NURSl 5315/l NURS5315l Examl 3l –l
Advancedl Pathophysiologyl Guidel |l UTAl
(Latestl 2026l Update)l 100%l Verifiedl
Questionsl &l Answersl |l Gradel A
Q:l leftl coronaryl artery
Answer:
-l leftl anteriorl descendingl artery:l bll tol anteriorl 2/3l ofl thel interventricularl septum,l antl
papillaryl msucle,l &l antl surfacel ofl thel leftl vent
-l leftl marginall artery:l bll tol leftl ventricle
-l leftl cirmcumflex:l bll tol laterall &l postl wallsl ofl thel leftl ventriclel &l leftl atruim
Q:l rightl coronaryl artery
Answer:
-l rightl coronaryl artery:l bll tol SAl &l AVl nodesl inl thel rightl atriuml &l bothl ventricles
-l rightl marginall artery:l bll tol thel anteriorl &l posteriorl portionsl ofl thel rightl ventricle
-l posteriorl descendingl artery:l bll tol posteriorl 1/3l ofl interventriulcarl septum,l posteriorl
wallsl ofl bothl ventricles,l &l posteromediall papillaryl muscles
Q:l rightl dominant
Answer:
posteriorl descendingl arteryl arisesl froml RCA
Q:l leftl dominant
Answer:
posteriorl descendingl arteryl arisesl froml thel leftl circumflexl artery
Q:l coronaryl arteryl occlusion
,Answer:
-l mostl commonl inl leftl anteriorl descendingl arteryl thenl RCAl andl leftl circumflex
Q:l leftl atrium
Answer:
-mostl posteriorl portionl ofl thel heart
-l whenl itl enlargesl itl canl causel dysphagial byl thel compressionl onl thel esophagusl orl canl
leadl tol hoarsenessl froml compressionl ofl thel leftl recurrentl laryngeall nerve
Q:l coronaryl arteryl disease
Answer:
-l riskl fcts:l advl age,l malel gender,l post-menopausall women,l familyl hx,l dyslipidemia,l
HTN,l smoking,l DM,l insulinl resistance,l obesity,l sedentaryl lifestyles,l highl fatl diet,l
increasel inl LDL,l chronicl kidneyl ds,l decreasel adiponectinl hormone,l NSAIDs
-l smokingl causesl releasel ofl catecholaminesl whichl causel vasconstrictionl andl HTNl
-l smokingl generatesl prodl ofl freel radicalsl thatl damagel thel endotheliall cells
-DMl =l endotheliall damage,l thickeningl ofl vessell walls,l increasedl thrombosisl &l deceasedl
prodl ofl nitricl acid
-l causel lumenl narrowingl &l mayl causel acutel ischemial whichl mayl bel relievedl prl
progressl tol anl MI;l chronicl ischemial mayl occurl w/l orl w/ol infarctionl andl leadl tol
cellularl damagel &l heartl failure
Q:l NSAIDs
Answer:
-l increasel coronaryl events
-l adversel effectsl onl myocardiall celll mitochondria
-l promotel productionl ofl toxicl reactivel O2l
-l alterl balancel b/wl thromboxanel &l prostacyclinl whichl promotesl pltl aggregation
Q:l Stablel angina
Answer:
-l chestl painl thatl isl causedl byl myocardiall ischemia
-l graduall lumenl narrowingl
-l occursl whenl O2l demandl increases
,-l painl isl severe,l feelsl likel al heavinessl orl pressure,l mayl radiatel tol thel neck,l jawl orl
leftl shoulder,l mayl bel accompaniedl byl pallor,l diaphoresis,l orl dyspnea
Q:l unstablel angina
Answer:
-l prolongedl orl recurrent
-increasesl inl severityl orl frequency
-l causedl byl al labilel thrombusl thatl doesl notl occludel bll flowl longerl thanl 20l min
-l EKGl willl showl Tl wavel inversion,l STl depressionl
-troponinl levelsl willl bel normal
Q:l Non-STl Elevationl Myocardiall Infarctionl (NSTEMI)
Answer:
-resultsl froml thrombusl thatl occludedl coronaryl bll flowl forl greaterl thanl 20l min&l resultsl
inl myocardiall necrosis
-l doesl notl involvel fulll thicknessl ofl thel ventricularl wall
-l EKGl willl showl STl depressionl orl Tl wavel inversion
Q:l STl Elevationl Myocardiall Infarctionl (STEMI)
Answer:
-l resultsl froml thrombusl permanentlyl blockingl coronaryl bll flowl
-l fulll thicknessl ventricularl wall
-l EKGl willl showl STl elevation
Q:l Evolutionl ofl MI
Answer:
cellularl injuryl d/tl ongoingl hypoxia->l myocytesl becomel cyanoticl ->l O2l reservesl usedl
