0630 - Pathology of MI - RM

Question 1

Outline Cell Injury

Answer 1

Process that occurs when cells are stressed so severely that they are no long able to adapt - e.g. O2 deprivation, toxins, infectious agents, physical trauma.
Can be reversible, or irreversible with death.

Question 2

Define Ischaemia

Answer 2

Significant decrease or loss of blood supply from impeded arterial flow or reduced venous drainage. Compromised supply of oxygen and metabolic substrates to end organ tissues, as well as impeding the clearing of toxins.

Question 3

Define infarction. What is the difference between venous and arterial?

Answer 3

Infection occurs in any tissue where there is sufficient ischaemia to cause tissue death or necrosis.
Arterial - complete blockage (usually by thrombus or embolism). Usually pale.
Venous - mechanical compression of vascular drainage, tissues are usually densely haemorrhagic.

Question 4

Define necrosis

Answer 4

Morphologic changes that follow cell death in living tissue. Both macroscopic and microscopic. Morphology due to denaturation of intracellular proteins, or enzymatic degradation of the cell.

Question 5

What are the four types of necrosis?

Answer 5

Coagulative (seen in MI and most infarctions)
Liquefactive (seen in cerebral infarct)
Caseous (seen in TB)
Fat (seen in pancreatitis)

Question 6

What is coagulative necrosis?

Answer 6

Characterised by denaturation of proteins due to infarction, with preservation of the cell outlines ‘ghost cells’ without nuclei. Structure is preserved, but nothing is alive.

Question 7

What is liquefactive necrosis?

Answer 7

Enzyme digestion is dominant, classic finding in abscesses and cerebral infarcts.

Question 8

What is caseous necrosis?

Answer 8

Distinctive form of necrosis, seen in TB.

Question 9

What is fat necrosis?

Answer 9

Focal areas of fat destruction ‘saponification’. Classic finding in pancreatitis as premature activation of enzymes in surrounding and distal tissues starts to break down the fat.

Question 10

Briefly outline coronary arteries

Answer 10

Heart supplied by right and left coronary arteries, both branches of ascending aorta. Left leads to circumflex and LAD, Right leads to right marginal and posterior interventricular.
INCLUDE IMAGE

Question 11

Define ischaemic heart disease.

Answer 11

Generic designation for closely related symptoms arising from myocardial ischaemia. Diminished coronary perfusion relative to myocardial demand.90% are due to coronary artery atherosclerosis.

Question 12

What are the 4 main syndromes of ischaemic heart disease?

Answer 12

Angina (stable/unstable/Prinzmetal)
Sudden Cardiac Death
Myocardial Infarction
Chronic ischaemic heart disease with heart failure.

Question 13

What are the three branches of ACS? What is the common precipitant?

Answer 13

Unstable angina, sudden cardiac death, MI

Precipitated by conversion of stable atherosclerotic plaque to an unstable atherosclerotic plaque.

Question 14

What factors can trigger acute plaque change?

Answer 14

Intrinsic - plaque structure and composition (thin cap)
Extrinsic - Mechanical stress, platelet reactivity
Rupture/fissuring
Erosion/ulceration
haemmorhage
In all cases - exposure of highly thrombogenic plaque constituents or haemorrhage into plaque, leading to thrombus formation and arterial occlusion.

Question 15

What are the risk factors for MI?

Answer 15

Unmodifiable - Male sex, increased age

Modifiable - Hypertension, smoking, diabetes, hypercholesterolaemia

Question 16

What is the pathogenesis of MI?

Answer 16

Acute plaque change leading to disrupted plaque. Platelets activate, and vasospasm may occur. Extrinsic coagulation pathway activates, increasing the thrombus size and within minutes, the artery completely occludes.

Question 17

What is the myocardial response to MI?

Answer 17

Ischaemia, with aerobic metabolism ceasing within seconds. Contractility lost within 60 seconds, and necrosis starts within 20-40 minutes, completing in 6 hours.

Question 18

What are some modifying factors for the myocardial response to MI?

Answer 18

Location, severity, and rate of development of occlusion
Size of vascular bed occluded
Duration of occlusion
Metabolic needs of myocardium
Extent of collateral vessels
Alterations in BP, HR, and cardiac rhythm.

Question 19

What is the difference between transmural and subendocardial infarcts?

Answer 19

Transmural has full thickness ischaemic necrosis of the ventricular wall in the area supplied by single affected artery.
Subendocardial has necrosis of the inner ⅓ of the wall. May involve several arteries, and is the least well-perfused area normally.

Question 20

What is the macro and micro appearance one day after MI?

Answer 20

Macro - subtle changes,dark mottling

Micro - coagulation necrosis, haemorrhage (from reperfusion), scant neutrophils, contraction bands.

Question 21

What is the macro and micro appearance two days after MI?

Answer 21

Macro - Mottled appearance with yellow/tan infarct centre

Micro - Coagulation necrosis (nuclei disappearing) and more neutrophils.

Question 22

What is the macro and micro appearance one week after MI?

Answer 22

Macro - hyperaemic border, with yellow/tan infarct centre.

Micro - Disintegration of necrotic myofibres (borders will be hardly visible), dying neutrophils, macrophages present.

Question 23

What is the macro and micro appearance two weeks after MI?

Answer 23

Macro - maximally yellow/tan and soft, with depressed infarct borders.
Micro - Phagocytosis, granulation tissue, and early fibrosis (lots of collagen with spindle cells).

Question 24

What is the macro and micro appearance two months after MI?

Answer 24

Macro - white scarring

Micro - Dense, collagenous scar.

Question 25

What are complications of MI (outside to inside)

Answer 25

Contractile dysfunction - immediate and ongoing
Conducting system - Arrhythmia
Pericardium - Pericarditis due to underlying inflammation - 2-3 days, resolves slowly.
Pericardial space - Effusion (Dressler’s Syndrome), haemopericardium/tamponade
Myocardium - Rupture 3-7 days post-MI, ventricular anuerysm
Endocardium - inflammation/mural thrombosis leading to thrombus/thromboembolism
Papillary muscles/valves - Dysfunction - rupture/fibrosis/ventricular dilation

Question 26

What is the difference between infarct extension and expansion?

Answer 26

Extension involves new necrosis adjacent to the existing infarct.
Expansion occurs as the necrotic muscle stretches - enlarges without further necrosis.