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MOD > Ischaemia and hypoxic injury > Flashcards

Ischaemia and hypoxic injury Flashcards

1
Q

define hypoxia

A

a state of reduced oxygen availability.

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2
Q

define ischemia

A

pathological reduction in blood flow to tissues.

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3
Q

what causes ischaemia

A

obstruction do to thrombosis.

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4
Q

Is ischaemia reversible

A

Yes if short duration

no is prolonged

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5
Q

what are 2 methods of artificial tissue perfusion

A

percutaneous coronary interventions for MI

thrombolysis for clots

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6
Q

why might reperfusion of ischema tissue might not be beneficial

A

1- tissue may be have undergone necrosis.

2-generation of reactive oxygen species by inflammatory cells can cause further injury

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7
Q

define reperfusion injury

A

generation of reactive oxygen species by inflammatory cells can cause further injury

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8
Q

define infrarction

A

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

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9
Q

what is the most common cause of most infarctions

A

arterial thrombus or embolism

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10
Q

what are the causes of infarction

A

thrombus and emboli
vasospasm
atheroma expansion
Extrinsic compression (e.g. tumour)
Twisting of vessel roots (e.g. volvulus)
Rupture of vascular supply (e.g. AAA)
Vasculitis- inflammation of the blood vessels.
Hyper viscosity- thick blood
Steal.- blockage just after splitting of an atery into 2 so blood flows through the path of least resistance.
Venous occlusion- Also causes infarction but it is uncommon

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11
Q

define red infarct

A

(haemorrhagic)

Dual blood supply / venous infarction- e.g lungs has 2 blood supplies bronchial and pulmonary.

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12
Q

define white infarct

A

Single blood supply hence totally cut-off

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13
Q

what shape are most infarcts

A

wedge shaped

obstruction upstream so all of down stream is affected.

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14
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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15
Q

Effects of vascular occlusion is variable and depends on four factors
these factors effect whether a tissue will become infected or not.

A

Nature of the blood supply
Rate of occlusion
Tissue vulnerability to hypoxia
Blood oxygen content

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16
Q

which organs have a dual blood supply

A

Lungs (pulmonary and bronchial arteries)
Liver (hepatic artery and portal vein)
Hand (radial and ulnar artery)

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17
Q

define watershed regions and give 2 examples

A

regions occur at the point of anastomosis between 2 vascular supplies.
splenic flexure and brain.

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18
Q

how does the rate of occlusion affect infarction

A

Slow developing occlusions are less likely to infarct tissues
Allows time for the development of alternative (collateral) perfusion pathways

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19
Q

Brain is 1 to 2% of total body weight but how much cardiac output and the oxygen of the body does it required

A

requires 15% of cardiac output and 20% of body oxygen consumption.

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20
Q

how long does it take the brain and heart to infarct without oxygen

A

brain-2-3 mins

heart- 20-30 mins

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21
Q

patients with what condition have reduced oxygen in the blood

A

Congestive cardiac failure
– Poor cardiac output and impaired pulmonary ventilation
– May develop an infarct with a normally inconsequential narrowing of the vessels!

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22
Q

define angina

A

chest pain due to ischemia / MI.

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23
Q

define stable angina

A

only comes about after physical exertion.

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24
Q

define unstable angina

A

develop chest pain more often at reduced levels of exercise or even at rest- indicates the plaque is enlarging and may even rupture.

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25
Q

what happens if you have ischamia of the brain

A

cerebrovascular disease.

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26
Q

what happens if you have ischamia of the the bowel

A

when you eat you need increase blood flow but if you cannot supply it due to volvulus then bowel dies.

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27
Q

what is the leading cause of death on both males and females

A

Ischaemic heart disease.

28
Q

what is ischema of the heart known as

A

isachemic heart disease.

29
Q

define cerebrovascular disease

A

Any abnormality of the brain caused by a pathological process involving the blood vessels
thrombus and embolism
bleeding (haemorrhagic)

30
Q

causes of isachemic stroke

A

Thrombosis secondary to atherosclerosis

Embolism (e.g. mural thrombus)

31
Q

causes of haemorrhagic stroke

A

Intracerebral haemorrhage (hypertensive)
Ruptured aneurysm in the circle of Willis (subarachnoid)
Berry anyersum- blockage in a blood vessel of the circle of willis.
If it burst then causes subarachnoid haemorrhage- pain in the back of the head.

32
Q

causes of ischaemic bowel disease

A

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

33
Q

what causes limb ischaema

A

Gangrene- Infarction of entire portion of limb (or organ)

Dry gangrene-Ischaemic coagulative necrosis only

Wet gangrene- Superimposed infection, Dry gangrene becomes wet gangrene is infected.

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

34
Q

define shock

A

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

35
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
anaerobic respiration-lactic acid.

