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Transcript of Pharmacologie testes
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USMLE WORLD STEP 1 PHARMACOLOGY
Question List
Pharmacology Q No: 1 Hepatobiliary system Pharmacology Q No: 42 Cardiology
Pharmacology Q No: 2 Blood vessels Pharmacology Q No: 43 Endocrinology
Pharmacology Q No: 3 Hematology Pharmacology Q No: 44 Hematology
Pharmacology Q No: 4 Head and neck Pharmacology Q No: 45 Dermatology
Pharmacology Q No: 5 Gastrointestinal system Pharmacology Q No: 46 Musculoskeletal
Pharmacology Q No: 6 Neurology Pharmacology Q No: 47 Neurology
Pharmacology Q No: 7 Head and neck Pharmacology Q No: 48 Gastrointestinal system
Pharmacology Q No: 8 Musculoskeletal Pharmacology Q No: 49 Neurology
Pharmacology Q No: 9 Neurology Pharmacology Q No: 50 Neurology
Pharmacology Q No: 10 N euro logy Pharmacology Q No: 51 Gastrointestinal system
Pharmacology Q No: 11 Blood vessels Pharmacology Q No: 52 Neurology
Pharmacology Q No: 12 Musculoskeletal Pharmacology Q No: 53 MusculoskeletalPharmacology Q No: 13 Head and neck Pharmacology Q No: 54 Oncology
Pharmacology Q No: 14 Neurology Pharmacology Q No: 55 Neurology
Pharmacology Q No: 15 Endocrinology Pharmacology Q No: 56 Blood vessels
Pharmacology Q No: 16 Neurology Pharmacology Q No: 57 Neurology
Pharmacology Q No: 17 Neurology Pharmacology Q No: 58 Hematology
Pharmacology Q No: 18 Blood vessels Pharmacology Q No: 59 Cardiology
Pharmacology Q No: 19 Pulmonology Pharmacology Q No: 60 Blood vessels
Pharmacology Q No: 20 Endocrinology Pharmacology Q No: 61 Neurology
Pharmacology Q No: 21 Neurology Pharmacology Q No: 62 Dermatology
Pharmacology Q No: 22 Genitourinary Pharmacology Q No: 63 Neurology
Pharmacology Q No: 23 Hematology Pharmacology Q No: 64 Endocrinology
Pharmacology Q No: 24 Neurology Pharmacology Q No: 65 Neurology
Pharmacology Q No: 25 Neurology Pharmacology Q No: 66 Cardiology
Pharmacology Q No: 26 Genitourinary Pharmacology Q No: 67 Cardiology
Pharmacology Q No: 27 Neurology Pharmacology Q No: 68 Neurology
Pharmacology Q No: 28 Cardiology Pharmacology Q No: 69 Pulmonology
Pharmacology Q No: 29 Neurology Pharmacology Q No: 70 Hematology
Pharmacology Q No: 30 Cardiology Pharmacology Q No: 71 Cardiology
Pharmacology Q No: 31 Cardiology Pharmacology Q No: 72 Renal
Pharmacology Q No: 32 Genitourinary Pharmacology Q No: 73 Neurology
Pharmacology Q No: 33 Neurology Pharmacology Q No: 74 Blood vessels
Pharmacology Q No: 34 Renal Pharmacology Q No: 75 Hematology
Pharmacology Q No: 35 Oncology Pharmacology Q No: 76 Musculoskeletal
Pharmacology Q No: 36 Endocrinology Pharmacology Q No: 77 Neurology
Pharmacology Q No: 37 Hepatobiliary system Pharmacology Q No: 78 Neurology
Pharmacology Q No: 38 Renal Pharmacology Q No: 79 Endocrinology
Pharmacology Q No: 39 Hepatobiliary system Pharmacology Q No: 80 Neurology
Pharmacology Q No: 40 Endocrinology Pharmacology Q No: 81 Pulmonology
Pharmacology Q No: 41 Cardiology Pharmacology Q No: 82 Head and neck
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USMLE WORLD STEP 1 PHARMACOLOGY
Parmacology ! No" #$ Neurology Parmacology ! No" %&' Pulmonology
Parmacology ! No" #( Hematology Parmacology ! No" %&) Blood vessels
Parmacology ! No" #' Pulmonology Parmacology ! No" %&* Cardiology
Parmacology ! No" #) Oncology Parmacology ! No" % Blood vessels
Parmacology ! No" #* Pulmonology Parmacology ! No" %&+ Renal
Parmacology ! No" ## Blood vessels Parmacology ! No" %$, Neurology
Parmacology ! No" #+ Neurology Parmacology ! No" %$% Blood vessels
Parmacology ! No" +, Endocrinology Parmacology ! No" %$& Cardiology
Parmacology ! No" +% Cardiology Parmacology ! No" %$$ Cardiology
Parmacology ! No" +& Neurology Parmacology ! No" %$( Cardiology
Parmacology ! No" +$ Genitourinary Parmacology ! No" %$' Genitourinary
Parmacology ! No" +( Oncology Parmacology ! No" %$) CardiologyParmacology ! No" +' Hepatobiliary system Parmacology ! No" %$* Neurology
Parmacology ! No" +) Musculoskeletal Parmacology ! No" %$# Head and neck
Parmacology ! No" +* Blood vessels Parmacology ! No" %$+ Neurology
Parmacology ! No" +# Neurology Parmacology ! No" %(, Musculoskeletal
Parmacology ! No" ++ Neurology Parmacology ! No" %(% Musculoskeletal
Parmacology ! No" %,, Genito urinary Parmacology ! No" %(& Cardiology
Parmacology ! No" %,% Renal Parmacology ! No" %($ Neurology
Parmacology ! No" %,& Musculoskeletal Parmacology ! No" %(( Hepatobiliary system
Parmacology ! No" %,$ Endocrinology Parmacology ! No" %(' Pulmonology
Parmacology ! No" %,( Neurology Parmacology ! No" %() Neurology
Parmacology ! No" %,' Hepatobiliary system Parmacology ! No" %(* Hematology
Parmacology ! No" %,) Pulmonology Parmacology ! No" %(# Pulmonology
Parmacology ! No" %,* Neurology Parmacology ! No" %(+ Blood vessels
Parmacology ! No" %,# Musculoskeletal Parmacology ! No" %', Endocrinology
Parmacology ! No" %,+ Blood vessels Parmacology ! No" %'% Hematology
Parmacology ! No" %%, Pulmonology Parmacology ! No" %'& Cardiology
Parmacology ! No" %%% Cardiology Parmacology ! No" %'$ Neurology
Parmacology ! No" %%& Blood vessels Parmacology ! No" %'( Neurology
Parmacology ! No" %%$ Neurology Parmacology ! No" %'' Cardiology
Parmacology ! No" %%( Gastrointestinal system Parmacology ! No" %') Endocrinology
Parmacology ! No" %%' Cardiology Parmacology ! No" %'* Endocrinology
Parmacology ! No" %%) Blood vessels Parmacology ! No" %'# Musculoskeletal
Parmacology ! No" %%* Pulmonology Parmacology ! No" %'+ Blood vessels
Parmacology ! No" %%# Neurology Parmacology ! No" %), Hematology
Parmacology ! No" %%+ Pulmonology Parmacology ! No" %)% Head and neck
Parmacology ! No" %&, Musculoskeletal Parmacology ! No" %)& Hepatobiliary system
Parmacology ! No" %&% Gastrointestinal system Parmacology ! No" %)$ Blood vessels
Parmacology ! No" %&& Cardiology Parmacology ! No" %)( Pulmonology
Parmacology ! No" %&$ Musculoskeletal Parmacology ! No" %)' Cardiology
Parmacology ! No" %&( Endocrinology Parmacology ! No" %)) Oncology
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USMLE WORLD STEP 1 PHARMACOLOGY
Parmacology ! No" &'$ Hematology Parmacology ! No" &+& Renal
Parmacology ! No" &'( Pulmonology Parmacology ! No" &+$ Cardiology
Parmacology ! No" &'' Neurology Parmacology ! No" &+( Dermatology
Parmacology ! No" &') Neurology Parmacology ! No" &+' Blood vessels
Parmacology ! No" &'* Head and neck Parmacology ! No" &+) Blood vessels
Parmacology ! No" &'# Cardiology Parmacology ! No" &+* Hepatobiliary system
Parmacology ! No" &'+ Blood vessels Parmacology ! No" &+# Neurology
Parmacology ! No" &), Hematology Parmacology ! No" &++ Renal
Parmacology ! No" &)% Musculoskeletal Parmacology ! No" $,, Cardiology
Parmacology ! No" &)& Neurology Parmacology ! No" $,% Hepatobiliary system
Parmacology ! No" &)$ Pulmonology Parmacology ! No" $,& Blood vessels
Parmacology ! No" &)( Endocrinology Parmacology ! No" $,$ Endocrinology
Parmacology ! No" &)' Blood vessels Parmacology ! No" $,( HematologyParmacology ! No" &)) Endocrinology Parmacology ! No" $,' Gastrointestinal system
Parmacology ! No" &)* Neurology Parmacology ! No" $,) Blood vessels
Parmacology ! No" &)# Blood vessels Parmacology ! No" $,* Neurology
Parmacology ! No" &)+ Hematology Parmacology ! No" $,# Renal
Parmacology ! No" &*, Endocrinology Parmacology ! No" $,+ Pulmonology
Parmacology ! No" &*% Genitourinary Parmacology ! No" $%, Endocrinology
Parmacology ! No" &*& Cardiology Parmacology ! No" $%% Endocrinology
Parmacology ! No" &*$ Pulmonology Parmacology ! No" $%& Neurology
Parmacology ! No" &*( Oncology Parmacology ! No" $%$ Neurology
Parmacology ! No" &*' Gastrointestinal system Parmacology ! No" $%( Hematology
Parmacology ! No" &*) Renal Parmacology ! No" $%' Blood vessels
Parmacology ! No" &** Blood vessels Parmacology ! No" $%) Neurology
Parmacology ! No" &*# Neurology Parmacology ! No" $%* Neurology
Parmacology ! No" &*+ Endocrinology Parmacology ! No" $%# Blood vessels
Parmacology ! No" , Musculoskeletal Parmacology ! No" $%+ Neurology
Parmacology ! No" % Hematology Parmacology ! No" $&, Pulmonology
Parmacology ! No" & Musculoskeletal Parmacology ! No" $&% Head and neck
Parmacology ! No" $ Blood vessels Parmacology ! No" $&& Blood vessels
Parmacology ! No" ( Genitourinary Parmacology ! No" $&$ Genitourinary
Parmacology ! No" ' Renal Parmacology ! No" $&( Blood vessels
Parmacology ! No" ) Endocrinology Parmacology ! No" $&' Musculoskeletal
Parmacology ! No" * Neurology Parmacology ! No" $&) Neurology
Parmacology ! No" # Neurology Parmacology ! No" $&* Gastrointestinal system
Parmacology ! No" + Endocrinology Parmacology ! No" $ Neurology
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USMLE WORLD STEP 1 PHARMACOLOGY
A. Peripheral nerve damage
B. Hepatocyte damage
C. Gastric mucosal damage
D. Serum sickness
E. Factitious disorder
Explanation:
sonia!id "#H$ is directly hepatoto%ic in &'()'* o+ patients causing
acute mild hepatic dys+unction ,ith transient increases in serum AS-
"SGP-$ A- "SGP-$ and /iliru/in and symptoms like +ever0 anore%ia0 and
nausea. -his adverse e++ect usually occurs during the +irst 1(2 months
o+ treatment and in most cases liver +unction tests return to /aseline
,ith continued #H therapy. n rare instances ho,ever severe hepatitis
and progressive liver dys+unction /iliru/inuria0 and 3aundice occur.
