Cardio quiz 2c

eem8u's version from 2016-12-17 05:28

Acute Coronary syndrome I


Clotting cascade
Question Answer
fx of factor Xconverts prothrombin II to thrombin IIa
fx of thrombin IIaconvert fibrinogen 1 >> fibrin Ia
fx of fibrin 1aforms of cross-linked fibrin CLOT (like a meshwork or cement w/in RBC’s & platelets are formed
role of tissue factor (released w/ trauma)activates factor X
role of factor VIIaactivates factor X (along with TFactor)


Antithrombotic mechanism - anticlotting factors
Question Answer
fx of antithrombinplatelet protein, inactivates thrombin IIa
***fx of heparan (on luminal surface) 1000x increased efficacy of antithrombin
***fx of thrombomodulinendothelia RECEPTOR that binds thrombin (inhibits fx) >> thrombin/thrombomodulin activate PROTEIN C
fx of Protein Cdegrade Factor Va and VIIa
fx of Protein Senhance function of protein C


Antithrombotic mechanisms - endothelium
Question Answer
fx of TPA (tissue plasminogen Activator)released by endothelial cells when clot is formed, cleaves plasminogen >> plasmin
***fx of plasmindegrade fibrin clot
***fx of prostacyclinreleased by endo >> platelet inactivation & vasodilation
fx of NOreleased by endo >> platelet inactivation & vasodilation
fx of adenosineconverted by endothelial cell from ADP >> platelet inactivation
***mechanism of platelet activationendothelium collagen & vWfactor exposed >> bind protein and platelets > activation >> release TXa2 / ADP >> activation of glycoprotein 2b/3a >> binds fibrinogen >> thrombus formation
****platelets release (2)tx2s, ADP


Pathogenesis of Coronary Thrombosis
Question Answer
fx of thromboxanereleased by platelet, causes vasoconstriction
fx of serotoninreleased by platelet, causes vasoconstriction
sequelae of vasoconstrictionhemodynamic stress on plaque & reduced coronary blood flow /reduce clearance of procoagulant
understand pathogenesis of thrombus formationslide 11, beginning with plaque rupture >>>>> 2 possible outcome unstable angina or MI


Myocardial Infarct
Question Answer
***2 functional sequelae of MIsystolic dysfx and diastolic dysfx (increased filling P >>> pulmonary congestion)
understand phases of remodelingslide 21.14 (thinning & fibrous scar >>> dilation & hypertrophy w/ COLLAGEN)
mechanism- hypertrophy in remodelingneurohormonal activation / increase in sympathetic tone (especially Angiotensin II)
2 mechanisms (general approaches) to prevent remodeling1- early perfusion (halt infarct) 2- counteract neurohormal activation via ACE-i and B-blocker (both increase survival)
*** MI Type 1plaque rupture w/ thrombus
***MI Type 2supply demand imbalance w/o rupture of plaque (vasospasm, fixed atherosclerosis, anemia, acute pressure drop as in anaphylaxis)
transmural MI - causetotal prolonged occlusion of coronary artery
****subendocardial MI - describe vulnerabilites of subendocardium (3)1- exposed to highest P’s 2- few collaterals 3- vessels w/ o2 must pass through contracting myocardium
****cocaine abuse - cause of ACS (3 mechanisms)vasospasm (decreased o2 supply), increased Hr (Increased O2 demand), atherosclerosis
plaque erosion (rather than rupture) more common in young women, smokers


****Clinical MI
Question Answer
know the differential diagnosis of Chest Pain (CV/ pulm/ GI)21.29 1- heart (pericardial syndromes, aortic dissection) 2- Pulm (PE, pneumonia, pneumothorax) 3- GI (esophageal spasm, acute cholecystitis)
Left circumflex a. >> infarct where & what 4 leadsLATERAL heart (1, avL, v5, v6)
Right coronary a. >> infarct where & what 3 leadsINFERIOR heart ( II, III, AvF)
LAD >> infarct where & what 4 leadsANTEROSEPTAL (V1-V4)
****leads specific to septumV1, v2
hyperacute T wave seen whenwithin minutes > hours of MI
deeper Q wave seen whenafter at least 1 day >>> months after MI


Question Answer
biomarkers of necrosistroponin (T, I, C), CK-MB, myoglobin
role of troponincontrol by Ca2+ >> mediate interaction b/t actin and myosin (cardiac and skeletal muscles)
troponin -cytosolic vs muscular poolsmall injury/elevation comes from cytosol first
****troponin - timing of rise / peak/ clearancerise 3-4 hrs / peak 18-36 hrs / 2 weeks to clear
****CK - timing of rise / peace / clearance 1< hours / peak < 1day / clear by 2 days **second MI**
biomarkers seen with (what forms of ACS)nonSTEMI (partial occlusion) and STEMI

