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Thieme Test Prep for the USMLE®

Learning Pharmacology
through Clinical Cases
Mario Babbini
Sandeep Bansal

I Thieme

,Learning Pharmacology through Clinical Cases

Mario Babbini, MD, PhD
Professor
Department of Pharmacology
Ross University School of Medicine
Portsmouth, Dominica, West Indies

Sandeep Bansal, MBBS, MD
Research Associate Professor
Course Director of Pharmacology
University of Illinois College of Medicine
Urbana-Champaign, Illinois, USA

Thieme
New York • Stuttgart • Delhi • Rio de Janeiro

,Acquisition Editor: Delia K. DeTurris Important note: Medicine is an ever-changing science
Managing Editor: Kenneth Schubach undergoing continual development. Research and clini-
Director, Editorial Services: Mary Jo Casey cal experience are continually expanding our knowledge,
Production Editor: Kenny Chumbley in particular our knowledge of proper treatment and
In-House Production Editor: Naamah Schwartz drug therapy. Insofar as this book mentions any dosage
International Rights Director: Heike Schwabenthan or application, readers may rest assured that the authors,
International Production Director: Andreas Schabert editors, and publishers have made every effort to ensure
Editorial Director: Sue Hodgson that such references are in accordance with the state of
International Marketing Director: Fiona Henderson knowledge at the time of production of the book.
International Sales Director: Louisa Turrell Nevertheless, this does not involve, imply, or express
Director of Sales, North America: Mike Roseman any guarantee or responsibility on the part of the publish-
Senior Vice President and Chief Operating Officer: Sarah ers in respect to any dosage instructions and forms of ap-
Vanderbilt plications stated in the book. Every user is requested to
President: Brian D. Scanlan examine carefully the manufacturers’ leaﬂets accompa-
nying each drug and to check, if necessary in consultation
Cover image: AdobeStock, ©pikselstock with a physician or specialist, whether the dosage sched-
ules mentioned therein or the contraindications stated by
the manufacturers differ from the statements made in the
present book. Such examination is particularly important
with drugs that are either rarely used or have been newly
released on the market. Every dosage schedule or every
Library of Congress Cataloging-in-Publication Data form of application used is entirely at the user’s own risk
Names: Babbini, Mario, author. | Bansal, Sandeep, author. and responsibility. The authors and publishers request ev-
Title: Thieme test prep for the USMLEª : learning pharmacology ery user to report to the publishers any discrepancies or
through clinical cases / Mario Babbini, Sandeep Bansal. inaccuracies noticed. If errors in this work are found after
Other titles: Learning pharmacology through clinical cases publication, errata will be posted at www.thieme.com on
Description: New York : Thieme, [2018]
the product description page.
Identifiers: LCCN 2017047835| ISBN 9781626234239 (softcover)
Some of the product names, patents, and registered de-
| ISBN 9781626234246 (eISBN)
Subjects: | MESH: Pharmacological Phenomena | Examination signs referred to in this book are in fact registered trade-
Questions | Case Reports marks or proprietary names even though speciﬁc refer-
Classification: LCC RM301.13 | NLM QV 18.2 | DDC 615.1076-- ence to this fact is not always made in the text. Therefore,
dc23 the appearance of a name without designation as propri-
LC record available at https://lccn.loc.gov/2017047835 etary is not to be construed as a representation by the
publisher that it is in the public domain.

© 2018 Thieme Medical Publishers, Inc.
Thieme Publishers New York
333 Seventh Avenue, New York, NY 10001 USA
+1 800 782 3488,

Thieme Publishers Stuttgart
Rüdigerstrasse 14, 70469 Stuttgart, Germany
+49 [0]711 8931 421,

Thieme Publishers Delhi
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Thieme Publishers Rio de Janeiro, Thieme Publicações Ltda.
Edifício Rodolpho de Paoli, 25º̵ andar
Av. Nilo Peçanha, 50 – Sala 2508
Rio de Janeiro 20020-906, Brasil
+55 21 3172 2297
This book, including all parts thereof, is legally protected
Cover design: Thieme Publishing Group by copyright. Any use, exploitation, or commercializa-
Typesetting by Prairie Papers tion outside the narrow limits set by copyright legisla-
tion without the publisher’s consent is illegal and liable
Printed in India by Replika Press Pvt Ltd.
to prosecution. This applies in particular to photostat
ISBN 978-1-62623-423-9
reproduction, copying, mimeographing or duplication of
Also available as an e-book: any kind, translating, preparation of microﬁlms, and elec-
eISBN 978-1-62623-424-6 tronic data processing and storage.