"Choice A$ Peripheral neuropathy is also a potential side e++ect o+ #H
therapy i+ simultaneous pyrido%ine is not administered. Ho,ever
peripheral neuropathy ,ould not cause the a/ove symptoms.
"Choice D$ Serum sickness drug hypersensitivity generally causes +ever
urticaria0 arthralgias0 proteinuria and lymphadenopathy 4(&' days a+ter
e%posure to the drug "antigen$. -his patient does not have arthralgias
or skin +indings.
Educational 5/3ective6
sonia!id "#H$ can /e directly hepatoto%ic causing acute mild hepatic
dys+unction in &'()'* o+ patients. n a smaller percentage o+ cases+rank hepatitis may develop causing +ever anore%ia and nausea.
5
Q NO 1:After a positive PPD test, a 64!earo"# $a"e %e&i's iso'ia(i# t)erap!* O'e$o't) "ater )e prese'ts +o$p"ai'i'& of fever, a'oreia a'# 'a-sea* W)at is t)e$ost "i.e"! +a-se of )is +-rre't s!$pto$s/
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USMLE WORLD STEP 1 PHARMACOLOGY
A. Atorvastatin and e!etimi/e
B. Atorvastatin and cholestyramine
C. Atorvastatin and gem+i/ro!il
D. Gem+i/ro!il and cholestyramine
E. #iacin and e!etimi/e
F. #iacin and gem+i/ro!il
Explanation:Bile acid(/inding resins "cholestyramine0 colestipol0 colesevelam$ ,ork
/y /inding to /ile acid in the gastrointestinal tract0 inter+ering ,ith
its enterohepatic circulation. D is reduced as a conse7uence0 /ecause
hepatic cholesterol is consumed in the re(synthesis o+ /ile acids0
,hich in turn increases the uptake o+ D +rom the circulation. Bile
acid production and secretion is increased &'(+old /ecause o+ the
interruption in the enterohepatic circulation o+ /ile acids. Bile acid(
/inding agents increase the cholesterol content o+ /ile0 increasing the
risk o+ gallstone +ormation. Fi/rates also increase the cholesterol
content o+ /ile0 and thus also increase the risk +or gallstones. Both
+i/rates and /ile acid(/inding resins should /e used ,ith caution in
patients ,ith pree%isting gall/ladder disease.
Educational 5/3ective6
Both gem+i/ro!il and cholestyramine increase cholesterol e%cretion /ythe liver. Along ,ith the reduction in serum D there is an increased
risk +or gallstone +ormation.
6
Q NO 2:A 40!earo"# Ca-+asia' fe$a"e as #ia&'ose# it) )!per"ipi#e$ia t)atrespo'#e# poor"! to #ietar! +)a'&es* Her past $e#i+a" )istor! is si&'ifi+a't fora+-te +)o"e+!stitis t)at re2-ire# a five#a! )ospita"i(atio'* Her fat)er #ie# of a$!o+ar#ia" i'far+tio' at t)e a&e of 34 a'# )er $ot)er )a# #ia%etes $e""it-s*W)i+) of t)e fo""oi'& #r-& +o$%i'atio's is $ost "i.e"! to pre+ipitate &a""sto'efor$atio' i' t)is patie't/
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USMLE WORLD STEP 1 PHARMACOLOGY
Complete /lood count
Hemoglo/in 8.' g9
Erythrocyte count ).) mln9mm:
Platelets 8''''9mm:
eukocyte count )4''9mm:
-he patient most likely received treatment ,ith6
A. Clindamycin
B. Gentamycin
C. Chloramphenicol
D. ;etronida!ole
E.
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USMLE WORLD STEP 1 PHARMACOLOGY
A. Acyclovir
B. Foscarnet
C. amivudine
D. Sa7uinavir
E. Ganciclovir
F. Amantadine
G. 5seltamivir
Explanation:
Foscarnet is a pyrophosphate analog that does not re7uire intracellular
activation. t directly inhi/its /oth D#A polymerase in herpesvirus and
reverse transcriptase in human immunode+iciency virus "H
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A.
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USMLE WORLD STEP 1 PHARMACOLOGY
A. Decreases calcium current in thalamic neurons
B. Decreases sodium current in cortical neurons
C. ncreases chloride current on multiple levels
D. Blocks #;DA receptors in hippocampal neurons
E. Blocks outgoing potassium current on multiple levels
Explanation:
?ecurrent or continuous generali!ed tonic(clonic sei!ures that last +or
more than :' minutes ,ithout a return to consciousness are called
status epilepticus. t is a li+e(threatening condition that has a
num/er o+ systemic e++ects0 including hypertension tachycardia0 cardiac
arrhythmias0 and lactic acidosis. -reatment o+ status epilepticus
should /e started immediately. t consists o+ the +ollo,ing6
&. Ben!odia!epines are the +irst(line drugs +or management o+ status
epilepticus. ora!epam is the drug o+ choice.
). Phenytoin "or +osphenytoin$ is administered simultaneously to
prevent the recurrence o+ sei!ures. Ben!odia!epines are pre+erred to
phenytoin +or initial sei!ure management /ecause /en!odia!epines have a
more rapid onset o+ action. -he onset o+ action o+ phenytoin is a/out
&4 minutes a+ter < in+usion/en!odia!epines /egin ,orking ,ithin a +e,
minutes.
+ sei!ure does not stop a+ter /en!odia!epines and phenytoin is
administered pheno/ar/ital is indicated. Alternatively mida!olam0
propo+ol0 or inhaled anesthetics may /e used to induce a state o+
general anesthesia.
10
Q NO 6:A 81!earo"# Ca-+asia' $a"e is %ro-&)t to t)e ER it) pro"o'&e# to'i+
+"o'i+ sei(-res* His ife sa!s t)at )e )a# a si$i"ar episo#e t)ree $o't)s a&o for)i+) )e as pres+ri%e# so$e $e#i+atio's t)at )e 'ever too.* 9: "ora(epa$ isa#$i'istere# i' t)e ER, a'# t)e sei(-res stop* A' i'trave'o-s i'f-sio' of a'ot)er
#r-& is si$-"ta'eo-s"! i'stit-te# to preve't sei(-re re+-rre'+e* W)i+) of t)efo""oi'& is t)e $ost "i.e"! $e+)a'is$ of a+tio' of t)e se+o'# #r-& i'f-se# i'
t)is patie't/
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USMLE WORLD STEP 1 PHARMACOLOGY
Phenytoin inhi/its neuronal high(+re7uency +iring /y reducing the
a/ility o+ sodium channels to recover +rom inactivation. -hus at high(+re7uency +iring rates the neuron /ecomes re+ractory to reactivation
and reduces sei!ure activity.
"Choice A$ Ethosu%imide acts /y /locking -(type calcium channels in the
thalamic neurons. t is +irst(line treatment +or a/sence sei!ures.
Ethosu%imide is not e++ective in status epilepticus.
"Choice C$ Ben!odia!epines0 /ar/iturates and alcohol /ind to the
component o+ GABAA receptor that is a ligand gated chloride channel.
-hese su/stances enhance the inhi/itory action o+ GABA on the receptor
and increase chloride current.
"Choices D and E$
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USMLE WORLD STEP 1 PHARMACOLOGY
A. Dia!epam
B. Amitriptyline
C. Propranolol
D. Car/ama!epine
E. Pra!osin
Explanation:
Classic signs and symptoms o+ anticholinergic to%icity include +ever0
mucosal and a%illary di!!iness0 cutaneous +lushing0 mydriasis0
cycloplegia0 and delirium "use the mnemonic @hot as a hare dry as a
/one0 red as a /eet0 /lind as a /at0 and mad as a hatter$. 5+ the
drugs listed0 amitriptyline has the most potent anticholinergic side
e++ects. Amitriptyline and the other tricyclic antidepressants have
these e++ects /ecause they /lock muscarinic receptors. 5verdose can
cause anticholinergic symptoms mimicking atropine to%icity.
"Choice A$ -ypical symptoms o+ /en!odia!epine overdose include sedation
anterograde amnesia and respiratory depression. Ben!odia!epines are
rarely +atal in overdose.
"Choice C$ Adverse e++ects associated ,ith nonselective :(adrenergic
/lockers include /ronchial constriction0 masked symptoms o+
hypoglycemia in dia/etics0 /radyarrhythmias0 ,orsening o+ ?aynaud
phenomenon0 and C#S depression.
"Choice D$ Car/ama!epine is an anticonvulsant used in sei!ure disorders
trigeminal neuralgia and /ipolar disorder. n overdose0 its to%ice++ects include stupor0 coma and increased sei!ure risk.
"Choice E$ Pra!osin is an al(adrenergic /locker used to treat
hypertension and urinary retention due to /enign prostatic hypertrophy.
ts ma3or adverse e++ect is hypotension "especially postural
hypotension$.
Educational 5/3ective6
Fever0 cutaneous +lushing0 dry oral mucosa0 dilated poorly reactive
pupils and con+usion are all signs o+ anticholinergic to%icity.
-ricyclic antidepressants0 particularly amitriptyline0 have
antimuscarinic side e++ects that may mimic atropine to%i city.
12
Q NO 7:A 46!earo"# '-rse is %ro-&)t to t)e e$er&e'+! roo$ it) +o'f-sio' a'#fever* O' p)!si+a" ea$, )er s.i' is f"-s)e#* Her ora" $-+osa is #r!, a'# )er p-pi"sare #i"ate# a'# poor"! respo'sive to "i&)t* A %ott"e of atropi'e is fo-'# i' )erpo+.et* W)i+) of t)e fo""oi'& #r-&s +a' +a-se a si$i"ar +"i'i+a" prese'tatio'/
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USMLE WORLD STEP 1 PHARMACOLOGY
A. Furosemide
B. Hydrochlorothia!ide
C. Spironolactone
D. Digo%in
E. Enalapril
F. Gly/uride
G. Acar/ose
Explanation:
-his patient has osteoporosis0 ,hich is re+lected /y her very lo, /one
density and her +ractured hip. Hydrochlorothia!ide is a diuretic agent
used to treat hypertension and to treat congestive heart disease. An
opportune side e++ect o+ hydrochlorothia!ide is that it increases the
a/sorption o+ calcium +rom the distal convoluted tu/ules0 making it an
ideal agent +or treating hypertension9CHE in a ,oman ,ho is also at
risk +or osteoporosis. Studies have sho,n that patients ,ho are on
thia!ide diuretics have relatively higher /one mineral densities.
Hydrochlorothia!ide has another +ortuitous side e++ectthe increased
renal calcium a/sorption causes hypocalciuria0 ,hich helps prevent
pain+ul renal stones in some patients.
"Choice A$ Furosemide is a loop diuretic used to treat hypertension and
CHF. t causes an increase in urinary calcium loss that could only,orsen osteoporosis in this ,oman.
"Choice C$ Spironolactone inhi/its action o+ other steroid hormones0
such as testosterone. -he antiandrogenic action o+ spironolactone is
utili!ed +or the treatment o+ hirsutism and androgen(dependent
malignancies. t does not have an a++ect on calcium homeostasis.