Acute Coronary Syndrome II — Treatment

Acute MI Medications
Question Answer
key distinction in txSTEMI vs. NSTEMI
****drugs w/ mortality benefit in MIB-blockers (if w/in 24 hours), Aspirin (no benefit with nitrates, CC blocker)
4 categories of medical therapy for all ACSanti- ischemia, anti-platelet, anti-coagulate and adjunctive
B-blocker- general fxanti-ischemic
B-blocker - mechanism and 3 outcomesreduce cardiac work / o2 demand >> 1- receive ischemic pain 2- prevent arrhythmia (electrical instability) 3- reduce infarct size
Nitrates - general fxanti-ischemic
Nitrates - mechanism (2)enhance coronary blood flow > coronary dilation // increase venous capcitiatnce > decrease preload > reduce wall stress
****drug contraindicated in hypotensionNitrates, if RV filling pressure drops (b/c of dilation) >> decreased output >> more hypotensive
***drug contraindicated in STEMI w/ RV (inferior) infarctnitrates >> b/c RV already has little contractile power >> decrease RV filling pressure >> significantly reduce CO
drug contraindication in allergy or active GI hemorrhageAspirin
Glycoprotein IIb/IIIa receptor antagonist - not used in STEMI when _____ administeredlytics (only use Glyco in cath lab)
****drug w/ greatest benefit in anterior MI /systolic dysfxACE-I (prevents remodeling)


Question Answer
Ca Channel blocker - general fxanti-ischemic
****Ca Channel blocker - effects (3)1- decrease preload (arterial vasodilation) & 2- lower blood pressure >> reduce wall stress 3 - antiangina
major risk of anti-thrombotics!bleeding
Aspirin / NSAID’s - general fxantiplatelet
****Aspirin / NSAID’s - mechanisminhibit production of thromboxane (which activates platelets)
Clopidogrel - general fxantiplatelet (thienopyridine derivative)
Clopidogrel - mechanismblock P2Y12 (ADP) R >> inhibit adenosine formation >> inhibit activation of more platelets
Prasugrel - general fxantiplatelet (thienopyridine derivative)
***Prasugrel - mechanismblock platelet P2Y12 (ADP) R >> inhibit adenosine formation >> inhibit activation of more platelets
Prasgurel vs Clopidogrel - efficacysee 24.14 prasugel = super clopidogrel b/c of cyp450 /BUT Prasugrel has higher bleeding risk!
Heparin - general fxAnticoagulation
UFH (unfractionated) heparin - mechanismbinds to antithrombin >> more potent inhibitor of 1- thrombin AND Factor xa
LMWH heparin - mechanismshorter chain - binds antithrombin and inhibits only factor Xa
Glycoprotein IIb/IIIa receptor antagonist- mechanisminhibit final common pathway of platelet aggregation
Glycoprotein IIb/IIIa receptor antagonist- general fxanti platelet
ACE-I - general fx(adjunctive) prevents remodeling
***Statins - general fx(adjunctive) benefits beyond low LDL .> plaque stabilize & improve endothelial c fx


Treatment for STEMI
Question Answer
recognize TIMI risk score componentsstratifies RISK in UA/NSTEMI for approp. tx >>> see 24.20 (high = 5-7, intermediate = 3-5)
primary goal of tx**reperfusion
tPA -mechanismplasminogen >> plasmin (dissolves fibrin-bound clot)
TPA has specificity forplasminogen **bound** to clot (ideal to leave unbound plasminogen for NORMAL meostatis)
preferred tx for elderly / bleeding riskprimary PCI
****preferred tx for cariogenic shockprimary PCI


MI complications
Question Answer
****bradycardia caused byRCA infarct >> SA node ischemia
tachycardia caused bypain/sympathetic response/decompensation
atrial fib caused byatrial ischemia or stretch
sx of right-sided failureJVD, hypotension (b/c of LV underfilling)
***tx for left-sided failurediuretics for volume overload (and HF medications)
sx of Left-sided failureCongestion / s3 heart sound, dyspnea, rales
ECG lead and pattern of posterior wall MILead 2 (mirror) = R waves (instead of Q) and ST depression w/ upright T waves
posterior wall MI- causedistal circumflex or distal RCA
dyskinetic LV wall can develop into _____LV aneurysm
****timing aneurysm vs psedoaneurysmweeks to months vs 2 weeks (when inflammation has weakened wall)
papillary muscle rupture sequelamitral rergurg >> HF and or death
papillary muscle MOST vulnerable to rupture posteromedial
Dressler syndromeautoimmune pericarditis (several weeks after MI)

