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Mechanism of Disease > Ischaemia, Infarction & Shock > Flashcards

Ischaemia, Infarction & Shock Flashcards

1
Q

How harmful is ischaemia?

A

Limited= cell injury reversible

Prolonged= irreversible cell damage, necrosis

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2
Q

What is therapeutic reperfusion? When will it work/not work?

A
  • Only if ischaemia is reversible
  • Will have no effect if not reversible (permanent damage)
  • Causes generation of reactive oxygen species by inflammatory cells causing further damage
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3
Q

Define infarction & infarct

A

Infarction=Ischaemic necrosis caused by occlusion of the arterial supply or venous drainage
Infarct=An area of infarction in tissues

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4
Q

What causes infarctions?

A
  • Majority= thrombosis & embolism most common within arteries
  • Other causes= vasospasm, atheroma expansion, twisting of vessels (volvulus), extrinsic compression (tumour), rupture of vascular supply (AAA), Venous occlusion
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5
Q

Describe the morphology of infarction

A
  • Red infarction (haemorrhagic)=dual blood supply/ venous infarction
  • White infarction (anaemic) = single blood supply hence totally cut-off
  • Most wedge shaped= obstruction occurs at upstream point, downstream area will be infarcted
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6
Q

Describe the histology of infarction

A
  • Coagulative necrosis

- Colliquative necrosis (brain)

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7
Q

What factors influence the degree of ischaemic damage?

A
  • Nature of the blood supply
  • Rate of occlusion
  • Tissue vulnerability to hypoxia
  • Blood oxygen content
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8
Q

How does nature of blood supply influence degree of ischaemic damage?

A
  • Alternative blood supply will mean less damage
  • Severe ischaemia required for infarction (lungs, liver, hands)
  • Kidneys, spleen, testis have single supplies hence vulnerable to infarction
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9
Q

How does rate of occlusion influence degree of ischaemic damage?

A
  • Slow developing occlusions less likely to infarct tissue
  • Allow time for development of alternative perfusion pathways
  • Coronary arteries
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10
Q

How does tissue vulnerability to hypoxia influence the degree of ischaemic damage?

A
  • The brain= very vulnerable, high O2 consumption

- The heart=slightly more resistant with cardiac myocyte death

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11
Q

How does blood O2 content influence the degree of ischaemic damage?

A
  • Reduced O2 in blood inc chances of infarction
  • Congestive cardiac failure=poor cardiac output
  • Watershed regions occurring at anastamosis
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12
Q

What clinical manifestations can occur in ischaemia in specific organs?

A
  • Heart (IHD, angina)
  • Brain (TIA/CVA)
  • Intestines (ischaemic bowel)
  • Extremities (peripheral vascular disease/gangrene)
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13
Q

Describe what cerebrovascular disease is

A
  • Any abnormality of the brain caused by a pathological process involving blood vessels
  • Includes thrombosis & embolism
  • Bleeding
  • Third leading cause of western death
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14
Q

What are the 2 types of cerebrovascular accident?

A
  • Causes of an ischaemic stroke=thrombosis secondary to atherosclerosis, embolism
  • Causes of haemorrhagic stroke=intracerebral haemorrhage, ruptured aneurysm in circle of Willis
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15
Q

What are the types of gangrene?

A
  • Wet= Superimposed infection
  • Dry= Ischaemic coagulative necrosis
  • Gas= Superimposed infection w/gas producing organism
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16
Q

Define shock

A
  • Physiological state characterized by a significant reduction of systemic tissue perfusion (severe hypotension) resulting in decreased O2 delivery to tissues.
  • Critical imbalance between O2 delivery & O2 consumption
17
Q

What are the cellular effects of shock?

A
  • Membrane ion pump dysfunction
  • Intracellular swelling
  • Leakage of intracellular contents into extracellular space
  • Inadequate regulation of intracellular pH
  • Anaerobic respiration= lactic acid
  • Initially reversible but quickly becoming irreversible
18
Q

What are the systemic effects of shock?

