L14- Ischaemia, Infarction & Shock Flashcards

1
Q

What is Hypoxia

A

Any state of reduced tissue oxygen availability

  • Generalised - whole body e.g. altitude, anaemia
  • Regional - specific tissues affected
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2
Q

What is Ischaemia

A

Pathological reduction in blood flow to tissues

  • Usually as a result of obstruction to arterial flow
  • commonly as a result of thrombosis / embolism
  • Ischaemia results in tissue hypoxia
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3
Q

How harmful is ischaemia? (Limited vs prolonged duration)

A

If limited / short duration —> cell injury reversible

Prolonged / sustained —> irreversible cell damage
Cell death occurs by necrosis (infarction)

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4
Q

Why can reperfusion of non-infarcted but ischaemic tissue be bad?

A
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5
Q

Whats is Infarction

A

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

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6
Q

Other causes of infarction?

A

Vasospasm (sudden blood vessel contraction)

Atheroma expansion

Extrinsic compression (e.g. tumour)

Twisting of vessel roots (e.g. volvulus)

Rupture of vascular supply (e.g. AAA)

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7
Q

Morphology of infarction : Red infarct vs White

A
Red infarction (haemorrhagic)
Dual blood supply / venous infarction
White infarction (anaemic)
Single blood supply hence totally cut-off
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8
Q

Why are most infarcts wedge shaped?

A

Obstruction usually occurs at an upstream point

The entire down-stream area will therefore be infarcted

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9
Q

What are the histological characteristics of infarcts

A
Coagulative necrosis (usually)
Colliquative necrosis (in the brain)
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10
Q

If a person dies suddenly (e.g. massive heart attack) what do you see in the tissues?

A

Nothing —>

No time to develop haemorrhage / inflammatory response

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11
Q

What factors influence the degree of ischaemic damage?

A

Nature of the blood supply (e.g is there a collateral supply present?)

Rate of occlusion (slow forming ones are less likely to infarct tissues)

Tissue vulnerability to hypoxia (The brain is vulnerable/ the heart is a bit more resistant)

Blood oxygen content (Reduced oxygen in the blood (anaemia etc.) increases the chances of infarction)

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12
Q

Clinical Manifestations of Ischaemia?

A

Ischaemic heart disease (angina / MI)

Cerebrovascular disease (TIA / CVA)

Ischaemic bowel

Peripheral vascular disease / gangrene

(Remember THE 5 Ps as well)

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13
Q

What is Cerebrovascular disease

A

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

Includes

  • Thrombosis and embolism (ischaemic)
  • Bleeding (haemorrhagic)
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14
Q

What is a Cerebrovascular accident

A

Stroke

Causes of an ischaemic stroke:

  • Thrombosis secondary to atherosclerosis
  • Embolism (e.g. mural thrombus)
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15
Q

What are the causes of a haemorrhagic stroke

A

Intracerebral haemorrhage (hypertensive)

Ruptured aneurysm in the circle of Willis (subarachnoid)

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16
Q

What is Ischaemic bowel disease

A

Usually caused by thrombosis or embolism in the superior or inferior mesenteric arteries

Presents with abdominal pain

17
Q

Limb ischaemia / infarction presentation

A

Gangrene
Infarction of entire portion of limb (or organ)

Dry gangrene
Ischaemic coagulative necrosis only

Wet gangrene
Superimposed infection

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

18
Q

What is Shock

A

A physiological state characterised by a significant reduction of systemic tissue perfusion (severe hypotension)

Which results in decreased oxygen delivery to the tissues.

19
Q

What can impaired tissue perfusion and oxygen deprivation lead to?

A

cellular hypoxia and derangement of critical biochemical processes at first cellular and eventually systemic levels.

20
Q

Cellular effects of shock…

A

Membrane ion pump dysfunction

Intracellular swelling

Leakage of intracellular contents into the extracellular space

Inadequate regulation of intracellular pH

Anerobic respiration —> build up of lactic acid

21
Q

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)

22
Q

Is shock reversible?

A

Initially it is, but then becomes irreversible as:

  • Cells start to die
  • End organs are damaged
  • Organs begin to fail
  • –> eventually leading to DEATH
23
Q

Types of shock

A

HYPOVOLAEMIC
(severe blood and fluid loss)

CARDIOGENIC
(heart suddenly can’t pump enough blood to meet your body’s needs)

DISTRIBUTIVE
(Anaphylactic, septic, toxic shock syndrome, neurogenic)

24
Q

What is Hypovolaemic shock

A

Intra-vascular fluid loss (blood, plasma etc)

↓ venous return to heart AKA “pre-load”

↓ stroke volume —> ↓ cardiac output

25
Q

What is the body’s response to Hypovolaemic shock?

A

Systemic vascular Resistance

26
Q

What are the causes of Hypovolaemic shock?

A

Haemorrhage:
-Trauma, gastrointestinal bleeding, ruptured haematoma , aneurysm

Non-haemorrhagic fluid loss:
-Diarrhoea, vomitting, heat stroke, burns

27
Q

What is Cardiogenic shock ?

A

Cardiac pump failure

28
Q

The 4 categories of Causes of Cardiogenic shock?

A

Myopathic (heart muscle failure e.g after M.I)

Arrythmia-related (abnormal electrical activity e.g AF)

Mechanical (problems with the valves)

Extra-cardiac (obstruction to blood outflow e.g PE, Anything that impairs cardiac filling or ejection of blood from heart)

29
Q

What is third spacing?

A

Acute loss of fluid into internal body cavities

30
Q

Types of Distributive shock: What is Septic shock and what happens during it

A

Severe, over-whelming systemic infections with Gram+ve, gram-ve bacteria or fungi

Inc in Cytokines / mediators —> VASODILATION

Pro-coagulation (DIC) —> Ischaemia

31
Q

Types of Distributive shock: What is Anaphylactic shock and what can cause it?

A

Severe type I hypersensitivity reaction

Sensitized individuals
Hospital e.g. drugs (penicillin etc)

Community e.g. peanuts, shellfish, or insect toxins

Small doses of allergen —> IgE cross-linking (stimulates mast cells) —> Vasodilation

Contraction of bronchioles / respiratory distress

Laryngeal oedema

Circulatory collapse —> shock / death

32
Q

Types of Distributive shock: What is Neurogenic shock

A

Spinal injury / anesthetic accidents

Loss of sympathetic vascular tone

Vasodilation —> shock

33
Q

Types of Distributive shock: What is Toxic shock syndrome

A

NOT the same as septic shock!!!!

S. aureus /S. pyogenes produce exotoxins “superantigens”

Non-specific binding of class II MHC to T cell receptors

Up to 20% of T cells can be activated at one time

Widespread release of massive amounts of cytokines leading to a decrease ↓SVR (systemic vascular resistance)