11 11 2014 Acute Coronary Syndrome

Question 1

Unstable angina and Non-ST-elevating Myocardial infarct (NSTEMI)

Answer 1

Both are caused by partially occlusive thrombus.

Both are non-Q wave MIs.

But NSTEMI is seen with myocardial necrosis

Question 2

ST- Elevation myocardial infarction (STEMI)

Answer 2

“Q-wave MI”

results from complete obstruction of coronary artery.

Question 3

Antithrombin

Answer 3

plasma protein that irreversibly binds to thrombin and other clotting factors and inactivates them.

Question 4

Protein C/S/ Thrombomodulin

Answer 4

inactivates “acceleration” (Factors 5a and 8a) in coagulation pathway.

Protein C is made by liver and is vit. K dependent. Activated by thrombin- thrombomodulin complexes. Degrades Factors 5a and 8a.

Thrombomodulin binds to thrombin – prevents it from converting fibrinogen to fibrin

Question 5

TFPI ( Tissue factor pathway inhibitor)

Answer 5

plasma serine protease inhibitor that is activated by coagulation of fact 10a.

10a- TFPI copmlex binds to and inactiavtes TF- 7a (usually triggered the extrinsic pathway)

Question 6

tPA (tissue Plasminogen activator)

Answer 6

protein secreted by endothelial cells in response to many triggers of clot formation.

It fleas protein plasminogen –> plasmin = enzymatically degrades fibrin clots.

Question 7

What is the major trigger for coronary thrombosis formation?

Answer 7

PLAQUE RUPTURE

caused by:

1. chemical factors that destabilize atherosclerotic lesion
   - enzymes that degrade interstitial matrix – make weak cap weaker
2. physical stress to which the lesions are subjected

Question 8

Exactly what happens when the plaque ruptures? ( what does it lead to?)

Answer 8

1. intraplaque hemorrhage = decrease vessel lumen/diameter
2. release of TF = activation of coagulation cascade
3. Exposure of sub endothelial collaged and Turbulent blood flow both
   = platelet activation and aggregation
   = Activation of coagulation cascade and vasoconstriction

= coronary thrombosis

Question 9

Role of dysfunctional endothelium in coronary thrombosis formation?

Answer 9

• decrease vasodilator effect
  = casues vasoconstriction –> coronary thrombosis
• decreases anti-thrombotic effect
  = causes coronary thrombosis

Question 10

Vasculitis as a cause of acute coronary syndrome

Answer 10

immune system attacks blood vessels = inflammation and endothelial injury

Question 11

Coronary embolism ( from endocarditis, artificial heart valves)

Answer 11

embolism of thrombus can occlude coronary artery.

Question 12

Severe coronary artery spasm

Answer 12

Cocaine induced
- increased SNS tone by blocking presynaptic uptake of norepinephrine and by enhancing the release of adrenal catecholamines
= vasospasm that decreases myocardial oxygen supply.

Increased myocardial demand (due to increased SNS) with decrease oxygen supply due to vasospasm

Question 13

Coronary trauma or aneurysm

Answer 13

weakens walls and causes injury.

Aneurysm causes stasis = thrombosis formation

Question 14

Troponin I and T

Answer 14

structurally unique to cardiac muscle.

If present you are having an MI – could be NSTEMI or STEMI

Begins to rise 3- 4 hrs after onset of discomfort
Peaks 18-36 hrs
Declines slowly allowing for detection between 10 to 14 days

Question 15

Creatine Kinase (CK) - MB

Answer 15

localized mainly in the heart but small amounts of CK-MB are found in tissues outside the heart
- uterus, prostate, gut, diaphram, and tongue

Also makes up 1-3% of creatine in skeletal muscle

• slightly suggestive of an MI

Starts to rise 3-8 hrs following infarction
Peaks at 24 hrs
Returns to normal within 48-72 hours

• not as sensitive for detecting MI as Troponin

Question 16

What happens after 4-12 hrs of MI infarction?

1. gross features
2. light microscope findings

Answer 16

1. occational darkening
2. none.
   if anything = waviness of fibers at the border
   - sarcolemmal disruption

Question 17

What happens after 12-24 hrs of MI infarction?

1. gross features
2. light microscope findings

Answer 17

1. Dark mottling
2. Ongoing coagulation necrosis
   Infiltration by neutrophils

Question 18

What happens after 1-3 days of MI infarction?

1. gross features
2. light microscope findings

Answer 18

Mottling with yellow-tan infarct center

interstitial infiltrate of neutrophils
Coagulation necrosis with loss of nuclei and striations

• complication = fibrous pericarditis if transmural infarct – inflammation extends to pericardium

Question 19

What happens after 4-7 days of MI infarction?

1. gross features
2. light microscope findings

Answer 19

hyperemic border; central yellow-tan softening

Dying neutrophils
Macrophage at infarct border
Disintegratin of dead myofibers

Question 20

What happens after 7-10 days of MI infarction?

1. gross features
2. light microscope findings

Answer 20

Maximally yellow-tan and soft with depressed red-tan margins

Well developed phagocytosis and fibrovascular granulation tissue at margins

Question 21

What happens after 10-14 days of MI infarction?

1. gross features
2. light microscope findings

Answer 21

Red gray depressed infarct borders

Well established granulation tissue with new blood vessels and collage deposition

Question 22

What happens after 2-8 weeks of MI infarction?

1. gross features
2. light microscope findings

Answer 22

Gray white scar, progressive form border toward core of infarct

Increased collagen deposition, with decreased cellularity

Question 23

What happens after 2 months of MI infarction?

1. gross features
2. light microscope findings

Answer 23

Scaring complete

Dense collagenous scar