36
Q

Systemic effects of shock

A

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

37
Q

Is shock reversible

A

Yes initially

No if prolonged.

38
Q

what are the consequences of untreated shock

A
  1. Cell death
  2. End-organ damage
  3. Multi-organ failure
  4. Death
39
Q

There are 3 types of shock

A

HYPOVOLAEMIC
CARDIOGENIC
DISTRIBUTIVE

40
Q

what are the subcategories of distributive shock

A 
ANAPHYLACTIC
SEPTIC 
TOXIC SHOCK SYNDROME
NEUROGENIC
Others
41
Q

what are the main events in hypovolaemic shock

A

Intra-vascular fluid loss (blood, plasma etc).
decreased venous return to heart AKA preload
decreased stroke volume so lower cardiac output.

42
Q

what are the compensation mechanisms for hypovalaemic shock

A
  • increase vasoconstriction so that heart rate increase which increases cardiac output.
  • cold, clammy, tachycardia, shut down and oliguria(to prevent more fluid loss)
43
Q

what cues hypovolaemic shock

A

Haemorrhage
Non-haemorrhgic fluid loss.- diarrhoea, vomitting, heat stroke and burns.
Third spacing- Acute loss of fluid into internal body cavities, third-space losses are common postoperatively

44
Q

what are the main events in cardiogenic shock

A

Cardiac pump failure, cardiac output is reduced

45
Q

How can you compensate for cardiogenic shock

A

increase systemic vascular resistance.

46
Q

what are the 4 main causes of cardiogenic shock

A

Myopathic (heart muscle failure)
Arrythmia-related (abnormal electrical activity)
Mechanical
Extra-cardiac (obstruction to blood outflow)

47
Q

what causes myopathic cardiogenic shock

A

MI infarction
right ventricular infarction- dilated cardiomyopathies.– “Stunned myocardium” following prolonged ischemia or cardiopulmonary bypass

48
Q

what are the Arrhythmia-related cardiogenic shock

A

Atrial and ventricular arrhythmias
Atrial fibrillation / flutter causes decreased cardiac output, by impairment of co-ordinated atrial filling of the ventricles.

Ventricular tachycardia, bradyarrhythmias, and complete heart block decrease cardiac output while ventricular fibrillation abolishes CO.

49
Q

what causes mechanical cardiogenic shock

A

Valvular defects (e.g. prolapse), ventricular septal defects

Atrial myxomas (benign tumour) , ruptured ventricular free wall aneurysm. Valvular

50
Q

what causes 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 (heart cannot dilate against pericardial sac as it is filled with fluid) etc

51
Q

define distributive shock

A

have the same volume of blood but tissue perfusion decreases because it dosen’t get as far.

52
Q

what is the main cause of distributive shock

A

decreased systemic vascular resistance

53
Q

how do you compensate for distributive shock

A

increase cardiac output- flushed and bounding heart.

54
Q

what are the 4 subtypes of distributive shock

A

SEPTIC SHOCK
ANAPHYLACTIC SHOCK
NEUROGENIC SHOCK
TOXIC SHOCK SYNDROME

55
Q

what causes septic shock

A

systemic infections

56
Q

what groups of people are more likely to get septic shock

A

Immunocompromised, elderly, very young

57
Q

how does septic shock cause vasodilation (molecules)

A

cytokines

58
Q

what causes anaphylactic shock

A

commonly drug allergy

Severe type I hypersensitivity reaction

59
Q

how does anaphylactic shock cause vasodilation

A

– Small doses of allergen causes IgE cross-linking
– Massive mast cell degranulation
– Vasodilation

60
Q

what are the consequences of vasodilation in anaphylactic shock

A

Contraction of bronchioles / respiratory distress
Laryngeal oedema
Decreased BP- struggling to breath.
Circulatory collapse resulting in shock / death

61
Q

what causes neurogenic shock

A

Spinal injury / anesthetic accidents

62
Q

how does neurogenic shock cause vasodilation

A

Loss of sympathetic vascular tone

Vasodilation

63
Q

what causes toxic shock

A

S. aureus / S. pyogenes exotoxins aka “superantigens

64
Q

how does toxic shock cause vasodilation

A

superantigens”- binds non-specifically to active lots of T ceels and lots of cytokines which decreases BP and decreases SVR.
causes vasodilation

65
Q

is toxi shock T cell specific and require antigen presenting etc.

A

NO

66
Q

define combined shock

A

Different types of shock can co-exist

67
Q

patients with septic shock can have a combined shock with

A 
–	Primary distributive component
•	Inflammatory and anti-inflammatory cascades ↑ vascular permeability / vasodilation
–	Hypovolemic component
•	Decreased oral intake
•	Insensible losses
•	Vomiting, diahorrhea
–	Cardiogenic component
•	Sepsis-related myocardial dysfunction

MOD (19 decks)

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