"Choice D$ -herapeutic digo%in levels do not lead to a signi+icant
alteration in calcium levels. Ho,ever0 digitalis to%icity is associated
,ith hypercalcemia. -his is not the correct ans,er /ecause the risk o+
digitalis to%icity +ar out,eighs any possi/le /ene+it o+ an increased
calcium level.
"Choice E$ Enalapril has not /een associated ,ith signi+icant change in
/one mineral density.
"Choice F and G$ Gly/uride and acar/ose are oral hypoglycemic agents
used to treat type ) dia/etes mellitus. Both o+ these medications have
an insigni+icant e++ect on /one mineral density.
Educational 5/3ective6
-hia!ide diuretics decrease urinary calcium e%cretion and may improve
/one density. Furosemide ,ill increase urinary calcium loss0 making it
a possi/le treatment +or hypercalcemia0 /ut not +or ,omen ,ith porus
/ones.
E%tremely important concept
13
Q NO 8:A 63!earo"# fe$a"e is )ospita"i(e# it) a )ip fra+t-re* Her %o'e #e'sit!,$eas-re# %! 2-a'titative ;ra! #e'sito$etr!, +orrespo'#s to t)e "oest 1
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USMLE WORLD STEP 1 PHARMACOLOGY
A. A
B. B
C. C
D. D
E. E
F. F
Explanation:GABA "y(amino/utyric acid$ is the main inhi/itory neurotransmitter in
the C#S. ts synthesis +rom glutamate is mediated /y glutamate
decar/o%ylase "GAD$ ,ithin neurons. ;eta/olism o+ GABA occurs /y means
o+ transamination per+ormed /y en!yme GABA transaminase "GABA(-$. Both
GAD and GABA(- use
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USMLE WORLD STEP 1 PHARMACOLOGY
"Choice A$ Ben!odia!epines0 /ar/iturates0 !olpidem and alcohol are all
GABA(agonists. -hey act /y /inding to GABAA receptor0 not to GABAitsel+.
"Choice C$ Stimulation o+ the GABAA receptor leads to activation o+ ion
channels and increased chloride in+lu% into the cell. GABA agonists do
not /ind to the ion channels directly they /ind to the receptor
/inding sites.
"Choices D0 E and F$ Stimulation o+ the GABA2 receptor leads to
activation o+ an inhi/itory G(protein ,ith a su/se7uent change in
activity o+ an ion channel. t results in inhi/ition o+ adenylyl
cyclase0 a decrease in calcium in+lu% and an increase in potassium
e++lu%.
Educational 5/3ective6
-he GABAA and GABAC receptors are ion channels0 ,hile the GABAB
receptor is linked to a G( protein. Ben!odia!epines0 !olpidem0
/ar/iturates and alcohol /ind to a component o+ GABAA receptors and
+acilitate the inhi/itory action o+ GABA in the C#S.
15
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USMLE WORLD STEP 1 PHARMACOLOGY
A. Acute dystonia
B. #euroleptic(induced Parkinsonism
C. Akathisia
D. -ardive dyskinesia
E. ;anic episode
F. #euroleptic malignant syndrome
G. Drug(induced delirium
Explanation:
E%trapyramidal symptoms "EPS$ occur +re7uently as side e++ects o+
typical antipsychotics /ut may also occasionally occur ,ith the use o+
atypical antipsychotics. -his patient has developed tardive dyskinesia
as a side e++ect o+ antipsychotic usage. -ardive dyskinesia is
characteri!ed /y involuntary pen oral movements such as /iting0
che,ing0 grimacing0 and tongue protrusions. nvoluntary choreoathetoid
movements o+ the head0 lim/s0 and trunk may also /e o/served. -he
condition usually arises /et,een +our months and +our years o+
treatment and may /e irreversi/le.
?isperidone is the atypical antipsychotic most likely to cause EPS
,hile clo!apine is the atypical antipsychotic least likely to cause
EPS. -here+ore tardive dyskinesia is /est managed /y decreasing the
dose or discontinuing the o++ending antipsychotic and replacing it ,ith
clo!apine. Because clo!apine is associated ,ith agranulocytosis0 it istypically considered to /e a medication o+ last resort.
"Choice A$ Acute dystonia can develop a/ruptly at any point /et,een
+our hours and +our days a+ter receiving an antipsychotic medication.
-he condition is characteri!ed /y muscle spasms or sti++ness0 tongue
protrusions or t,isting opisthotonus0 and oculogyric crisis "a +orced
sustained elevation o+ the eyes in an up,ard position$. -reatment o+
acute dystonia is ,ith antihistamines "eg0 diphenhydramine$ or
anticholinergics "eg0 /en!tropine or trihe%yphenidyl$.
"Choice B$ Parkinsonism can also occur0 developing /et,een +our days
and +our months a+ter receiving an antipsychotic medication. t
presents ,ith cog,heel rigidity0 masked +acies0 /radykinesis0 pill(
rolling +inger tremors and shu++ling gait. -reatment is ,ith
anticholinergics such as /en!tropine.
"Choice C$ Akathisia is a su/3ective +eeling o+ restlessness that
compels patients to constantly move around. t can occur at anytime
during treatment ,ith antipsychotics.
"Choice E$ Acute mania is marked /y grandiose delusions "millions o+
dollars are held in trust +or them the President calls them they are
chosen /y God +or a magni+icent purpose etc.$. Flight o+ ideas and
pressured speech /ecome very intense and hyperactivity and impulsivity
/ecomes more pronounced.
"Choice F$ #euroleptic malignant syndrome is a rare and potentially
+atal syndrome characteri!ed primarily /y delirium +ever muscle
rigidity0 and autonomic insta/ility.
16
Q NO 10:A 6
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USMLE WORLD STEP 1 PHARMACOLOGY
"Choice G$-he hallmark o+ delirium is con+usion ora clouding o+ the
sensorium. Patients may appear some,hat da!ed and unclear a/out theirsurroundings. Disorientation to time and place are common accompanying
+eatures.
Educational 5/3ective6
-ardive dyskinesia is characteri!ed /y involuntary perioral movements
such as /iting0 che,ing0 grimacing0 and tongue protrusions. nvoluntary
choreoathetoid movements o+ the head0 lim/s0 and trunk may also /e
o/served. -he condition usually arises /et,een +our months and +our
years o+ treatment and may/e irreversi/le.
17
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USMLE WORLD STEP 1 PHARMACOLOGY
A. Epinephrine
B. Phenylephrine
C. Dopamine
D. Edrophonium
E. Esmolol
Explanation:
Dopamine is uni7ue among adrenergic stimulators due to its a/ility to
simultaneously increase /oth myocardial contractility and renal /lood
+lo,. Because o+ this uni7ue e++ect dopamine is used to increase renal
per+usion in lo,( output cardiac states0 such as hypovolemic and
cardiogenic shock. Dopamine e%ecutes its renal e++ects via stimulation
o+ D& adrenergic receptors in the ,alls o+ renal /lood vessels. -hese
D& adrenergic receptors are also located in the splanchnic and
mesenteric arteries0 ,hich are also dilated /y dopamine=s e++ects.
Dopaminergic increases in renal /lood +lo, results in increasedglomerular +iltration0 increased urinary output0 and increased sodium
e%cretion.
-he dose o+ dopamine that a++ects Dl receptors o+ renal arteries also
acts as an agonist on & receptors o+ myocardium0 increasing /oth heart
rate and myocardial contractility0 leading to overall increases in
cardiac output. Systolic /lood pressure su/se7uently increases due to
the rise in cardiac output. Higher doses o+ dopamine stimulate al(
adrenoreceptors in the arteries o+ skin and viscera "including
kidneys$0 resulting in vasoconstriction.
See the ta/le /elo, +or comparison o+ the e++ects o+ dopamine ,ith
epinephrine "a and agonist$ and phenylephrine "a agonist$.
"Choice A$ Epinephrine stimulates /oth I and adrenoreceptors and
increases myocardial contractility and cardiac output " stimulation$0
,hile decreasing renal /lood +lo, "al stimulation$.
18
Q NO 11:A $e#i+a" st-#e't is +o'#-+ti'& a p)ar$a+o"o&! eperi$e't* He i'f-sesDr-& ; i'trave'o-s"! over #iffere't #ose ra'&es a'# $eas-res severa" i$porta't)e$o#!'a$i+ para$eters* Grap)s p"otti'& t)e re+or#e# $eas-re$e'ts of re'a"%"oo# f"o a'# +ar#ia+ o-tp-t +)a'&e it) i'+reasi'& #oses of Dr-& ; are s)o'%e"o* W)i+) of t)e fo""oi'& is $ost "i.e"! to %e t)e #r-& -se# i' t)e eperi$e't/
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USMLE WORLD STEP 1 PHARMACOLOGY
"Choice B$ Phenylephrine is a selective agonist o+ a(adrenoreceptors
that does not a++ect :& receptors o+ myocardium. Stimulation o+ alreceptors causes renal splanchnic and mesenteric vasoconstriction.
"Choice D$ Edrophonium is a short(acting cholinesterase inhi/itor used
in the diagnosis o+ myasthenia gravis. -hrough its cholinergic e++ects
edrophonium reduces heart rate0 cardiac conduction0 and cardiac
contractility.
"Choice E$ Esmolol is a cardioselective /locker ,ith a short duration
o+ action. Esmolol decreases heart rate0 myocardial contractility0 and
cardiac conduction ,ithout a++ecting renal /lood +lo,.
Educational 5/3ective6
o, doses o+ dopamine stimulate /oth Dl receptors in renal and
splanchnic /lood as ,ell as & receptors o+ the myocardium0 leading to
increases in /oth renal /lood +lo, and myocardial contractility. 5n the
other hand0 high doses o+ dopamine stimulate I& receptors0 resulting in
peripheral vasoconstriction.
19
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USMLE WORLD STEP 1 PHARMACOLOGY
A. ?heumatoid arthritis progression
B. ;ethotre%ate side e++ect
C. Prednisone side e++ect
D. ndomethacin side e++ect
E. 5mepra!ole side e++ect
Explanation:
-his patient presents ,ith a pathologic +racture o+ a lum/ar verte/ra.
A pathologic +racture is one that results +rom a +orce signi+icantlyless than that re7uired to +racture a normal /one. nderlying /one
pathology is generally present. Patients taking as little as J.4mg o+
daily prednisone +or longer than si% months can develop osteoporotic
/one changes0 and :'(4'* o+ patients on prolonged systemic
glucocorticoids may develop pathologic verte/ral /ody +ractures. ong
term use o+ systemic steroids is thought to promote osteoporosis /y
causing decreased synthesis o+ /one matri%0 inhi/iting the intestinal
action o+ vitamin D to promote calcium a/sorption0 and causing
increased parathyroid hormone levels.
"Choice A$ ?heumatoid arthritis "?A$ is an autoimmune in+lammatory
disorder that predominantly a++ects synovial 3oints in the hands and
+eet0 /ut also a++ects larger 3oints like the ,rists and shoulders.
nterverte/ral /ody 3oints lack a synovial space. ?A ,ould /e unlikely
to directly cause a pathologic thoracolum/ar verte/ral +racture.
"Choices B0 D and E$ ;ethotre%ate0 #SADs and proton pump inhi/itorsare not kno,n to cause osteoporosis.
Educational 5/3ective6
5steoporosis is a common cause o+ pathological verte/ral +ractures.
Chronic systemic use o+ corticosteroids like prednisone promotes
osteoporosis and there+ore may cause such +ractures.
