug dosing, therapeutic response,
effective treatment of disease, biotransformation, and pharmacotherapy, and to prescribe safe and appropriate
treatment for patients, you should be able to
1.
define and explain pharmacogenomics, single nucleotide polymorphism (SNP), and allele.
2.
explain how genetic variants contribute to variability in drug response, paying specific attention to
genetic variations in phase I and II enzymes, glucose 6-phosphate dehydrogenase (G6PD), and
transporters.
3.
compare and contrast examples of variations in drug response within single gene loci and multiple gene
loci (e.g., warfarin).
4.
explain the genetic variations associated with the pharmacokinetic and pharmacodynamic responses of
warfarin therapy.
Clinical Trials
In order to explain how the United States approves therapy for the safe and effective use in the population, you
should be able to
1.
define lead compound, no-effect dose, minimum lethal dose, and median lethal dose and explain their
purposes and usefulness.
2.
explain the goals and limitations of preclinical testing.
3.
explain key terminology associated with clinical trial testing, such as control, randomized, double-blind,
4.
5.
single-blind, open label, parallel trial, crossover trial, endpoint, and surrogate endpoint.
define the various phases of clinical trials and explain the scope and purpose of each phase.
define investigational new drug, institutional review board, and new drug application.
CPR II- PHAR- DSA/CIS- Cholinergic Drugs (Kruse)
1. In order to explain the physiologic effects of autonomic drugs, you should be able to describe the outcomes
of cholinergic receptor stimulation at effector organs throughout the body, specifically the smooth muscle of
the eye, blood vessels, lung, gastrointestinal track, and bladder, cardiac muscle, adrenal medulla, and
glands.
2. In order to explain the intended and unintended consequences of autonomic drugs, you should be able to
explain parasympathetic nervous system response to the administration of cholinergic agonists and
cholinergic antagonists, and select drugs to minimize adverse effects of cholinergic agonists.
3. In order to treat a patient experiencing muscarinic acetylcholine receptor blockade, you should be able to
identify and explain symptoms of muscarinic receptor antagonism and select appropriate pharmacologic
therapy to reverse anticholinergic effects.
4. In order to treat symptoms associated with myasthenia gravis, you should be able to recognize symptoms
of decreased acetylcholine signaling at the neuromuscular junction, select a drug mechanism for
appropriate treatment, and explain anticipated adverse effects.
5. In order to treat symptoms associated with airway restriction (e.g., wheezing, difficulty breathing), you
should be able to select appropriate receptors to activate or inhibit as part of a treatment strategy that will
result in positive clinical outcomes.
6. In order to treat symptoms associated with decreased secretions (e.g., eye, salivary gland), you should be
able select appropriate treatment and identify key receptors involved in drug mechanism of action.
7. In order to treat patients presenting with urinary incontinence, you should be able to select appropriate drug
therapy and anticipate anticipated adverse effects.
8. In order to treat patients presenting with difficulty urinating, you should be able to select appropriate drug
therapy and anticipate anticipated adverse effects.
9. In order to treat patients who wish to stop smoking, you should be able to explain the mechanism of action
of varenicline, identify anticipated adverse effects, and choose appropriate management strategies if
adverse events occur.
10. In order to reverse neuromuscular blockade, you should be able to select drugs or combination of drugs to
restore normal muscle function while minimizing adverse effects.
11. In order to explain the effects of ganglionic blocking drugs, you should be able to explain the physiological
response when a nicotinic neuronal acetylcholine receptor antagonist is administered to an anesthetized
patient.
CPR II- PHAR- LECT- BPH and Erectile Dysfunction Pharmacology (Sheehy)
1. List male lower urinary tract symptoms (LUTS) and explain how α1 adrenergic receptor antagonists relieve
LUTS.
2. Contrast the specificity of terazosin, doxazosin, alfuzosin, tamsulosin, and silodosin.
3. Predict the adverse effects based on the specificity of the α1 adrenergic receptor antagonists mentioned in
#2.
4. Relate androgen metabolism in a prostate epithelial cell to the mechanism of prostate enlargement during
benign prostatic hyperplasia (BPH) and to the mechanism of action of steroid 5α reductase inhibitors in the
treatment of BPH.
5. Describe why α1 adrenergic receptor antagonists are a dynamic remedy and steroid 5α reductase
inhibitors are a structural remedy in the treatment of BPH.
6. Summarize the mechanism of action of sildenafil, vardenafil, tadalafil, and avanafil in the context of the
physiology of penile erection.
7. Outline key differences in duration of action and onset in the PDE-5 inhibitors listed in #6.
8. Assess why phosphodiesterase-5 inhibitors are contraindicated in patients taking organic nitrates for
angina pectoris.
9. Discuss why priapism is a medical emergency and understand the consequences and treatment options for
priapism.
10. Name alternatives to PDE-5 treatment for erectile dysfunction and contrast the mechanism of action of
alprostadil with the mechanism of action of PDE-5 inhibitors.
CPR II- PHAR- DSA/LECT- Drugs Used in Chronic Ischemic Heart Disease (IHD) (Konorev)
1.
2.
3.
4.
Explain pharmacological strategies used in the treatment of different types of angina pectoris.
List nitrovasodilator drugs, and describe mechanisms of their vasodilatory and antiplatelet effects.
Describe the production and role of nitric oxide in maintaining vascular tone.
Describe the rationale behind using sublingual, buccal, and transdermal routes of administration of nitrates,
as opposed to oral administration of these drugs.
5. Describe sensitivity of different types of vessels towards vasodilatory activity of nitrates, and the role of
reduced thiols in the activation of nitrates to nitric oxide.
6. Describe clinical use and therapeutic effects of nitrovasodilators in different types of angina.
7. Describe adverse effects of nitrates.
8. Describe mechanisms of developing of nitrate tolerance.
9. Identify an important nitrate drug interaction.
10. List cardioactive and non-cardioactive calcium channel blocker drugs (CCBs) used in angina.
11. Describe mechanisms of beneficial action of CCBs in different types of angina pectoris.
12. Distinguish between cardioactive and non-cardioactive CCBs in terms of their effects in angina pectoris
and adverse effects.
13. Describe how beta blockers may be useful in the treatment of angina pectoris, their adverse effects and
contraindications.
14. Describe the rationale for using beta-blockers, CCBs and nitrates in combination therapy of angina
pectoris.
CPR II- PHAR- DSA/CIS - Drugs for Lipid Disorder (Kruse)
1. For the problem of hyperlipidemia, and in order to treat elevated triglyceride (TG) levels, you should be
able to select an appropriate medication to lower TG levels and be able to describe the drug’s mechanism
of action.
2. For the problem of hyperlipidemia, and in order to treat elevated low-density lipoprotein (LDL) levels, you
should be able to select an appropriate medication to lower LDL levels and be able to describe the drug’s
mechanism of action.
3. For the problem of hyperlipidemia, and in order to treat elevated LDL levels, you should be able to select
an HMG-CoA reductase inhibitor (statin) based on potency of reducing LDL levels.
4. For the problem of hyperlipidemia, and in order to treat elevated TG and LDL levels, you should be able to
select an appropriate medication that lowers TG and/or LDL levels, list expected adverse effects, be able to
identify plasma markers that indicate adverse drug reactions.
5. For the problem of hyperlipidemia, and in order to lower elevated cholesterol levels, you should be able to
compare and contrast the mechanisms of action and adverse effects of bile acid sequestrants and
cholesterol absorption inhibitors.
6. For the problem of hyperlipidemia, and in order to lower elevated cholesterol levels, you should be able to
describe dietary changes that have a positive effect on overall cholesterol levels.
7. For the problem of hyperlipidemia, and in order to change levels of measured components of total
cholesterol (e.g., LDL, TG, HDL), you should be able to select a drug (or combination of drugs) that will
have the greatest impact on lowering LDL, lowering TG, or raising HDL levels.
CPR II- PHAR- DSA/LECT/CIS- Drugs for Cardiac Arrhythmias (Konorev)
1. List cell types exhibiting pacemaker and fast action potentials in the heart; describe currents that contribute
to the fast action potential in the heart.
2. Describe currents that contribute to slow (pacemaker) action potential in the heart, and anatomical
locations of cells that exhibit slow action potential in the heart.
3. Recognize sodium channel as a target of the class 1 antiarrhythmic drugs; describe regulation of sodium
current by this channel and its activation-inactivation cycle.
4. Characterize parameters that describe interaction of class 1 drugs with sodium ion channel protein (statedependent block, kinetics of dissociation, charge of the drug molecule).
5. Define general electrophysiological mechanisms of action of class 1A antiarrhythmic drugs, representative
drugs, their pharmacodynamics, general indications, and adverse effects.