A
  • Alterations in the serum pH=acidaemia
  • Endothelial dysfunction= vascular leakage
  • Stimulation of inflammatory & anti-inflammatory cascades
  • End-organ damage=ischaemia
19
Q

What are the types of shock?

A
  • Hypovolaemic
  • Cardiogenic
  • Distributive (anaphylactic, septic, toxic shock syndrome, neurogenic)
20
Q

Describe hypovolaemic shock

A
  • intra-vascular fluid loss (blood, plasma)
  • dec venous return
  • dec stroke volume so dec cardiac output
  • inc systemic vascular resistance = vasoconstriction
21
Q

What are causes of hypovolaemic shock?

A
  • Haemorrhage (trauma, GI bleeding, ruptured haematoma, AAA)
  • Non-haemorrhagic fluid loss (diarrhoea, vomiting, heat stroke, burns)
  • Acute loss of fluid into internal body cavities
  • Third-space loss= common postoperatively & intestinal obstruction, pancreatitis, cirrhosis
22
Q

What is cardiogenic shock?

A
  • Cardiac pump failure
  • dec cardiac output
  • inc systemic vascular resistance
23
Q

What are the 4 categories of cardiogenic shock?

A
  • 60-90% mortality
  • Myopathic (heart muscle failure)
  • Arrhythmia-related
  • Mechanical
  • Extra-cardiac (obstruction to blood outflow)
24
Q

What are the causes of myopathic cardiogenic shock?

A
  • Myocardial infarction
  • Right ventricular infarction, dilated cardiomyopathies
  • stunned myocardium
25
Q

What are causes of arrhythmia-related cardiogenic shock? What does this lead to?

A
  • Atrial & ventricular arrhythmias
  • Atrial fibrillation/flutter
  • Ventricular tachycardia, bradyarrhythmia, complete heart block
  • Leads to dec cardiac output
26
Q

What are causes of mechanical cardiogenic shock?

A
  • Valvular defects (prolapse)
  • Ventricular septal defects
  • Atrial myxomas
  • Ruptured venticular free wall aneurysm
27
Q

What are causes of extra-cardiac cardiogenic shock?

A
  • Anything that impairs cardiac filling/ ejection of blood from heart
  • Massive pulmonary embolism
  • Tension pneumothorax
  • Severe constrictive pericarditis
  • Pericardial tamponade
28
Q

What happens in distributive shock?

A
  • dec systemic vascular resistance due to severe vasodilation
  • inc cardiac output = flushing
29
Q

What is septic shock?

A
  • 35-60% mortality within 1 month
  • Severe over-whelming systemic infections w/gram +ve/-ve bacteria or fungi
  • inc cytokines/mediators= vasodilation
  • Pro-coagulation=ischaemia
30
Q

What is anaphylactic shock?

A
  • Severe type I hypersensitivity reaction
  • Sensitized individuals (penicillin, peanuts)
  • Small doses of allergen= IgE cross-linking
  • Laryngeal oedema
  • Massive mast cell degranulation
  • vasodilation
  • Contraction of bronchioles/ respiratory distress
  • Circulatory collapse-shock/death
31
Q

What is neurogenic shock?

A
  • Spinal injury/anaesthetic accident
  • Loss of sympathetic vascular tone
  • Vasodilation=shock
32
Q

What is toxic shock syndrome?

A
  • S.aureus/S.pyogenes produce exotoxins(superantigens)
  • Don’t require processing by antigen-presenting cells
  • Non-specific binding of class II MHC to T cell receptors
  • Widespread release of massive amounts of cytokines= dec systemic vascular resistance
33
Q

What are the combinations of shock that can occur and what happens in them?

A
  • Primary distributive component (inflammation & anti-inflammatory cascades inc vascular permeability/vasodilation)
  • Hypovolemic component (dec oral intake, insensible losses, vomiting, diarrhoea)
  • Cardiogenic component (sepsis-related myocardial dysfunction)

Mechanism of Disease (18 decks)

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