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Flashcards in Acute Coronary Syndromes Deck (62):
1

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

Tissue factor

2

Intrinsic pathway

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

3

Extrinsic pathway

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.

4

Antithrombin

Plasma protein that inactivates thrombin

5

Protein C/thrombomodulin

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

6

Tissue factor pathways inhibitor (TFPI)

Yeah its pretty much what it sounds like

7

Mechanisms of clot lysis

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

8

How do plaques adhere to injured epithelium

Bind to von Willibrand factor and collagen.

9

Thromboxane A2

Pro-thrombotic factor that binds to platelets

10

ADP

Causes platelet aggregation

11

How does endothelium prevent the actions of ADP?

Turns it into adenosine.

12

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

Prostacyclin and NO. Also convert ADP.

13

How does prostacyclin and NO induce vasodilation prevent thrombus formation?

Because increased blood flow prevents contact between procoagulant factors.

14

Major cause of coronary artery thrombosis?

Plaque rupture

15

Two chemical factors that destabilize fibrous caps?

MMP (matrix metalloproteinase)
T-lymphocyte cytokines that inhibit collagen synthesis

16

Most prone part of cap to rupture?

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

17

When do MIs usually occur

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

18

What is the first step in coronary thrombogenesis?

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

19

Functional sequellae of MI

Impaired contractility (systolic dysfunction)
Impaired relaxation (diastolic dysfunction)

20

How do MIs cause systolic dysfunction

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

21

How do MIs cause diastolic dysfunction

Reduced compliance because its energy dependent too.

22

Stunned myocardium

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

23

Ischemic preconditioning

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

24

Remodeling definition and process

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

25

Why is infarct expansion so dangerous?

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

Signs: new gallop sounds, new/worsening pulmonary congestion

26

What is the product that stimulates ventricular hypertrophy during late remodeling

Local ang II release

27

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

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

Inflammatory disorders like vasculitis

Peripartum female (can have spontaneous coronary dissection)

Cocaine abuse

28

How does cocaine abuse cause ACS?

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

29

Types of Myocardial Infarction

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

Types of type 2 MI

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

31

Q-wave MI

Transmural infarction

32

Non q-wave MI.

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

33

Presentation of ACS?

Ischemic discomfort at rest

34

Sign of ACS

Either ST segment elevation or non ST segment elevation

35

Non ST segment elevation ACS

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

36

ST segment elevation ACS

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

37

Nonocclusive ruptured plaque leading to thrombus causes

Unstable angina, NSTEMI

38

Occlusive ruptured plaque leading to thrombus causes

STEMI.

39

Increasing severity of ACS

Unstable angina -> NSTEMI -> STEMI

40

Most critical distinction to make

NSTEMI or STEMI

41

Clinical symptoms of MI

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

Who is likely to have an MI without symptoms?

Diabetics

43

Physical findings of MI

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

44

Why can an MI cause MR?

Because papillary muscle doesn't function properly.

45

Differential for MI

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

46

ECG findings of USA or NSTEMI

T wave inversion, ST depression or normal

47

Are biomarkers elevated in USA?

No

48

Are biomarkers elevated in NSTEMI

yes

49

ECG evolution with STEMi

See slides

50

Definition of STEMI

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

51

Definition of NSTEMI

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

52

Pathophysiology of STEMI

Total or near total occlusion of coronary artery

53

Pathophys of NSTEMI

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

54

Management of STEMI

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

55

Management of NSTEMI

Depends on TIMI score

56

Cardiac biomarkers

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

57

Troponins

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

Where is troponin released from first?

Cytosolic pool, but if injury persists, then muscular pool

59

When do levels of troponin rise and peak?

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

60

Creatine Kinase

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

61

Kinetics of CK

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

62

Can biomarkers be normal early in ACS?

Yes 100%.