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Systems 2: Cardiovascular > Pathophysiology of Ischaemia and Infarction > Flashcards

Pathophysiology of Ischaemia and Infarction Flashcards

1
Q

What is the definition of ischaemia?

A
  • Supply of oxygen to a tissue/organ is not enough for the demand of the tissue/organ
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2
Q

What are the 4 types of hypoxia?

A
  • Hypoxic
  • Anaemic
  • Stagnant
  • Cytotoxic
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3
Q

What causes hypoxic hypoxia?

A
  • Low inspired O2 level

- Normal inspired O2 but low PaO2

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4
Q

What causes anaemic hypoxia?

A
  • Normal O2 inspiration but blood abnormal
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5
Q

What causes stagnant hypoxia?

A

Normal inspired O2 but abnormal delivery

  • Occlusion of vessels
  • Systemic (e.g. shock)
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6
Q

What causes cytotoxic hypoxia?

A
  • Normal inspired O2 but abnormalities at the tissue level
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7
Q

What factors affect oxygen supply?

A
  • Inspired O2
  • Pulmonary function
  • Blood constituents
  • Blood flow
  • Integrity of vasculature
  • Tissue mechanisms
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8
Q

What factors affect tissue demand?

A
  • Type of tissue

- Activity of tissue above baseline

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9
Q

In ischaemic heart disease what are the supply issues?

A
  • Coronary artery atheroma
  • Cardiac failure
  • Pulmonary function
  • Pulmonary oedema (LVF)
  • Anaemia
  • Previous MI
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10
Q

What demand issues relate to ischaemic HD?

A
  • Heart has a high demand

- Increases on exercise and stress

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11
Q

What type of atheroma will cause stable angina?

A
  • Established
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12
Q

What type of atheroma will cause unstable angina?

A
  • Complicated
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13
Q

What are the functional effects of ischaemia?

A
  • Blood/O2 supply doesn’t meat demand so demand increases further leading to angina
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14
Q

What is released due to this lack of O2/blood supply?

A
  • Lactic acid from anaerobic respiration

- Ultimately, if not converted back into pyruvate leads to cell death

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15
Q

What are the clinical effects of ischaemia?

A
  • Dysfunction
  • Pain
  • Physical damage to specialised cells that can’t be replaced
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16
Q

What is the definition of infarction?

A
  • Ischaemic necrosis within a tissue/organ by occlusion of either the arterial supply or venous drainage
17
Q

What does the scale of damage caused by infarction depend on?

A
  • Time period
  • Tissue/organ affected
  • Pattern of blood supply
  • Previous disease
18
Q

What is coagulative necrosis and where does it occur in response to infarction?

A

Dead tissue arrangement is left for a few days following infarction i.e. in the heart

19
Q

What is colliquitive necrosis and where does it occur in response to infarction ?

A

Dead tissue is liquefied into a liquid viscous mass i.e. the brain

20
Q

What order does the myocardium lose it’s ability to function following infarction?

A
  • Anaerobic metabolism (a few seconds after)
  • Loss of myocardial contractility (<2 mins)
  • Ultrastructural changes (a few minutes)
21
Q

What are the ultrastructural changes following ischaemia?

A
  • Myofibrillar relaxation
  • Glycogen depletion
  • Cell and mitochondrial swelling
  • All are reversible unless ischaemia is very long
22
Q

On investigation what can be seen less that 24 hours following an infarct?

A
  • No visual inspection change

- Swollen mitochondria on electron microscopy

23
Q

What changes can be seen 24-48 hours post infarct?

A
  • Pale infarct
  • Red infarct
  • Acute inflammation at edges of infarct
24
Q

What structures does a pale infarct occur?

A
  • Myocardium
  • Spleen
  • Kidney
  • Solid tissue
25
Q

What structures does a red infarct occur?

A
  • Lung
  • Liver
  • Loose tissue
26
Q

What can be seen 72 hours after pale infarct?

A
  • In a pale infarct, yellow white and red periphery
27
Q

What can be seen 72 hours after red infarct?

A

Little change

28
Q

What can be seen microscopically 72 hours after?

A
  • Chronic inflammation
  • Macrophages
  • Granulation tissue
  • Fibrosis
  • Neutrophil polymorphs
29
Q

What is the end result following an infarction (if survival)

A
  • Scar tissue replaces tissue damage
30
Q

What is the process of scar tissue formation in an MI?

A
  • Cell death
  • Acute inflammation
  • Macrophages phagocytose dead cells
  • Granulation tissue
  • Collagen deposition
  • Scar formation
31
Q

Where does ischaemic necrosis extent from and to in a transmural infarction?

A

The full width of the myocardium

32
Q

What is a subendocardial infarction?

A
  • Ischaemic necrosis mostly limited to zone of myocardium beneath the endocardial lining
33
Q

How are acute infarcts classified?

A
  • Elevation of the ST segment on the ECG
34
Q

What classifies a non STEMI?

A
  • No elevation of the ST segment

- Serum troponin level risen

35
Q

What do non-STEMI’s correlate with?

A
  • A subendocardial infarct

Systems 2: Cardiovascular (19 decks)

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