6. Describe electrophysiological mechanisms of action of class 1B antiarrhythmic drugs, representative drugs,
their pharmacodynamics, general indications, and adverse effects.
7. Distinguish between class 1A and class 1B agents in terms of their kinetics of dissociation from sodium
channels, effects on potassium channels, and proarrhythmic adverse effects.
8. Describe electrophysiological mechanisms of action of class 1C antiarrhythmic drugs, representative drugs,
indications, and adverse effects.
9. Briefly outline the results of the CAST trial.
10. Describe mechanisms of regulation of the pacemaker action potential currents by sympathetic nervous
system.
11. Describe the effects of class 2 agents on the impulse generation and propagation in the heart.
12. Describe clinical use of class 2 agents in treatment of cardiac arrhythmias.
13. Recognize potassium channels as targets of the class 3 antiarrhythmic drugs; describe roles of potassium
channels in the regulation of resting and action potentials.
14. Describe the electrophysiological effects of potassium channel blockade by class 3 agents, and
representative drugs.
15. Describe the effects of amiodarone on the heart, its pharmacokinetics and pharmacokinetic drug
interactions, indications and adverse actions.
16. Recognize L-type calcium channel as a target of the class 4 antiarrhythmic drugs; describe effects of these
drugs on pacemaker action potential in the heart.
17. List antiarrhythmic class 4 agents, their clinical indications and side effects.
18. Describe adenosine as an antiarrhythmic agent, its mechanism of action and targeted cell type,
electrophysiological effects, and clinical indications.
CPR II- PATH- DSA/LECT/CIS/ Path Quiz - Pulmonary Pathology (Singh)
Chapter 16 – The Upper airways, Ear, and Neck (pages 735-742)
1. Review the anatomy and, where applicable, the normal histology of the upper airways (nose and sinus),
ears, and neck.
2. Compare and contrast infectious and allergic inflammation of the nose (rhinitis) and sinus (sinusitis),
including etiologic factors, responsible micro-organisms, treatment, and complications.
3. Recognize the pathogenesis, clinical presentation, and histologic features of an inflammatory sinonasal
polyp.
4. Describe unique features of sinusitis, including sequelae of obstruction, means of bacterial entry, and
complications of sinusitis arising from spread to adjacent tissues.
5. Recognize various forms of fungal sinusitis, the organisms responsible, and how they vary in presentation
and prognosis. Review Robbins, 9th ed, chapter 8, pp 389-90 to review rhinocerebral mucormycosis.
6. Describe the clinical presentation and associated histopathology of Granulomatous Polyangiitis in the sinus
tract.
7. Describe the clinical and (where applicable) radiographic presentations of the following tumors of the
sinonasal tract:
a. Angiofibroma
b. Schneiderian papilloma
c. Olfactory neuroblastoma
d. NUT carcinoma
e. Nasopharyngeal carcinoma
f. Extranodal NK/T cell lymphoma
Describe the histologic and other defining features as outlined in the lecture and reading assignments.
8. Recognize the clinical and pathologic features of the following lesions of the larynx: vocal cord nodule,
squamous papilloma, squamous carcinoma, and be able to compare and contrast prognostic and
management implications of each.
9. List the microbial agents responsible for acute and chronic otitis media, describe their clinical presentations
and associated complications (including cholesteatoma).
10. Understand how the pathologic basis of otosclerosis produces the symptoms associated with this disease
process.
11. Compare and contrast branchial cleft cysts and thyroglossal duct cysts in terms of presentation,
embryologic derivation, and histology.
12. Review features of carotid body tumors: be able to describe their embryologic derivation, clinical and
radiographic presentation, and the histologic features that allow for the diagnosis.
Chapter 15 – The Lung (pages 669-724)
13. Describe the embryologic/fetal development of the lung as outlined in your textbook (Robbins, 9th ed.), and
the resultant normal histologic features of the upper and lower respiratory tract, including the cellular
structure and function of the alveolar sac.
14. Describe the mechanisms behind the development of the following congenital anomalies, know how to
recognize them clinically/radiographically, and understand the complications associated with them:
a. Pulmonary hypoplasia
b. Foregut cysts
c. Congenital pulmonary adenomatoid malformations
d. Pulmonary sequestrations
e. Tracheoesophageal fistulas
15. Compare and contrast various types of atelectasis, including possible etiologies and respective clinical
presentations.
16. Define pulmonary edema from a pathophysiologic and morphologic standpoint and recognize the various
mechanisms and etiologies resulting in pulmonary edema. Apply your understanding of the disease
process to recognize how various therapeutic options work.
17. Understand the process by which Acute Respiratory Distress Syndrome (ARDS) occurs, including major
predisposing conditions, the involved pathologic mechanisms, and associated clinical/diagnostic features.
18. Review features of Neonatal Respiratory Distress Syndrome (NRDS) (Robbins chapter 10, pp 457-459),
and be able to describe the pathogenesis and clinical features of this disease process.
19. Define Acute Interstitial Pneumonia, and be able to describe its clinical presentation, associated
histopathology, and prognosis.
20. Recognize the clinical spectrum of obstructive lung disease, from chronic bronchitis to emphysema, and
compare and contrast their respective etiologies, pathophysiology, clinical presentation, diagnostic
features, and prognosis.
21. Describe the unique genetics and pathophysiology that underlie α1-antitrypsin deficiency.
22. Compare and contrast the various mechanisms underlying asthma, including associated immune
mechanisms, contributing factors, and disease classifications. Understand the progression of asthma with
subsequent complications, including airway remodeling and status asthmaticus.
23. Define bronchiectasis, and be able to describe its clinical presentation, contributing etiologies, and
complications. Review diagnostic features of Allergic Bronchopulmonary Aspergillosis (ABPA), Cystic
Fibrosis (Robbins chapter 10, pp 466-471), and Kartagener syndrome.
24. Recognize basic characteristics of interstitial/restrictive lung diseases, including contributing factors, clinical
and radiographic presentations, related histopathology, and related clinical course/prognosis for the
following entities:
a. Usual interstitial pneumonia (UIP)
b. Non-specific interstitial pneumonia (NSIP)
c. Cryptogenic organizing pneumonia (COP)
d. Sarcoidosis
e. Hypersensitivity pneumonia
f. Desquamative interstitial pneumonia (DSIP)
g. Respiratory bronchiolitis-interstitial lung disease (RB-ILD)
h. Langerhans cell histiocytosis (LCH)
i. Pulmonary alveolar proteinosis (PAP)
25. Describe how the following pneumoconiosis develop: Silicosis, Coal workers’ pneumoconiosis, and
Asbestosis. Evaluate possible routes of exposure and associated pathology, clinical disease, and
prognosis.
26. Understand the pathophysiology of pulmonary embolism, and recognize potential risk factors and facets of
the clinical presentation. Describe associated complications, including cor pulmonale and pulmonary
infarction.
27. Define pulmonary hypertension from a pathophysiologic standpoint and describe the basic underlying
mechanism and typical clinical presentation. Recognize associated histopathologic lesions.
28. Compare and contrast the pathogenesis and clinical features of diffuse pulmonary hemorrhage syndromes,
including Goodpasture syndrome, Polyangiitis with Granulomatosis, and Idiopathic Pulmonary
Hemosiderosis.
29. Recognize the clinical/radiographic features of lobar pneumonia, and understand the progression of
associated pathologic changes and complications.
30. Compare and contrast the various types of community-acquired bacterial pneumonia, with specific focus on
commonly responsible microbiologic agents: S. pneumoniae, H. influenza, S. aureus, K. pneumoniae, M.
catarrhalis, P. aeruginosa, L. pneumophilia, and Mycoplasma pneumoniae. Be knowledgeable about
associated clinical/radiographic features and histopathologic features.
31. Describe the pathogenesis of community-acquired viral pneumonia, with specific focus on Influenza,
SARS, Respiratory syncytial virus, human Metapneumovirus. Describe associated clinical, radiographic,
and histopathologic features. Regarding influenza, understand the concept of antigenic shift and antigenic
drift.
32. Recognize clinical/radiographic features of aspiration pneumonia and lung abscess and be able to describe
various responsible etiologies.
33. Understand the progression of pulmonary tuberculosis and hallmark clinical and pathologic features.
Review Robbins, 9th ed, chapter 8, pp 371-376.
34. Recognize agents responsible for chronic pneumonia, especially fungal infections to include
Histoplasmosis, Blastomycosis, and Coccidiomycosis. Refer to Robbins, 9th ed, chapter 8, pp 388-389 to
review pulmonary Aspergillosis. Compare and contrast the means of exposure (including any endemic
geographic areas) for these infections. Apply your knowledge of the histopathology of these causative
organisms to be able to diagnose them microscopically.