,

Table of Contents
Preface................................................................................................................................................. vii

1 Acromegaly...........................................................................................................................................1

2 Acute Lymphoblastic Leukemia..................................................................................................... 9

3 Asthma................................................................................................................................. .............. 17

4 Atrial Fibrillation.............................................................................................................................. 25

5 Bipolar Disorder............................................................................................................................... 37

6 Breast Cancer..................................................................................................................................... 43

7 Cardiogenic Shock............................................................................................................................ 51

8 Crohn’s Disease................................................................................................................................. 59

9 Chronic Kidney Disease.................................................................................................................. 69

10 Chronic Obstructive Pulmonary Disease................................................................................... 79

11 Drug Abuse......................................................................................................................................... 87

12 Epilepsy............................................................................................................................................... 95

13 Essential Hypertension................................................................................................................. 105

14 General Anesthesia........................................................................................................................ 115

15 Glaucoma.......................................................................................................................................... 125

16 Gout.................................................................................................................................................... 133

17 Graves’ Disease................................................................................................................................ 143

18 Growth Retardation and Hypogonadism................................................................................. 153

19 Heart Failure.................................................................................................................................... 163

20 Hematopoietic Cell Transplantation......................................................................................... 175

21 Hodgkin’s Lymphoma................................................................................................................... 183

22 Hormonal Contraception............................................................................................................. 191

23 Human Immunodeficiency Virus Infection............................................................................ 201

24 Infective Endocarditis................................................................................................................... 211

25 Iron Deficiency Anemia................................................................................................................ 219

26 Liver Cirrhosis ................................................................................................................................ 227

27 Lung Cancer..................................................................................................................................... 237
v

,

28 Megaloblastic Anemia................................................................................................................... 245

29 Migraine............................................................................................................................................ 251

30 Myasthenia Gravis.......................................................................................................................... 259

31 Myocardial Infarction................................................................................................................... 269

32 Parkinson’s Disease....................................................................................................................... 281

33 Peptic Ulcer Disease....................................................................................................................... 291

34 Perimenopause and Osteoporosis............................................................................................. 299

35 Pheochromocytoma...................................................................................................................... 309

36 Pneumonia....................................................................................................................................... 319

37 Polycystic Ovarian Syndrome..................................................................................................... 327

38 Primary Adrenal Deficiency (Addison’s Disease)................................................................... 337

39 Prostate Cancer............................................................................................................................... 347

40 Psoriasis............................................................................................................................................ 355

41 Pulmonary Embolism................................................................................................................... 363

42 Rheumatoid Arthritis.................................................................................................................... 371

43 Schizophrenia.................................................................................................................................. 383

44 Solid Organ Transplantation....................................................................................................... 393

45 Stroke................................................................................................................................................. 401

46 Systemic Lupus Erythematosus.................................................................................................. 411

47 Torsade de Pointes......................................................................................................................... 419

48 Type 1 Diabetes Mellitus............................................................................................................... 425

49 Type 2 Diabetes Mellitus............................................................................................................... 435

50 Urinary Tract Infection................................................................................................................. 445

Index.......................................................................................................................................................... 451