20
Q NO 12:A 3B!earo"# fe$a"e it) a "o'& )istor! of r)e-$atoi# art)ritis a'#pepti+ -"+er #isease prese'ts to t)e e$er&e'+! roo$ it) a+-te "o %a+. pai'after too 2-i+."! sitti'& #o' o'to a )ar#oo# +)air* S)e reports t)at s)eta.es $a'! $e#i+atio's, a'# )as %ee' for severa" !ears* ;ra! s)os afra+t-re of t)e fo-rt) "-$%ar verte%ra* W)i+) of t)e fo""oi'& $a! )ave+o'tri%-te# to t)is i'-r!/
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USMLE WORLD STEP 1 PHARMACOLOGY
A.
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USMLE WORLD STEP 1 PHARMACOLOGY
+our drugs listed re7uire mono phosphorylation /y a virally(encoded
kinase. Because these drugs are activated en!ymatically0 the structuralprotein composition o+ the virus does not a++ect drug sensitivity.
"Choice E$-he drug degradation rate is not responsi/le +or di++erences
in viral suscepti/ility to acyclovir.
Educational 5/3ective6
;ono phosphorylation o+ acyclovir /y a viral thymidine kinase is the
+irst "and rate(limiting$ step in the conversion o+ acyclovir to its
active triphosphate +orm. Acyclovir and related drugs "eg0 +amciclovir0
valaciclovir$ are more e++ective against herpes simple% virus and
varicella !oster virus than cytomegalovirus and Epstein(Barr virus.
22
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USMLE WORLD STEP 1 PHARMACOLOGY
A. Diarrhea
B. #asal congestion
C. Cough
D. Dry mouth
E. Fre7uent urination
Explanation:
Antihistaminics0 or Hi histamine receptor /lockers0 are very use+ul
drugs in the treatment o+ allergy. Hi receptor /lockers decrease the
activity o+ this receptor /y increasing the proportion o+ inactive Hi
receptors0 via a process kno,n as reverse /lockade. n addition to
/locking Hi receptors0 +irst(generation antihistaminics have
antimuscarinic0 antiadrenergic and anti serotonergic properties.
n motion sickness0 the muscarinic ;i and histaminic Hi path,ays are
stimulated0 resulting in the nausea and vomiting o+ motion sickness.
Because o+ their anti muscarinic and antihistaminic properties0 +irst(
generation antihistaminic drugs like mecli!ine and dimenhydrinate are
e++ective at preventing these symptoms. 5ther +irst generation drugs
are also e++ective0 /ut are generally avoided /ecause o+ their sedating
properties. Scopolamine has only antimuscarinic e++ects and is also
e++ective at preventing the symptoms o+ motion sickness.
Side e++ects o+ antimuscarinics include /lurry vision0 dry mouth0
palpitations0 urinary retention and constipation. -he options in
choices A0 B0 C and E occur ,ith stimulation rather than /lockade o+
the muscarinic path,ay.
Educational 5/3ective6
Antimuscarinic agents and antihistamines ,ith antimuscarinic action are
most e++ective +or motion sickness prevention.
23
Q NO 14:A B!earo"# trave"er prese'ts to !o-r offi+e for a ro-ti'e +)e+.-p* Hei"" %e "eavi'& for a +r-ise 'et ee., a'# as.s for a #r-& t)at o-"# preve't t)esevere 'a-sea a'# vo$iti'& )e eperie'+es o' s)ips* After re+o$$e'#i'& t)eappropriate #r-&, !o- ar' a%o-t )i+) of t)e fo""oi'& si#e effe+ts/
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USMLE WORLD STEP 1 PHARMACOLOGY
A. Do,n regulation o+ leptin activity
B. ncreased insulin release
C. Decreased insulin resistance
D. ncreased +ree +atty acid levels
E. Do,nregulation o+ adiponectin
Explanation:
-hia!olidinediones "-LD4$ e%ert their glucose(lo,ering e++ect /y
decreasing insulin resistance. -LDs /ind to pero%isome proli+erator
activated receptor gamma "PPA?(gamma$0 ,hich is a transcriptional
regulator o+ the genes involved in glucose and lipid meta/olism. 5ne o+
the most crucial genes regulated /y PPA?(gamma is adiponectin0 ,hich is
a cytokine secreted /y +at tissue "adipocytokine$. Adiponectin levels
are lo, in type ) dia/etes ,hich -LDs alter. As the glucose lo,ering
e++ect o+ -LDs re7uires alteration in gene transcription and protein
synthesis0 it takes days to ,eeks a+ter initiation o+ therapy to
o/serve a signi+icant reduction in glucose levels. -LDs do not cause
hypoglycemia. -he main side e++ects o+ -LDs are +luid retention0 ,eight
gain0 and the precipitation o+ congestive heart +ailure +rom +luid
retention.
"Choice A$ eptin is the hormone secreted /y +at cells. t is
responsi/le +or appetite suppression and decreased insulin resistance0
,hich is mediated via the central nervous system. Although PPA?(gamma
activation increases +at cell mass0 circulating leptin levels are
essentially unchanged. Some studies have sho,n that PPA?(gamma
activation leads to suppression o+ the transcription o+ the leptin
24
Q NO 15:A 'e #r-& is %ei'& #eve"ope# for t)e treat$e't of #ia%etes* T)is #r-&
a+tivates t)e peroiso$e pro"iferatora+tivate# re+eptor &a$$a ?PPAR&a$$a@, a'-+"ear re+eptor a'# tra's+riptio' fa+tor* A+tivatio' of t)is re+eptor o-"# $ost"i.e"! res-"t i' )i+) of t)e fo""oi'&/
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USMLE WORLD STEP 1 PHARMACOLOGY
gene. -he activity o+ leptin is not signi+icantly altered ,ith PPA?
gamma activation0 ho,ever."Choice B$ PPA?(gamma is present in small amounts in pancreatic /eta
cells. -LDs do not directly alter insulin secretion6 ho,ever0 as
insulin resistance diminishes0 circulating levels o+ insulin tend to
decrease overtime.
"Choice D$ PPA?(gamma activation leads to an increase in +at mass
secondary to the increased di++erentiation o+ preadipocytes into mature
adipocytes. -he movement o+ +ree +atty acids into +at cells is
increased0 and circulating +ree +atty acids levels decrease.
"Choice E$ Adiponectin is a ne,ly(discovered cytokine secreted /y +at
cells. Adiponectin levels are decreased in patients ,ith type )
dia/etes mellitus. 5ne o+ the mechanisms /y ,hich PPA?(gamma activation
decreases insulin resistance is /y increased e%pression o+ the
adiponectin gene.
Educational 5/3ective6
-LDs activate PPA?(gamma0 ,hich is the nuclear receptor that alters the
transcription o+ genes responsi/le +or +at and lipid meta/olism.
-hia!olidinediones "-LD4$ e%ert their glucose(lo,ering e++ect /y
decreasing insulin resistance.
25
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USMLE WORLD STEP 1 PHARMACOLOGY
A. Capsular polysaccharide vaccine
B. Pilus protein vaccine
C. ipopolysaccharide vaccine
D. Penicillin
E. Sul+ametho%a!ole
F. ?i+ampin
Explanation:
-he gram stain description o+ gram(negative cocci in pairs makes the
etiologic agent o+ this in+ection most likely #eisseria meningitidis.
Because the agent is transmitted /y direct contact ,ith contaminated
respiratory secretions or air/orne droplets0 +amily mem/ers and otherclose contacts o+ persons ,ith meningococcal disease are at high risk
o+ ac7uiring the disease or /ecoming carriers and must receive
immediate prophyla%is.
?i+ampin has /een used success+ully since the &82'=s +or
chemoprophyla%is +or house hold mem/ers and close contacts o+ patients
,ith invasive meningococcal disease and is the most likely chemo
prophylactic agent to /e administered in this su/3ect. ?i+ampin is used
+or chemoprophyla%is /ecause it penetrates ,ell into the respiratory
tract and ,ill eliminate nasopharyngeal coloni!ation. ?i+ampin=s most
nota/le side e++ect is an orange discoloration o+ secretions "urine0
/reast milk and tears$0 and patients should /e alerted to the +act that
contact lenses ,ill /e permanently stained orange. Also0 remem/er that
ri+ A;P in @A;Pli+ies CMP145 and ,ill increase the meta/olism o+ drugs
such as ,ar+arin that are processed /y this system.
"Choice A$ hile penicillin is the pre+erred agent +or treatment o+ #.
meningitidis in+ections0 it is not use+ul +or prophyla%is ,here
ri+ampin0 +ollo,ed /y ce+tria%one0 is the drug o+ choice. -he reason
+or this is that only ri+ampin and the third generation cephalosporins
have /een sho,n to eliminate nasal carriage.
"Choice E$ Sul+ametho%a!ole ,as historically used as chemoprophyla%is
+or contacts o+ an inde% case o+ meningococcal disease0 /ut presently
this ,ould not /e a correct choice due to the +act that #. meningitidis
26
Q NO 16:A 18!earo"# $a"e is )ospita"i(e# it) )ea#a+)e, 'a-sea a'# fever* A
p)!si+a" ea$i'atio' is si&'ifi+a't for 'e+. stiff'ess* Gra$'e&ative +o++i i' pairsare revea"e# #-ri'& CS $i+ros+op!* W)i+) of t)e fo""oi'& is t)e %est a! topreve't i'fe+tio' i' )is +"ose +o'ta+ts/
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USMLE WORLD STEP 1 PHARMACOLOGY
has developed ,idespread resistance to sul+onamides0 so these drugs are
no longer used.
Educational 5/3ective6
?i+ampin is most typically used as chemoprophyla%is o+ meningococcal
meningitis. t must /e prescri/ed to all close contacts o+ any patient
,ho has active disease ,ithin ) ,eeks o+ diagnosis in order to /e
e++ective.
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USMLE WORLD STEP 1 PHARMACOLOGY
A. Dia!epam
B. Haloperidol
C. Ben!tropine
D. Physostigmine
E. ;etoprolol
F. Atropine
G. -hiamineH. ;orphine
. #alo%one
Explanation:
-his patient most likely has Nimson >eed "Datura stramonium$ poisoning.
-his condition is also called as @Gardener=s mydriasis. Nimson >eed
produces to%ins "/elladonna alkaloids$ that possess strong
anticholinergic properties. Nimson ,eed and atropine poisoning are
strikingly similar. Blockade o+ visceral muscarinic receptors produces
the +ollo,ing e++ects6
&. Heart6 diminished vagal tone at the SA node causes relative
tachycardia.
). Blood vessels6 vasoconstriction via muscarinic receptor /lockade in
endothelial cells results in decreased nitric o%ide synthesis. n spite
o+ this e++ect atropine poisoning is associated ,ith cutaneous+lushing the pathogenesis o+ this e++ect is unkno,n.
:. G6 delayed gastric emptying0 decreased intestinal motility0 and
secretion.
1. ?espirators=6 /ronchodilatation.
4. G6 urinary retention via detrusor rela%ation and contraction o+ the
e%ternal urethral sphincter.
2. Secretions6 decreased lacrimation "dry eyes$0 salivation "dry mouth$
and s,eating "dry and hot skin$. Atropine decreases one=s a/ility to
s,eat0 contri/uting to hyperthermia.
J. Eye6 mydriasis "dilated pupils$ and cycloplegia "ina/ility to +ocus
on the near o/3ects /lurry vision$.