35. Describe pneumonias that occur in immunocompromised settings, with specific emphasis on Pneumocystis
and Mycobacterium avium. Be aware of the post-transplant state as a form of significant
immunocompromise, and describe infections that can occur in this setting. Differentiate findings in
opportunistic infections from transplant rejection.
36. Understand the genetic and environmental risk factors for primary lung carcinoma.
37. Compare and contrast the risk factors, precursor lesions, clinical/radiographic presentation, histologic
features, behavior, and treatment implications of the following primary pulmonary tumors:
a. Adenocarcinoma
b. Squamous carcinoma
c. Small cell carcinoma
d. Carcinoid tumor
e. Atypical carcinoid tumor
38. Review table 15-11 in Robbins to understand clinical manifestations of anatomic spread of pulmonary
carcinoma.
39. Compare and contrast the various paraneoplastic syndromes that can occur in pulmonary carcinoma,
including their mechanisms of action and clinical presentations.
40. Recognize the importance of determining whether a pulmonary tumor is a metastatic malignancy, and
clinical/radiographic features that provide clues to the diagnosis.
41. Review additional miscellaneous lung tumors as mentioned in Robbins: Hamartoma,
Lymphangioleiomyomatosis, and Inflammatory Myofibroblastic Tumors. Understand the clinical
presentation and means of diagnosis for all 3 entities.
42. Compare and contrast transudative vs exudative pleural effusions (including empyema), the basic
mechanisms underlying the distinction, and common examples of each. Understand how these various
effusions present and manifest in terms of the color and character of the fluid produced.
43. Understand the basic pathophysiologic mechanisms that underlie tension vs. spontaneous pneumothorax,
and recognize how they present clinically.
44. Describe the risk factors, clinical/radiographic presentation, gross and histopathologic features, and
prognosis of mesothelioma.
45. Any micro-organism discussed in the lecture series or covered by the reading material should be reviewed
as necessary in Clinical Microbiology Made Ridiculously Simple, 6th Ed. It will be expected that students
understand the relevant gram staining and morphologic/growth characteristics allowing for recognition of
bacteria within the content of the course. The staining characteristics of fungal and mycobacterial
organisms should be recognized. Morphologic features of cytomegalovirus should be recognized.
46. Be able to describe the typical radiographic patterns that result from the following pathologic entities
(Special Session: Pathology-Radiology correlations lecture):
 Normal chest x-ray
 Bronchopneumonia
 Lobar pneumonia
 Abscess
 Bronchiectasis
 Acute respiratory distress syndrome
 Idiopathic pulmonary fibrosis
 Histoplasmosis
 Bronchioloalveolar Carcinoma
 Pulmonary edema
 Pneumothorax
Resource: High-Yield Imaging: Chest (1st Ed.) Muller N. Elsevier, c2010. ISBN: 978-1416061618.
Available electronically through the library Clinical Key database.
47. Define and utilize the following vocabulary
 Hypoxemia
 Dyspnea
 Tachypnea
 Hemoptysis
 Rhinorrhea
 Epistaxis
 Bronchoscopy/bronchoscopic
 Thoracoscopy/thoracosopic
 Emaciated
 Lavage
CPR II- PATH/PHYS- DSA/CIS- Pulmonary Function Tests (Dobson/Karius)
1.
2.
3.
4.
5.
6.
Review the volumes and capacities of the lung (DSA).
Describe the components of pulmonary functions testing (DSA)
Explain the importance of FVC, FEV1, and the FEV1/FVC. (DSA)
List the variables that affect lung volumes. (CIS)
Recognize common clinical indications/contraindications for spirometry. (CIS)
Compare and contrast obstructive and restrictive lung diseases as they relate to: (CIS)
• FVC
• FEV1 /FVC
• Diffusion capacity
7. When given a patient presentation and appropriate PFT data, be able to distinguish between obstructive
and restrictive diseases.
CPR II- PHAR- LECT- Drugs for Thromboembolic Disorder (Wolff)
1. Recognize different types of drugs used in thromboembolic disorders (anticoagulant, antiplatelet, and
fibrinolytic drugs).
2. Describe mechanisms of action of indirect thrombin inhibitors, and distinguish between different
preparations of heparins. List representative drugs, their general clinical indications and
contraindications.
3. Describe heparin-induced thrombocytopenia, mechanisms of development and approach to treatment.
4. Contract the mechanism of indirect inhibition of factor Xa by fondaparinux and its clinical indications
and consequences versus heparins.
5. Describe parenteral direct thrombin inhibitors, representative drugs, and their mechanisms of action,
clinical indications and adverse effects.
6. Describe the mechanism of action, pharmacokinetics, indications and adverse effects of warfarin.
7. List causes of high variability in therapeutic warfarin concentrations between individuals (genetic
make-up, disease states).
8. List pharmacokinetic and pharmacodynamic drug interactions of warfarin.
9. List oral factor Xa inhibitors, their clinical indications, and advantages and disadvantages as compared
with warfarin.
10. Recognize an oral direct thrombin inhibitor drug, clinical indications for its use, and advantages and
disadvantages as compared with warfarin.
11. List antidotes for anticoagulant drugs.
12. Describe lab tests that are used to monitor activity of anticoagulant drugs in treated patients.
13. Describe antiplatelet drugs, their mechanisms of action (aspirin, ADP receptor blockers and GP IIa/IIIB
blockers) and general clinical indications.
14. Describe individual variability in therapeutic effect of clopidogrel due to a genetic make-up.
15. List phosphodiesterase inhibitor drugs that are used as antiplatelet agents, their mechanisms of action
and clinical uses.
16. Describe types and mechanisms of action of fibrinolytic (thrombolytic) drugs, their general clinical
indications, and adverse effects.
17. Recognize the difference between tissue-type plasminigen activators and other fibrinolytic drugs in terms of
inducing systemic fibrinogenolysis.
CPR II- PHAR- LECT- Drugs for Heart Failure (Wolff)
1. Distinguish between chronic systolic heart failure, diastolic heart failure, high-output heart failure,
right-sided heart failure and acute decompensated heart failure
2. Describe the compensatory changes in patients with heart failure in terms of preload and afterload
3. Define the terms inotropic agent and chronotropic agent.
4. Recognize prototypical angiotensin-converting enzyme (ACE) inhibitors, and the angiotensin receptor
blockers (ARB) and the angiotensin receptor blocker/neprilysin inhibitor.
5. Describe the mechanisms of action and notable adverse effects for the above drug classes, and explain
the rationale for their use in the treatment of heart failure.
6. Recognize prototypical sympathetic agonists and antagonists, describe their mechanism of action and
notable adverse effects, and explain their usage and limitations when treating heart failure.
7. Recognize the prototypical "funny current" inhibitor, describe its mechanism of action and explain its
usage in the treatment of heart failure.
8. Recognize prototypical K+-losing and –sparing diuretics (more follows in diuretics session), explain the
purpose for using K+-losing diuretics to treat heart failure.
9. Explain the purpose of aldosterone inhibition when treating post-myocardial infarction heart failure.
10. Describe the therapeutic role of digoxin and the mechanisms by which its beneficial actions and
notable adverse effects occur including interaction with K+-losing diuretics.
11. Recognize prototypical direct vasodilators, describe their mechanisms of action and their notable
adverse effects, and describe the clinical utility of vasodilators when treating heart failure.
12. Recognize the prototypical phosphodiesterase inhibitor used to treat heart failure and describe its
mechanism of action and limitations.
13. Compare and contrast the agents used to treat heart failure with respect to their effects on preload,
afterload and inotropy.
CPR II- PHYS- DSA/LECT- Sleep and EEG (Karius)
In order to learn this material, you should review and understand:
 Respiratory Control mechanisms (from CP1)
 General neurophysiology (action potentials, synapse).
In order to understand and explain sleep-disordered breathing, you should be able to:
1. Describe how the circadian rhythm is generated, including genetic components. (DSA)
2. Describe how entrainment of the genetically determined circadian rhythm to the environment occurs
(DSA).
3. Compare and contrast the waves commonly recorded in the waking EEG. (DSA)
4. Compare and contrast REM and NREM sleep (DSA)
5. Describe how attention, sensory stimulation, and age change the EEG. (DSA)
6. Compare and contrast sleep induction with the induction of REM sleep.
7. Describe how arousal from sleep occurs.
8. Compare and contrast the normal waking EEG with that recorded during NREM (slow wave) and REM
sleep.
