Ischaemia and infarction Flashcards

1
Q

ischaemia

A

relative lack of blood supply to tissue/ organ leading to inadequate oxygen supply to meet needs of tissue/ organ: hypoxia

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2
Q

types of hypoxia

A

hypoxic, anaemic,

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3
Q

hypoxic hypoxia

A

low inspired oxygen or normal inspired oxygen but low partial pressure of oxygen

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4
Q

anaemic hypoxia

A

normal inspired oxygen but blood abnormal

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5
Q

stagnant hypoxia

A

normal inspired oxygen but abnormal oxygen delivery eg occlusion of vessel (local) and shock (systemic)

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6
Q

cytotoxic hypoxia

A

normal inspired oxygen but abnormal at tissue level

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7
Q

factors affecting oxygen supply

A

inspired oxygen, pulmonary function, blood constituents, blood flow, integrity of vasculature, tissue mechanisms

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8
Q

factors affecting oxygen demand

A

tissue type, activity of tissue above baseline value

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9
Q

ischaemic heart disease

A

supply issues- coronary artery atheroma, cardiac failure, pulmonary function- other disease or pulmonary oedema, anaemia, previous MI
demand issues- heart has high intrinsic demand, exertion/ stress

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10
Q

clinical correlation between ischaemic heart disease and atheroma

A

ulcerated/ fissured plaques leads to thrombosis which leads to ischaemia and or infarction

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11
Q

functional effects of ischaemia

A

blood oxygen supply fails to meet demand due to decreased supply and increased demand or both. related to rate of onset. can be general, chronic, acute on chronic

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12
Q

cellular effects of ischaemia

A

different tissues have variable oxygen requirement and variably susceptible to ischaemia, neurons, heart cells, renal tubular cells affected more than fat, bone etc

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13
Q

clinical effects of ischaemia

A

dysfunction, pain, physical damage

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14
Q

outcome of ischaemia

A

no clinical effect, resolution, infarction

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15
Q

aetiology of infarction

A

thrombosis, embolism, strangulation eg gut, trauma

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16
Q

scale of damage of ischamia and infarction depends on

A

time period, tissue organ, pattern of blood supply, previous disease

17
Q

types of necrosis

A

coagulative and colliquitive

18
Q

myocardial ischaemia process and time

A

anaerobic metabolism and onset of ATP depletion, loss of myocardial contractility, ultrastructural changes eg myofibrillar relaxation, glycogen depletion, cell and mitochondrial swelling. all happens within a few mins. 20-30mins means irreversible damage. 20-40 mins myocyte necrosis. 1 hour to injury to microvasculature

19
Q

appearances of infarcts over time

A

less than 24 hours swollen mitochondria, 24-48 hours acute inflammation initially at edge of infarct, loss of specialised cell features, 72 hours- chronic inflammation, macrophages remove debris, granulation tissue, fibrosis

20
Q

pale infarcts occur in

A

myocardium, spleen, kidney, solid tissues. turn yellow and red periphery after 72 hours

21
Q

red infarcts occur in

A

lung, liver loose tissues, previously congested tissue, venous occlusion, secondary/ continuing blood supply. little change after 72 hours

22
Q

end result of infarct

A

scar replaces area of tissue damage (more white) and shape depends on territory of occluded vessel

23
Q

reparative processes of myocardial infarction

A

cell death, acute inflammation, macrophage phagocytosis of dead cells, granulation tissue, collagen deposition, scar formation

24
Q

transmural infarction

A

ischaemic necrosis affects full thickness of the myocardium

25
Q

acute infarcts are classified according to

A

whether there is elevation of the ST segments on the ECG.

26
Q

non stemi

A

no ST segment elevation but a significantly serum troponin level. thought to correlate with a subendocardial infarct

27
Q

effects infarction

A

site of dependent, size of infarct, death, dysfunction, contribution of previous disease/ infarction

28
Q

complications of myocardial infarction

A

sudden death, arrhythmias, angina, cardiac failure, cardiac rupture, papillary muscle, reinfarction, pericarditis, papillary muscle dysfunction, pulmonary embolism secondary to deep vein thrombosis, mural thrombosis, ventricular aneurysm, dresslers syndrome