O. C#S6 hallucinations0 agitation and delirium.
Atropine=s antimuscarinic e++ects can /e counteracted /y increasing the
concentration o+ acetylcholine in the synaptic cle+t. ncreased
acetylcholine concentrations are produced /y cholinesterase inhi/itors
that suppress acetylcholine degradation. Physostigmine0 a
cholinesterase inhi/itor can /e used +or treatment o+ atropine
overdose.
"Choice A$ Dia!epam is a long(acting /en!odia!epine that +acilitates
GABA action /y increasing the +re7uency o+ chloride channel opening.
Dia!epam is used to treat sei!ures associated ,ith atropine poisoning
/ut does not a++ect muscarinic cholinergic receptors.
"Choice B$ Haloperidol is a neuroleptic drug that /locks dopamine
receptors in the C#S. t also has anticholinergic and antihistamine
properties.
28
Q NO 17:A 3
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USMLE WORLD STEP 1 PHARMACOLOGY
"Choice C$ Ben!tropine is a centrally acting anti(cholinergic
medication used +or treatment o+ idiopathic and drug inducedParkinson=s disease. ts administration ,ould increase the patient=s
symptoms.
"Choice E$ ;etoprolol is a selective (adrenergic receptor antagonist.
t is used to treat angina acute coronary syndromes heart +ailure0
hypertension and arrhythmias. ;etoprolol does not have any e++ect on
muscarinic cholinergic receptors.
Educational 5/3ective6
-he mnemonic +or the clinical mani+estations o+ atropine poisoning is6
@/lind as a /at0 mad as a hatter0 red as a /eet. Hot as a hare0 dry as
a /one0 the /o,el and /ladder lose their tone0 and the heart runs
alone. Atropine is a reversi/le cholinergic antagonist that acts
selectively on muscarinic receptors. ts e++ects can /e reversed /y
cholinesterase inhi/itors "physostigmine$.
29
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USMLE WORLD STEP 1 PHARMACOLOGY
A. Dia!o%ide
B. #itroprusside
C. Hydrala!ine
D. Esmolol
E. #icardipine
F. Fenoldopam
Explanation:
-he management o+ hypertensive emergency re7uires immediate /ut gradual
/lood pressure reduction over minutes to hours to minimi!e target organ
damage. ntravenous therapy is necessary to allo, immediate e++ects and
the pre+erred and optimal parenteral agent ,ill vary according to the
patient=s clinical situation and presence o+ coe%isting conditions and
disease states.
Fenoldopam is a ne,er0 novel intravenous agent that is a /en!a!epines
derivative o+ dopamine. n contrast to dopamine0 itis a selective
dopamine(i receptor agonist ,ith no e++ect on alpha or /eta receptors.
Dopamine(i receptor stimulation activates adenylyl cyclase and raises
intracellular cyclic A;P0 resulting in vasodilation o+ most arterial
/eds0 especially renal0 mesenteric0 and coronary /eds. -he main e++ect
is a signi+icant reduction in systemic vascular resistance. Stimulation
o+ dopamine(receptors in the kidneys not only improves renal /lood
+lo,0 /ut also leads to increased sodium and ,ater e%cretion. -hus
+enoldopam is the only availa/le intravenous agent that improves renal
per+usion ,hile it lo,ers /lood pressure.
Fenoldopam is indicated +or short term management o+ severe
hypertension and can /e sa+ely used in all hypertensive emergencies. tmay /e e%ceptionally /ene+icial in patients ,ith concomitant renal
insu++iciency.
"Choices A and C$ Although dia!o%ide and hydrala!ine are /oth arterial
vasodilators0 neither agent therapeutically improves renal per+usion.
Both agents cause signi+icant re+le% sympathetic activation0 resulting
in increased heart rate and contractility and e%tensive sodium and
+luid retention. -hey are usually considered third line agents and are
not recommended in hypertensive emergencies ,ith aortic dissection.
Hydrala!ine is considered sa+e and use+ul in pregnancy related
hypertensive emergency.
"Choice B$ #itroprusside is a very potent direct acting arterial and
venous vasodilator. Due to its +avora/le pharmacokinetics pro+ile
"7uick onset and short duration o+ action$0 it is considered the most
e++ective agent +or most cases o+ hypertensive emergency. #itroprusside
causes slight re+le% sympathetic activation0 and thus can cause modesttachycardia and sodium and +luid retention. Since nitroprusside is
meta/oli!ed to cyanide and thiocyanate0 the primary limiting +actor to
its use is the risk +or cyanide to%icity ,ith prolonged use0 high
doses0 and renal insu++iciency.
"Choice D$ Esmolol is a short acting selective /eta(i receptor
antagonist that decreases heart rate contractility0 and cardiac output.
t has an immediate onset o+ action and upon discontinuation o+
esmolol the e++ects are reversed ,ithin )' minutes. Esmolol can cause
/radycardia0 le+t ventricular dys+unction0 and /ronchospasm. t is
mainly used in the setting o+ postoperative hypertension and may /e
30
Q NO 18:A 'e #r-& t)at is -se# to treat )!perte'sive e$er&e'+ies +a-sesarterio"ar #i"atio'* 9t a"so i'+reases re'a" perf-sio' a'# pro$otes 'atri-resis*T)e #r-& #es+ri%e# a%ove is $ost si$i"ar it) )i+) of t)e fo""oi'& a&e'ts/
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USMLE WORLD STEP 1 PHARMACOLOGY
pre+erred in critical patients ,here rapid ,ithdra,al o+ drug e++ects
is needed."Choice E$ #icardipine is a dihydropyridine calcium channel /locker
that ,orks /y /locking calcium channels in the vascular smooth muscle
and the myocardium0 resulting in rela%ation o+ smooth muscles and
coronary arteries. Because nicardipine causes signi+icant arterial
vasodilation0 it can cause mild to moderate tachycardia. 5ther side
e++ects include +lushing0 headache0 and venous irritation. Since
nicardipine has a longer hal+ li+e compared to other agents0 the
hypotensive e++ect may /e prolonged and rapid titration o+ the agent is
di++icult.
Educational 5/3ective6
Fenoldopam is a ne,er parenteral agent that is classi+ied as a
selective dopamine(& receptor agonist. t causes arteriolar dilation
and natriuresis leading to decreased systemic vascular resistance and
/lood pressure reduction. Since +enoldopam is the only intravenous
agent that improves renal per+usion0 it may /e e%ceptionally /ene+icial
in hypertensive patients ,ith concomitant renal insu++iciency.
31
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USMLE WORLD STEP 1 PHARMACOLOGY
A. Decreased activity o+ /acterial catalase(pero%idase
B. ncreased activity o+ en!ymes involved in cell ,all polysaccharide
synthesis
C. Altered structure o+ /acterial ri/osomal proteins
D. Altered structure o+ en!ymes involved in D#A ,inding(un,inding
E. Altered structure o+ en!ymes involved in ?#A synthesis
Explanation:
-he treatment o+ active ;yco/acterium tu/erculosis in+ection is /est
accomplished through the use o+ isonia!id and ri+ampin in addition to
any com/ination o+ streptomycin0 pyra!inamide0 etham/utol or
+luoro7uinolone. Because streptomycin is one o+ the older drugs in the
aminoglycoside +amily0 /acterial resistance to this anti/iotic is
,idespread. As a result streptomycin usage is currently limited to the
treatment o+ tu/erculosis plague0 and tularemia. ike all other
aminoglycosides0 streptomycin can only /e administered parenterally0
and it ,orks /y inhi/iting the /acterial :'S ri/osomal su/unit
"ultimately preventing /acterial protein synthesis$. ;utations o+ the
genes that encode ri/osomal proteins are responsi/le +or aminoglycoside
resistance /ecause they modi+y the ri/osomal /inding sites +or these
drugs.
"Choice A$ Decreased activity o+ /acterial catalase(pero%idase is one
mechanism o+ myco/acterial resistance to isonia!id. ;yco/acterial
catalase(pero%idase is re7uired +or the initial en!ymatic conversion o+
isonia!id to its active meta/olite ,ithin the myco/acterial cells
,ithout this en!yme isonia!id is una/le to inhi/it myco/acterialmycolic acid synthesis.
"Choice B$ ncreased activity o+ en!ymes involved in cell ,all
polysaccharide synthesis is the means /y ,hich myco/acteria develop
resistance to etham/utol. Etham/utol inter+eres speci+ically ,ith
myco/acterial peptidoglycan cell ,all synthesis through an unclear
mechanism that appears to di++er +rom that o+ isonia!id. -his drug is
ine++ective against organisms other than myco/acteria.
"Choice D$ Structural alteration o+ en!ymes involved in D#A ,inding(
un,inding is the means /y ,hich many microorganisms /ecome resistant to
+luoro7uinolone anti/iotics. Fluoro7uinolones inhi/it the /acterial
en!yme D#A gyrase "topoisomerase $.
"Choice E$ Structural alteration o+ en!ymes involved in ?#A synthesis
is the mechanism through ,hich organisms /ecome resistant to ri+ampin.
?i+ampin inhi/its the /acterial D#A(dependent ?#A polymerase0 there/y
preventing the transcription o+ D#A into m?#A.
Educational 5/3ective6
-he aminoglycoside streptomycin inhi/its protein synthesis /y
inactivating the :'S "small$ ri/osomal su/unit.
Q Decreased activity o+ /acterial catalase(pero%idase is one mechanism
o+ myco/acterial resistance to isonia!id.
Structural alteration o+ en!ymes involved in ?#A synthesis "D#A(
dependent ?#A polymerase$ is the mechanism through ,hich organisms
/ecome resistant to ri+ampin.
32
Q NO 19:9so"ates of M* t-%er+-"osis o%tai'e# fro$ a 4!earo"# H9 :positive $a"e#e$o'strate resista'+e to a '-$%er of a'ti%ioti+s* W)i+) of t)e fo""oi'& %estep"ai's resista'+e to strepto$!+i' i' t)ese %a+teria/
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USMLE WORLD STEP 1 PHARMACOLOGY
A. Steady decrease in /oth - and DH- levels
B. First concordant increase0 then concordant decrease in - and DH-
levels
C. Discordant decrease in DH- level
D. First discordant increase0 then discordant decrease in DH- level
E. #o change in - and DH- levels
Explanation:
Pulsatile release o+ gonadotropin(releasing hormone "Gn?H$ +rom the
hypothalamus is the natural state o+ human +unctioning causing release
o+ gonadotrophins +rom the pituitary that in turn stimulates release o+
testosterone in a man. -estosterone is converted to DH- in target
tissues /y the en!yme 4(alpha reductase. Alternatively i+ Gn?H levels
are constantly elevated. ?ather than pulsed the secretion o+
luteini!ing hormone "H$ and +ollicle(stimulating hormone "FSH$ +rom
the pituitary ,ill /e suppressed.
A num/er o+ Gn?H analogs such as leuprolide0 have /een generated /y
amino acid su/stitutionsalterations that allo, longer hal+ lives and
increased activity. euprolide is a long(acting Gn?H analog that causes
continuous Gn?H activity. -he result is ultimately a suppression o+ the
pituitagonadal a%is +or the duration o+ treatment although there is a
/rie+ period o+ initial stimulation sometimes called a @start up+lare. An increase in gonadotrophin levels during the initial +lare(up
period causes an increase in /oth testosterone and DH- levels "a
concordant increase$. Soon the start up +lare /urns out and /oth
testosterone and DH- are typically suppressed to castrate levels. -hese
ye, lo, levels o+ androgens are use+ul +or the treatment o+ androgen(
dependent cancers such as prostate cancer.