vi

,

Preface
This book is a collection of clinical cases student can perform the action, then he or
designed to promote the learning of she should be able to answer the question
pharmacology by using case studies. Working correctly. The explanation includes both the
with cases is the best way to involve students reasons why a given answer is correct and
in the learning process because: why the distractors are wrong.
▶▶Every case shows a real situation, very Many questions are related to the highest
close to those seen in every day practice. levels of Bloom’s taxonomy (e.g., interpretation
▶▶Every case can elicit several problems of data and the solution of problems) rather
that must be solved. In other words, it is than being simple recall questions.
a problem-based learning process. The rationale for this book is related to the
current trend in medical education. Today,
▶▶Every case not only requires the
it is more and more evident that the mere
knowledge of several disciplines but
memorization of information provided by
also the application of this knowledge to
books is insufficient for meaningful learning.
specific clinical situations.
In other words “knowledge that cannot be used
The format of each case is the following: is useless.” It is the application of knowledge
▶▶Each case provides relevant data that counts. A vast array of medical problems
(presenting complaint and its history, is available in the literature today, but there
past medical history, family history, are few books related to the pharmacology of
drug history, physical examination, lab clinical cases. The driving idea of this book is
findings, diagnosis, pharmacotherapy) to link the clinical case to the application of
to identify the main features of the basic knowledge, primarily in physiology,
case, along with a set of statements that pathology, and microbiology, as well as to
describe the case follow-up. explain the reasons for using specific drugs
▶▶Each case has a series of multiple-choice in real clinical problems, with the goal of
questions. promoting critical thinking skills.
–– Some questions address the The main audience of the book is medical
knowledge of basic disciplines school students. However, the book could also
(mainly, physiology, pathology, and be useful for students in other medical fields,
microbiology) the student needs to including pharmacists, physician assistants,
assess the case. and nurses.
–– Other questions are related Pharmacology and clinical medicine
to the pharmacotherapy of are fast-evolving disciplines. The authors
the disease. These questions have referred to reliable sources in order
encompass the pharmacokinetics, to provide information in accordance with
mechanism of action, adverse currently accepted standards. However, the
authors are aware that in several instances,
effects, contraindications, and the
the pharmacotherapy of disease is still
interactions of all drugs used for the
controversial. We have tried, as much as
pharmacotherapy of the case.
possible, to avoid questions addressing
The questions are designed to prepare controversial issues.
students for the United States Medical This book is not intended to be a substitute
Licensing Examinion (USMLE) Step 1 and Step for pharmacology textbooks. Students are
2. Four to six choices are provided for each strongly advised to consult their textbooks of
question, but for all questions there is only pharmacology for more in-depth coverage of
one best answer. the subject matter.
Each question has a learning objective,
the correct answer, and an explanation. Mario Babbini, MD, PhD
The learning objective is a brief behavioral Sandeep Bansal, MBBS, MD
statement written using an action verb. If a

vii

, Case 1 Acromegaly

G.A., a 40-year-old man, complained to his physician of difficulty seeing objects in the
periphery, excessive sweating, and gradual enlargement of his hands and feet. His shoe size
had increased by two sizes in the last 2 years, and his wedding ring also had to be resized. He
had recently started snoring, and he would waken in the morning with a headache. His facial
skin had also become oilier.
Physical examination showed a man with a slightly protruding lower jaw. His vital signs
were as follows: blood pressure 130/88 mm Hg, pulse 80 bpm, respirations 22/min.
The patient’s skin was thickened, and excessive perspiration was noted on his hands and
feet. Visual field examination revealed temporal hemianopia. Dental examination showed
increased dental spacing.
Pertinent laboratory results on admission were as follows:

Blood hematology
▶▶ Blood glucose, fasting: 130 mg/dL (normal, 70–110)
▶▶ Growth hormone (GH) suppression test: GH 20 ng/mL (normal, < 2)
▶▶ Insulin-like growth factor 1 (IGF-1) 890 ng/mL (normal, 138–410)
▶▶ Prolactin: 50 ng/mL (normal, < 20)
▶▶ Free testosterone: 2.5 pg/mL (normal for age 40, 6.8–21.5)
▶▶ Luteinizing hormone (LH): 2.2 U/L (normal 6–23)
▶▶ Follicle-stimulating hormone (FSH): 1.3 U/L (normal 4–25)

MRI scan of the head
Pituitary macroadenoma encroaching on the optic chiasma.

Colonoscopy
Normal, with no evidence of tumor growth.

The diagnosis was acromegaly due to GH-secreting adenoma. G.A. was scheduled for
transsphenoidal resection of the adenoma.
Six weeks postsurgery, G.A. felt much better, and his peripheral vision had also improved.
However, a lab exam showed that his GH and IGF-1 levels were still high due to the extrasellar
invasion of the adenoma. He was thus started on therapy with a somatostatin analogue and
a dopamine agonist.

,1 Acromegaly

Questions 5. Which of the following signal trans-
duction pathways best describes the
1. G.A. was diagnosed with a growth hor- molecular mechanism of octreotide action
mone–secreting adenoma. Which of the fol- to suppress somatotroph function?
lowing types of cells constitute a major part A. S
timulation of adenylyl cyclase
of this adenoma? B. C
losure of potassium channels
A. B
asophilic cells C. A
ctivation of mitogen-activated protein
B. A
cidophilic cells kinase
C. C
hromophobe cells D. I nhibition of adenylyl cyclase
D. N
ull cells E. O
pening of calcium channels

