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MoD > L10 - Ischaemia, infarction, shock > Flashcards

L10 - Ischaemia, infarction, shock Flashcards

1
Q

what is hypoxia?

A

reduced oxygen availability in tissues which causes cell injury by reducing aerobic oxidative respiration.

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2
Q

are the effects of hypoxia reversible?

A

yes can be reversible or result in adaption - prolonged hypoxia causes cell death (irreversible)

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3
Q

what effect does chronic hypoxia have at a cellular level?

A

atrophy prolonged - necrosis

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4
Q

what are the causes of hypoxia?

A
  • cardio respiratory failure - low ambient oxygen (e.g. altitude) - anemia - carbon monoxide poisoning - ischaemia
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5
Q

what might cause inadequate blood oxygenation?

A

cardio respiratory failure low ambient oxygen (e.g. altitude)

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6
Q

what might cause a decreased blood oxygen-carrying capacity?

A

anaemia carbon monoxide poisoning

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7
Q

what does localised tissue hypoxia result from?

A

reduction in blood flow to an organ or tissues - not generalised like hypoxia

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8
Q

what is the most common obstruction to arterial supply leading to ischaemia?

A

atherosclerosis embolism thrombosis

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9
Q

which is more severe, Non-ischaemic (generalised) hypoxia or Ischaemia?

A

Ischaemia injures tissues faster / more severely NB: hypoxia is impaired oxygen supply only - other metabolites such as glucose still supplied for respiration - complete block in ischaemia

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10
Q

is rapid restoration of blood flow always therapeutic for ischaemia?

A

only if ischaemia is limited/short duration if it’s prolonged you will have necrosis and oxygen will not be able to reverse it.

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11
Q

what is ischaemia?

A

Localised tissue hypoxia due to decreased blood flow to an organ or tissue

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12
Q

what is infarction?

A

Tissue necrosis as a consequence of ischaemia (i.e. ischaemic necrosis)

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13
Q

does ischaemia most commonly occur as a result of arterial or venous obstruction

A

arterial NB: both are possible

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14
Q

What is ischaemia-reperfusion injury?

A

generation of reactive oxygen species (ROS) by sudden repercussion of ischaemic (dysfunctional) tissues

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15
Q

what generates reactive oxygen species (ROS)?

A

inflammatory cells - cause further cell damage

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16
Q

why is ischaemia-reperfusion injury clinically relevant?

A
  • forms injury - up to 50% of infarct bay be due to IRPI generally reperfusion is still better than infarction
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17
Q

what is an “infarct”?

A

an area of infarction in a tissue

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18
Q

what are the main causes of infarction? and most commonly in which type of vessel?

A

thrombosis/embolism, rupture/thrombosis or atherosclerotic plaque arterial

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19
Q

what are causes, other than atherosclerosis, of infarction?

A

– Vasospam – 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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20
Q

what is venous occlusion?

A

blockage of veins also causes infarction but is uncommon

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21
Q

what is the most common clinical. outcome of infarction?

A

venous obstruction and congestion but no infarction

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22
Q

which type of organs are vulnerable to venous infarction?

A

organs with a single venous outflow

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23
Q

infarction can be classified morphologically by what?

A

colour

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24
Q

what are the two. types of infarction?

A

red infarction (haemorrhagic) white infarction (anaemic)

