CPPS 306 QUESTIONS WITH CORRECT ANSWERS 2025

CPPS 306 QUESTIONS WITH CORRECT
ANSWERS 2025
BosentanV-VCORRECTVANSWERV-
firstVdrugVforVtheVantagonismVofVETAVandVETBV(didn'tVworkVthatVwell,VdueVtoVnoVvasodilationVpathways)
V

mainVuseVpulmonaryVhypertension

AmbrisentanV-VCORRECTVANSWERV-ETAVselectiveVtheoreticallyVprovidesVanVantihypertensiveVeffectV
allowedVETBVreceptorsVtoVreleaseVNOVfromVendothelialVcellsV
mainVuseVpulmonaryVhypertension

NOVnitricVoxideV-VCORRECTVANSWERV-NOVcanVbeVthoughtVofVasVaVvasorelaxantVequivalentVofVET
NOVisVreleasedVfromVtheVendothelialVcellsVintoVvascularVsmoothVmuscle
promotesVtheVactivityVofVguanylateVcyclaseV(sGC)VwhichVthenVpromotesVcyclicVGMP
thisVreducesVintracellularVCA2+VresultingVinVvasodilation

RiociguatV-VCORRECTVANSWERV-
directlyVstimulatesVactivityVofVsolubleVguanylateVcyclaseV(usedVforVpulimaryVhypertension)V
loweringVintercellularVcalcium

ProstacyclinV-VCORRECTVANSWERV-mainlyVusedVforVpulmonaryVhypertensionV
stimulatesVACVtoVproduceVmoreVcAMP,VwhichVreducesVintercellularVCA2+
thereforeVprostacyclinVrelaxesVbloodVvesselsVinVtheVpulmonaryVcirculation

EndothelialVderivedVhyperpolarizingVfactorV(EDHF)V-VCORRECTVANSWERV-
ReleaseVofVEDHFVresultsVinVopeningVofVcalciumVchannel,VandVhyperpolarizationV
hyperpolarizationVinhibitsVcalciumVchannel,VpreventingVentryVofVCa2+VintoVtheVvasscularVsmoothVmussleV
resultingVinVrelaxationV(dilationVoverVconstriction)

ThiazidesV(group)V-VCORRECTVANSWERV-mostVcommonlyVusedVdiretic

FurosemideV-VCORRECTVANSWERV-
LoopVdireticV(forcesVpeopleVtoVgoVtoVtheVbathroomValot<VhighVchanceVthatVpatientVstopsVtakingVmedicatio
nVbeacuseVofVthis)

SpironolactoneV-VCORRECTVANSWERV-K+VsparingVdireticVpreventsVpotasiumVloss

AngiotensisnVIIV-VCORRECTVANSWERV-BindsVtoVtheVAT1VreceptorV
mainVphysiologicalVactionsVincludeV
AldosteroneVsynthesisVandVsecretionV
NaClVreabsorptionV
AntidiureticVhormoneV(ADH)VreleaseV

******vasoconstrictionVthroughVanVincreaseVinVCa2+VinVtheVvascularVsmoothVmuscle

RamiprilV-VCORRECTVANSWERV-allVACEVinhibitorsVendVinV-pril

, inhibitsVvasoconstrictionV
inhibitsValdosteroneVsecretionV(NaVretention)
InhibitsVNaCLVreabsobtionV
inhibitVADHVreleaseV
****increasedVvasodilationVthroughVBK

resultVDecreasedVSVR
andVanVincreaseVinVnatriuresisVandVdiuresis

LosartanV-VCORRECTVANSWERV-AngiotensingVreceptorVblockersV(ARBs)
noVeffectVonVbradykininV
lessVcough
lessVangioedema

AliskirenV-VCORRECTVANSWERV-DirectVreninVinhibitorsV(DRI)
theoryVpatientsV'resistant'VtoVotherVRASVinhibitorsVmightVrespondVwellVtoVDRIV
practiceVDRIVhasVnotVbeenVpopular,VfirstVinVtheVlineVofVdrugs

NifedipineV-VCORRECTVANSWERV-(-ipine)
DihydropyridinesVactVonVtheVvasculatureV>Vheart
pharmacodynamicsV
vasodilationV(primary)
arterial>venous
reducesVcontractilityV
*****mainlyVdilates

VerapamilVandVDiltiazemV-VCORRECTVANSWERV-non-dihydropyridines
bothVhaveVaVgreaterVimpactVonVtheVheartVthanVdihydropyridinesVbutVstill,VretainVvascularVeffectsV
pharmacodynamicVactionsV
reduceVheartVrate
reduceVcontractilityV
vasodilation

nifedipineV-VCORRECTVANSWERV-rapidVonsetVcalciumVblocker

AmlodipineV-VCORRECTVANSWERV-slowerVonsetVcalciumVblocker

PropranololV-VCORRECTVANSWERV-BetaVantagonistVblockers
(-lol)V
pharmacodynamicVactions
decreaseVheartVrate,VcontractilityV(b1)
decreaseVreninVsecretionV(b1)
decreaseVSNSVactivityV(b1)

reducesVBPVbyVreducingVcardiacVoutputV
andVbyVreducingVactivationVofVRAS

MetoprololV-VCORRECTVANSWERV-BetaVblockerVB1
cardioselective

propranololV-VCORRECTVANSWERV-BetaVblockerVB1VandVB2