2. G.A. was found to have increased fast- 6. G.A. was prescribed a dopamine ago-
ing glucose levels. Which of the following nist. Which of the following drugs was
was most likely the cause of this finding? most likely administered?
A. S
uppression of glucagon secretion A. B
romocriptine
B. I ncreased glycogenesis B. C
abergoline
C. A
ntagonism of insulin action C. O
lanzapine
D. D
ecreased excretion of glucose in urine D. S
umatriptan
E. I ncreased cortisol levels E. B
uspirone

3. G.A. was found to have decreased 7. Nausea is a common adverse effect of
blood levels of testosterone. Which of the dopamine agonists. Which of the following
following was most likely the cause of this brain structures is most likely the primary
decrease? site of the action that mediates this adverse
effect?
A. G
H-induced inhibition of Leydig cell
function A. F
rontal cortex
B. P
rolactin-induced increase of B. A
mygdala
gonadotropin release C. A
rea postrema
C. I ncreased somatostatin release D. P
araventricular nucleus
D. G
H-induced impairment of Sertoli cell E. V
estibular nuclei
function
8. Which of the following could most
4. G.A. felt well after surgical resection likely develop as an adverse effect of
of his adenoma. However, because of the octreotide early in the course of treatment
residual tumor, his GH and IGF-1 levels of acromegaly?
were still high. He started a therapy with
A. K
yphosis
a somatostatin analogue. Which of the fol-
lowing drugs was most likely prescribed? B. C
holelithiasis
C. H
yperprolactinemia
A. O
ctreotide
D. E
sophageal varices
B. L ansoprazole
E. A
bdominal pain
C. S
omatropin
D. S
unitinib
E. L euprolide

2

, Answers and Explanations

9. G.A. did not respond adequately to ▶▶ Thyrotrophs (thyroid-stimulating
the octreotide and cabergoline therapy. hormone [TSH]-secreting cells):
He was subsequently prescribed pegvi- basophilic
somant. Which of the following phrases A See correct answer explanation.
best describes the mechanism of action of C Chromophobe cells are cells that
pegvisomant? stain poorly with histology dyes and look
A. I nhibition of growth hormone release pale under the microscope.
D Null cells are lymphocytes that lack
B. B
lockade of somatostatin receptors
characteristic surface markers that are
C. A
ctivation of insulin-like growth factor found on B and T lymphocytes. They are
1 receptors not the hormone-secreting cells of the
D. A
ctivation of growth hormone receptor anterior pituitary.
E. B
lockade of growth hormone receptors
▶▶ Learning objective: Describe the effects of
growth hormone on glucose metabolism.
10. Which of the following signs and
symptoms of acromegaly are unlikely to
resolve with drugs that reduce growth hor- 2. Answer: C
mone release or its action? Growth hormone antagonizes the function
of insulin, resulting in decreased periph-
A. S
oft tissue changes
eral utilization of glucose and increased
B. P
rognathism
gluconeogenesis. Normally, GH release
C. H
yperglycemia peaks during sleep, and, in concert with
D. O
iliness of skin other hormones, such as cortisol, helps to
E. H
yperhidrosis maintain glucose levels within the nor-
mal range to provide a continuous supply
of glucose to the vital organs. However, in
cases of GH-secreting adenoma, GH lev-
Answers and els are constantly high, which results in
increased blood glucose levels that could
Explanations lead to diabetes mellitus. G.A.’s fasting glu-
cose levels were above the normal range of
▶▶ Learning objective: Describe the histology of 70 to 110 mg/dL, indicating the antagoniz-
the anterior pituitary gland. ing effects of GH on insulin activity.
A Glucagon secretion is not suppressed
1. Answer: B by growth hormone. Moreover, suppres-
The cells of the anterior pituitary gland sion of glucagon secretion would not cause
are classified as acidophils or basophils, increased blood glucose levels.
depending on their affinity for acidic or B Glycogenesis is decreased, not
basic histology dyes, respectively. Acido- increased, due to antagonism of insulin
philic cells look red and basophilic cells actions.
look blue under the microscope. The five D Glucose is normally filtered by the
types of anterior pituitary cells can be sub- glomerulus and is completely reabsorbed
divided as follows: by the renal tubules. When blood glucose is
> 200 mg/dL, it exceeds the renal reabsorp-
▶▶ Somatotrophs (GH-secreting cells):
tion capacity, and glucose starts appearing
acidophilic
in the urine. Decreased renal excretion of
▶▶ Lactotrophs (prolactin-secreting cells):
glucose cannot occur in the presence of
acidophilic
high blood glucose.
▶▶ Corticotrophs (adrenocorticotropic
E Increased cortisol levels could cause
hormone [ACTH]-secreting cells):
hyperglycemia, but cortisol levels are not
basophilic
increased by GH-secreting adenoma. Actu-
▶▶ Gonadotrophs (FSH- and LH-secreting
ally, the anterior pituitary adenoma could
cells): basophilic

