Ischaemia And Infarction Flashcards

1
Q

Hypoxic hypoxia

A

Low inspired O2

Or normal inspired O2 but low PaO2

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2
Q

Anaemic hypoxia

A

Normal inspired O2 but blood is abnormal

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3
Q

Stangnant hypoxia

A

Normal inspired O2 but abnormal delivery from local occlusion of vessel or systemic effects eg shock

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4
Q

Cytotoxic hypoxia

A

Normal inspired O2 but abnormal at tissue level

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5
Q

Factors affecting oxygen supply

A
Inspired O2
Pulmonary function
Blood constituents
Blood flow
Integrity of vasculature
Tissue mechanisms
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6
Q

Factors affecting oxygen demand

A

Different types of tissue

Activity of tissues above baseline value

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7
Q

Causes of supply issues in is ischaemic heart disease

A

Coronary artery atheroma, cardiac failure, pulmonary disease or oedema (LVF), anaemia, previous MI

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8
Q

Cause of demand issues in is ischaemic heart disease

A

Heart has high Intrinsic demand, exertion/stress

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9
Q

Atheroma types in coronary artery

A

Established - stable angina(on exertion)

Complicated - unstable angina (at rest)

Ulcerated/fissured - thrombosis then ischaemia/infarction

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10
Q

Clinical consequences of ischemia

A
MI
TIA
Cerebral infarction
Abdominal aortic aneurysm
Peripheral vascular disease
CF
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11
Q

blood flow formula

A

Q= difference in Pressure over resistance

Resistance is worked out with radius and constants and length and viscosity

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12
Q

Biochemical effects of ischemia

A

Only anaerobic respiration so less ATP

Lactate produces and the acid damages tissue

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13
Q

Clinical effects/symptoms of ischemia

A

Dysfunction
Pain
Physical damage

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14
Q

Outcomes of ischemia

A

No clinical effects
Resolution with or without therapeutic intervention
Infarction

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15
Q

Causes of infarction

A

Thrombosis
Embolism
Strangulation eg gut
trauma

Occlusion of either arterial supply or venous drainage

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16
Q

what is coagulative necrosis and where does it happen

A

Goes hard eg heart, lung

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17
Q

Colliquitive necrosis

A

Eg brain, draws fluid

18
Q

Onset time of anaerobic metabolism and ATP depletion in MI

19
Q

Onset of loss of myocardial contractility (heart failure) in MI

A

Less than 2 minutes

19
Q

Onset of loss of myocardial contractility (heart failure) in MI

A

Less than 2 minutes

20
Q

Onset of ultrastructural changes in MI eg myofibrillar relaxation, glycogen depletion, cell and mitochondrial swelling

A

A few minutes

21
Q

When does severe ischaemia become irreversible in MI

A

20-30 minutes

22
Q

Onset of myocyte necrosis (disruption of sarcolemmal membrane and leakage of cell contents) in MI

A

20-40 minutes

23
Q

Onset of injury to microvasculature in MI

A

Over an hour

24
Changes of appearance of infarcts at under 24 hours
No visual but under EM swollen mitochondria at under 12 hours
25
Changes of appearance of infarcts at 24-48 hours
Pale infarct eg myocardium, spleen , kidney (solid tissues) Or Red infarct eg lung, liver (loose tissues, previously congested tissue, second/continuing blood supply, venous occlusion Microscopically, acute inflammation initially at edges, loss of specialised cell features
26
Changes in appearance of infarcts at 72hours
Pale infarct with red periphery Red little change Chronic inflammation, MQ to remove debris, granulation tissue, fibrosis
27
End result appearance of infarcts
Scar replaces tissue damage
28
Reparative processes in myocardial infarction
``` Cell death Acute inflammation Macrophages phagocytosing dead cells Granulation tissue Collagen deposition (fibrosis) Scar formation ```
29
4-12 hours of myocardial infarction
Early coagulation necrosis, odema and haemorrhage
30
12-24 hours of myocardial infarction
Ongoing coagulation necrosis, myocyte changes, early neutrophilic infiltrate
31
1-3 days of myocardial infarction
Coagulation necrosis again, loss of nuclei and striations, brisk neutrophilic infiltrate
32
3-7 days of myocardial infarction
Disintegration of dead myofibres, dying neutrophils, early phagocytosis
33
7-10 days of myocardial infarction
Well developed phagocytosis, granulation tissue at margins
34
10-14 days of myocardial infarction
Well established granulation tissue with new blood vessels and collagen deposition
35
2-8 weeks of myocardial infarction
Increased collagen deposition, decreased cellularity
36
>2 months of myocardial infarction
Dense collagenous scar
37
Transmural infarction
Ischemic necrosis affects full thickness of myocardium
38
Subendocardial infarction
Ischemic necrosis mostly limited to a zone of myocardium under the endocardial lining of the heart
39
What type of infarct correlates with Non-stemi
Subendocardial