9. When given a polysomnogram and patient presentation, be able to:
a. Identify the occurrence of sleep-disordered breathing
b. Compare and contrast the physiologic differences between occlusive and central sleep apneas
c. Explain the physiologic effects of the apnea as seen on the polysomnogram.
CPR II- PHAR- DSA/CIS- Anti-fungal, Anti-influenza, and Anti-TB Pharmacology (Sheehy)
1. Explain the mechanism of action, mechanism of resistance and prominent adverse effects of varying antifungal pharmacological agents including amphotericin B, flucytosine, the azoles, and the echinocandins.
2. Associate the efficacy of oseltamivir, zanamivir, peramivir, amantadine, and rimantadine with the life cycle
of the influenza virus.
3. Differentiate between first line pharmacological treatment regimens that are appropriate for patients with
active tuberculosis and those patients with a reactive purified protein derivative (PPD) skin test.
4. Describe the mechanisms of action and key adverse effects of anti-tuberculosis medications used as first
and second line therapies in the treatment of tuberculosis.
5. Recall mechanisms of resistance of anti-tuberculosis medications used as first and second line therapies in
the treatment of tuberculosis.
____________________________________________________________________
Exam 2
LEARNING OBJECTIVES
CPR II- PHAR- LECT- Drugs for Asthma and COPD (Iszard)
1. Understand and describe what medications are used to treat patients for asthma or chronic obstructive
pulmonary disease (COPD). The student will be able to distinguish key differences and similarities between
the medications selected in the treatment of asthma and COPD.
2. Understand and discuss the indications, cautions and adverse effects of bronchodilators, inhaled
corticosteroids and leukotriene antagonists used in treatment and management of patients with asthma or
COPD.
3. Understand and describe the mechanisms of how corticosteroids, oral and IV steroids and leukotriene
pathway inhibitors exert their effect in the treatment of asthma and COPD.
4. In order to treat patients with asthma and COPD, the student will be able to make discernments between
different pharmacological drugs and select the best course of treatment for a clinical scenario.
CPR II- PATH- LECT/CIS- Renal Pathology (Putthoff)
(Renal/Lower GU/Male GU)
Glomerular disease
1. Fully discuss those pathologic entities/disorders of major human systems which may result in edema
(localized vs. generalized)
2. Relate the entities which may exhibit edema to plasma protein anomalies and compare/contrast with those
that are primarily hydrostatic in nature
3. Compare and contrast clinical renal syndromes specific to primary renal glomerular disease and those that
indicate primary renal tubular disease. Provide specific examples of each. See Key Concepts (R. 899), and
Robbins text pages 898 and 899
4. Compare and contrast the basic causes, clinical findings and specific kidney diseases associated with
acute and chronic kidney failure
5. Define azotemia and uremia. Distinguish and explain pre-renal and post-renal azotemia
6. Delineate the major organ systems that are prominently affected by the clinical syndrome of uremia and
list/explain the most common and specific pathologic findings associated with each organ system
7. Define the major GFR landmarks in the progression of renal disease and list the specific term associated
with each major stepwise progression (see posted PPs and correlate with mechanisms of progression in
glomerular diseases in the text (R pp 908, 909),
8. Explain the vital role of the endothelial cell and its varying cellular and molecular adaptations in small
vessels and the microvasculature, especially as they relate to (renal) afferent/efferent arterioles and
glomerular capillary loops
9. Define and diagram the renal glomerulus and describe the morphology, spatial location and function of
each of the following component structures: afferent arteriole, efferent arteriole, vascular pole of the
glomerulus, macula densa, juxtaglomerular granular cells, fenestrated endothelium, glomerular basement
membrane, visceral epithelial cells (podocytes), filtration slits and diaphragms, mesangial cells and
mesangial matrix, extraglomerular mesangium, Bowmans capsule, parietal epithelial cells, urinary space
and urinary pore. Correlate with Figs. 20-1, 20-2. 20-3 and Key Concepts R. 903.
10. List the major glomerular syndromes (Table 20-3) and succinctly describe the clinical characteristics and
associations that make each a discernible entity
11. Diagram, compare and contrast the terms “diffuse, focal, segmental and global” as they are used to
describe distribution and involvement of glomeruli and as they aid in the distinction and clinical differential
diagnosis of glomerular diseases on biopsy reporting. Associate those with major features of glomerular
involvement due to electron-dense deposits reflecting immune complex lesional localizations (see Figure
20-5) and pathologic responses of the glomerulus to injury (see text pp. 902/903). Expand the discussion of
glomerular injury to include major cellular and soluble injury mediators and epithelial cell injury to include
the concept of podocytopathy
12. Compare and contrast major immunologic phenomena, especially in situ immune complex formation and
circulating immune phenomena localizing in areas related to the basement membrane - complex
depositions, which figure prominently in many cases of glomerular injury. Provide specific examples of
disorders exhibiting each (note Table 20-4, Figure 20-4 and Key Concepts, p. 906). See Table 20-5 as a
key reference source for the GNs and noted corrections to the table as explained in posted PPs and class.
13. Clearly describe the major clinical findings, signs and symptoms of nephritic syndrome.
14. Describe the etiology, epidemiology, risk factors, clinical (note salient features of children vs. adults)
presentation, pathogenesis and pathologic findings of acute (diffuse) proliferative glomerulonephritis
especially focusing upon that due to antecedent streptococcal infection (see Figure 20-9)
15. Describe specific pathologic features of the GFM that are characteristic of patients who manifest nephritic
syndrome and hematuria
16. Define the clinical syndrome of rapidly progressive glomerulonephritis (RPGN) and describe/categorize its
three major diagnostic types (See Table 20-6)
17. Describe the epidemiology, clinical associations, clinical course & pathologic findings in RPGN
18. Describe in detail the pathophysiologic lesion(s) that result in crescent formation and specific
histomorphologic findings that occur in “crescentic extracapillary glomerulonephritis”. See Figure 20-10.
19. Discuss pathologic features that affect the basement membrane in RPGN and their relationship to the
clinical features of “nephritic syndrome”. See Key Concepts pp 913-914
20. Compare and contrast Type 1 RPGN - anti-GBM disease & Goodpasture Syndrome (note Figure 20-4 B
and E)
21. Compare and contrast the clinical findings and epidemiology of Type II and Type III RPGN and provide
specific examples of each
22. List the four major clinical/laboratory findings that constitute nephrotic syndrome and describe the general
sequential pathophysiologic and clinical features derived thereof, for each (R. p. 914) and major patient
complications associated with nephrotic syndrome
23. Distinguish between primary and secondary causes of nephrotic syndrome (Key Concepts p. 922, 923)
24. List the major primary renal diseases associated with “pure” nephrotic syndrome and describe the
epidemiology and pathophysiologic features of each, focusing upon minimal change disease and
membranous glomerulopathy
25. List and describe all salient characteristics of the most common primary disorder (GN) exhibiting nephrotic
syndrome in US children. Especially note its typical clinical presentation, laboratory findings at
presentation, and (positive/negative) light, immunofluorescent and ultrastructural microscopic defining
characteristics
26. In terms of #25, discuss appropriate approach to treatment and response to therapy
27. Describe the clinical presentation, clinical associations, laboratory findings, pathologic features, clinical
course and approach to treatment for each of the following (types of focal segmental glomerulosclerosis):
Primary disease: idiopathic focal segmental glomerulonephritis
HIV-associated nephropathy
Ablative nephropathy of progressive renal disease
Genetic mutational forms
28. List and describe all salient characteristics of the most common (GN) disorder exhibiting (primarily)
nephrotic syndrome in US adults. Especially note its typical clinical presentation, laboratory findings at
presentation, and light (H&E/special stains), immunofluorescent and ultrastructural defining characteristics.
29. In terms of #28, discuss appropriate treatment (for both primary and secondary forms) and response to
therapy
30. Describe the clinical presentation, clinical associations, laboratory findings, pathologic findings, clinical
course and approach to treatment for the following GN disorders with mesangial proliferation
characteristics (note Figures 20-16 and 20-17)
membranoproliferative Type I (primary vs. secondary)
membranoproliferative Type II (dense deposit disease)
IgA nephropathy (emblematic of isolated glomerular abnormality)
31. Define chronic glomerulonephritis and the major clinical and pathologic associations that are associated
and characteristic of this entity.
32. Delineate the inheritance patterns, epidemiology, clinical findings, pathogenesis, pathologic features, &
clinical course of Alport Syndrome & thin basement membrane disease (in both genders)
33. Compare and contrast primary renal (GN) disease vs. secondary renal (GN) disease. Explain which are
definable “diseases” versus those are that are “patterns”.