upl ->l glycogenl storesl decreasel andl glycolysisl notl ablel tol supplyl alll neededl energyl tol
heart->l lessl ATPl prodl ->H+l ionsl &l lacticl acidl accumulatel froml anaerobicl metabolisml -
>l K,l Ca,l &l Mgl lostl froml cellsl ->l myocardiall cellsl deprivedl ofl nutrientsl losel
contractilityl &l resultl inl diminishedl contractionl ->l ischemicl cellsl releasel catecholaminesl
whichl furtherl stressesl heartl &l increasesl riskl ofl arrythmiasl &l heartl failurel ->l norepil
decreasesl insulinl secretionl &l hyperglycemial occursl (seenl 72l hrl afterl MI)l ->l angiotensinl
, 2l releasedl causingl vasoconstrictionl ->l increasesl afterload&l myocardiall wrkload->l
necrosisl afterl 20l min->l areal ofl necrosisl detl fxnl ofl heartl andl clinicall manifestations
Q:l reperfusionl injury
Answer:
causedl whenl bll flowl restored;l triggersl releasel ofl toxicl O2l radicals,l Cal influx,l &l pHl
changesl thatl causel persistentlyl openl mitochondriall permeabilityl transitionl presl &l
contributel tol cellularl death
Q:l structurall changesl withl MI
Answer:
-l hypoxicl injuryl thatl mayl causel necrosis
-l impairmentl ofl myocardiall contractionl forl hrsl tol daysl causedl byl electrolytel alterationsl
andl releasel ofl O2l radicals
-l mayl progressl tol heartl failure,l shockl orl dysrythmias
-l myocardiall hibernatingl :l persistentl hypoxicl tissl undergol adaptationl tol survivel untill
perfusionl isl restored
-l myocardiall remodeling:l neurohormonall processl associatedl withl hrtl failurel whichl resultsl
inl hypertrophy,l scarring,l &l decreasedl contraction
Q:l MIl CM
Answer:
-l suddenl severel chestl painl (crushing)l thatl mayl radiatel tol back,l neck,l jaw,l shoulderl orl
leftl arm
-l N/Vl
-l tacycardia,l newl cardiacl murmurs,l pulmonaryl crackles,l cooll andl clammy
-l cardiacl tropl increased
Q:l myocardiall ischemia
Answer:
Tl wavel inversionl
bloodl supplyl decreased
Q:l myocardiall injury
Advancedl Pathophysiologyl Guidel |l UTAl
(Latestl 2026l Update)l 100%l Verifiedl
Questionsl &l Answersl |l Gradel A
Q:l leftl coronaryl artery
Answer:
-l leftl anteriorl descendingl artery:l bll tol anteriorl 2/3l ofl thel interventricularl septum,l antl
papillaryl msucle,l &l antl surfacel ofl thel leftl vent
-l leftl marginall artery:l bll tol leftl ventricle
-l leftl cirmcumflex:l bll tol laterall &l postl wallsl ofl thel leftl ventriclel &l leftl atruim
Q:l rightl coronaryl artery
Answer:
-l rightl coronaryl artery:l bll tol SAl &l AVl nodesl inl thel rightl atriuml &l bothl ventricles
-l rightl marginall artery:l bll tol thel anteriorl &l posteriorl portionsl ofl thel rightl ventricle
-l posteriorl descendingl artery:l bll tol posteriorl 1/3l ofl interventriulcarl septum,l posteriorl
wallsl ofl bothl ventricles,l &l posteromediall papillaryl muscles
Q:l rightl dominant
Answer:
posteriorl descendingl arteryl arisesl froml RCA
Q:l leftl dominant
Answer:
posteriorl descendingl arteryl arisesl froml thel leftl circumflexl artery
Q:l coronaryl arteryl occlusion
,Answer:
-l mostl commonl inl leftl anteriorl descendingl arteryl thenl RCAl andl leftl circumflex
Q:l leftl atrium
Answer:
-mostl posteriorl portionl ofl thel heart
-l whenl itl enlargesl itl canl causel dysphagial byl thel compressionl onl thel esophagusl orl canl
leadl tol hoarsenessl froml compressionl ofl thel leftl recurrentl laryngeall nerve
Q:l coronaryl arteryl disease
Answer:
-l riskl fcts:l advl age,l malel gender,l post-menopausall women,l familyl hx,l dyslipidemia,l
HTN,l smoking,l DM,l insulinl resistance,l obesity,l sedentaryl lifestyles,l highl fatl diet,l
increasel inl LDL,l chronicl kidneyl ds,l decreasel adiponectinl hormone,l NSAIDs
-l smokingl causesl releasel ofl catecholaminesl whichl causel vasconstrictionl andl HTNl
-l smokingl generatesl prodl ofl freel radicalsl thatl damagel thel endotheliall cells
