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Cardio > Acute Coronary Syndromes > Flashcards

Acute Coronary Syndromes Flashcards

1
Q

What do endothelial cells start to express when exposed to inflammatory mediators?

A

Tissue factor

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2
Q

Intrinsic pathway

A

Contact activation pathway
Factor XII converted into XIIa, which turns factor XI into XIa, which IX into IXa, which complexes with factor VIIIa.

This complex converts factor X into factor Xa. Xa and Va convert prothrombin into thrombin. Thrombin converts fibrinogen into fibrin. And we have a cross linked fibrin clot

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3
Q

Extrinsic pathway

A

Factor VII converted to VIIa by trauma. Simultaneously Tissue factor exposed due to trauma. VIIa and Tissue factor cleave X to Xa.

Xa, along with Va, convert prothrombin to thrombin, which converts fibrinogen to fibrin.

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4
Q

Antithrombin

A

Plasma protein that inactivates thrombin

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5
Q

Protein C/thrombomodulin

A

Thrombin receptor on endothelial cells so its unable to cleave fibrinogen to fibrin

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6
Q

Tissue factor pathways inhibitor (TFPI)

A

Yeah its pretty much what it sounds like

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7
Q

Mechanisms of clot lysis

A

Blood clots initiate the secretion of TPA from endothelial cells, which converts plasminogen to plasmin. Plasmin degrades fibrin clots.

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8
Q

How do plaques adhere to injured epithelium

A

Bind to von Willibrand factor and collagen.

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9
Q

Thromboxane A2

A

Pro-thrombotic factor that binds to platelets

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10
Q

ADP

A

Causes platelet aggregation

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11
Q

How does endothelium prevent the actions of ADP?

A

Turns it into adenosine.

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12
Q

Two factors released by endothelial cells that prevent platelet aggregation and increase blood flow

A

Prostacyclin and NO. Also convert ADP.

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13
Q

How does prostacyclin and NO induce vasodilation prevent thrombus formation?

A

Because increased blood flow prevents contact between procoagulant factors.

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14
Q

Major cause of coronary artery thrombosis?

A

Plaque rupture

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15
Q

Two chemical factors that destabilize fibrous caps?

A

MMP (matrix metalloproteinase)

T-lymphocyte cytokines that inhibit collagen synthesis

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16
Q

Most prone part of cap to rupture?

A

Shoulder of cap due to stress. Can also rupture because of myocardial contraction or high intraluminal blood pressure

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17
Q

When do MIs usually occur

A

Early morning hours because physiologic stress is highest. High BP, high blood viscosity, high sympathetic tone

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18
Q

What is the first step in coronary thrombogenesis?

A

Dysfunction of the endothelium. Vasoconstriction becomes the favored state. Thromboxane and serotonin will promote vasoconstriction.

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19
Q

Functional sequellae of MI

A 
Impaired contractility (systolic dysfunction)
Impaired relaxation (diastolic dysfunction)
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20
Q

How do MIs cause systolic dysfunction

A

Hypokinesis (reduced contraction) or Akinesis, or dyskinesis (bulging out during contraction)

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21
Q

How do MIs cause diastolic dysfunction

A

Reduced compliance because its energy dependent too.

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22
Q

Stunned myocardium

A

Reversible injury to myocytes after MI. Contractile function is restored days to weeks later.

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23
Q

Ischemic preconditioning

A

Episodes of ischemia actually make tissue resistant to subsequent episodes. This occurs during stable angina.

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24
Q

Remodeling definition and process

A

Process of ventricular reorganization after infarct. First the infarct zone will thin and elongate. This is also known as infarct expansion. Then spherical dilation will occur with increased interstitial collagen

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25
Q

Why is infarct expansion so dangerous?

A

Because its associated with higher mortality and a higher rate of complications like HF.

Signs: new gallop sounds, new/worsening pulmonary congestion

26
Q

What is the product that stimulates ventricular hypertrophy during late remodeling

A

Local ang II release

27
Q

Nonatherosclerotic causes of ACS in young patients or somebody with no risk factors

A

Mechanical valves or infective endocarditis – cause emboli that occlude coronaries.

Inflammatory disorders like vasculitis

Peripartum female (can have spontaneous coronary dissection)

Cocaine abuse

28
Q

How does cocaine abuse cause ACS?

A

Vasospasm decreases oxygen supply, increased HR + inotropy cause increased demand. Also associated with increased atherosclerosis.