34. List the systemic diseases generally associated with nephritic syndrome; the systemic diseases associated
with nephrotic syndrome, and those that may be “mixed” or variable
35. Describe the fundamental pathogenesis/classification of diabetes mellitus, diabetic nephropathy and its
clinical importance in US and worldwide populations.
36. Fully describe the spectrum and range of major morphologic changes in diabetic nephropathy, focusing
upon the kidney parenchyma, papillae, glomeruli, and blood vessels/interstitium (succinct review in
chapters 20, 21 and 24). Very succinctly note common diabetic ocular complications (esp. cataract
formations and retinopathy), and diabetic neuropathy.
37. Describe the fundamental pathogenesis and spectrum of glomerular lesions which may be observed in
cases of SLE.
38. Explain all salient elements in the pathogenesis of Henoch-Schönlein purpura and its spectrum of clinical
manifestations. Describe its morphologic features in the glomerulus (by light microscopy and
immunofluorescence), skin lesions (surface and dermal blood vessels), and its relationship to IgA
nephropathy.
39. Succinctly note the general pathophysiologic features and glomerular manifestations of bacterial
endocarditis/other systemic infections as they primarily affect the glomerulus, fibrillary glomerulonephritis,
and glomerular manifestations of Goodpasture syndrome, microscopic polyangiitis, and granulomatosis
with polyangiitis (formerly known as Wegener granulomatosis).
Tubulointerstitial disease
40. Define acute tubular injury and describe in detail the following aspects of this type of kidney injury (AKI)
(and ATN, see Figure 20-22):
etiology
pathophysiology
histomorphologic aspects
clinical course & prognosis
41. Fully describe the features and electrolyte issues of acute kidney failure especially as they relate to
stages/clinical phases, and complications therein
42. Describe in detail the following aspects of tubulointerstitial nephritis/ acute pyelonephritis:
Definitions and related disorders
Etiology/ infectious agents (R. p. 930)
Pathophysiology
histomorphologic aspects
43. Fully define chronic pyelonephritis and discuss its major etiologic factors, including VUR
44. List the major causes of papillary necrosis (Table 20-9) and delineate the male-female ratio, time course,
role of infection and pathologic features of each
45. Describe analgesic nephropathy and its histomorphologic consequences
46. Describe the epidemiology, predisposing conditions & mineral constituency of renal calculi
47. Note and fully discuss renal tubular epithelial damage and sequelae due to Bence Jones proteins. Indicate
etiology, morphologic features and potential renal consequences
48. Define benign nephrosclerosis and discuss its pathogenesis
49. Recognize and describe the gross pathologic changes associated with benign nephrosclerosis (Figures 2036/37)
50. Describe the pathologic changes associated with accelerated nephrosclerosis (Figure 20-38) and contrast
them with those of benign nephrosclerosis
51. Discuss the sequence of events considered important in the pathogenesis of accelerated nephrosclerosis
52. Describe the vessel alterations that characterize blood vessels associated with the clinical syndrome of
malignant hypertension
53. Discuss the clinical manifestations of malignant hypertension and define those aspects and consequences
which indicate it is a medical emergency
54. Describe the lesions responsible for renal artery stenosis, indicate their clinical importance, patient settings
and treatment approach
55. Succinctly compare and contrast the clinical settings, diagnosis of, pathogenesis and prognosis/treatment
of typical HUS, atypical HUS, and TTP
56. Describe the overlapping morphologic and pathophysiologic changes associated with the above thrombotic
microangiopathies (note Key Concepts, p. 943)
57. Briefly describe the pathogenesis, morphologic changes and risk factors associated with atherosclerotic
ischemic renal disease, atheroembolic renal disease, diffuse cortical necrosis, and renal infarcts
Anomalies/cystic disease/obstruction/stones
58. List the major congenital anomalies and defects that affect the kidney and discuss the relative occurrence
and clinical significance of each.
59. Compare and contrast the epidemiology, pathologic features, clinical features, complications, associations
and the clinical course of (Figure 20-44):
Autosomal dominant (adult) polycystic kidney disease
Autosomal recessive (childhood) polycystic kidney disease
60. Delineate the major subtypes, epidemiology, pathologic features, clinical features, complications and
clinical course of cystic diseases of the renal medulla, i.e.
Medullary sponge kidney
Nephronophthisis and adult-onset medullary cystic disease
Multicystic renal dysplasia
Acquired (dialysis-associated) cystic disease
Simple cysts
(See Table 20-11 with corrections as noted in posted PP)
61. Comprehensively discuss those entities that may be associated with urinary tract obstruction and their
clinical import/consequences and treatment approach
62. List and explain the spectrum of urolithiasis manifestations including incidence, etiology/pathogenesis,
mineral constituencies (what is most common? Table 20-12), clinical associations and salient acute/chronic
clinical consequences
Renal neoplasia
63. List and describe benign renal neoplasms and their classification
64. Note Table 20-10. Renal disease related to nonrenal neoplasms
65. Describe the unique epidemiologic, syndromic, clinical and pathologic features of renal papillary adenoma,
angiomyolipoma, and oncocytoma
66. Describe the clinical relevancy and associations of familial renal cancer syndromes, i.e those with VHL,
hereditary leiomyomatosis/RCC, hereditary papillary carcinoma and BHD syndrome
67. Fully discuss renal cell carcinoma (RCC) with emphasis on cytogenetic, genetic findings and clinical
correlations. How are these reflected in the classification of these neoplasms? Figure 20-50/51.
68. Describe the unique clinical, pathologic/molecular and morphologic features of clear cell RCC, papillary
RCC and chromophobe RCC
69. Describe the significance of stage and histologic features in terms of prognosis of RCC
70. Fully describe and discuss renal urothelial carcinoma, its incidence and unique characteristics
71. Succinctly describe metastatic disease to the kidney
Regional-related pediatric neoplasia
72. Comprehensively discuss neuroblastoma and its accurate placement in the differential diagnosis of
abdominal mass in a child. Include relevant clinical, laboratory/molecular biologic and prognostic features
of this malignancy
73. Describe the primary location and clinical, genetic, pathologic, syndromic and morphologic features of
Wilms tumor, including prognostic indicators, and issues related to second primary tumors as a
consequence of therapy
[Review R. pp. 475 – 481].
Ureters
74. Delineate and discuss diseases, disorders and neoplasms that may affect the ureters, primarily and
secondarily, i.e.
- congenital anomalies
- inflammatory conditions
- tumors and tumor-like lesions
- obstructive lesions (see Table 21-1, p. 961R)
- sclerosing retroperitoneal fibrosis
Urinary Bladder
75. Briefly discuss clinical complications that may occur with congenital anomalies associated with the urinary
bladder, e.g.
- diverticulae, exstrophy, vesicoureteral reflux, and urachal cysts.
76. Describe and explain the common clinical presentations and pathologic changes associated with acute and
chronic cystitis.
77. List and discuss etiologies (organisms etc.) and predisposing factors for acute and chronic cystitis
78. Explain the clinical and pathophysiologic relationship between cystitis and pyelonephritis
79. Describe the basic pathologic features of interstitial cystitis, malacoplakia (Figure 21-5), polypoid cystitis,
nephrogenic adenoma, cystitis cystica/cystitis glandularis, and squamous metaplasia. Explain how you
accurately diagnose these entities
80. Summarize the inflammatory disorders and metaplasias of the bladder and discuss their common clinical
presentations
81. Comprehensively explain the classification of urinary bladder neoplasms from precursor lesions to
infiltrating malignancies
Urinary Bladder continued and Urethra
82. Delineate and discuss the relevant clinical features of papillary lesions of the urinary bladder. Incorporate in
the discussion the full spectrum of benign and malignant lesions in this category, including PUNLMP
83. List and explain the nature of malignant mesenchymal and non-epithelial tumors of the urinary bladder with
emphasis on pediatric vs. adult lesions
84. Describe the unique epidemiologic, clinical and pathological features of urothelial carcinoma
85. Discuss and delineate the classification of transitional cell neoplasia with emphasis on diagnosis, growth
patterns (flat lesions vs. papillary, Figure 21-6), cytogenetic findings, staging significance and salient
clinical correlates in this category of neoplasia
86. Describe the significance of stage and histopathologic features in terms of prognosis of urinary bladder
carcinoma
87. Compare and contrast the unique etiologic, clinical, epidemiologic, pathologic and morphologic features of
adenocarcinoma, squamous cell carcinoma, and other uncommon (in the US) primary malignancies of the
urinary bladder, including mesenchymal and secondary tumors
88. Comprehensively discuss the common and major causes of bladder outlet obstruction (males vs. females)
89. Comprehensively list the most common diseases, inflammations/infections (including salient aspects of
regional infections), including clinical presentations, and neoplastic lesions of the urethra
90. Compare and contrast gonococcal urethritis vs. non-gonococcal urethritis (specifying organisms and type)
and clinically-relevant gender-specific issues.
