Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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.

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

are the effects of hypoxia reversible?

A

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

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

what effect does chronic hypoxia have at a cellular level?

A

atrophy prolonged - necrosis

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

what are the causes of hypoxia?

A
  • cardio respiratory failure - low ambient oxygen (e.g. altitude) - anemia - carbon monoxide poisoning - ischaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what might cause inadequate blood oxygenation?

A

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

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

what might cause a decreased blood oxygen-carrying capacity?

A

anaemia carbon monoxide poisoning

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

what does localised tissue hypoxia result from?

A

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

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

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

A

atherosclerosis embolism thrombosis

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

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

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

what is ischaemia?

A

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

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

what is infarction?

A

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

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

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

A

arterial NB: both are possible

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

What is ischaemia-reperfusion injury?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what generates reactive oxygen species (ROS)?

A

inflammatory cells - cause further cell damage

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

what is an “infarct”?

A

an area of infarction in a tissue

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

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

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

what is venous occlusion?

A

blockage of veins also causes infarction but is uncommon

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

what is the most common clinical. outcome of infarction?

A

venous obstruction and congestion but no infarction

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

which type of organs are vulnerable to venous infarction?

A

organs with a single venous outflow

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

infarction can be classified morphologically by what?

A

colour

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

what are the two. types of infarction?

A

red infarction (haemorrhagic) white infarction (anaemic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what tissues would experience a red infarction?

A
  • dual blood supply - venous infarction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what tissues would experience a white infarction?

A
  • single blood supply (totally cut off)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Most infarcts are wedge-shaped – why?

A

vascular supply is upstream or proximal in tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what type of necrosis is seen in infarction?

A

coagulative (connective tissue remains) NB: not true in the brain, liquactive bc no connective tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
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 into infarcted tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what gross morphological features would you see in a patient 1-2 days after a myocardial infarction?

A

Pale red / oedematous

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what microscopic morphological features would you see in a patient 1-2 days after a myocardial infarction?

A

oedema with early neutrophil infiltration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what gross morphological features would you see in a patient 3-4 days after a myocardial infarction?

A

yellow with haemorrhagic edge

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what microscopic morphological features would you see in a patient 3-4 days after a myocardial infarction?

A

coagulative necrosis with macrophage infiltration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

what gross morphological features would you see in a patient 1-3 weeks after a myocardial infarction?

A

pale/thin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

what microscopic morphological features would you see in a patient 1-3 weeks after a myocardial infarction?

A

granulation tissue formation

36
Q

what microscopic morphological features would you see in a patient 3-6 weeks after a myocardial infarction?

A

dense fibrous scar

37
Q

what gross morphological features would you see in a patient 3-6 weeks after a myocardial infarction?

A

dense fibrous scar

38
Q

when would you begin to see a dense fibrous scar after a myocardial infarction?

A

3-6 weeks after

39
Q

when would you begin to see granulation tissue formation after a myocardial infarction?

A

1-3 weeks

40
Q

what is low-flow. infarction?

A

infarction in areas of diminished blood flow in vulnerable anatomical regions

41
Q

what is “portal” vasculature?

A

Blood supplied via other parenchymal capillary beds

42
Q

give examples of portal vasculature?

A

Anterior pituitary (via hypothalamus) renal tubules (via glomeruli)

43
Q

what are “watershed” regions?

A

Point of anatomoses between 2 vascular supplies

44
Q

give examples of watershed regions?

A

Splenic flexure colon (SMA,IMA), myocardium (ventricles & coronary art), regions in the brain

45
Q

what is shock?

A

A pathophysiological state of reduced systemic tissue perfusion resulting in decreased oxygen delivery to the tissues

46
Q

is shock reversible?

A

Shock is initially reversible but rapidly becomes irreversible

47
Q

what is the physiological result of shock?

A

cell death due to hypoxia -> end-organ damage -> organ failure _> death

48
Q

why is it important to recognise shock fast?

A

can rapidly result in multi-organ failure (and then death) due to cell death (hypoxia)

49
Q

what factors contribute to mean arterial pressure?

A

cardiac output total peripheral resistance

50
Q

what factors determine cardiac output?

