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MOD > MOD 14 - Ischaemia & hypoxic injury > Flashcards

MOD 14 - Ischaemia & hypoxic injury Flashcards

1
Q

what is hypoxic injury

A

any state of reduced tissue O2 availability (general & regional)

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2
Q

what is ischaemia

A

pathological reduction in blood flow to tissue

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3
Q

what will happen if reperfusion of non-infarcted but ischaemic tissues always good

A

generation of reactive oxygen species by inflammatory cells causes further damage

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4
Q

what is infarction

A

ischaemic necrosis caused by occlusion of the arterial supply or venous drainage

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5
Q

what is the most common cause of infarction

A

thrombosis and embolism - most commonly within arteries

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6
Q

what does red infarction indicate?

A

haemorrhagic - dual blood supply/venous infarction

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7
Q

what does white infarction mean?

A

single blood supply hence totally cut off

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8
Q

what are the factors influence the degree of ischaemic damage

A

nature of the blood supply, rate of occulsion, tissue vulnerability to hypoxia , blood oxygen content

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9
Q

how long will irreversible cell damage occur if brain tissue is deprived of oxygen

A

3 to 4 minutes

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10
Q

how long will irreversible cell damage occur if heart tissue is deprived of oxygen

A

20 to 30 minutes

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11
Q

what is cerebrovascular disease

A

any abnormality of the brain caused by a pathological process involving the blood vessels

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12
Q

what are the causes of haemorrhagic stroke

A

intracerebral harmorrhage (hypertensive), ruptured aneurysm in the circle of Willis (subarachnoid)

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13
Q

what are cerebrovascular accidents

A

ischaemic stroke

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14
Q

what are some examples of some ischaemia around the body

A

heart - ischaemic haert disease (angina)

brain - cerebrovascular disease (TIA/CVA)

intestines - ischaemic bowel

extremities - peripheral vascular disease/gangrene

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15
Q

what are ischaemic bowel disease

A
  • usually caused by thrombosis or embolism in the superior or inferior mesenteric arteries,
  • presents with abdominal pain
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16
Q

what is shock?

A

a physiological state characterised by a significant reduction of systemic tissue perfusion (severe hypotension) resulting in decreased oxygen delivery to the tissues

17
Q

what are the consequences of shock?

A

shock result in a critical imbalance between oxygen deliver and oxygen consumption

impaired tissue perfusion and ultimately prolonged oxygen deprivation leads to cellular hypoxia and derangement of critical biochemical processes at first cellular and eventually systemic levels

18
Q

what are the effect of shock at a cellular level

A

membrane ion pump dysfunction, intracellular swelling, leakage of intracellular contents into the extracellular space, inadequate regulation of intracellular pH
anaerobic respiration - lactic acid

19
Q

what are the systemic effects of shock

A

Alterations in the serum pH (acidaemia)
Endothelial dysfunction vascular leakage
Stimulation of inflammatory and anti-inflammatory cascades
End-organ damage (ischaemia)

20
Q

what are the different types of shock?

A

hypovolaemic, cardiogenic, distributive (anaphylactic, spetic, toxic shock syndrome, neurogenic)

21
Q

what is hypovolaemic shock

A

intra-vascular fluid loss (blood, plasma etc)

decreased venous return to heart AKA ‘pre-load’

decreased stroke volume - decreased cardiac output

22
Q

what can compensate for hypovolaemic shock

A

increase systemic vascular return (vasoconstrict)

23
Q

what are the cause of hypovolaemic shock

A

haemorrhage, non-haemorrhagic fluid loss - diarrhoea, vomiting, burns

24
Q

what is third spacing

A

acute loss of fluid into internal body cavities - common postoperatively and in intestinal obstruction

25
Q

what is cardiogenic shock

A

cardiac pump failure

decrease cardiac output

26
Q

how can you compensate for cardiogenic shock

A

increase systemic venous return (vasocontrict)

27
Q

what are the causes of cardiogenic shock

A

1 - myopathic (heart muscle failure)

2 - arrythmia-related (abnormal electrical activity)

3- mechanical

4 - extra-cardiac (obstruction to blood outflow)

28
Q

what can be some examples of myopathic cardiogenic shock

A

MI, Right ventricular infarction, dilated cariomyopathies

29
Q

what can be some examples of arrhythmia-related cardiogenic shock

A
  • atrial and ventricular arrhythmias
  • AF - arrhythmia & disorientated filling and emptying
  • ventricular tachycardia, bradyarrhythmias and complete heart block
30
Q

what can be some examples of mechanical cardiogenic shock

A

valvular defect, ventricular septal defects, atrial myoxmas, ruptured ventricular free wall aneurysm

31
Q

what can be some examples of extra-cardiac cardiogenic shock

A

Anything that impairs cardiac filling or ejection of blood from heart
Massive pulmonary embolism, tension pneumothorax,
Severe constrictive pericarditis, pericardial tamponade et

32
Q

what is distributive shock

A
  • decreased systemic venous return due to severe vasodilation
33
Q

how can you compensate for distributive shock

A

increase cardiac output - flushed/bounding heart

34
Q

what is septic distributive shock

A

severe, over-wheming systemic infections

35
Q

what can cause septic distributive shock

A

increase cytokines/mediators - vasodilation & can also cause Disseminated Intravascular coagulation

36
Q

what can anaphylactic distributive shock

A

severe type 1 hypersensitivity reaction - sensitised individuals, small doses of allergen - IgE cross-linking

37
Q

how does anaphylactic distributive shock work

A
  • Sensitized individuals
    Hospital e.g. drugs (penicillin etc)
    Community e.g. peanuts, shellfish, or insect toxins
    Small doses of allergen
  • IgE cross-linking
  • massive mast cell degranulation
  • vasodilation
  • contraction of bronchioles/respiratory distress
  • laryngeal oedema
  • circulatory collapse

shock/death

38
Q

how does neurogenic shock cause problem?

A

spinal injury/aesthetic accidents - loss of sympathetic vascular tone - vasodilation - shock

39
Q

how is toxic shock syndrome caused

A

S. aureus/ S. pyogenes produce exotoxins - superantigens - non-specific binding of class II MHC to T cell receptors - widespread release of massive amounts of cytokines - decreased systemic venous return

MOD (19 decks)

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