2.01 - Pathology Of Myocardial Infarction Flashcards Preview

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Flashcards in 2.01 - Pathology Of Myocardial Infarction Deck (32):
1

What is ischaemia?

Loss of blood supply from impeded arterial flow or reduced venous drainage. This compromises the supply of oxygen and metabolic substrates (e.g. glucose)

2

What is Infarction?

Infarction occurs in any tissue in which there is sufficient ischaemia to cause death or tissue necrosis. 

3

Describe an arterial infarction

A complete blockage of an artery by thrombosis or embolism

4

What is a venous infarction?

Venous infarctions occur when there is compression of the vascular supply. E.g. in hernias when the bowel may fold on itself and cut off blood supply

5

What is necrosis?

The morphologic changes that follow cell death in a living tissue

6

What are the morphlogic appearances of necrosis due to?

Denaturation of intracellular proteins and enzymatic degradation of the cell

7

What are the four types of necrosis?

Coagulative

Liquefactive

Caseous

Fat

8

Describe coagulative necrosis

Most common type of necrosis in ischaemia

Denaturtion of proteins with preservation of the cell outlines.

Classic finding in myocardial infarction and most forms of tissue infarction

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9

Describe Liquefactive necrosis

Classic finding in abcesses and cerebral infarct

Enzyme degradation dominant

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10

Describe caseous necrosis

Distinctive form of necrosis.

Classic finding in TB

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11

Describe Fat Necrosis

Focal areas of fat destruction. 

Classic finding in pancreatitis --> release of pancreatic enzymes that then travel to distant sites

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12

What are the four main classifications for ischaemic heart disease?

Angina (Stable, Unstable, Prinzmetal)

Sudden Death

Myocardial infarction

Chronic ischaemic heart disease with heart failure

13

Describe the pathogenesis of Ischaemic Heart Disease (IHD)

90% due to coronary artery atherosclerosis. This decreases coronary perfusion relative to myocardial demand

14

What factors of the atherosclerotic plaques determine the risk for developing IDH?

The number of plaques

The distrobution of plaques (are they on proximal vessels?)

The structure of the plaques

The degree of narrowing they cause 

How quickly the plaques evolve

15

What are some risk factors for Myocardial Infarction?

Male

Risk factors for atherosclerosis (hypertension, cigarette smoking, diabetes mellitus, hypercholesterolaemia)

16

Describe acute plaque change

When the nature and structure of an atherosclerotic plaque changes due to certain intrinsic (plaque structure and composition) and extrinsic (mechanical stress, platelet reactivity).

Plaque change can result in rupture (leading to thrombi or emboli), erosion/ulceration and haemorrhage.

17

Describe the events in coronary artery occlusion

Acute plaque change leads to a disrupted plaque

This results in adhesion, aggregation and activation of platelets.

The extrinsic pathway of coagulation is stimulated and the thrombus increases in size

Within minutes the coronary artery can become completely occluded

18

Describe the response of the myocardium to ischaemia

Cessation of aerobic glycolysis within seconds --> lactic acidosis

Loss of contractility within 60 seconds

Severe ischaemi for 20-40mins will lead to some necrosis 

Complete necrosis in 6 hours

This depends on the location, severity and rate of development of the occlusion

19

Compare and Contrast Transmural and Subendocardial Infarction

Transmural: full thicknes ischaemic necrosis of ventricular wall. Distribution of a single coronary artery. 

Subendocardial: ischaemic necrosis limited to inner third of ventricular wall. May involve the distribution of several coronary artery

20

Describe the macroscopic and microscopic morphologic changes in myocardial infarction after four hours

Micro: thin wavy myocytes

21

Describe the macroscopic and microscopic morphologic changes in myocardial infarction after one day

Macro: subtle changes, dark mottling

Micro: coagulation necrosis, haemorrhage, scant neutrophils, contraction bands

22

Describe the macroscopic and microscopic morphologic changes in myocardial infarction after two days

Macro: mottled appearance with yellow/tan infarct centre and is soft to touch

Micro: coagulation necrosis, neutrophils

23

Describe the macroscopic and microscopic morphologic changes in myocardial infarction after one week

Macro: hyperaemic border with central tan softening

Micro: disintegration of necrotic myofibres, dying neutreophils, macrophages

24

Describe the macroscopic and microscopic morphologic changes in myocardial infarction after two weeks

Macro: maximally yellow/tan and soft, depressed infarct borders

Micro: phagocytosis, granulation tissue, early fibrosis

25

Describe the macroscopic and microscopic morphologic changes in myocardial infarction after two months

Macro: white scarring

Micro: dense collagenous scar

26

What is the outside-->inside system to understanding the complications of MI

Outside to inside:

Contractile dysfunction, conducting system, pericardium, pericardial space, myocardium, endocardium, papillary muscles/valves

27

What are the complications of MI?

Contractile dysfunction

Arrhythmias

Pericarditis

Haemopericardium & cardiac tamponade

Myocardial rupture

Infarct extension/expansion

Ventricular aneurysm

Mural thrombus

Papillary muscles dysfunction

28

Describe the consequences of contractile dysfunction in MI

Immediate and ongoing

Left ventricular failure --> hypotension and pulmonary oedema

29

Describe the consequences of haemoepicardium and cardiac tamponade in MI

Haemoepicardium: Escape of blood from the ventricles in to the pericardial cavity. Occurs through a rupture of the myocardium

Cardiac tamponade: Constriction of the heart with decreased diastolic filling. usually fatal

 

30

Compare infarct extension and infarct expansion

Extension: new necrosis adjcent to the existing infarct

Expansion: weak necrotic muscle stretches, the infarct enlarges in size without further necrosis

31

Describe mural thrombus

Local inflammation of the endocardium. Abnormal contractility results in blood stasis.

Both contribute to thrombus formation and the potential for a thromboembolism

32

Describe the timeline of complications in MI

Arrhythmia: Immediate leading to sudden death. Can also be ongoing i.e. bundle branch block

Contractile Dysfunction: Immediate, within 60 seconds. Cardiogenic shock, chronic left ventricular failure

Pericarditis: 2-3 days usual

Myocardial rupture: 3-7 days when necrotic myocardium at it’s weakest

Mural thrombosis with risk of embolism: Highest rist at 10 days, lasting for 3 months

Aneurysm: Late complication