91. Define and explain reactive arthritis and the noteworthy-associated clinical triad
92. Delineate and discuss the pathologic nature and clinical features of urethral caruncle, benign epithelial
tumors of the urethra and primary carcinoma of the urethra. How common is the latter? Proximal entities
vs. distal?
Penis
93. Describe the pathologic nature, etiology and clinical features of hypospadias, epispadias, phimosis and the
uncircumcised penis. Note complications thereof
94. Explain the fundamental pathophysiology of balanoposthitis, the conditions/infectious agents often
associated, and complications, with persistence
95. Discuss and delineate the incidence and manifestations of benign and malignant penile tumors
96. List and discuss the major pathologic and clinical features of HPV infections of the penis and scrotum, their
classification and subtypes including oncoprotein associations, essential nature of related lesions (benign
or malignant) and potential for progression in men. Succinctly explain how the latter differs from HPV
infections in females
97. Fully explain, compare and contrast bowenoid papulosis, CIS, Bowen disease and invasive squamous cell
carcinoma. Note the most salient clinical, differential diagnosis and treatment features
Testis, Epididymis and Scrotum
98. Explain the essential pathologic features of cryptorchidism, its tendency for histologic degeneration,
propensity for malignant transformation and relevant surgical aspects of orchiopexy.
99. Discuss and organize the following in terms of pathologic change and clinical manifestations of ….(as they
relate to the testis and epididymis):
Regressive changes
Inflammation
Non-specific epididymitis and orchitis
Granulomatous orchitis
Gonorrhea
TB
Syphilis
100. Define; note the natural history and clinical/surgical issues of
Testicular torsion
Neonatal type
Adult type
Spermatic cord and paratesticular tumors (in children and adults)
101. A. List the (predominantly primary) testicular tumors and discuss their incidence, age group,
presentation, etiologic associations, familial predispositions, type-specific hormone elaboration/biomarkers,
classification, propensity for metastases, and prognosis (note clinical features of testicular germ cell tumors
(p. 979), i.e.
Germ cell tumors
Seminomatous (Figures 21-23/24)
Non-Seminomatous [NSGCT]
Embryonal
Yolk sac
Choriocarcinoma
Teratoma
Mixed tumors
Tumors of sex-cord-gonadal stroma
Leydig cell tumors
Sertoli tumors
Gonadoblastoma
Testicular lymphoma
102.
Define and explain the clinical significance of certain common lesions of the tunica vaginalis, i.e.
hydrocele, hematocele, chylocele, spermatocele and varicocele.
Prostate (Figures 21-30/31)
103.
Fully discuss (the following) major disease categories of the prostate, including incidence, pathologic
basis, clinical manifestation(s), prognostic features, salient molecular biologic associations and
classification schemes of
Inflammation/Infection
Including acute bacterial, chronic bacterial, chronic abacterial,
granulomatous prostatitis, etc.,
Benign enlargement (Figure 21-33)
104.
Detail the incidence, age grouping, etiology and pathogenesis, glandular location at inception,
hormonal issues of proliferation or impaired cell death, clinical features, treatment and issues of
obstruction, and
Adenocarcinoma (and subtypes)
A. Comprehensively note and discuss incidence, morbidity and mortality, ethnic predilections,
role of androgens (and noteworthy aspects of the androgen receptor gene product including nucleotide molecular biologic features therein), fundamental genetic/molecular
biologic associations with malignant transformation and their clinical import, glandular
location and pathogenesis, PIN, infiltrating morphology (see Figure 21-37), Gleason scoring
(Figure 21-38) and its prognostic implications, clinical course, typical sites of metastases,
the clinical utility of PSA (including density and velocity issues), and clinical implications of
BRCA2 and PCA3. Note: Key Concepts, R. p. 989.
B. Explain the anatomic nature of localized spread (and inherent clinical issues) in secondary
malignant involvement of the prostate.
105.
Note and explain variations or subtypes of prostate cancers including variations of differentiation (i.e.
squamous, mucinous and neuroendocrine) and their clinical implications. List and describe mesenchymal
tumors and lymphoreticular neoplasms arising in (or involving) the prostate and those described in
Miscellaneous tumors and tumor-like conditions of the prostate.
Global Overarching
106. Understand that, increasingly, clinical genetic/molecular biologic information derived from research
laboratories and clinical trials throughout the world, changes and virtually revolutionizes our understanding
of human disease today, and for the foreseeable future.
107. In terms of #106, and as you study the kidney, lower GU tract and male genital system delineate those
major aspects of inheritance or sporadic mutation of the human genome or epigenome that are reflected in
the major categories of acute or chronic human disease [referable to the genitourinary tract], whether it is
reactive/proliferative in nature, infectious, autoimmune, metaplastic, hamartomatous or truly neoplastic.
108. In terms of neoplasia and malignancy of the genitourinary tract, focus upon those elements necessary
for diagnosis (including major histomorphologic aspects and prominent genetic/molecular biologic
features), prognosis (including those major histomorphologic aspects known to confer a better or worse
prognosis and/or related genetic/molecular biologic features) and upon those elements of therapy that tend
to be global responses within or for a salient category of neoplasia/malignancy.
109. In terms of essential knowledge and understanding, read and know the material encapsulated in each
Key Concepts box in Robbins, 9ed, Chapters 20 and 21.
110. With a goal to achieving clarity of understanding and application, comprehensively construct differential
diagnoses and accurately discuss the diseases, disorders and neoplasms in learning objectives 1 – 109 in
patient case presentations in interactive settings - (CIS) sessions.
CPR II- PHAR- LECT- Diuretics (Wolff)
1.
2.
3.
4.
5.
6.
7.
8.
9.
Distinguish between diuretics, natriuretics and aquaretics and give examples of each.
List the common clinical indications when using diuretics alone or in combination.
Explain why some diuretics are potassium-losing and others are potassium-sparing.
Give examples of loop diuretics, and explain their mechanism and site of action, key adverse effects, and a
feature that distinguishes one from the others.
Give examples of thiazide diuretics, and explain their mechanism and site of action, key clinical use and
adverse effects.
Give examples of potassium-sparing diuretics, and explain their mechanisms and sites of action, clinical
utility and key adverse effects, and the manners by which agents acting at their sites of action differ from
each other.
Give an example of a carbonic anhydrase inhibitor diuretic, its site of action, and principal uses.
Give examples of osmotic diuretics, explain what this means and describe potential adverse effects.
Give examples of aquaretics, and explain their mechanism and site of action, key uses and adverse
effects.
CPR II- PHAR- LECT- Pulmonary Hypertension (Wolff)
1. Describe how bone morphogenic protein receptor type II and appetite suppressants such as fenfluramine
have been associated with pulmonary hypertension etiology.
2. Describe the purpose of vasoreactivity testing in pulmonary hypertension
3. Compare the routes of administration and the associated adverse effects of prostacyclin analogs used to
treat pulmonary arterial hypertension.
4. Compare endothelin-1 receptor antagonists used to treat pulmonary hypertension with respect to
receptor selectivity, receptor binding reversibility, adverse effects associated with their use, and the
potential for significant drug interactions.
5. List phosphodiesterase type 5 inhibitors and a guanylate cyclase sensitizer used to treat pulmonary
arterial hypertension, observed desired and adverse effects, and differences between them.
6. Explain why combination therapy is often used when treating pulmonary hypertension.
CPR II- PHAR- LECT- Drugs for Hypertension (Wolff)
1. Review the classification of hypertension, its types, and consequences.
2. Recognize that lifestyle modifications should be implemented to the extent possible before starting the
patient on antihypertensive medications that typically must be taken for the remainder of their life.
3. Demonstrate an overall appreciation of the potential sites in the body that can be targeted in some
manner to lower blood pressure.
4. List current first-line drug classes for treating hypertension.
5. Understand the site and general mechanism of action of diuretics used to lower blood pressure, and
circumstances that influence diuretic choice.
6. Extend earlier understanding of calcium channel blockers to now include rationale for their utilization as
antihypertensive agents.
7. Understand the rationale, sites and mechanisms of action of the various agents that lower blood
pressure by suppressing the renin-angiotensin-aldosterone system, and, for each class, their
characteristic adverse effects, contraindications, and notable drug interactions.
8. Discuss the use of agents inhibiting the renin-angiotensin system in patients with renovascular
hypertension.
