Pharmacologie testes

8/11/2019 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: 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: 15 Endocrinology Pharmacology Q No: 56 Blood vessels


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: 25 Neurology Pharmacology Q No: 66 Cardiology

Pharmacology Q No: 26 Genitourinary Pharmacology Q No: 67 Cardiology


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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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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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

4


5/73


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/


6/73


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.


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/


7/73


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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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


9/73


A.


10/73


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/


11/73


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$


12/73


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$.


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'/


13/73


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.


-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


14/73


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


15/73


"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%.


-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


16/73


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


17/73


"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.


-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


18/73


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/


19/73


"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,.


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


20/73


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.


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!/


21/73


A.


22/73


+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.


;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


23/73


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.


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/


24/73


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'&/


25/73


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.


-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


26/73


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/


27/73


has developed ,idespread resistance to sul+onamides0 so these drugs are

no longer used.


?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.


28/73


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


29/73


"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.


-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


30/73


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/


31/73


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.


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


32/73


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.


-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/


33/73


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.


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


34/73


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'/


35/73


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+


36/73



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


37/73


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


38/73


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.


#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


39/73


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.


-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


40/73


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,.


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/


41/73


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.


;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/


42/73


43/73


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'/


44/73


-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.


-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


45/73


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.


-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/


46/73


A. uinidine

B. idocaine

C. Flecainide

D. Do+etilideE.


47/73


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$


48/73


49/73


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/


50/73


Gn?H receptor. -hey are indicated in prostate cancer0 precocious

pu/erty and endometriosis.


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


51/73


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.


52/73


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.


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

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