29
Q

Types of Myocardial Infarction

A

Type 1 – classic case of plaque rupture
Type 2 – Supply/demand imbalance without plaque rupture
Type 3 – Cardiac death
Type 4/5 – MI in the setting of a revascularization procedure.

30
Q

Types of type 2 MI

A

Vasospasm or endothelial dysfunction (prinzmetal/cocaine)
Fixed atherosclerosis causing supply-demand imbalance
Supply-demand balance alone (syndrome X)

31
Q

Q-wave MI

A

Transmural infarction

32
Q

Non q-wave MI.

A

Subendocardial ischemia – few collaterals there and exposed to highest pressures from ventricle

33
Q

Presentation of ACS?

A

Ischemic discomfort at rest

34
Q

Sign of ACS

A

Either ST segment elevation or non ST segment elevation

35
Q

Non ST segment elevation ACS

A

Can be unstable angina, Non-q wave MI, or even a Q wave MI (very rarely)

36
Q

ST segment elevation ACS

A

Generally a q-wave MI, but sometimes (rare) can be a non-q wave MI.

37
Q

Nonocclusive ruptured plaque leading to thrombus causes

A

Unstable angina, NSTEMI

38
Q

Occlusive ruptured plaque leading to thrombus causes

A

STEMI.

39
Q

Increasing severity of ACS

A

Unstable angina -> NSTEMI -> STEMI

40
Q

Most critical distinction to make

A

NSTEMI or STEMI

41
Q

Clinical symptoms of MI

A 
Chest pain more severe, longer duration, with greater radiation than normal. Does not improve with rest or nitroglycerin.
Sympathetic discharge (diaphoresis, tachycardia, nausea, clammy skin)
Shortness of breath (LV volume rises, so backs up to lungs)
42
Q

Who is likely to have an MI without symptoms?

A

Diabetics

43
Q

Physical findings of MI

A

S4 (noncompliant LV)
S3 (volume overload and systolic dysfunction)
Systolic murmur (may come from papillary muscle dysfunction leading to MR)
Fever

44
Q

Why can an MI cause MR?

A

Because papillary muscle doesn’t function properly.

45
Q

Differential for MI

A

Pericarditis, pleuritis (pain w/inspiration and diffuse ST ele)
Aortic dissection (ripping pain, BP asymmetry, widened mediastinum on CXR)
PE
Acute cholecystitis

46
Q

ECG findings of USA or NSTEMI

A

T wave inversion, ST depression or normal

47
Q

Are biomarkers elevated in USA?

A

No

48
Q

Are biomarkers elevated in NSTEMI

A

yes

49
Q

ECG evolution with STEMi

A

See slides

50
Q

Definition of STEMI

A

Prolonged chest discomfort unrelieved by nitroglycerin with ST segment elevation on EKG and rise in cardiac markers

51
Q

Definition of NSTEMI

A

Angina at rest for longer than 20 minutes without ST segment elevation but with cardiac biomarkers.

52
Q

Pathophysiology of STEMI

A

Total or near total occlusion of coronary artery

53
Q

Pathophys of NSTEMI

A

Abrupt decrease in myocardial O2, thrombus formation or an atherosclerotic plaque

54
Q

Management of STEMI

A

Immediate reperfusion with a preferred door to balloon time of <90 minutes

55
Q

Management of NSTEMI

A

Depends on TIMI score

56
Q

Cardiac biomarkers

A

Troponin (T, I, or C)
Creatine Kinase Myocardial Band (CK-MB)
Myoglobin

57
Q

Troponins

A

Control calcium mediated interactions between actin and myosin that are released into circulation from muscle and cytosolic reserves during necrosis. TNI and TNT are highly sensitive and specific for myocardial necrosis.

58
Q

Where is troponin released from first?

A

Cytosolic pool, but if injury persists, then muscular pool

59
Q

When do levels of troponin rise and peak?

A

Rise within 3-4 hours. Peak at 18-36 and decline slowly

60
Q

Creatine Kinase

A

Enzyme involved in ATP generation. Found in heart (CK-MB) but also in muscle (MM) and brain (BB). Also in uterus prostate gut.

61
Q

Kinetics of CK

A

Faster release and peak (24h) then cTn, returns to normal faster.

62
Q

Can biomarkers be normal early in ACS?

A

Yes 100%.

Cardio (23 decks)

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