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CARD - 1 > Pathophysiology of Ischaemia and Infarction > Flashcards

Pathophysiology of Ischaemia and Infarction Flashcards

1
Q

Define ischaemia.

A

Lack of blood supply to tissues —> oxygen/nutrient shortage

(Can be due to supply or demand)

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2
Q

Define hypoxia.

A

Inadequate oxygen supply to meet the needs of the tissue or organ.

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3
Q

How can anaemics become hypoxic?

A

They inspire normal amount of oxygen, but lack of haemoglobin leads to inadequate delivery to tissues.

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4
Q

What are the four types of hypoxia?

A
  1. hypoxic hypoxia - low oxygen levels inspired or low PaO2
  2. anaemic hypoxia - due to anaemia
  3. stagnant hypoxia - abnormal delivery can be local, e.g. occlusion of vessel or systemic, e.g shock
  4. cytotoxic hypoxia - normal inspired O2 but abnormal at tissue level
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5
Q

How can the tissue itself affect oxygen supply?

A

Different tissues will have different oxygen demands dependent on workload and amount of activity.

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6
Q

What is atherosclerosis (an atheroma)?

A

Localised accumulation of lipid and fibrous tissue in intima of arteries.

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7
Q

What condition will arise from an atheroma in a coronary artery?

A

Stable angina.

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8
Q

What condition will arise from a complicated atheroma in a coronary artery?

A

Unstable angina.

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9
Q

What will result from ulcerated/fissured atheromatous plaques?

A

Thrombosis which can lead to ischaemia or infarction.

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10
Q

What is a thrombus?

A

A blood clot inside a blood vessel, that may obstruct the blood flow inside the circulatory system.

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11
Q

What can result from an atheroma in the aorta?

A

Aortic aneurysm - an unusual swelling of the aorta, large aneurysms can be fatal, if it ruptures can lead to huge internal, fatal bleed.

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12
Q

What might atherosclerosis lead to?

A

MI, TIA (transient ischaemic attack), cerebral infarction, abdominal aortic aneurysm, peripheral vascular disease, cardiac failure.

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13
Q

How do atheromas affect blood flow?

A

The change in vessel wall structure can lead to thrombus formation.
Blood flow is massively controlled by radius of lumen (to power of 4), so even a small decrease in blood flow can lead to a massive decrease in flow and a huge drop in oxygen delivery –> ischaemia and infarction.

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14
Q

What are the three classifications of ischaemia and how do they differ?

A

Acute - will be able to see changes (sudden onset)
Chronic - might go unnoticed for a while but just progressively worsen
Acute-on-chronic - sudden worsening of an already chronic disease

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15
Q

What are the biochemical consequences of ischaemia?

A

Cells may have to resort to anaerobic metabolism leading to the production of L-lactate (this would normally be turned back into pyruvate on repaying the oxygen debt but as this doesn’t happen can lead to toxic build up) –> cell death.

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16
Q

What are the cellular consequences of ischaemia?

A

Different cells have varying needs for oxygen and will be variably susceptible to ischaemia.

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17
Q

What are the clinical effects of ischaemia?

A

Dysfunction
Pain, e.g. claudication (pain in calf muscles)
Physical damage, specialised cells are often damaged first and most.

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18
Q

What are the possible outcomes of ischaemia?

A

1 - no clinical effect.
2 - resolution (w or w/o therapeutic intervention).
3 - infarction.

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19
Q

Define infarction.

A

Ischaemic necrosis within a tissue or organ in living body produced by occlusion of either the arterial supply or venous drainage.

20
Q

What is the aetiology of infarction?

A

Cessation of blood flow, for example due to thrombosis, embolism, strangulation (e.g. gut) or trauma (cut or ruptured vessel).

21
Q

What is the scale of damage in ischaemia or infarction dependent on? (4)

A

Time period, tissue/organ, patterns of blood supply, previous disease.

22
Q

Describe the pathophysiology of infarction.

A

Anaerobic metabolism leads to build up of toxic metabolites, leading to cell death and liberation of enzymes which break down the tissue.

23
Q

Distinguish between coagulative and colliquitive necrosis.

