Brainscape's Knowledge GenomeTM

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


See full index

Systems: Cardiovascualar AB > Pathophysiology of Ischaemia and Infarction > Flashcards

Pathophysiology of Ischaemia and Infarction Flashcards

1
Q

Hypoxia

A

Relative lack of blood supply to tissue/organ leading to inadequate O2 supply to meet needs of tissue tissue/organ

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

Classes of hypoxia

A
  • Hypoxic
  • Anaemic
  • Stagnant
  • Cytotoxic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Hypoxic hypoxia

A

Low inspired O2 level Or

Normal inspired O2 but low PaO2

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

Anaemic hypoxia

A

Normal inspired O2 but blood abnormal

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

Stagnant hypoxia

A

Normal inspired O2 but abnormal delivery due to

  • Local (occlusion of vessel)
  • Systemic (shock)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Cytotoxic hypoxia

A

Normal inspired O2 but abnormal at tissue level

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

Factors affecting oxygen supply

A
  • Inspired O2
  • Pulmonary function
  • Blood constituents
  • Blood flow
  • Integrity of vasculature
  • Tissue mechanisms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Factors affecting oxygen demand.

A
  • Tissue itself: different tissues have different requirements
  • Activity of tissue above baseline value
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What can cause supply issues in ischaemic heart disease?

A
  • Coronary artery atheroma
  • Cardiac failure
  • Pulmonary function other disease
  • Pulmonary oedema
  • Anaemia
  • Previous MI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What can cause demand issues in ischaemic heart disease?

A
  • Heart has high intrinsic demand

- Exertion/ stress

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

Atheroma/ atherosclerosis

A

Localised accumulation of lipid and fibrous tissue in intima of arteries

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

What does established atheroma in coronary artery lead to?

A

Stable angina

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

What does complicated atheroma in coronary artery lead to?

A

Unstable angina

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

What do ulcerated/ fissured plaques lead to?

A

Thrombosis causing ischaemia/infarction

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

What does atheroma in the aorta lead to?

A

Aneurysm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the consequences of atheroma?

A
  • MI
  • TIA
  • Cerebral infarction-
  • AAA
  • PVD
  • Cardiac failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How does atheroma lead to ischaemia and infarction??

A
  • Change in vessel wall leads to thrombosis
  • Thrombosis decreases the radius of the vessel
  • Leads to decrease in flow causing decrease in oxygen transport
  • Leads to ischaemia/infarction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the functional effects of ischaemia?

A
  • Blood/O2 supply fails to meet demand due to decreased supply and or increased demand
  • Related to rate of onset
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How can the effects of ischaemia be categorised?

A
  • Acute
  • Chronic
  • Acute-on-chronic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the biochemical effects of ischaemia?

A
  • In anaerobic metabolism pyruvate is converted to L-lactate
  • There is a build up in cytotoxic lactate which leads to decreased oxygen
  • The acidic environment leads to cell death
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the cellular effects of ischaemia?

A

Different tissues have variable O2 requirement and are variably susceptible to ischaemia

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

What are the clinical effects of ischaemia?

A
  • Dysfunction
  • Pain
  • Physical damage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are the outcomes of ischaemia?

A
  • No clinical effect
  • Resolution versus therapeutic intervention
  • Infarction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Infarction

A

Ischaemic necrosis within a tissue/organ in living body produced by occlusion of either the arterial supply or venous drainage

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

What is the aetiology of infarction?

A

Cessation of blood flow

26
Q

What may cause cessation of blood flow?

A
  • Thrombosis
  • Embolism
  • Strangulation
  • Trauma
27
Q

What factors is the scale of damage of ischaemia/infarction dependent on?

A
  • Time period
  • Tissue/organ
  • Pattern of blood supply
  • Previous disease
28
Q

How does anaerobic metabolism lead to the breakdown of tissue?

A

Anaerobic metabolism causes cell death. When cells die there is a liberation of enzymes which in turn bring about the breakdown of tissues

29
Q

Coagulative necrosis

A

Coagulative necrosis is a type of accidental cell death typically caused by ischemia or infarction. In coagulative necrosis the architecture of dead tissue is preserved for at least a couple of days.

30
Q

Colliquitive necrosis

A

Liquefactive necrosis (or colliquative necrosis) is a type of necrosis which results in a transformation of the tissue into a liquid viscous mass

31
Q

Where does coagulative necrosis occur?

A
  • Heart

- Lung

32
Q

Where doe colliquitive necrosis occur?

A

Brain

33
Q

How does myocyte death occur in infarction?