A

heart rate (parasympathetic or sympathetic) stroke volume (venous return)

51
Q

what factors contribute to venous return?

A

blood volume respiratory pump skeletal pump

52
Q

what are the 3 main types of shock?

A

hypovolaemic cardiogenic distributive

53
Q

what are different types of distributive shock?

A

• ANAPHYLACTIC • SEPTIC • TOXIC SHOCK SYNDROME • NEUROGENIC

54
Q

what is hypovolaemic shock?

A

Intra-vascular fluid loss (blood, plasma etc) - ↓ venous return to heart AKA “pre-load” - ↓ stroke volume → ↓ cardiac output

55
Q

how can you compensate for hypovolaemic shock?

A

increase the systemic vascular resistance / vasoconstrictor

56
Q

what are causes of hypovolaemic shock?

A

haemorrhage non-haemorrhage fluid loss: - diarrhoea - vomiting - heat stroke - burns

57
Q

what is “Third spacing”?

A

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
Q

what is cardiogenic shock?

A

Cardiac pump failure - ↓ CO

59
Q

what are the 4 categories of causes of caridogenic shock?

A

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

60
Q

what is distributive shock?

A

↓ SVR due to severe vasodilation

61
Q

what is septic shock?

A
  • Severe, over-whelming systemic infections - increase in cytokines and inflammatory mediators = extreme vasodilation
62
Q

what is anaphylactic shock?

A

severe type 1 hypersensitivity reaction Massive mast cell degranulation → – Vasodilation

63
Q

what is neurogenic shock?

A

disruption of the autonomic pathways within the spinal cord - spinal injury/anaesthetic accidents - loss of sympathetic vascular tone = vasodilation = shock

64
Q

what is toxic shock syndrome?

A

• 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
Q

you can have a combination of shock sub-types, true or false?

A

true

66
Q

what is the mortality rate for septic shock?

A

35 – 60% die within one month of the onset

67
Q

what is the mortality rate for cardiogenic shock?

A

60 – 90% mortality

68
Q

what is gangrene?

A

Infarction of entire portion of limb (or organ)

69
Q

what are the 3 types of gangrene?

A

dry wet gas

70
Q

what is dry gangrene?

A

Ischaemic coagulative necrosis only

71
Q

what is wet gangrene?

A

Gangrene with superimposed infection

72
Q

which type of Gangrene is with superimposed infection?

A

wet or gas

73
Q

what is gas gangrene?

A

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

74
Q

what type of gangrene would clostridium perferinges cause?

A

gas

75
Q

what 4 factors influence the degree of ischaemic damage?

A
  1. NATURE OF THE BLOOD SUPPLY 2. THE RATE OF OCCLUSION 3. THE TISSUE VULNERABILITY TO HYPOXIA 4. THE BLOOD OXYGEN CONTENT
76
Q

which organs have dual blood supply?

A

lungs liver hand NB: Tissues with a dual vascular supply are generally resistant to infarction of a single vessel

77
Q

which organs have end-arterial circulations (artery only blood supply) hence are vulnerable to infarction?

A

kidneys spleen testis

78
Q

are slow developing occlusions, less or more likely to infarct tissues?

A

less ALLOWS TIME FOR DEVELOPMENT OF ALTERNATIVE PERFUSION PATHWAYS (COLLATERAL SUPPLY)

79
Q

which is the most vulnerable organ to hypoxia?

A

brain

80
Q

If a neurone is deprived of oxygen, how long does it take to undergo irreversible cell damage?

A

3 – 4 MINUTES

81
Q

If a cardiomyocyte is deprived of oxygen, how long does it take to undergo irreversible cell damage?

A

20 – 30 MINUTES

82
Q

If a cardio fibroblast is deprived of oxygen, how long does it take to undergo irreversible cell damage?

A

hours

83
Q

how long after myocardial infarction would you see this?

A

3-4 days

yellow with red (haemorrhagic) edge

84
Q

how long after myocardial infarction would you see this?

A

1-2 days

pale red/odematous

85
Q

how long after myocardial infarction would you see this?

A

3-6 weeks after

dense fibrous scar

86
Q

what type of infarct is this?

A

watershed infarct

MoD (19 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions