Acute Coronary Syndromes Flashcards Preview

Cardio > Acute Coronary Syndromes > Flashcards

Flashcards in Acute Coronary Syndromes Deck (62)
Loading flashcards...
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)