Ischaemia, Infarction & Shock (14) Flashcards

(58 cards)

1
Q

Hypoxia

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Ischaemia

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

If ischaemic for short duration

A

Cell injury reversible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

If prolonged/sustained ischamia

A

Irreversible cel damage/cell death occurs by necrosis/infarction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Therapeutic reperfusion

A

Good if reversible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Examples of therapeutic reperfusion

A

PCI for MI or thrombolysis for stroke

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Reperfusion injury

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Infarction

A

Ischaemic necrosis caused by occlusion of arterial supply/venous daring

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Infarct

A

Area of infarction in tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Red infarction

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

White infarction

A

Anaemic, single blood supply hence totally cut off

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What shape are most infarcts?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Histological characteristic of infarction

A

Usually coagulative necrosis (in brain - colliquative)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

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

A

Kidneys, spleen, testis (single supplies)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Heart hypoxia

A

Cardiac myocyte death takes 20-30mins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Clinical manifestations

A

Heart - IHD/stable angina/MI

Brain - cerebrovascular disease (TIA/CVA)

Intestines - ischaemic bowel

Extremities - peripheral vascular disease/gangrene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Cerebrovascular disease

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Causes of ischaemic stroke

A

Thrombosis secondary to atherosclerosis, embolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Causes of haemorrhagic stroke

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Causes of ischaemic bowel disease

A

Thrombosis/embolism in superior/inferior mesenteric arteries

25
What does IBD present with?
Abdominal pain
26
Gangrene
Infarction of entire portion of limb/organ
27
Dry gangrene
Ischaemic coagulative necrosis only
28
Wet gangrene
Superimposed infection
29
Gas gangrene
Superimposed infection with gas producing organism e.g. clostridium perfringens
30
What is shock?
Physiological state, significant reduction of systemic tissue perfusion (severe hypotension) > decreased oxygen delivery to tissues
31
Shock results in a critical imbalance between
Oxygen delivery and oxygen consumption
32
Cellular effects of shock
Membrane ion pump dysfunction, intracellular swelling, leakage of intracellular contents into extracellular space, inadequate regulation of intracellular pH, anaerobic respiration > lactic acid
33
Systemic effects of shock
Alteration in the serum pH (academia), endothelial dysfunction > vascular leakage, stimulation of inflammatory and anti-inflammatory cascades, end-organ damage (ischaemia)
34
Results of prolonged shock
Cell death, end-organ damage, multi-organ failure, death
35
Hypovolaemic shock
Intra-vascular fluid loss (blood, plasma etc)
36
Mechanism of hypovolaemic shock
Decrease venous return to heart (pre-load), decrease stroke volume > decrease cardiac output, decrease mean arterial blood pressure. Need vasoconstriction increase SVR
37
Haemorrhagic causes of hypovolaemic shock
Trauma, GI bleed, ruptured haematoma, haemorrhagic pancreatitis, fractures, ruptured aortic, abdominal/left ventricular free wall aneurysm
38
Non-haemorrhagic causes of hypovolaemic shock
Diarrhoea, vomiting, heat stroke, burns, third spacing
39
Third spacing
Acute loss of fluid into internal body cavities, common postoperatively and in intestinal obstruction, pancreatitis/cirrhosis (draws in fluid)
40
Cardiogenic shock
Cardiac pump failure, decreased CO and arterial pressure
41
Causes of cardiogenic shock
1. Myopathic (muscle failure) 2. Arrhythmia-Related 3. Mechanical 4. Extra-cardiac (obstruction to blood outflow)
42
Myopathic shock causes
MI (>40% LV myocardium), RV infarction/dilated cardiomyopathies, 'stunned myocardium' - following prolonged ischaemic/cardiopulmonary bypass
43
Arrhythmia-related cardiogenic shock causes
Atrial and ventricular arrhythmias
44
Atrial fibrillation and shock
Flutter > decrease CO by impairment of co-ordinated atrial filling of ventricles
45
Ventricular tachycardia, bradyarrhythmias and complete heart block and shock
While ventricular fibrillation, abolishes CO
46
Mechanical cardiogenic shock
Valvular defects (prolapse), ventricular septal defects, atrial myxomas (non-cancerous tumour - often grows on atrial septum), rupture ventricular free wall aneurysm
47
Extra-cardiogenic shock causes
P.E, tension pneumothorax, severe constrictive pericarditis, pericardial tamponade (impairs cardiac filling/ejection of blood from heart)
48
Pericardial tamponade
Blood filling pericardial sac usually aids dilation
49
Distributive shock sub-types
Septic, anaphylactic, neurogenic shock, toxic shock syndrome
50
Distributive shock
Decrease SVR due to severe vasodilation, compensate by increasing CO > flushed/bounding heart
51
Septic shock
Severe systemic infections - gram +ve/-ve bacteria/fungi
52
Who gets septic shock?
Immunocompromised, elderly, very young
53
What happens in septic shock
Increase in cytokines/mediators > vasodilation > pro coagulation (DIC) > ischaemia > wide spread clotting and thrombosis > use of all clotting factors > haemorrhage > death
54
Anaphylactic shock
Severe type 1 hypersensitivity reaction, small doses of allergy > IgE cross-linking, mast cell degranulation > vasodilation > respiratory distress/laryngeal oedema/circulatory collapse
55
Who gets anaphylactic shock?
Sensitised individuals
56
Neurogenic shock
Spinal injury/anaesthetic accidents, loss of sympathetic vascular tone, vasodilation > shock
57
Toxic shock syndrome
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
Treatment of shock
O2, fluid, antibiotics