"Choice A$ >ith the use o+ a Gn?H analog androgen levels are suppressed
a+ter a transient increase so the @decrease only option here cannot /e
correct. Suppression o+ testosterone and DH- ,ithout an initial +lare
is seen ,ith the use o+ Gn?H antagonists.
"Choices C and D$ euprolide has no e++ect on 4(alpha reductase
activity. -here+ore the changes in testosterone and DH- levels are
al,ays concordant +ollo,ing leuprolide administration. Finasteride is a
4(alpha(reductase inhi/itor used +or the treatment o+ /enign prostatic
hypertrophy. t prevents the conversion o+ testosterone to DH-0 causing
a discordant decrease in DH- levels.
"Choice E$ -he purpose o+ administering a Gn?H is to change androgen
levels "testosterone and DH- levels$ so @no change cannot possi/ly /e
correct.
Educational 5/3ective6
euprolide is a Gn?H agonist that causes +irst a transient increase0
then a decrease in /oth testosterone and DH- levels. Finasteride causes
a discordant decrease in DH- level.
33
Q NO 20:A 6
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USMLE WORLD STEP 1 PHARMACOLOGY
A. Amo%icillin
B. ?i+ampin
C. ;etronida!ole
D. Flucona!ole
E. Cimetidine
F. 5mepra!ole
G. 5ral contraceptives
Explanation:
As ,ith many other medications phenytoin is meta/oli!ed /y hepatic P14'
o%idase. Plasma drug level0 e++icacy0 and the severity o+ side e++ects
are directly in+luenced /y the rate o+ meta/olism o+ phenytoin. -he
+ollo,ing +eatures o+ phenytoin meta/olism are important6
&. Hepatic hydro%ylation o+ phenytoin is dose(dependent. >hen lo, doses
o+ phenytoin are administered0 a su++icient num/er o+ en!yme molecules
are availa/le0 and the drug is eliminated rapidly. Higher doses o+
phenytoin may +ully saturate the en!yme hence0 increasing the dose
a/ove the saturation limit causes an ina/ility to meta/oli!e the drug
and a rapid rise in plasma levels. Even a small increase in phenytoin
intake a/ove the prescri/ed dose may lead to severe to%icity.
). Phenytoin is an inducer o+ P14' o%idase. nduction o+ this en!yme
increases the consumption o+ many medications that are meta/oli!ed /y
the liver0 such as oral contraceptives. >hen the P14' o%idase system isinduced0 the serum concentration o+ such medications ,ill decrease0
there/y reducing e++icacy.
:. Because phenytoin is meta/oli!ed /y P14' en!ymes its level i+
a++ected ,hen it is co(administered ,ith other medications that induce
or inhi/it the P14' system. -he co(administration o+ phenytoin ,ith
P14' inducers decreases concentration o+ phenytoin in plasma and
diminishes its e++ectiveness. Some P14' inducers are /ar/iturates
ri+ampin0 car/ama!epine0 griseo+ulvin0 and chronic alcohol consumption.
P14' inhi/itors slo, hepatic meta/olism0 ,hich increases the to%icity
o+ phenytoin. Some o+ P14' inhi/itors are isonia!id0 cimetidine0
macrolides0 a!ole anti+ungals0 and grape 3uice.
"Choices A and F$ Amo%icillin and omepra!ole do not a++ect the hepatic
meta/olism o+ phenytoin.
"Choices C and G$ Both metronida!ole and oral contraceptives are
meta/oli!ed /y hepatic P14' o%idase0 /ut these t,o drugs neither induce
nor inhi/it the activity o+ P14' o%idase.
"Choices D and E$ Flucona!ole and cimetidine inhi/it P14' en!ymes and
increase the concentration o+ phenytoin in the serum.
Educational 5/3ective6 Phenytoin meta/olism depends on the +unction o+
hepatic P14' o%idases and is dose(dependent. Drugs that induce hepatic
microsomal en!ymes "pheno/ar/ital0 car/ama!epine0 and ri+ampin$ enhance
phenytoin meta/olism and decrease its serum concentration. Mou should
kno, all o+ the commonly(prescri/ed medications that are meta/oli!ed /y
the P14' system and you should kno, ,hich drugs induce or inhi/it the
+unction o+ these en!ymes.
34
Q NO 21:A 1!earo"# Ca-+asia' fe$a"e is %ro-&)t to t)e ER after a to'i++"o'i+sei(-re* S)e as #ia&'ose# it) epi"eps! severa" !ears a&o a'# )as %ee's-++essf-""! treate# it) p)e'!toi'* 5"oo# tests revea" )er p"as$a p)e'!toi' "eve"to %e "o* S)e states t)at s)e )as %ee' +o$p"ia't it) )er $e#i+atio'* W)i+) oft)e fo""oi'& #r-&s $a! %e respo'si%"e for t)is patie'ts +o'#itio' if +oa#$i'istere# it) p)e'!toi'/
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USMLE WORLD STEP 1 PHARMACOLOGY
A.
nsulin
B. Platelet(derived gro,th +actor "PDGE$
C. lnterleukin() "()$
D. Atrial natriuretic peptide
E. &0 )4(dihydro%3cholecalci+erol
F. Gamma(amino/utyric acid "GABA$
Explanation:
Atrial natriuretic peptide "A#P$ and nitric o%ide "#50 endothelium
derived rela%ing +actor$ are hormones that e%ert their intracellular
e++ects /y /inding a receptor protein that also has a guanylate cyclase
en!ymatic a/ility. -his is kno,n as the cG;P second messenger system.
-he cG;P second messenger system is similar to the cA;P second
messenger system in that hormone /inding causes +ormation o+ a cyclic
nucleotide monophosphate +rom a nucleotide triphosphate. -hese systems
are also similar in that the cyclic nucleotide monophosphate is a/le to
activate a protein kinase to carry out the intracellular e++ects o+ the
hormone and also in that the e++ect o+ the hormone is terminated /y
degradation o+ the cyclic nucleotide monophosphate /y
phosphodiesterase. -he cG;P system is di++erent /ecause the receptor
and guanylate cyclase are part o+ the same protein "as opposed to the
cA;P system0 ,hich consists o+ +our distinct proteins$. -his receptor
guanylate cyclase protein e%ists in /oth transmem/rane +orm "+or A#P$
and in a +ree cytosolic +orm "+or #5 ,hich can +reely di++use through
cell mem/ranes.
Sildena+il causes a net increase in the intracellular cG;P
concentration /y inhi/iting cG;P phosphodiesterase in target cells.-his e++ect is similar to that o+ nitric o%ide "#5$ and atrial
natriuretic peptide "A#P$ in that these hormones activate a cG;P second
messenger system upon /inding to their speci+ic receptors0 and
activation o+ the cG;P second messenger system ,ill also lead to
increased intracellular cG;P. t is important to note though that #5
and A#P increase intracellular cG;P /y a di++erent mechanism than that
o+ the drug sildena+il ,hich inhi/its /reakdo,n o+ cG;P /y inhi/iting
phosphodiesterase. -hese hormones increase production o+ cG;P they do
not decrease degradation o+ cG;P as sildena+il does.
"Choice A$ nsulin acts /y the tyrosine kinase second messenger system.
"Choice B$ Platelet(derived gro,th +actor "PDGF$ is a +actor that
stimulates cell gro,th and division including angiogenesis. t also
acts via a tyrosine kinase receptor.
"Choice C$ lnterleukin() "()$ is a cytokine that primarily +unctions
in an autocrine manner ,here/y activated - lymphocytes providecostimulus to themselves /y secreting () and producing ()
receptors.
"Choice E$ &0 )4(dihydro%==cholecalci+erol is the active +orm o+
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USMLE WORLD STEP 1 PHARMACOLOGY
Educational 5/3ective6
Sildena+il is a selective inhi/itor o+ the cG;P phosphodiesterase0 anduse o+ this drug ,ill prevent degradation o+ cG;P leading to higher
intracellular levels. #itric o%ide and atrial natriuretic peptide act
via a cG;P second messenger system "#5 /eing primarily responsi/le +or
causing erection$0 and /inding o+ these hormones to their receptors
,ill also increase intracellular cG;P concentrations.
36
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USMLE WORLD STEP 1 PHARMACOLOGY
H/ &:.) g9d
>BC &&''9mm:
Platelet &O''''9mm:
>hich o+ the +ollo,ing drugs is most likely to /e associated ,ith this
patient=s conditionR
A. Heparin
B. Argatro/an
C. >ar+arin
D. tPA
E. Aspirin
F. -iclopidine
G. A/ci%ima/
H. Cilosta!ol
37
Q NO 23:A 60!earo"# $a"e +o$es to t)e p)!si+ia's offi+e +o$p"ai'i'& of $o-t)-"+ers a'# fever* His past $e#i+a" )istor! is si&'ifi+a't for "o'&ter$ )!perte'sio'a'# a' episo#e of tra'sie't is+)e$i+ atta+. )i+) o++-rre# o'e $o't) a&o a'#"aste# 8< $i'-tes* His +o$p"ete %"oo# +o-'t s)os
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USMLE WORLD STEP 1 PHARMACOLOGY
Explanation:
Antiplatelet drugs ,ork /y one o+ three /asic mechanisms6 &$ +ormationo+ ligands "aspirin decreases throm/o%ane A) +ormation$0 )$ /locking
interaction o+ ligands ,ith receptors on platelets "clopidogrel and
ticlopidine ,ork as ADP antagonists$0 or :$ inter+ering ,ith
intracellular signaling "cilosta!ol and dipyridamole increase cA;P /y
decreasing phosphodiesterase activity$.
-iclopidine and clopidogrel are use+ul in the treatment and prevention
o+ ischemic strokes0 acute coronary syndrome and peripheral vascular
disease. -hese agents can /e com/ined ,ith aspirin to get an additive
antiplatelet e++ect0 as the mechanism o+ action o+ ticlopidine and
clopidogrel is di++erent +rom aspirin. Sometimes patients are allergic
to or cannot tolerate aspirin or clopidogrel "the t,o +irst line drugs$
and in those patients ticlopidine is the other option. 5ther,ise
ticlopidine is rarely used due to the occurrence o+ serious side
e++ects. #eutropenia is seen in a/out percent o+ patients on
ticlopidine and typically presents ,ith +ever and mouth ulcers. -hough
this is rare0 it is a serious complication and complete /lood count
should /e monitored /i,eekly +or the +irst three months.
"Choice A$ Heparin usually causes throm/ocytopenia /ut not neutropenia.
"Choice G$ A/ci%ima/ and other /9a inhi/itors are also associated
,ith signi+icant throm/ocytopenia typically ,ithin )1 hours. -hey are
typically used in acute coronary syndrome and a+ter stent placement.
"Choices B0 C0 D0 E and H$ -hese drugs do not cause neutropenia.
Educational 5/3ective6
#eutropenia is seen in a/out percent o+ patients on ticlopidine and
typically presents ,ith +ever and mouth ulcers. -hough this is rare0
itis a serious complication and complete /lood count should /e
monitored /i,eekly +or the +irst three months.
38
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USMLE WORLD STEP 1 PHARMACOLOGY
A.
