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Y2 MECHANISMS OF DISEASE > Ischaemia, Infarction & Shock > Flashcards

Ischaemia, Infarction & Shock Flashcards

1
Q

What is the definition of hypoxia?

A

When the oxygen saturation of tissues falls

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2
Q

What is the definition of ischaemia?

A

the interruption/disturbance of blood flow to cells and tissues

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3
Q

What is the relationship between ischaemia and hypoxia?

A

ischaemia ALWAYS results in hypoxia

hypoxia can occur without ischaemia e.g. anaemia

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4
Q

How is the oxygen supply and metabolite supply affected in hypoxia?

A

There is an impaired oxygen supply only

Other metabolites are still supplied to the tissue

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5
Q

How is the metabolite supply affected in ischaemia?

A

There is a decreased supply of metabolites, including glucose

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6
Q

What is the consequence of lack of glucose in ischaemia?

A

glycolytic anaerobic respiration fails due to lack of glucose

the build up of metabolites impairs anaerobic respiration further

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7
Q

What is the consequence of the reduced metabolite supply in ischaemia on the tissues?

A

Ischaemia will injure tissues faster and more severely than hypoxia

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8
Q

What is the main cause of ischaemia?

A

vascular occlusion

this can be arterial or venous

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9
Q

What are the 3 main causes of vascular occlusion?

A
  1. severe atherosclerosis
  2. thrombosis
  3. embolism
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10
Q

What are the 6 rarer causes of ischaemia?

A
  1. vasospasm
  2. vasculitis
  3. extrinsic compression (e.g. tumour)
  4. twisting of vessel roots (e.g. volvulus)
  5. rupture of vascular supply
  6. cardiac failure
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11
Q

What happens if ischaemia is limited and only occurs for a short duration?

A

Any cell injury is reversible

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12
Q

What is primary percutaneous coronary intervention used for?

A

Myocardial ischaemia/infarction

It allows for rapid restoration of blood flow to allow for reversible cell injury

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13
Q

What happens if ischaemic injury is prolonged or sustained?

A

Irreversible cell damage

This leads to necrosis

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14
Q

What is tissue necrosis called when it is caused by ischaemia?

A

infarction

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15
Q

What do the variable effects of vascular occlusion depend on (4 factors)?

A
  1. nature of the blood supply
  2. the rate of occlusion
  3. tissue vulnerability to hypoxia
  4. blood oxygen content
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16
Q

How does the nature of the blood supply affect whether vascular occlusion will cause damage?

A

an alternative blood supply means that vascular occlusion causes less damage

severe ischaemia is required for infarction

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17
Q

In which 3 organs is severe ischaemia less likely to occur due to a dual blood supply?

A
  1. lungs = pulmonary and bronchial arteries
  2. liver - hepatic artery and portal vein
  3. hand - radial and ulnar artery
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18
Q

In general, what kind of tissues are resistant to infarction of a single vessel?

A

tissues with a dual blood supply

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19
Q

Why are the kidneys, spleen and testis more vulnerable to both arterial and venous infarction?

A

they have end-arterial circulations

this means an artery only blood supply

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20
Q

What type of organs are more vulnerable to venous infarction?

A

organs with a single venous outflow (testis/ovary)

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21
Q

How does the rate of occlusion affect the severity of the effects of vascular occlusion?

Why?

A

Slow developing occlusions are less likely to lead to infarction

This allows time for the development of alternative perfusion pathways (collateral supply)

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22
Q

What is the state of the anastomoses in the heart under normal circumstances?

A

there are small anastomoses that connect the major branches of the coronary artery system

they have minimal flow

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23
Q

What is significant about the anastomoses in the coronary artery system when a coronary arterial branch becomes occluded?

A

If a coronary arterial branch becomes slowly occluded, the flow can be directed through the anastomoses

Infarction can be avoided even if the main arterial branch is totally occluded

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24
Q

If a neurone in the brain is deprived of oxygen, how long does it take for it to undergo irreversible cell damage?

A

3 - 4 minutes

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25
Q

If a cardiac myocyte or cardiac fibroblast is deprived of oxygen, how long does it take for irreversible cell damage to occur?

A

cardiac myocyte - 20-30 mins

cardiac fibroblast takes hours

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26
Q

Why does it take longer for irreversible cell damage to occur in a cardiac fibroblast compared to a myocyte?

A

fibroblasts are not as metabolically active as heart muscle cells

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27
Q

How does blood oxygen content affect the severity of the effects of vascular occlusion?