9. Understand the sites and mechanisms of action of the various sympatholytic agents used to lower blood
pressure, and, for each, their characteristic adverse effects, contraindications, and notable drug
interactions.
10. Understand the sites and mechanisms of action of direct-acting vasodilators used to lower blood
pressure, and, for each, their characteristic adverse effects, contraindications, and notable drug
interactions.
11. Recognize the impact of co-morbid conditions and patients in special populations on drug choice.
12. Recognize the drugs used to treat the hypertensive disorders of pregnancy.
CPR II- CLMD- DSA- ECG Module + Competency Assessment (Johnston)
1. Interpret ECG’s and or rhythm strips that include the following examples:
 Normal
 Premature atrial contractions (PAC’s)
 Atrial fibrillation
 Atrial flutter
 Supraventricular Tachycardia
 Multifocal Atrial Tachycardia
 Junctional Rhythm
 Premature Ventricular Contractions
 Ventricular Tachycardia
 Ventricular Fibrillation
 AV Blocks (1st, 2nd, 3rd degree)
 Right Bundle Branch Block
 Left Bundle Branch Block
 Hemiblocks
 Hypertrophy (Ventricular)
 Myocardial Infarction
 Pericarditis
 Hyperkalemia
 Hypokalemia
CPR II- CLMD- DSA/CIS- Dyspnea on exertion/Cough/SOB (Hubbard)
DSA titles include: Obstructive and Restrictive Lung Disease, Pulmonary HTN/OSA, Pleural and Mediastinal
Disease, Approach to Dyspnea, Approach to Cough, Uncommon causes of Hypoxia, Cancers of the
Respiratory System, Acute Respiratory Distress Syndrome, Venous Thromboembolism
At the conclusion of this module, the student will
1. Outline major cardiac, pulmonary, renal, and other causes of dyspnea on exertion.
2. Utilize history and physical findings to differentiate between cardiac, pulmonary, renal, and other causes of
resting or exertional dyspnea and cough.
3. Describe the MRC Dyspnea Scale, and apply it to clinical scenarios to assist in treatment decisions.
4. Plan a directed evaluation of a patient with dyspnea on exertion, dyspnea, or cough to determine the
diagnosis and severity of the disorder.
5. Describe the 6-minute walk test and its utility in the diagnosis and management of patients with dyspnea
and dyspnea on exertion.
6. Describe the GOLD criteria, and apply it to clinical scenarios to assist in management of patients with
COPD.
7. Apply the current asthma guidelines in management of patients with this disorder.
8. Create a management plan for patients with dyspnea on exertion, dyspnea, and cough from the common
cardiac, pulmonary, renal, and other causes. Where possible, outline contributions from other
professionals (physician and non-physician) and their roles in the management plan.
CPR II- CLMD- DSA/CIS- Cough and Fever (Hubbard)
Upon completion of this section, the student will
1. Identify patients at risk for the development of pneumonia.
2. Describe patients at risk for developing active tuberculosis, or harboring latent tuberculosis.
3. Recognize common signs and symptoms of pneumonia and tuberculosis.
4. Develop a differential diagnosis of pulmonary infections etiologies, and a plan to evaluate them.
5. Describe preventative strategies for populations vulnerable to lower pulmonary infections, and the utility of
screening measures for populations at risk.
6. Outline a plan of treatment for patients with community-acquired pneumonia, healthcare-associated
pneumonia, and tuberculosis.
CPR II- CLMD- DSA/Module/CIS- Chest Pain (Johnston)
1. Develop a differential diagnosis for chest pain
2. Recognize potentially lethal causes of chest pain, including the salient features of each differential
diagnosis
3. Compare and contrast stable and Unstable Angina (UA)
4. Utilize appropriate laboratory tests and imaging studies to best support the correct diagnosis
5. Discuss treatments for chest pain, including stable and unstable angina
CPR II- CLMD- DSA/CIS- Dyspnea and Cough (Tyler)
At the end of this session, the student will be able to…
1. Investigate common differential considerations for a patient presenting with cough and dyspnea within the
realm of cardiac, pulmonary, and renal disorders.
2. Discuss the general approach in a patient presenting with cough and dyspnea due to the following:
a. Granulomatosis with polyangiitis
b. Churg-Strauss
c. Sarcoidosis
d. Hypersensitivity pneumonia
e. Cryptogenic organizing pneumonia
f. Idiopathic pulmonary fibrosis
3. Explore associations with the diagnoses as mentioned above by noting the typical clinical manifestations,
diagnostic implications, epidemiology, and general pathophysiologic processes of each disease.
CPR II- CLMD- DSA/CIS- Hypoxia (Hubbard)
DSA titles include: Obstructive and Restrictive Lung Disease, Pulmonary HTN/OSA, Pleural and Mediastinal
Disease, Approach to Dyspnea, Approach to Cough, Uncommon causes of Hypoxia, Cancers of the
Respiratory System, Acute Respiratory Distress Syndrome, Venous Thromboembolism
At the conclusion of this module, the student will
1. Outline major cardiac, pulmonary, renal, and other causes of hypoxia.
2. Utilize history and physical findings to differentiate between cardiac, pulmonary, renal, and other causes of
hypoxia.
3. Plan a directed evaluation of a patient with hypoxia to determine the diagnosis and severity of the disorder.
4. Describe the 6-minute walk test, and its utility in the diagnosis and management of patients with hypoxia.
5. Apply the current asthma guidelines in management of patients with this disorder.
6. Create a management plan for patients with hypoxia from the common cardiac, pulmonary, renal, and
other causes. Where possible, outline contributions from other professionals (physician and non-physician)
and their roles in the management plan.
CPR II- CLMD- DSA/CIS- Chest pain/angina/discomfort (Khalid)
DSA titles include: Shock, ACS (NSTEMI) and STEMI
1.
2.
3.
4.
Understand the clinical presentation, diagnosis and treatment of Acute coronary syndrome (NSTEMI).
Understand the clinical presentation, diagnosis and treatment of STEMI.
Review the complications of STEMI.
Understand the different types of shock with focus on Cardiogenic shock
CPR II- CLMD- DSA/CIS- Dyspnea (Johnston)
1.
2.
3.
4.
5.
Explain the definition of Heart Failure (HF) and recognize the different etiologies associated with HF.
Identify disorders that can mimic HF (Differential Diagnosis).
Recognize the risk factors associated with HF.
Explain the common symptoms and signs associated with HF.
Compare and contrast the differences between the American College of Cardiology (ACC) and American
Heart Association (AHA) STAGES of HF and the New York Heart Association (NYHA)
function/classification of HF.
6. Recognize the different types of HF and identify precipitating causes of HF.
7. Utilize appropriate tests (lab, imaging) to support diagnosis of HF.
8. Explain both non-pharmacologic and pharmacologic treatment of HF.
CPR II- CLMD- DSA/CIS- Approach to Lightheadedness, Dizziness, and Syncope (Selby)
1. Develop, work through, and narrow a differential diagnosis for patients presenting with lightheadedness,
dizziness, and/or syncope.
2. Identify and discuss relevant historical and physical exam findings that will aid in evaluating patients
presenting with lightheadedness, dizziness, and/or syncope.
3. Recommend and interpret common diagnostic tests that will aid in evaluating patients presenting with
lightheadedness, dizziness, and/or syncope.
4. Discuss the common risk factors, causes, clinical presentation, diagnosis, and treatment of the following
medical conditions:
-Cardiac syncope including hypertrophic cardiomyopathy (HCM)
-Reflex syncope
-Orthostatic syncope
-Pulmonary Embolism
-Diabetes insipidus
CPR II- CLMD- DSA/CIS- Palpitations (Johnston)
1.
2.
3.
4.
5.
6.
Maintain awareness of definitions of palpitations
Apply focused questions relevant to the chief complaint
Interpret arrhythmias on ECG’s and rhythm strips
Recognize different etiologies of palpitations
Apply appropriate tests to evaluate palpitations
Utilize appropriate treatment (pharmacologic/electrical) when indicated
CPR II- CLMD- DSA/CIS- Approach to Fatigue and General weakness (Selby)
1. Develop, work through, and narrow a differential diagnosis for patients presenting with fatigue and/or
generalized weakness.
2. Identify and discuss relevant historical and physical exam findings that will aid in evaluating patients
presenting with fatigue and/or generalized weakness.
3. Recommend and interpret common diagnostic tests that will aid in evaluating patients presenting with
fatigue and/or generalized weakness.
4. Discuss the common risk factors, causes, clinical presentation, diagnosis, and treatment of the following
medical conditions:
Hyponatremia
Hyperkalemia
Obstructive sleep apnea
Heart failure
CPR II- CLMD- DSA/CIS- Fever (Tyler)
1. Define fever as it relates to basic physiology, host defense mechanisms, and expected ranges.
2. Describe hyperthermia and its distinction from fever while relating common entities that are associated with
its occurrence.