-DMl =l endotheliall damage,l thickeningl ofl vessell walls,l increasedl thrombosisl &l deceasedl
prodl ofl nitricl acid
-l causel lumenl narrowingl &l mayl causel acutel ischemial whichl mayl bel relievedl prl
progressl tol anl MI;l chronicl ischemial mayl occurl w/l orl w/ol infarctionl andl leadl tol
cellularl damagel &l heartl failure
Q:l NSAIDs
Answer:
-l increasel coronaryl events
-l adversel effectsl onl myocardiall celll mitochondria
-l promotel productionl ofl toxicl reactivel O2l
-l alterl balancel b/wl thromboxanel &l prostacyclinl whichl promotesl pltl aggregation
Q:l Stablel angina
Answer:
-l chestl painl thatl isl causedl byl myocardiall ischemia
-l graduall lumenl narrowingl
-l occursl whenl O2l demandl increases
,-l painl isl severe,l feelsl likel al heavinessl orl pressure,l mayl radiatel tol thel neck,l jawl orl
leftl shoulder,l mayl bel accompaniedl byl pallor,l diaphoresis,l orl dyspnea
Q:l unstablel angina
Answer:
-l prolongedl orl recurrent
-increasesl inl severityl orl frequency
-l causedl byl al labilel thrombusl thatl doesl notl occludel bll flowl longerl thanl 20l min
-l EKGl willl showl Tl wavel inversion,l STl depressionl
-troponinl levelsl willl bel normal
Q:l Non-STl Elevationl Myocardiall Infarctionl (NSTEMI)
Answer:
-resultsl froml thrombusl thatl occludedl coronaryl bll flowl forl greaterl thanl 20l min&l resultsl
inl myocardiall necrosis
-l doesl notl involvel fulll thicknessl ofl thel ventricularl wall
-l EKGl willl showl STl depressionl orl Tl wavel inversion
Q:l STl Elevationl Myocardiall Infarctionl (STEMI)
Answer:
-l resultsl froml thrombusl permanentlyl blockingl coronaryl bll flowl
-l fulll thicknessl ventricularl wall
-l EKGl willl showl STl elevation
Q:l Evolutionl ofl MI
Answer:
cellularl injuryl d/tl ongoingl hypoxia->l myocytesl becomel cyanoticl ->l O2l reservesl usedl
upl ->l glycogenl storesl decreasel andl glycolysisl notl ablel tol supplyl alll neededl energyl tol
heart->l lessl ATPl prodl ->H+l ionsl &l lacticl acidl accumulatel froml anaerobicl metabolisml -
>l K,l Ca,l &l Mgl lostl froml cellsl ->l myocardiall cellsl deprivedl ofl nutrientsl losel
contractilityl &l resultl inl diminishedl contractionl ->l ischemicl cellsl releasel catecholaminesl
whichl furtherl stressesl heartl &l increasesl riskl ofl arrythmiasl &l heartl failurel ->l norepil
decreasesl insulinl secretionl &l hyperglycemial occursl (seenl 72l hrl afterl MI)l ->l angiotensinl
, 2l releasedl causingl vasoconstrictionl ->l increasesl afterload&l myocardiall wrkload->l
necrosisl afterl 20l min->l areal ofl necrosisl detl fxnl ofl heartl andl clinicall manifestations
Q:l reperfusionl injury
Answer:
causedl whenl bll flowl restored;l triggersl releasel ofl toxicl O2l radicals,l Cal influx,l &l pHl
changesl thatl causel persistentlyl openl mitochondriall permeabilityl transitionl presl &l
contributel tol cellularl death
Q:l structurall changesl withl MI
Answer:
-l hypoxicl injuryl thatl mayl causel necrosis
-l impairmentl ofl myocardiall contractionl forl hrsl tol daysl causedl byl electrolytel alterationsl
andl releasel ofl O2l radicals
-l mayl progressl tol heartl failure,l shockl orl dysrythmias
-l myocardiall hibernatingl :l persistentl hypoxicl tissl undergol adaptationl tol survivel untill
perfusionl isl restored
-l myocardiall remodeling:l neurohormonall processl associatedl withl hrtl failurel whichl resultsl
inl hypertrophy,l scarring,l &l decreasedl contraction
Q:l MIl CM
Answer:
-l suddenl severel chestl painl (crushing)l thatl mayl radiatel tol back,l neck,l jaw,l shoulderl orl
leftl arm
-l N/Vl
-l tacycardia,l newl cardiacl murmurs,l pulmonaryl crackles,l cooll andl clammy
-l cardiacl tropl increased
Q:l myocardiall ischemia
Answer:
Tl wavel inversionl
bloodl supplyl decreased
Q:l myocardiall injury