Haloperidol
B. Physostigmine
C. Dia!epam
D. #eostigmine
E. Edrophonium
Explanation:
Atropine can /e administered prior to /ronchoscopy to decrease
respiratory mucous secretions and promote /ronchodilation. Ho,ever0
this patient is no, mani+esting symptoms o+ 5#S and peripheral anti(
muscarinic to%icity. n the elderly "patients J' years o+ age$
atropine=s hal+(li+e may /e prolonged +rom its usual : hours to up to
&'(:' hours due to reduced clearance0 causing an increased
suscepti/ility to to%icity. An organic delirium or psychosis can result
+rom /lockade o+ muscarinic receptors in the C#S. n severe atropine
overdose0 C#S e++ects may progress to coma and respiratory +ailure.
Peripherally0 atropine can cause6 dry and +lushed skin0 hyperthermia
"atropine +ever$0 mydriasis and cycloplegia0 /ronchodilation0
tachycardia constipation and urinary retention.
Physostigmine inhi/its acetylcholinesterase /oth peripherally and
centrally "a tertiary amine0 physostigmine is capa/le o+ crossing the
/lood(/rain /arrier$. -he increased acetylcholine availa/ility
counteracts atropine=s /lockade o+ muscarinic cholinergic receptors.
"Choice A$ -he antipsychotic haloperidol may sedate this patient and
suppress his C#S symptoms0 /ut it ,ould not reverse the otheranticholinergic mani+estations "e.g. mydriasis0 tachycardia$ o+ his
atropine to%icity.
"Choice C$ Dia!epam is sedating and is sometimes used to treat
atropine(induced agitation. Ho,ever0 it ,ould not reverse the
peripheral antimuscarinic e++ects. "Choices D and E$ -hese are
anticholinesterase drugs ,ith actions similar to physostigmine.
Ho,ever0 they /oth have a 7uaternary ammonium structure that prevents
penetration o+ the /lood(/rain /arrier at moderate doses. -hese drugs
,ould thus +ail to alleviate the patient=s 5#S symptoms.
Educational 5/3ective6
-he tertiary amine physostigmine can reverse /oth the C#S and
peripheral symptoms o+ severe atropine to%icity. -he anticholinesterase
agents neostigmine and edrophonium have a 7uaternary ammonium structure
that limits C#S penetration.
39
Q NO 24:A 0B!earo"# $a"e i'patie't a%o-t to -'#er&o %ro'+)os+op! ispre$e#i+ate# it) i'tra$-s+-"ar atropi'e a'# %e+o$es a+-te"! rest"ess,#isorie'te#, a'# +o$%ative* O' p)!si+a" ea$i'atio', )is p-pi"s are i#e"!#i"ate# a'# 'o'rea+tive to "i&)t* A' EO $o'itor s)os si'-sta+)!+ar#ia* W)i+) of t)e fo""oi'& a&e'ts i"" reverse aFi of t)is patie'ts
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USMLE WORLD STEP 1 PHARMACOLOGY
A. Glomerular +iltration rate "GF?$
B. E++ective renal plasma +lo,
C. e+t ventricular e3ection +raction "EP$
D. Hepatic /lood +lo,
E. Cere/ral /lood +lo,
Explanation:
General anesthesia encompasses loss o+ consciousness0 analgesia0
amnesia0 skeletal muscle rela%ation and inhi/ition o+ re+le%es. -his
comple% o+ symptoms occurs due to the inhi/ition o+ electrical activity
o+ neurons. ;ost o+ inhalation anesthetics0 /ar/iturates0 and
/en!odia!epines achieve C#S depression /y in+luencing GABA receptors
and increasing the inhi/itory action o+ GABA. nhaled anesthetics have
also /een sho,n to a++ect potassium channels in the neuronal mem/ranes
and lock them in the state o+ hyperpolari!ation. -hey may also a++ect
nicotinic and glycine receptors.
Apart +rom their desira/le action on C#S inhalation anesthetics a++ect
almost all organ systems o+ the /ody.
&. Cardiovascular e++ects include myocardial depression that leads to a
decrease in cardiac output and an increase in atrial and ventricular
pressures. Hypotension associated ,ith +luorinated anesthetics is a
result o+ decrease in cardiac output.
). ?espiratory6 all inhalation anesthetics0 e%cept nitrous o%ide0 are
respiratory depressants. -hey decrease tidal volume and minute
ventilation and cause hypercapnia. Another undesira/le e++ect is thesuppression o+ mucociliary clearance0 ,hich may predispose to
postoperative atelectasis. Halothane and sevo+lurane have
/ronchodilation properties and are pre+erred in patients ,ith asthma.
:. n the /rain0 +luorinated anesthetics decrease vascular resistance
and lead to an increase in cere/ral /lood +lo,. t is an undesira/le
e++ect as it results in increased intracranial pressure.
1. n kidneys0 inhaled anesthetics decrease glomerular +iltration rate0
increase renal vascular resistance and decrease renal plasma +lo,.
4. Fluorinated anesthetics decrease hepatic /lood +lo,.
"Choices A and B$ ?enal +unction in general anesthesia is characteri!ed
/y decrease in glomerular +iltration rate and decrease in renal plasma
+lo,.
"Choice C$ Fluorinated anesthetics are myocardial depressants. -hey
decrease cardiac output ,hich leads to hypotension.
"Choice D$ Fluorinated anesthetics decrease hepatic /lood +lo,.
Educational 5/3ective6
Almost all volatile anesthetics increase cere/ral /lood +lo,. t is an
undesira/le e++ect as it results in increased CP. 5ther important
e++ects o+ inhalation anesthetics are myocardial depression0
hypotension0 respiratory0 depression and decreased renal +unction.
40
Q NO 25:A 6!earo"# $a"e is -'#er&oi'& a $aor s-r&i+a" pro+e#-re -'#er&e'era" a'est)esia* A f"-ori'ate# i')a"e# a'est)eti+ ?isof"-ra'e@ is -se# toa+)ieve t)e #esira%"e #ept) of +e'tra" 'ervo-s s!ste$ #epressio'* A' i'+reasei' )i+) of t)e fo""oi'& para$eters is $ost "i.e"! to )appe' #-ri'& t)ea'est)esia i' t)is patie't/
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USMLE WORLD STEP 1 PHARMACOLOGY
A. Anti(progestin
B. nhi/ition o+ progesterone synthesis
C. Prostaglandin agonist
D. nhi/ition o+ cell division
E. Anti(glucocorticoid
F. Anti(mineralocorticoid
Explanation:
;i+epristone "previously called ?(1O2$ is an a/orti+acient approved /y
the EDA +or clinical use. t can /e used +or therapeutic a/ortions up
to 18 days a+ter conception. ;i+epristone is a progesterone antagonist
,ith an a++inity +or the progesterone receptor +ive times that o+
natural progesterone.
Progesterone is necessary +or implantation and maintenance o+
pregnancy. >hen its e++ects are antagoni!ed /y mi+epristone0 there is
decidual necrosis and e%pulsion o+ the products o+ conception. -he
success rate o+ mi+epristone at inducing medical termination o+
pregnancy is a/out O'*6 ho,ever0 the success rate is higher ,hen
mi+epristone is com/ined ,ith the prostaglandin analog misoprostol.
"Choice B$ Epostane and trilostane inhi/it the +ormation o+
progesterone +rom pregnenolone /y inhi/iting the en!yme :((
hydro%ysteroid dehydrogenase. -hese agents have /een studied +or use in
the medical termination o+ pregnancy0 /ut their success rates have /een
7uite limited.
"Choice C$ Endogenous prostaglandin causes uterine contraction andcervical dilatation0 important steps in the process o+ la/or.
Prostaglandin analogues have /een used +or years in the medical
termination o+ pregnancy. -he prostaglandin(E& analogue0 misoprostol0
is availa/le +or clinical use in com/ination ,ith the a/orti+acient0
mi+epristone. ";isoprostol has limited success in pregnancy termination
,hen used alone0 /ut enhances the e++icacy o+ mi+epristone.$
Additionally0 misoprostol is sometimes used +or the prevention o+
#SAD(induced gastrointestinal ulceration.
"Choice D$ Folic acid antagonists like methotre%ate inhi/it tropho/last
division thus decreasing tropho/last survival0 hindering implantation
and encouraging e%pulsion. n studies methotre%ate has a higher success
rate ,hen com/ined ,ith vaginal misoprostol. ;ethotre%ate is also used
+or the treatment o+ ectopic pregnancy.
"Choices E and F$ ;i+epristone has mild anti(glucocorticoid and anti(
mineralocorticoid e++ects. Ho,ever0 these e++ects do not contri/ute to
its utility as an agent +or the medical termination o+ pregnancy.
Educational 5/3ective6
;i+epristone is an anti(progestin agent that can /e used to terminate
early pregnancy. -he prostaglandin(E& analogue0 misoprostol0 is
availa/le +or clinical use in com/ination ,ith the a/orti+acient0
mi+epristone.
41
Q NO 26:A !earo"# Ca-+asia' fe$a"e %e&i's treat$e't it) t)e a%ortifa+ie't$ifepristo'e si ee.s after )er "ast $e'str-a" perio#* S)e eperie'+es a%#o$i'a"+ra$ps, 'a-sea a'# va&i'a" %"ee#i'& soo' after i'itiati'& t)erap!* W)i+) of t)efo""oi'& effe+ts is $ost "i.e"! respo'si%"e for t)is patie'ts s!$pto$s/
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USMLE WORLD STEP 1 PHARMACOLOGY
A. Decreased sodium e++lu%
B. ncreased calcium in+lu%
C. ncreased potassium in+lu%
D. ncreased cA;P concentration
E. -roponin sensiti!ation to calcium
Explanation:
Digo%in inhi/its #a(K(A-Pase0 causing an increase in intracellular
sodium0 ,hich in turn decreases the transmem/rane sodium gradient that
acts as the driving +orce o+ the #a(Ca transporter. -his leads tocalcium accumulation in the cell. n e%citation(contraction coupling0
,hen a cardiac myocyte is depolari!ed sodium and calcium enter the cell
and potassium e%its. -his depolari!ation causes the release o+ a large
amount o+ calcium +rom the sarcoplasmic reticulum ,ithin the cell0 and
this high calcium concentration allo,s the /inding o+ calcium to
troponin C and su/se7uent actin(myosin cross /ridge +ormation and
muscle contraction. -he greater the intracellular calcium
concentration0 the greater the contraction ,ill /e. Cardiac rela%ation
then occurs via se7uestration o+ calcium /ack into the sarcoplasmic
reticulum.
43
Q NO 28:9' a patie't it) severe"! i$paire# "eft ve'tri+-"ar f-'+tio', 9: #i&oi'a#$i'istratio' i'+reases +ar#ia+ o-tp-t a'# #e+reases ri&)t atria" press-re a'#p-"$o'ar! +api""ar! e#&e press-re* W)i+) of t)e fo""oi'& is t)e i'itia" +e""-"areve't tri&&eri'& t)is respo'se to #i&oi'/
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USMLE WORLD STEP 1 PHARMACOLOGY
-hus calcium gluconate should not /e given to patients +or hyperkalemia
in the setting o+ digo%in to%icity. Digo%in and potassium compete ,itheach other +or #a(K( A-Pase thus digo%in to%icity results in
hyperkalemia. Hypokalemia ,orsens digo%in to%icity.
"Choice A$ Digo%in e%erts its e++ect on the #a(K(A-Pase thus causing
decreased sodium e++lu% +rom the cardiac myocyte.
"Choice B$ Digo%in causes decreased calcium e++lu%0 not increased
calcium in+lu%. High levels o+ intracellular calcium are necessary +or
e%citation(contraction coupling leading to contraction o+ the myocyte.