3

, 1 Acromegaly

compress the surrounding corticotroph analogues are used for the treatment of acro-
cells and impair corticotropin release to megaly. Octreotide, and the long-acting agent
decrease cortisol synthesis in the adrenal lanreotide, are commonly used somatostatin
cortex. analogues. These are small peptide drugs that
are administered by subcutaneous or intra-
▶▶ Learning objective: Describe the likely causes muscular injection. Octreotide elimination
of decreased gonadal function in a patient half-life is approximately 80 minutes, com-
with a pituitary mass. pared to 1 to 3 minutes for somatostatin, thus
making it a more suitable agent for thera-
3. Answer: A peutic indications. It is usually administered
A pituitary tumor mass, especially a mac- subcutaneously three times a day, but its long-
roadenoma (functional or nonfunctional) acting, slow-release form can be administered
can press against other cell types in the intramuscularly every 4 weeks. Lanreotide is
anterior pituitary to impact their func- a longer-acting somatostatin analogue. The
tion. In case of a nonfunctional pituitary sustained-release formulation of lanreotide is
adenoma, usually the first cells impacted administered intramuscularly every 10 to 14
are GH-secreting cells, and then in sequen- days, and the extended-release formulation is
tial order, gonadotrophs, thyrotrophs, and administered every 4 weeks. The goal of the
corticotrophs are impacted. G.A. had a GH- therapy is to reduce the symptoms, reduce GH
secreting macroadenoma that possibly had levels to < 2.5 ng/mL with GH suppression test
caused pressure effects to impair gonado- (normal, < 2 ng/mL), and bring the insulin-like
troph function, resulting in decreased growth factor 1 (IGF-1) levels within the age-
gonadotropin (LH and FSH) secretion. and gender-specific normal limits.
Decreased gonadotropin levels result in Although surgery (transsphenoidal
decreased stimulation of Leydig cells to resection of adenoma) is the first-line treat-
synthesize and release testosterone. ment for most patients with acromegaly, its
B G.A. had hyperprolactinemia. However, effectiveness depends on factors such as (1)
high prolactin levels would inhibit gonado- size of the tumor, (2) the tumor’s invasive-
tropin-releasing hormone (GnRH) from the ness, and (3) the skill of the surgeon. Initial
hypothalamus, which in turn would impair, remission with surgery can be achieved
not increase, gonadotropin release. in about 80% of patients who have micro-
C Somatostatin release is not increased adenoma and about 40 to 60% with mac-
in acromegaly due to GH-secreting ade- roadenoma. Drug therapy is attempted for
noma. Moreover, somatostatin does not patients who do not respond well to surgery
impact Leydig cell function. and for initial responders with recurrence of
D GH does not impact Sertoli cell func- signs and symptoms. In patients with acro-
tion. Moreover, Sertoli cells have to do with megaly with an invasive tumor invading
spermatogenesis, and not with testoster- the cavernous sinus or the nearby optic chi-
one synthesis and release. asma, surgery helps in debulking the tumor
and rapidly relieving the signs and symp-
▶▶ Learning objective: Describe the toms, such as temporal hemianopia, caused
pharmacology of somatostatin analogues. by compression of the tumor mass on the
surrounding structures. However, it is diffi-
4. Answer: A cult to remove the entire invasive adenoma;
Growth hormone release from the somato- thus increased GH levels and signs and
trophs of the anterior pituitary is regulated symptoms of acromegaly can appear soon
by hypothalamic hormones: GH-releasing after initial debulking of tumor. Drug ther-
hormone (GHRH) and somatostatin (SST). apy is used for further management of these
GHRH stimulates and SST inhibits the patients, as was initiated for G.A.
release of GH. B Lansoprazole is a H+/K+ adenosine
Somatostatin has a half-life of 1 to 3 min- triphosphatase (ATPase) (gastric proton
utes, making it unsuitable for long-term treat- pump) inhibitor that is used for the treat-
ment of acromegaly. Therefore, somatostatin ment of acid-peptic disease.
4

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