A

reduced oxygen content in the blood means that tissues are more vulnerable to infarction

e.g. anaemia

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28
Q

Why does an infarct occur in a normally inconsequential narrowing of vessels in congestive heart failure?

A

There is poor cardiac output and impaired pulmonary ventilation

Infarct occurs due to impaired oxygenation of the tissues

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29
Q

What 5 categories are looked for when looking at morphological changes of an infarct?

A
  1. location
  2. colour
  3. shape
  4. type of necrosis
  5. histological changes over time
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30
Q

What is the name of the locations that are looked for when identifying an infarct?

A

watershed regions

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31
Q

What is a watershed region?

A

a point of anastomoses between 2 vascular supplies

Infarcts are more likely to occur here

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32
Q

What are examples of common watershed regions?

A
  1. splenic flexure in colon
  2. myocardium
  3. regions in the brain
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33
Q

What are the two types of infarction and their colour?

A
  1. red infarction (haemorrhagic)

2. white infarction (anaemic)

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34
Q

Where do red infarctions tend to be found?

A

In regions with a dual blood supply

or venous infarctions

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35
Q

Where do white infarctions tend to be found?

A

in regions with a single blood supply

36
Q

What shape are most infarcts?

A

wedge shaped

37
Q

Why are most infarcts wedge-shaped?

A
  1. vascular supply is up-stream in the tissue
  2. the vascular branches expand as you get deeper into the tissue
  3. if obstruction occurs at an upstream point, the entire down-stream area will be infarcted
38
Q

What is the main type of necrosis seen in infarction?

A

coagulative necrosis

39
Q

What is the type of necrosis seen in an infarction of the brain?

A

colliquative/liquefactive necrosis

40
Q

As duration of cellular injury progresses, what are the 4 events that occur?

A
  1. biochemical alterations leading to cell death
  2. ultrastructural changes
  3. light microscopic changes
  4. gross morphological changes
41
Q

What gross and microscopic features will be seen 0-4 hours after cellular injury?

A

there will be no changes seen

42
Q

Between 4-12 hours, what gross and microscopic features will be seen in coagulative infarction?

A

gross - occasional dark mottling

microscopic - oedema, haemorrhage - this is the start of coagulative necrosis

43
Q

Between 12-24 hours, what gross and microscopic features will be seen in coagulative infarction?

A

gross - dark mottling

microscopic - ongoing coagulative necrosis

44
Q

Between 1-3 days, what gross and microscopic features will be seen in coagulative infarction?

A

gross - yellow with haemorrhagic edge

microscopic - oedema with early neutrophil infiltration

45
Q

Between 3-7 days, what gross and microscopic features will be seen in coagulative infarction?

A

gross - yellow centre becomes soft

microscopic - dying neutrophils with macrophage infiltration

46
Q

Between 1-2 weeks, what gross and microscopic features will be seen in coagulative infarction?

A

gross - red-grey colour

microscopic - granulation tissue formation

47
Q

Between 2-8 weeks, what gross and microscopic features will be seen in coagulative infarction?

A

gross - fibrous scar

microscopic - increased collagen leading to scar formation

48
Q

Under what conditions is therapeutic reperfusion of ischaemia a good thing?

A

tissue reperfusion is generally good

ONLY if the ischaemia is reversible

49
Q

What happens if ischaemia is NOT reversible, but therapeutic reperfusion is still performed?

A

reperfusion of infarcted tissues has no effect

this is because the damage caused by infarction cannot be reversed

50
Q

What is reperfusion injury?

A

the generation of reactive oxygen species by sudden reperfusion of ischaemic (dysfunctional) tissues

this damages the tissues

51
Q

How can reperfusion injury affect the function of salvaged tissue?

A

the function of the salvaged tissue may be delayed for hours to days

52
Q

Why is reperfusion injury clinically relevant?

A

around 50% of the final infarct may be due to reperfusion injury

generally, reperfusion is better than infarction

53
Q

What is the definition of shock?

A

a pathophysiological state of reduced systemic tissue perfusion resulting in decreased oxygen delivery to the tissues

54
Q

How does shock affect oxygen balance of tissues?

A

it causes a critical imbalance between oxygen delivery and oxygen requirements of the tissues

55
Q

What can impaired tissue perfusion and prolonged oxygen deprivation in shock lead to?

A
  1. cell death due to hypoxia
  2. end-organ damage
  3. multi-organ failure
  4. death
56
Q

Can shock be reversible?

A

It is initially reversible, but rapidly becomes irreversible

57
Q

Essentially, what is shock the result of?

