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EMS - Mechanisms of Disease > Ischaemia, Infarction & Shock (14) > Flashcards

Ischaemia, Infarction & Shock (14) Flashcards

1
Q

Hypoxia

A

Any state of reduced tissue oxygen availability (generalised - whole body/regional - specific tissues)

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2
Q

Ischaemia

A

Pathological reduction in blood flow to tissues, result of obstruction usually due to thrombosis/embolism > tissue hypoxia

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3
Q

If ischaemic for short duration

A

Cell injury reversible

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4
Q

If prolonged/sustained ischamia

A

Irreversible cel damage/cell death occurs by necrosis/infarction

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5
Q

Therapeutic reperfusion

A

Good if reversible

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6
Q

Examples of therapeutic reperfusion

A

PCI for MI or thrombolysis for stroke

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7
Q

Reperfusion injury

A

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

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8
Q

Infarction

A

Ischaemic necrosis caused by occlusion of arterial supply/venous daring

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9
Q

Infarct

A

Area of infarction in tissues

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10
Q

Causes of infarction

A

Thrombosis, embolism, vasopasms (narrow), atheroma expansion, extrinsic compression (tumour), twisting of vessel roots (volvulus), rupture of vascular supply (AAA), venous occlusion

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11
Q

Red infarction

A

Haemorrhagic, dual blood supply/venous infarction (blood supply damaged so leaks)

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12
Q

White infarction

A

Anaemic, single blood supply hence totally cut off

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13
Q

What shape are most infarcts?

A

Wedge-shaped, obstruction usually occurs upstream, entire down-stream will be infarcted

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14
Q

Histological characteristic of infarction

A

Usually coagulative necrosis (in brain - colliquative)

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15
Q

Effects of vascular occlusion vary on..

A
  1. Nature of blood supply
  2. Rate of occlusion
  3. Tissue vulnerability to hypoxia
  4. Blood oxygen content
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16
Q

Nature of blood supply

A

Lung (pulmonary and bronchial arteries), liver (hepatic artery, portal vein), hand (radial and ulnar artery), severe ischameia for infarction

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17
Q

Which organs are more vulnerable to infarction due to the nature of their blood supply?

A

Kidneys, spleen, testis (single supplies)

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18
Q

Heart hypoxia

A

Cardiac myocyte death takes 20-30mins

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19
Q

Brain hypoxia

A

Neurone deprived of oxygen irreversible cell damage occurs 3-4 mins, brain is 1-2% of total body weight but requires 20% body oxygen consumption and 15% cardiac output

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20
Q

Clinical manifestations

A

Heart - IHD/stable angina/MI

Brain - cerebrovascular disease (TIA/CVA)

Intestines - ischaemic bowel

Extremities - peripheral vascular disease/gangrene

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21
Q

Cerebrovascular disease

A

Any abnormality of the brain caused by pathological process involving blood vessels

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22
Q

Causes of ischaemic stroke

A

Thrombosis secondary to atherosclerosis, embolism

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23
Q

Causes of haemorrhagic stroke

A

Intracerebral haemorrhage (hypertensive), Ruptured aneurysm in the circle of Willis (subarachnoid)

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24
Q

Causes of ischaemic bowel disease

A

Thrombosis/embolism in superior/inferior mesenteric arteries

25
Q

What does IBD present with?

A

Abdominal pain

26
Q

Gangrene

A

Infarction of entire portion of limb/organ

27
Q

Dry gangrene

A

Ischaemic coagulative necrosis only

28
Q

Wet gangrene

A

Superimposed infection

29
Q

Gas gangrene

A

Superimposed infection with gas producing organism e.g. clostridium perfringens

30
Q

What is shock?