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25
what tissues would experience a red infarction?
- dual blood supply - venous infarction
26
what tissues would experience a white infarction?
- single blood supply (totally cut off)
27
Most infarcts are wedge-shaped – why?
vascular supply is upstream or proximal in tissue
28
what type of necrosis is seen in infarction?
coagulative (connective tissue remains) NB: not true in the brain, liquactive bc no connective tissue
29
If a person dies suddenly (e.g. massive heart attack) what do you see in the tissues?
nothing no time to develop haemorrhage/inflammatory response into infarcted tissues
30
what gross morphological features would you see in a patient 1-2 days after a myocardial infarction?
Pale red / oedematous
31
what microscopic morphological features would you see in a patient 1-2 days after a myocardial infarction?
oedema with early neutrophil infiltration
32
what gross morphological features would you see in a patient 3-4 days after a myocardial infarction?
yellow with haemorrhagic edge
33
what microscopic morphological features would you see in a patient 3-4 days after a myocardial infarction?
coagulative necrosis with macrophage infiltration
34
what gross morphological features would you see in a patient 1-3 weeks after a myocardial infarction?
pale/thin
35
what microscopic morphological features would you see in a patient 1-3 weeks after a myocardial infarction?
granulation tissue formation
36
what microscopic morphological features would you see in a patient 3-6 weeks after a myocardial infarction?
dense fibrous scar
37
what gross morphological features would you see in a patient 3-6 weeks after a myocardial infarction?
dense fibrous scar
38
when would you begin to see a dense fibrous scar after a myocardial infarction?
3-6 weeks after
39
when would you begin to see granulation tissue formation after a myocardial infarction?
1-3 weeks
40
what is low-flow. infarction?
infarction in areas of diminished blood flow in vulnerable anatomical regions
41
what is "portal" vasculature?
Blood supplied via other parenchymal capillary beds
42
give examples of portal vasculature?
Anterior pituitary (via hypothalamus) renal tubules (via glomeruli)
43
what are "watershed" regions?
Point of anatomoses between 2 vascular supplies
44
give examples of watershed regions?
Splenic flexure colon (SMA,IMA), myocardium (ventricles & coronary art), regions in the brain
45
what is shock?
A pathophysiological state of reduced systemic tissue perfusion resulting in decreased oxygen delivery to the tissues
46
is shock reversible?
Shock is initially reversible but rapidly becomes irreversible
47
what is the physiological result of shock?
cell death due to hypoxia -\> end-organ damage -\> organ failure \_\> death
48
why is it important to recognise shock fast?
can rapidly result in multi-organ failure (and then death) due to cell death (hypoxia)
49
what factors contribute to mean arterial pressure?
cardiac output total peripheral resistance
50
what factors determine cardiac output?
heart rate (parasympathetic or sympathetic) stroke volume (venous return)
51
what factors contribute to venous return?
blood volume respiratory pump skeletal pump
52
what are the 3 main types of shock?
hypovolaemic cardiogenic distributive
53
what are different types of distributive shock?
• ANAPHYLACTIC • SEPTIC • TOXIC SHOCK SYNDROME • NEUROGENIC
54
what is hypovolaemic shock?
Intra-vascular fluid loss (blood, plasma etc) - ↓ venous return to heart AKA “pre-load” - ↓ stroke volume → ↓ cardiac output
55
how can you compensate for hypovolaemic shock?
increase the systemic vascular resistance / vasoconstrictor
56
what are causes of hypovolaemic shock?
haemorrhage non-haemorrhage fluid loss: - diarrhoea - vomiting - heat stroke - burns
57
what is "Third spacing"?
Third-spacing occurs when too much fluid moves from blood vessels into the interstitial or "third" space - the nonfunctional area between cells. This can cause potentially serious problems such as edema, reduced cardiac output, and hypotension.
58
what is cardiogenic shock?
Cardiac pump failure - ↓ CO
59
what are the 4 categories of causes of caridogenic shock?
– Myopathic (heart muscle failure) – Arrythmia-related (abnormal electrical activity) – Mechanical – Extra-cardiac (obstruction to blood outflow)
60
what is distributive shock?
↓ SVR due to severe vasodilation
61
what is septic shock?
- Severe, over-whelming systemic infections - increase in cytokines and inflammatory mediators = extreme vasodilation
62
what is anaphylactic shock?
severe type 1 hypersensitivity reaction Massive mast cell degranulation → – Vasodilation
63
what is neurogenic shock?
disruption of the autonomic pathways within the spinal cord - spinal injury/anaesthetic accidents - loss of sympathetic vascular tone = vasodilation = shock
64
what is toxic shock syndrome?
• NOT the same as septic shock • S. aureus / S. pyogenes produce exotoxins “superantigens” • Do not require processing by antigen-presenting cells • 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 ↓SVR
65
you can have a combination of shock sub-types, true or false?
true
66
what is the mortality rate for septic shock?
35 – 60% die within one month of the onset
67
what is the mortality rate for cardiogenic shock?
60 – 90% mortality
68
what is gangrene?
Infarction of entire portion of limb (or organ)
69
what are the 3 types of gangrene?
dry wet gas
70
what is dry gangrene?
Ischaemic coagulative necrosis only
71
what is wet gangrene?
Gangrene with superimposed infection
72
which type of Gangrene is with superimposed infection?
wet or gas
73
what is gas gangrene?
Superimposed infection with gas producing organism e.g. clostridium perferinges
74
what type of gangrene would clostridium perferinges cause?
gas
75
what 4 factors influence the degree of ischaemic damage?
1. NATURE OF THE BLOOD SUPPLY 2. THE RATE OF OCCLUSION 3. THE TISSUE VULNERABILITY TO HYPOXIA 4. THE BLOOD OXYGEN CONTENT
76
which organs have dual blood supply?
lungs liver hand NB: Tissues with a dual vascular supply are generally resistant to infarction of a single vessel
77
which organs have end-arterial circulations (artery only blood supply) hence are vulnerable to infarction?
kidneys spleen testis
78
are slow developing occlusions, less or more likely to infarct tissues?
less ALLOWS TIME FOR DEVELOPMENT OF ALTERNATIVE PERFUSION PATHWAYS (COLLATERAL SUPPLY)
79
which is the most vulnerable organ to hypoxia?
brain
80
If a neurone is deprived of oxygen, how long does it take to undergo irreversible cell damage?
3 – 4 MINUTES
81
If a cardiomyocyte is deprived of oxygen, how long does it take to undergo irreversible cell damage?
20 – 30 MINUTES
82
If a cardio fibroblast is deprived of oxygen, how long does it take to undergo irreversible cell damage?
hours
83
how long after myocardial infarction would you see this?
3-4 days yellow with red (haemorrhagic) edge
84
how long after myocardial infarction would you see this?
1-2 days pale red/odematous
85
how long after myocardial infarction would you see this?
3-6 weeks after dense fibrous scar
86
what type of infarct is this?
watershed infarct

MoD (19 decks)

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