Pathology of MI

Pathophysiology of MI
Question Answer
most common cause of decreased blood supply to heartatherosclerotic CAD (90&)
hyperthyroidism - mechanismincreased oxygen demand (increased cardiac work)
MI - sequence of eventsplaque changes (rupture, erosion, ulceration ) >> platelet adherence & activation >> micro thrombus >> vasopasum (from platelet-mediated factors) >> Tissue factor released coagulation pathway activated >> thrombus >> partial/full occlusion
2 gross categories of MItransmural (full/near full thickness) vs subendocardial (inner 1/3 or 1/2)
****regional subendo MI - causetransient or partial obstruction of coronary artery (vs circumferential subendo)
****circumferential subendo MI - causeprolonged severe hypotension or severe stenosis
2 complications of transmuralventricular rupture, pericarditis
ECG - subendo vs transmural MINonST (partial obstruction) vs ST (complete obstruction)
multifocal microinfarct - mechanism**only small intramural vessels**
***multifocal microinfarct - 3 possible causesvasospasm (cocaine!), micro emboli (DIC/sickle cell), vasculitis
multifocal microinfarct - 2 outcomesSCD (fatal arrhythmia) or dilated CM


Infarct zones
Question Answer
anterior 2/3 of septumLAD
anterior wallLAD
lateral wallLCX (circumflex)
R ventricular wallRCA
****postero/basal wall of LVRCA
posterior 1/3 of septumRCA
most vulnerable region of heartsubendocardium


MI- Cellular Damage
Question Answer
reversible cell damage characterized by**hydropic change (failure of Na/K pump) = swelling
reversible cell damage - mechanismaerobic metabolism > eventual ATP defieicny > Na/K pump fail >> Na / h20 influx >> swelling
irreversible cell damage characterized bydamage and destruction of organelles (loss of nuclei) >> release of biomarkers (troponin, CK-MB, etc.)
ireversible cell damage - mechanism**disruption of sarcolemma
ireversible cell damage - occurs after ____ minutes of ischemia20-30
benefits of reperfusion diminish after ____ hours6-12 (tissue no longer salvageable)


****MI - Gross Findings
Question Answer
not apparent, general untilat least 12 hours (or longer if more collaterals have developed)
4-12 hours+/- dark mottling (reddish blue stagnated blood)
12-24 hrs***dark mottling (reddish blue stagnated blood)
1-3 daysmottling w/ yellow-tan infarct (due to neutrophils)
4-7 dayshyperemic border (start of granulation tissue, start of scar) & yellow-tan center (macrophages)
7-10 daysMaximal yellow-tan and soft with depressed red-tan margins
2-8 weeksgrey-white scar >> fibrosis
complete scarring by2 months (will look the same 10 years later)


***MI-microscopic features - see 23,33
Question Answer
****<4 - day hoursWAVY fibers (23.27)
stain to detect ischemia in early-post MI deathstain for complement C5b-9
1-3 dayscoagulative necrosis w/ **NEUTROPHILS (coagulation looks like pink streaky bands)
1-2 weeksMphage / fibroblast / granulation tissue
***3-4 weeksloos granuatlion tissue w/ TYPE III collagen
> 2 monthsamorphous pink collagenous plug (see 23.31, 23.33) - TYPE I collagen (seen in blue on stain)


Complications of MI
Question Answer
myocardial rupture - timing2-4 days post MI (peak necrosis) // but can occur anytime w/in 2 weeks
myocardial rupture - sequelaecardiac tamponade (heart strangling in blood)
ventricular aneurysm - causeinadequate scar formation post-MI
acute pericarditis - timing2-3 days post MI
dressler syndrome - defineautoimmune pericarditis
dressler syndrome - timingweeks-months post MI
****anterior transmural complications (3)rupture, aneurysm, mural thrombi
****posterior transmural complication (1)conduction block (b/c RCA)


Question Answer
inflammation - mechanismperfusion brings more neutrophils
intracellular ca - mechanismoverload (due to damaged sarcolemma) >> activates proteins >> more damage
oxidative stress- mechanismformation of reactive o species w/ no antioxidant defenses (compromised during ischemia)
Reperfusion injury- gross findinghemorrhage
***Reperfusion injury - microscopic findingcontraction bands (due to excess calcium) see 23.45