A

Physiological state, significant reduction of systemic tissue perfusion (severe hypotension) > decreased oxygen delivery to tissues

31
Q

Shock results in a critical imbalance between

A

Oxygen delivery and oxygen consumption

32
Q

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

33
Q

Systemic effects of shock

A

Alteration in the serum pH (academia), endothelial dysfunction > vascular leakage, stimulation of inflammatory and anti-inflammatory cascades, end-organ damage (ischaemia)

34
Q

Results of prolonged shock

A

Cell death, end-organ damage, multi-organ failure, death

35
Q

Hypovolaemic shock

A

Intra-vascular fluid loss (blood, plasma etc)

36
Q

Mechanism of hypovolaemic shock

A

Decrease venous return to heart (pre-load), decrease stroke volume > decrease cardiac output, decrease mean arterial blood pressure. Need vasoconstriction increase SVR

37
Q

Haemorrhagic causes of hypovolaemic shock

A

Trauma, GI bleed, ruptured haematoma, haemorrhagic pancreatitis, fractures, ruptured aortic, abdominal/left ventricular free wall aneurysm

38
Q

Non-haemorrhagic causes of hypovolaemic shock

A

Diarrhoea, vomiting, heat stroke, burns, third spacing

39
Q

Third spacing

A

Acute loss of fluid into internal body cavities, common postoperatively and in intestinal obstruction, pancreatitis/cirrhosis (draws in fluid)

40
Q

Cardiogenic shock

A

Cardiac pump failure, decreased CO and arterial pressure

41
Q

Causes of cardiogenic shock

A
  1. Myopathic (muscle failure)
  2. Arrhythmia-Related
  3. Mechanical
  4. Extra-cardiac (obstruction to blood outflow)
42
Q

Myopathic shock causes

A

MI (>40% LV myocardium), RV infarction/dilated cardiomyopathies, ‘stunned myocardium’ - following prolonged ischaemic/cardiopulmonary bypass

43
Q

Arrhythmia-related cardiogenic shock causes

A

Atrial and ventricular arrhythmias

44
Q

Atrial fibrillation and shock

A

Flutter > decrease CO by impairment of co-ordinated atrial filling of ventricles

45
Q

Ventricular tachycardia, bradyarrhythmias and complete heart block and shock

A

While ventricular fibrillation, abolishes CO

46
Q

Mechanical cardiogenic shock

A

Valvular defects (prolapse), ventricular septal defects, atrial myxomas (non-cancerous tumour - often grows on atrial septum), rupture ventricular free wall aneurysm

47
Q

Extra-cardiogenic shock causes

A

P.E, tension pneumothorax, severe constrictive pericarditis, pericardial tamponade (impairs cardiac filling/ejection of blood from heart)

48
Q

Pericardial tamponade

A

Blood filling pericardial sac usually aids dilation

49
Q

Distributive shock sub-types

A

Septic, anaphylactic, neurogenic shock, toxic shock syndrome

50
Q

Distributive shock

A

Decrease SVR due to severe vasodilation, compensate by increasing CO > flushed/bounding heart

51
Q

Septic shock

A

Severe systemic infections - gram +ve/-ve bacteria/fungi

52
Q

Who gets septic shock?

A

Immunocompromised, elderly, very young

53
Q

What happens in septic shock

A

Increase in cytokines/mediators > vasodilation > pro coagulation (DIC) > ischaemia > wide spread clotting and thrombosis > use of all clotting factors > haemorrhage > death

54
Q

Anaphylactic shock

A

Severe type 1 hypersensitivity reaction, small doses of allergy > IgE cross-linking, mast cell degranulation > vasodilation > respiratory distress/laryngeal oedema/circulatory collapse

55
Q

Who gets anaphylactic shock?

A

Sensitised individuals

56
Q

Neurogenic shock

A

Spinal injury/anaesthetic accidents, loss of sympathetic vascular tone, vasodilation > shock

57
Q

Toxic shock syndrome

A

NOT SAME AS SEPTIC SHOCK, S.aureus/S.pyogenes produce exotoxins ‘superantigens’ non-specific binding of class 2 MHC to T cell receptors (up to 20% of T cells activated at once), widespread release of cytokines, decrease SVR

58
Q

Treatment of shock

A

O2, fluid, antibiotics

EMS - Mechanisms of Disease (21 decks)

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