A

decreased systemic tissue perfusion

or mean arterial pressure

58
Q

What factors contribute to mean arterial pressure (MAP)?

A

MAP = CO x SVR

systemic vascular resistance is the same as total peripheral resistance

59
Q

What factors affect cardiac output?

A

heart rate and stroke volume

60
Q

What is the main factor influencing SVR?

A

arteriolar radius

this depends on how dilated or constricted the vessels are

61
Q

What are the causes of shock?

A

anything that causes either:

  1. decreased cardiac output
  2. decreased systemic vascular resistance
62
Q

What are the 3 types of shock?

A
  1. hypovolaemic
  2. cardiogenic
  3. distributive
63
Q

What are the stages involved in hypovolaemic shock?

A
  1. there is intravascular fluid loss (blood, plasma)
  2. reduced venous return to the heart
  3. this reduces stroke volume, and therefore cardiac output
64
Q

How does the body compensate for hypovolaemic shock?

A

vasoconstriction increases SVR

this means blood is directed away from the peripheries and towards vital organs

heart rate is increased

65
Q

How would a patient in hypovolaemic shock feel/present?

A

cool/clammy due to less blood going to the peripheries

due to compensation, they may have normal blood pressure

66
Q

What are the 2 categories of causes of hypovolaemic shock?

A
  1. haemorrhage

2. non-haemorrhagic fluid loss

67
Q

What tends to cause haemorrhage that leads to hypovolaemic shock?

A
  1. trauma, GI bleeding, ruptured haematoma
  2. haemorrhagic pancreatitis, fractures
  3. ruptured aortic, abdominal or left ventricular wall aneurysm
68
Q

What tends to cause non-haemorrhagic fluid loss?

A
  1. diarrhoea, vomiting, heat stroke, burns

2. third spacing

69
Q

What is third spacing?

A

acute loss of fluid into internal body cavities

70
Q

When are third-space losses common?

A
  1. post-operatively

2. in intestinal obstruction, pancreatitis or cirrhosis

71
Q

What causes cardiogenic shock?

A

cardiac pump failure

this leads to reduced cardiac output

72
Q

How is cardiogenic shock compensated for?

A

increase in SVR

this reduces blood flow to the extremities

73
Q

What are the 4 categories of cardiogenic shock?

A
  1. myopathic
  2. arrhythmia-related
  3. mechanical
  4. extra-cardiac
74
Q

What causes myopathic cardiogenic shock?

A

failure of the heart muscle

75
Q

What causes arrhythmia related cardiogenic shock?

A

abnormal electrical activity

76
Q

What causes mechanical cardiogenic shock?

A

acquired or developmental defects

77
Q

What causes extra-cardiac cardiogenic shock?

A

obstruction to blood outflow

78
Q

In what conditions can myopathic cardiogenic shock be seen?

A
  1. myocardial infarction
  2. cardiomyopathies
  3. “stunned myocardium” following cardiopulmonary bypass
79
Q

What is arrhythmia-related cardiogenic shock and in what conditions is it seen?

A

there is nothing wrong with the cardiac muscle, but it is not beating correctly

seen in atrial or ventricular arrhythmias

there is impaired ventricular contraction/filling, reducing cardiac output

80
Q

In what conditions is mechanical cardiogenic shock seen?

A

any defects relating to blood flow through the heart

  1. valvular defects
  2. ventricular septal defects
  3. atrial myxomas
81
Q

What are examples of conditions that cause extra-cardiac cardiogenic shock?

A

anything outside the heart that impairs cardiac filling or ejection of blood from the heart

  1. massive pulmonary embolism
  2. tension pneumothorax
  3. severe constrictive pericarditis
  4. pericardial tamponade
82
Q

What causes distributive shock?

A

there is a decrease in systemic vascular resistance due to severe vasodilation

83
Q

How does the body compensate for distributive shock and how would this present?

A

Increase in cardiac output

Patient appears warm and flushed with a bounding heart beat

84
Q

What are the 4 sub-types of distributive shock?

A
  1. septic shock
  2. anaphylactic shock
  3. neurogenic shock
  4. toxic shock syndrome
85
Q

What causes septic shock and toxic shock syndrome?

A

cytokines causing severe vasodilation

86
Q

What causes anaphylactic shock and neurogenic shock?

A

anaphylactic shock is due to mast cells

neurogenic shock is due to loss of sympathetic tone

87
Q

What is meant by “mixed shock”?

A

when different types of shock can co-exist

Y2 MECHANISMS OF DISEASE (36 decks)

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