A
  • Coronary arterial obstruction leads to decreased blood flow to region of the myocardium
  • This results in ischaemia and rapid myocardial dysfunction
  • Overall resulting in myocyte death
34
Q

Timeline of infarction: seconds

A

Anaerobic metabolism sets in and onset of ATP depletion

35
Q

Timeline of infarction: <2min

A

Loss of myocardial contractility leading heart failure

36
Q

Timeline of infarction: a few minutes

A

Ultrasound changes can be seen:

  • Myofibrillar relaxation
  • Glycogen depletion
  • Cell and mitochondrial swelling
37
Q

Timeline of infarction: 20-40 minutes

A
  • Myocyte necrosis

- Disruption of the integrity of the sarcolemma membrane causes leakage of intracellular macromolecules: blood tests

38
Q

Timeline of infarction: >1 hr

A

Injury to the microvasculature

39
Q

When will severe ischaemia lead to irreversible damage?

A

20-30 minutes

40
Q

What is the appearance of the infarct less than 24 hrs after occurrence?

A
  • No change on visual inspection

- A few hrs to 12 hrs post insult able to see swollen mitochondria on electron microscopy

41
Q

What is the appearance of the infarct 24-48 hrs after occurrence?

A
  • Pale infarct: myocardium, spleen, kidney, solid tissues
  • Red infarct: loose tissues, previously congested tissue; second/continuing blood supply, venous occlusion
  • Microscopically: acute inflammation initially at edge of infarct; loss of specialised cell features
42
Q

What is the appearance of the infarct 72 hours onwards after occurrence?

A
  • Pale infarct- yellow/white and red periphery
  • Red infarct- little change
  • Microscopically: chronic inflammation: macrophages remove debris; granulation tissue; fibrosis
43
Q

What is the end result of infarcts?

A
  • Scar replaces area of tissue damage
  • Shape depends on territory of occluded vessel
  • Reperfusion injury
44
Q

What reparative processes occur after myocardial infarction?

A
  • Cell death
  • Acute inflammation
  • Macrophage phagocytosis of dead cells
  • Granulation tissue
  • Collagen deposition (fibrosis)
  • Scar formation
45
Q

Histological timeline of MI:4-12hrs

A
  • Early coagulation necrosis
  • Oedema
  • Haemorrhage
46
Q

Histological timeline of MI: 12-24 hrs

A
  • Ongoing coagulation necrosis
  • Myocyte changes
  • Early neutrophilic infiltrate
47
Q

Histological timeline of MI: 1-3 days

A
  • Coagulation necrosis
  • Loss of nuclei and striations
  • Brisk neutrophilic infiltrate
48
Q

Histological timeline of MI: 3-7 days

A
  • Disintegration of dead myofibres
  • Dying neutrophils
  • Early phagocytosis
49
Q

Histological timeline of MI: 7-10 days

A
  • Well developed phagocytosis

- Granulation tissue at margins

50
Q

Histological timeline of MI: 10-14 days

A

-Well established granulation tissue with new blood vessels and collagen deposition

51
Q

Histological timeline of MI: 2-8 weeks

A
  • Increased collagen deposition

- Decreased cellularity

52
Q

Histological timeline of MI:>2 months

A

Dense collagenous scar

53
Q

Transmural infarction

A

Ischaemic necrosis affects full thickness of the myocardium

54
Q

Subendothelial infarction

A

Ischaemic necrosis mostly limited to a zone of myocardium under the endocardial lining of the heart

55
Q

What are the histological features of transmural/subendocardial infarctions?

A
  • Features are the same
  • Granulation tissue stage
  • Fibrosis
  • Possibly shorter time in the subendoccardial infarct
56
Q

How are acute infarcts classified?

A

According to whether there is elevation of the ST segment on the ECG

57
Q

Non-STEMI

A
  • No ST segment elevation but significantly elevated serum troponin level
  • Thought to correlate with a subendocardial infarct
58
Q

What are the effects of infarction dependent on?

A
  • Site dependent
  • Size of infarct
  • Death, dysfunction
  • Contribution of previous disease/ infarction
59
Q

When can complications following MI arise?

A
  • Immediate
  • Early
  • Late
60
Q

What can complications of MI include?

A
  • Sudden death
  • Arrhythmias
  • Angina
  • Cardiac failure
  • Cardiac rupture (ventricular wall, septum, papillary muscle)
  • Reinfarction
  • Pericarditis
  • Pulmonary embolism secondary to DVT
  • Papillary muscle dysefunction (necrosis/rupture) leading mitral incompetence
  • Mural thrombosis
  • Ventricular aneurysm
  • Dressler’s syndrome

Systems: Cardiovascualar AB (42 decks)

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