3. Discuss the etiology of fever relating common categories in consideration of differential causes and their
associated prevalence.
4. Explore characteristics of common, and less common, causes of fever and hyperthermia.
5. Identify alarm symptoms attributed with the occurrence of fever in relation to clinical manifestations and
differential diagnoses that would be associated with these alarm symptoms.
6. Delineate important history-taking considerations in a patient presenting with fever relating the quality, time
course, and associated symptoms necessary to formulate an accurate diagnosis.
7. Given a patient presenting with fever, apply typical clinical manifestations, epidemiology, and diagnostic
considerations for the following:
a. Endocarditis
b. Heart Failure
c. Myocarditis
d. Primary Vasculitis Syndromes
i. Granulomatosis with polyangiitis
ii. Microscopic polyangiitis
iii. Polyarteritis nodosa
e. Pulmonary embolism
f. Tick-borne illness
CPR II- CLMD- DSA/CIS- Edema (Kirila)
1. Determine symptoms that the patient presents with/complains of/admits to on review of systems, that
correlate with edema or an underlying cause
2. Distinguish edema from tissue swelling
3. Distinguish among Lymphedema, Lipedema, and other types of edema and potential combinations
4. Differentiate location and distribution of edema based on patient’s history in addition to physical findings on
exam
5. Generate a differential diagnosis for edema focusing on the potentially life-threatening and the most
common
6. Determine extrinsic factors that are contributing to edema
7. Prioritize diagnostic testing to evaluate edema
8. Revise differential diagnosis of edema based on changes in patient presentation and/or results of
diagnostic testing
______________________________________________________________________________
Exam 3
LEARNING OBJECTIVES
CPR II- CLMD- DSA/CIS- Approach to Oliguria and Proteinuria (Selby)
1. Develop, work through, and narrow a differential diagnosis for patients presenting with oliguria and/or
proteinuria.
2. Identify and discuss relevant historical and physical exam findings that will aid in evaluating patients
presenting with oliguria and/or proteinuria.
3. Recommend and interpret common diagnostic tests that will aid in evaluating patients presenting with
oliguria and/or proteinuria.
4. Discuss the common risk factors, causes, clinical presentation, diagnosis, and treatment of the following
medical conditions:
-Chronic kidney disease
-Acute kidney injury
-Nephrotic syndrome
-Nephritic syndrome
CPR II- CLMD- DSA/CIS- Approach to Acid base disorders (Selby)
1.
2.
3.
4.
5.
6.
Discuss and identify basic acid-base physiology
Be able to accurately interpret an arterial blood gas (ABG) via a systematic
process
Discuss the normal values on an ABG for pH, HCO3-, and PCO2
Discuss meaning and be able to calculate anion gap and osmolar gap when appropriate
Discuss how acid-base disturbances are compensated from clinical standpoint
Apply appropriate compensatory formulas for any given acid-base disturbance
– i.e. determine if simple or mixed acid-base disorder is present
7. Discuss how to use delta-delta gap in patients with HAGMA to assess for coexistent NAGMA or metabolic
alkalosis
8. Discuss clinical presentation and common causes of high anion gap metabolic acidosis
– Also common causes of high osmolar gap metabolic acidosis
9. Discuss the effect of acidosis and alkalosis on serum potassium levels
10. Discuss meaning and be able to calculate urine anion gap when appropriate
11. Discuss common causes of normal anion gap metabolic acidosis (NAGMA)
12. Discuss clinical presentation and pathophysiology of renal tubular acidosis type 1, 2, and 4 and be able to
differentiate between them
13. Discuss clinical presentation and common causes of metabolic alkalosis
14. Discuss clinical presentation and common causes of respiratory acidosis and respiratory alkalosis
CPR II- CLMD- DSA/CIS- Hematuria/Dysuria/Nocturia/Urinary Incontinence (Tyler)
Dysuria/Nocturia/Urinary Incontinence
1. Define nocturia, dysuria, and urinary incontinence along with the associated pathophysiologic processes
commonly attributed to each.
2. Differentiate nocturia and dysuria in relation to their defining characteristics and differential diagnoses.
3. Explore common causes of nocturia, dysuria, and urinary incontinence that would contribute to a
reasonable differential diagnosis list and demonstrates overlap of these symptoms.
4. Given a patient with nocturia, dysuria, and urinary incontinence identify important historical elements
needed in investigating an accurate primary diagnosis.
5. Explain the most common differential considerations for nocturia relating epidemiology, expected history
associations, clinical manifestations, and general diagnostic considerations for the following:
a. Benign Prostatic Hypertrophy
b. Congestive Heart Failure (volume redistribution)
c. Cystitis
d. Urinary Incontinence
e. Diabetes Mellitus
f. Diuretic Use
g. Urinary Stone Disease
h. Acute bacterial prostatitis
Hematuria
At the end of this session, the student will be able to…
6. Distinguish between macroscopic (gross) hematuria and microscopic hematuria relating specific laboratory
parameters in defining each.
7. Identify glomerular and non-glomerular causes of hematuria.
8. Relate the findings of hematuria to the following illnesses, or diseases, as it relates to the association of
hematuria, clinical manifestations, basic pathophysiology, and diagnosis:
a. Renal cell carcinoma
b. IgA nephropathy
c. Medullary sponge kidney
CPR II- CLMD- DSA/CIS- Cardiac, Pulmonary, and Renal Pediatric Pearls 1 & 2 (Newman)
1.
2.
3.
4.
5.
List the 3 components of the pediatric assessment triangle
List the 3 components of cardiopulmonary arrest in children
Identify the common clinical signs and symptoms seen in patients with asthma
List common triggers for asthmatics
Describe the different classifications of asthma
a. Intermittent
b. Mild persistent
c. Moderate persistent
d. Severe persistent
6. Differentiate between asthma and other causes of wheeze/cough
7. Describe the etiology/clinical findings present in the following conditions
a. Croup
b. Epiglottitis
c. Bronchiolitis
d. Pneumonia
e. Asthma
f. Anaphylaxis (and the 3 most important agents used in treatment)
g. Foreign body aspiration
8. Differentiate between well-controlled and poorly-controlled asthma
9. Identify those patients needing maintenance therapy for asthma
10. Speak knowledgably about Asthma Action Plans
11. List the clinical features used in assessing a patient’s degree of respiratory distress
12. Identify barriers to good asthma control and offer suggestions on how these barriers might be
mitigated/eliminated
13. List the mainstays of treating a patient suffering an acute asthma exacerbation
a. Oxygen
b. Albuterol
c. Steroids
14. Diagnose acute post-streptococcal glomerulonephritis
15. Name the prognostic indicator of long-term renal damage in children with Henoch-Schonlein Purpura
16. List the signs and symptoms of urinary tract infections (UTI’s) in children
17. Name the acceptable methods of urine collection when sending a urine sample for culture and sensitivity
18. Describe the criteria for the diagnosis of a UTI in a child
19. Name the most common urinary pathogens in children
20. Describe the recommendations for imaging in children with UTI’s
21. List the most common causes of obstructive uropathy in children
22. Explain the significance of the different grades of vesicoureteral reflux in pediatric patients
23. Identify appropriate first-line antibiotic choices for the empiric treatment in a child with a UTI/pyelonephritis
24. List the indications for referral of a pediatric patient with a UTI to a specialist.
25. Develop a differential diagnosis for a newborn with tachypnea.
26. Describe the newborn pulse oximetry screening test used to detect critical congenital heart disease prior to
discharge from the nursery
27. Identify each of the following critical congenital heart defects as cyanotic or non-cyanotic
a. Coarctation of the aorta
b. Transposition of the great arteries
c. Hypoplastic left heart
d. Tetralogy of fallot
e. Double outlet R ventricle
f. Ebstein’s anomaly
g. Pulmonary atresia
h. Single ventricle
i. Total anomalous pulmonary return
j. Tricuspid atresia
k. Truncus arteriosis
28. List the criteria for referring a patient with a heart murmur to a cardiologist
29. Locate electronically and be able to use the following:
a. Clinical Practice Guideline for Screening and Management of High Blood Pressure in Children and
Adolescents. Pediatrics. 2017;140(3)
b. Fourth Report (January 2004)
30. Describe how an inappropriately sized blood pressure cuff effects the blood pressure reading
CPR II- CLMD- CIS- Comprehensive Clinical Review (Tyler/Selby/Johnston/Hubbard)
1. See the above presentation LO’s by these physicians for the LOs for this review presentation.