"Choice C$ -he #a(K(A-Pase causes K in+lu% and #a e++lu%. Digo%in acts
to inhi/it the #a(K(A-Pase.
"Choice D$ Cyclic A;P "cA;P$ is an important second messenger in
e%citation(contraction coupling though digo%in has no e++ect on the
production o+ cA;P. cA;P is +ormed +rom AlP /y adenylyl cyclase0 the
activity o+ ,hich is stimulated /y /eta agonists. cA;P increases the
conductance o+ the calcium channels in the sarcoplasmic reticulum. As a
result0 more calcium can enter the cell and strengthen the +orce o+
contraction.
"Choice E$ Digo%in does not cause increased troponin sensitivity to
calcium. #e, drugs are /eing developed to increase the sensitivity o+
calcium.
Educational 5/3ective6
-he mechanism o+ action o+ digitalis is the inhi/ition o+ the #a(K(
A-Pase in cardiac pacemaker cells leading to A< nodal /lockade
"increased diastolic +illing time +or greater contraction /y the Frank(
Starling mechanism$ and increased contractility +rom increased
intracellular calcium.
44
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USMLE WORLD STEP 1 PHARMACOLOGY
A. Chlorproma!ine
B. Haloperidol
C. Liprasidone
D. -hiorida!ine
E. 5lan!apine
F. Clo!apine
Explanation:-hiorida!ine is an anti(psychotic medication that may cause retinal
deposits that resem/le retinitis pigmentosa.
"Choice A$ Chlorproma!ine is associated ,ith corneal deposits.
"Choice B$ Haloperidol is associated ,ith e%trapyramidal symptoms.
"Choice C$ Liprasidone is associated ,ith prolonged -.
"Choice E$ 5lan!apine is associated ,ith ,eight gain.
"Choice F$ Clo!apine is associated ,ith agranulocytosis and sei!ures.
Educational 5/3ective6
-hiorida!ine causes retinal deposits that resem/le retinitis
pigmentosa. Chlorproma!ine is associated ,ith corneal deposits.
45
Q NO 29:A 63!earo"# $a"e prese'ts to !o-r offi+e it) i$paire# visio'* He sa!st)at t)e pro%"e$s it) )is visio' starte# a "o'& ti$e a&o a'# &ra#-a""! pro&resse#overti$e* His past $e#i+a" )istor! is si&'ifi+a't for "o'&sta'#i'& s+)i(op)re'iaeffe+tive"! +o'tro""e# %! $e#i+atio's* Op)t)a"$os+op! s-&&ests t)e #ia&'osis ofreti'itis pi&$e'tosa i' t)is patie't* W)i+) of t)e fo""oi'& a'tips!+)oti+ a&e'ts )as$ost "i.e"! %ee' -se# i' t)is patie't/
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A. uinidine
B. idocaine
C. Flecainide
D. Do+etilideE.
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Explanation:
An e++ect typical o+ the class ll antiarrhythmic agents isdemonstrated on this graph ,here potassium e++lu% +rom the cell
"negative /lack line$ as ,ell as the length o+ the action potential is
prolonged ,hile the movement o+ sodium "positive /lue line$ and calcium
"positive /lack line$ are relatively una++ected. Do+etilide "Choice D$0
i/utilide0 amiodarone and sotalol are representative o+ class
agents.
"Choice A$ uinidine is a class A antiarrhythmic agent. t /locks
sodium channels and has the e++ect on phase ' depolari!ation and phase
: repolari!ation.
"Choice B$ idocaine is a class B antiarrhythmic agent and acts /y
/locking sodium channels only in veri rapidly depolari!ing cells. t
does not have much e++ect on potassium e++lu%.
"Choice C$ Flecainide is a class C antiarrhythmic agent. t /locks
sodium channels and primarily acts /y slo,ing phase ' depolari!ation.
"Choice E$
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USMLE WORLD STEP 1 PHARMACOLOGY
A. Progesterone antagonist
B. Estrogen antagonist
C. Androgen antagonist
D. Aromatase inhi/itor
E. Gn?H antagonist
Explanation:
5/esity0 oligomenorrhea0 hyperandrogenism "hirsutism0 acne$ and
in+ertility in a young ,oman are suggestive o+ polycystic ovarian
syndrome "PC5S0 Stein(eventhal syndrome$. -his disease is
characteri!ed /y increased circulating androgens and H0 and a high
H9FSH ratio. Hypersecretion o+ H /y the anterior pituitary is
considered a primary a/normality in PC5S. ncreased H stimulates
secretion o+ androgens /y ovarian theca cells. Elevated H and androgen
levels coupled ,ith decreased ESH levels lead to dysregulation o+ the
menstrual cycle and anovulation due to +ailure o+ +ollicular
maturation. Decreased +re7uency o+ ovulation in PC5S causes menstrual
irregularities "oligomenorrhea$ and in+ertility. nopposed estrogen
in+luence on the endometrium leads to endometrial proli+eration and an
increased risk o+ endometrial carcinoma. 5ther complications o+ PC5S
include dia/etes mellitus due to peripheral insulin resistance and an
increased risk o+ cardiovascular disease due to elevated triglycerides
and cholesterol.
n+ertility in P5DS is treated ,ith clomiphene and ,eight loss.Clomiphene structurally resem/les estrogen and reacts ,ith estrogen
receptors in the 5#S "Choice B$. >hen estrogens are secreted in
su++icient 7uantities0 they elicit negative +eed/ack on the
hypothalamus and inhi/it production o+ gonadotropin(releasing hormone
"Gn?H$. Clomiphene /locks these receptor sites there/y suppressing
negative +eed/ack on the hypothalamohypophysial a%is /y estrogen. -he
result o+ clomiphene therapy is continued secretion o+ gonadotropins
despite normal or elevated estrogen levels. ncreased amounts o+ ESH
and H ultimately stimulate ovulation.
"Choice A$ ;i+epristone "?1O2$ is a progesterone antagonist. +
administered to pregnant ,omen0 this drug inter+eres ,ith the action o+
progesterone causing +ailure o+ maintenance o+ the endometrium and
sensiti!ation o+ the uterus to procontractile hormones such as PGE()
there/y inducing a/ortion.
"Choice C$-he androgen antagonists cyproterone and +lutamide
competitively inhi/it the action o+ androgens /y interacting ,ith
receptors on the target cells. Flutamide is used occasionally +or the
treatment o+ prostate cancer though Gn?H agonists are pre+erred0 ,hile
cyproterone is indicated to treat hirsute +emales.
"Choice D$ Aromatase inhi/itors include anastro!ole and letro!ole. -hey
inhi/it peripheral conversion o+ androgens into estrogens and are used
in ,omen ,ith estrogen(receptor(positive /reast cancer.
"Choice E$ Gn?H agonists include leuprolide and goserelin. Continuous
administration o+ these drugs inhi/its production o+ gonadotropin(
releasing hormone /y the hypothalamus /y causing do,nregulation o+ the
49
Q NO 32:A 8!earo"# $i"#"! o%ese o$a' is treate# for i'ferti"it!* Her $e'str-a"+!+"es are irre&-"ar o++-rri'& o'+e ever! to to t)ree $o't)s* Ea$i'atio' s)os)irs-tis$* O'+e treat$e't is starte#, )er ser-$ pro&estero'e "eve" i'+reasess)arp"! a'# se+retor! +)a'&es are 'ote# o' e'#o$etria" sa$p"i'&* W)i+) of t)efo""oi'& a&e'ts )as %ee' $ost "i.e"! -se# i' t)is patie't/
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USMLE WORLD STEP 1 PHARMACOLOGY
Gn?H receptor. -hey are indicated in prostate cancer0 precocious
pu/erty and endometriosis.
Educational 5/3ective6
5/esity0 oligomenorrhea and in+ertility are seen in patients ,ith
polycystic ovarian syndrome "P5DS$. n+ertility in P5DS occurs due to
anovulation resulting +rom a/normal FSH and H levels. Clomiphene is an
estrogen antagonist that increases secretion o+ gonadotropins and
stimulates ovulation.
50
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USMLE WORLD STEP 1 PHARMACOLOGY
A. Beta(/lockers +or hypertension
B. Cimetidine +or peptic ulcer disease
C. /upro+en +or osteoarthritis
D. A @/a/y aspirin +or stroke prevention
E. An over(the(counter multivitamin
Explanation:
;ost over(the(counter vitamins contain B2.
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USMLE WORLD STEP 1 PHARMACOLOGY
A. Cardiac muscle cell damage
B. Bone marro, suppression
C. ?enal tu/ular dys+unction
D. Hepatocyte necrosis
E. Pulmonary hypertension
Amphotericin B is the drug o+ choice +or many systemic mycoses. t is
also the most to%ic anti+ungal medication. -he most dangerous adverse
e++ect o+ amphotericin B is its nephroto%icity. Amphotericin B causes
/oth a decrease in the glomerular +iltration rate and direct to%ic
e++ects on the tu/ular epithelium. Anemia and electrolyte a/normalities
may stem +rom amphotericin B(associated nephroto%icity. Hypokalemia and
hypomagnesemia are common0 due to an increase in the mem/rane
permea/ility o+ the distal tu/ule. Hypokalemia can cause ,eakness and
arrhythmias. ECG +indings in hypokalemia include -(,ave +lattening0 S-(
segment depression0 prominent ,aves0 and premature atrial and
ventricular contractions. Pro+ound hypokalemia can cause ventricular
tachycardia or +i/rillation.
"Choice A$ Do%oru/icin and daunoru/icin are associated ,ith
irreversi/le dose(dependent cardioto%icity. -his is not a side e++ect
o+ amphotericin B.
"Choice B$ Bone marro, suppression is associated ,ith chloramphenicol0
!idovudine0 phenyl/uta!one0 and gold( containing medications. Bone
marro, suppression ,ould not cause ECG changes.
"Choice D$ Acetaminophen and halothane are e%amples o+ medications thatcan cause liver necrosis. Amphotericin B is not hepatoto%ic.
"Choice E$ Busul+an and /leomycin are e%amples o+ the drugs that cause
pulmonary +i/rosis and can lead to pulmonary hypertension.
Educational 5/3ective6
Hypokalemia and hypomagnesemia are common electrolyte distur/ances in
patients undergoing treatment ,ith amphotericin B. Hypokalemia and
hypomagnesemia re+lect an increase in distal tu/ular mem/rane
permea/ility.
52
Q NO 34:A 40!earo"# Ca-+asia' $a"e -'#er&oi'& treat$e't it) a$p)oteri+i' 5for #isse$i'ate# )istop"as$osis +o$p"ai's of ea.'ess a'# pa"pitatio's* A' ECGrevea"s fre2-e't pre$at-re ve'tri+-"ar %eats* 9f +a-se# %! #r-& toi+it!, t)ese 'esi&'s a'# s!$pto$s are $ost "i.e"! re"ate# to
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A. #(acetylcysteine
B. Folinic acid
C. Filgrastim
D. Fomepi!ole
E. De%ra!o%ane
F. Ami+ostine
Explanation:
Cisplatin is a platinum(containing compound that e%erts its
chemotherapeutic e++ect /y +orming a reactive o%ygen species that can
+orm D#A cross links. -he most prominent adverse e++ect associated ,ith
use o+ cisplatin is nephroto%icity. -his drug causes acute tu/ular
in3ury0 and a signi+icant percentage o+ patients ,ill develop mild
renal insu++iciency a+ter the +irst course o+ therapy i+ preventative
measures are not taken.
Ami+ostine is a thiol(/ased cytoprot