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MoD > 14 - Ischaemia, infarction and shock > Flashcards

14 - Ischaemia, infarction and shock Flashcards

1
Q

Why is reperfusion of non-infarcted but ischaemic tissues not always good?

A

Generation of reactive oxygen species by inflammatory cells causes further cell damage === reperfusion injury

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2
Q

Main causes of infarctions

A

Thrombosis and embolism

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3
Q

Other causes of infarctions

A 
vasopasm
artheroma expansion
extrinsic compression
twisting of vessel roots (volvulus)
rupture of vascular supply (AAA)
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4
Q

Infarction morphology

A

Red (haemorrhagic)

White (anaemic)

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5
Q

what necrosis in the brain

A

colliquative

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6
Q

most popular necrosis

A

coagulative

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7
Q

if someone dies of a sudden heart attack what histology do you see?

A

nothing! as no time to develop haemorrhage / inflammatory response

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8
Q

factors affecting the degree of ischaemic damage

A

nature of the blood supply
rate of occlusion
tissue vulnerability to hypoxia
blood o2 content

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9
Q

most vulnerable organs for infarction

A

kidneys, spleen, testis

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10
Q

a slow rate of occlusion makes you more or less likely to have an infarct?

A

less likely as it allows development of collateral perfusion pathways

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11
Q

blood oxygen content

A

anaemia increases chance of infarction

congestive heart failure - poor CO and impaired pulm. vent. may develop an infarct with normally inconsequential narrowing of the vessels

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12
Q

shock definition

A

physiological state characterised by significant reduction of systemic tissue perfusion (severe hypotension) resulting in decreased O2 delivery to the tissues

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13
Q

shock’s effects 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 resp –> lactic acid

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14
Q

shock’s effects at a systemic level

A

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

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15
Q

Shock and reversibility

A

Shock is initially reversible but rapidly becomes irreversible

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16
Q

Result of shock

A

Cell death
End-organ damage
Multi-organ failure
Death

17
Q

Classification of shock

A

Hypovolaemic
Cardiogenic
Distributive

18
Q

Types of distributive shock

A

Anaphylactic
Septic
Toxic shock syndrome
Neurogenic

19
Q

Hypovolaemic shock

A

Intra-vascular fluid loss (blood, plasma etc)
Decrease in venous return to heart aka pre-load
Lower stroke volume therefore low CO

20
Q

How to compensate for hypovolaemic shock

A

Increase blood volume

21
Q

Causes of hypovolaemic shock

A

Haemorrhage - trauma, GI, rupture, fractures, aneurysm rupture

Non-haemorrhagic - diarrhoea, vomiting, heat stroke, burns

Third spacing

22
Q

What is third spacing?

A

Acute loss of fluid into internal body cavities

Third-space losses are common post-op and in GI obstruction, pancreatitis or cirrhosis

23
Q

Cardiogenic shock - why? how to compensate?

A

Cardiac pump failure with low CO

How to compensate -> increase in systemic vascular resistance

24
Q

Causes of cardiogenic shock

A

Myopathic (heart muscle failure)
Arrythmia related
Mechanical
Extra cardiac (obstruction to blood flow)

25
Q

Extra cardiac cardiogenic shock e.g.s

A

Anything that impairs cardiac filling or ejection of blood from heart

Massive PE, tension PT, severe constrictive pericarditis, pericardial tamponade

26
Q

Distributive shock

A

Decrease in systemic vascular resistance due to severe vasodilation

Compensate via increasing CO

27
Q

Septic shock which organisms? who’s at risk? pathophysiogical features

A

Gram +ve, -ve bacteria or fungi and affects immunocompromised, elderly, very young

Increase in cytokines/mediators leading to vasodilation

Pro-coagulation (DIC)

28
Q

Anaphylactic shock - pathophysiology

A

Severe type I hypersensitivity rxn

Small doses of allergen = IgE cross-linking

Massive mast cell degranulation which = vasodilation

29
Q

Anaphylactic shock - body’s rxn

A

Contraction of bronchioles/ resp. distress

Laryngeal oedema
Circulatory collapse -> shock/death

30
Q

Neurogenic shock

A

Spinal injury / anaesthetic accidents = loss of sympathetic vascular tone

Vasodilation -> shock

31
Q

Toxic shock syndrome

A

NOT SAME AS SEPTIC SHOCK

32
Q

Toxic shock syndrome - causative organism

A

S. aureus

S. pyogenes

33
Q

Toxic shock syndrome - pathophysiology

A

do not require processing by APCs

non-specific binding of MHC II to T cell receptors with up to 20% of T cells being activated at once

Widespread cytokine release = decrease in SVR

MoD (20 decks)

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