A

Coagulative necrosis - dead material forms gel-like substance in which structural integrity of tissue is maintained, seen in infarction of heart and lung
Colliquitive necrosis - digestive of dead cells forms viscous liquid, seen in infarction of brain

24
Q

Describe how blockages in vessels of the heart lead to myocyte death.

A

Coronary arterial obstructive leads to decreased blood flow to region of myocardium leading to ischaemia, rapid myocardial dysfunction and myocardial death.

25
Q

Describe the changes that occur during myocardial ischaemia leading to infarction and at what time scales these occur.

A

Anaerobic metabolism onset of ATP depletion - seconds.
Loss of myocardial contractility (–> heart failure) - less than 2 min.
Ultrastructural changes (myofibrillar relaxation glycogen depletion, cell and mitochondrial swelling ?reversible) - few mins.

26
Q

For how long does severe ischaemia need to go untreated before there is irreversible damage?

A

20-30 mins.

27
Q

What is involved in myocyte necrosis and how long does it take to happen?

A

20-40 mins. Involves disruption of integrity of sarcolemmal membrane –> leakage of intracellular macromolecules (troponin can be picked up in blood tests).

28
Q

After one hour, what does the infarction cause?

A

Damage to the microvasculature.

29
Q

How do the appearances of infarcts change over time?

A

Less than 24 hrs -
no change on visual inspection
12 post insult, see swollen mitochondria on electron microscopy
24-48 hrs -
pale infarct - e.g. myocardium, spleen, kidney, solid tissues
red infarct - e.g. in lung and liver
loose tissues, previously congested tissue, second/continuing blood supply, venous occlusion
microscopically - acute inflammation initially at edge of infarct, loss of specialised cell features.
72 hrs onwards -
pale infarct - yellow/white and red periphery
little change to red infarct
microscopically - chronic inflammation, macrophages remove debris, granulation tissue, fibrosis

30
Q

What is the end appearance of an infarct?

A

Scar replaces area of tissue damage. Shape depends on territory of occluded vessel. Reperfusion injury.

31
Q

What are the reparative processes in MI?

A 
Cell death
acute inflammation 
macrophage phagocytosis of dead cells
granulation tissue
collagen deposition (fibrosis)
scar formation
32
Q

What happens in hours 4-12 of an MI?

A

early coagulation necrosis, oedema, haemorrhage

33
Q

What happens in hours 12-24 of an MI?

A

ongoing coagulation necrosis, myocyte changes, early neutrophilic infiltrate

34
Q

What happens in days 1-3 of an MI?

A

Coagulation necrosis, loss of nuclei and striations, brisk neutrophilic infiltrate

35
Q

What happens in days 3-7 of an MI?

A

Disintegration of dead myofibres, dying neutrophils, early phagocytosis

36
Q

What happens in days 7-10 of an MI?

A

Well developed phagocytosis, granulation tissues at margins.

37
Q

What happens in days 10-14 of an MI?

A

Well established granulation tissue with new blood vessels and collagen deposition.

38
Q

What happens in weeks 2-8 of an MI?

A

Increased collagen deposition, decreased cellularity.

39
Q

What happens after two months of an MI?

A

Dense collagenous scar.

40
Q

Define transmural infarction.

A

Ischaemic necrosis affects full thickness of myocardium.

41
Q

Define subendocardial infarction.

A

Ischaemic necrosis mostly limited to a zone of myocardium under the endocardial lining of the heart.

42
Q

What differs in the histological features of the transmural and subendocardial infarction.

A

Subendocardial infarct possibly slightly shortened repair time compared to transmural.

43
Q

What is a non-STEMI?

A

No ST elevation in ECG, but elevated serum troponin level.

44
Q

What are STEMIs thought to correlate with?

A

Subendocaridal infarcts.

45
Q

What are the effects of the infarction dependent on?

A

site dependent, within body and organ.
size of infarct
death, dysfunction (pain)
contribution of previous disease or infarction

46
Q

Complications of MI can be immediate, early or late, give examples of possible complications.

A

Sudden death, arrhythmias, angina, cardiac failure, cardiac rupture - ventricular wall, septum, papillary muscle, reinfarction, pericarditis, pulmonary embolism secondary to DVT, papillary muscle dysfunction - necrosis or rupture –> mitral incompetence, mural thrombosis, ventricular aneurysm, Dressler’s syndrome.

CARD - 1 (28 decks)

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