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Cardiovascular System > Pathology of Ischaemia and Infarction > Flashcards

Pathology of Ischaemia and Infarction Flashcards

1
Q

What is Ischaemia

A

• Relative lack of blood supply to tissue/organ leading to inadequate O2 supply to meet the needs of tissue/organ: hypoxia

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2
Q

Types of Hypoxia (4)

A

Hypoxic
Anaemic
Stagnant
Cytotoxic

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3
Q

Hypoxic (2)

A

a) Low inspired O2 level

b) Normal inspired O2 but low PaO2

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4
Q

Anaemic

A

a) Normal inspired O2 but blood abnormal (carrying capacity)

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5
Q

Stagnant (3)

A

Normal inspired air but abnormal delivery

a) Local e.g. occlusion of vessel
b) Systemic e.g. shock

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6
Q

Cytotoxic

A

a) Normal inspired O2 but abnormal at tissue level

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7
Q

Factors affecting oxygen supply (6)

A
  1. Inspired O2
  2. Pulmonary function
  3. Blood constituents
  4. Blood flow
  5. Integrity of vasculature
  6. Tissue mechanisms
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8
Q

Factors affecting oxygen demand

A
  1. Tissue itself- different tissues have different requirements
  2. Activity of tissue above baseline value
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9
Q

What causes supply issues (6)

A 
Coronary atheroma
Cardiac failure
Pulmonary function
Pulmonary oedema
Anaemia
Previous
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10
Q

What causes demand issues

A

High intrinsic demand

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11
Q

What is atheroma/atherosclerosis

A

Localised accumulation of lipid and fibrous tissue in the intima of arteries

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12
Q

Established atheroma in coronary artery =

A

Stable angina

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13
Q

Complicated atheroma in coronary artery

A

Unstable angina

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14
Q

Ulcerated/fissured plaques (2)

A

Thrombosis

Ischaemia/Infarction

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15
Q

Atheroma in the aorta

A

Aneurysm

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16
Q

Clinical consequences of Atheroma in the aorta (7)

A
  • MI
  • TIA (transient ischaemic attack)
  • Cerebral Infarction
  • Abdominal aneurysm
  • Peripheral vascular disease
  • Cardiac failure
  • Coronary artery disease
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17
Q

Effects of Atheroma on Blood Flow (3)

A

Vessel Wall
Blood Flow
Resistance

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18
Q

Blood flow (Q) =

A

Pressure gradient/ Resistance

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19
Q

Poiseuille’s formula demonstrates

A

Relationship between radius and resistance

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20
Q

Function effects of ischaemia

A

Blood/O2 supply fails to meet demand due to decreased supply and increased demand

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21
Q

General effects of ischaemia

A

Acute

Chronic

22
Q

Biochemical effects of ischaemia

A

Anaerobic metabolism

cell death

23
Q

Cellular effects of ischaemia

A

Different tissues have different O2 requirements

High metabolic are more susceptible

24
Q

Clinical effects of ischaemia (3)

A

a) Dysfunction
b) Pain
c) Physical damage- specialised cells

25
Q

Outcomes of Ischaemia (3)

A

a) No clinical effect
b) Resolution versus therapeutic intervention
c) Infarction

26
Q

What is Infarction

A

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

27
Q

Cessation of blood supply can be caused by (4)

A
  1. Thrombosis
  2. Embolism
  3. Strangulation e.g. gut
  4. Trauma- cut/ruptured vessel
28
Q

What is the scale of damage of ischaemia/infarction dependent on (4)

A
  1. Time period
  2. Tissue/organ
  3. Pattern of blood supply
  4. Previous disease
29
Q

How does infarction lead to the break down of tissues

A

Anaerobic metabolism leads to cell death with liberates the enzymes and causes the breakdown of tissues

30
Q

What is coagulative necrosis and where does it occur

A

. heart and lung- semi-solid debris due to the presence of protein fibres

31
Q

What is colliquative necrosis and where does it occur

A

brain- characterized by the digestion of dead cells to form a viscous liquid mass.

32
Q

What does coronary arterial obstruction cause

A

Myocardial dysfunction and myocyte death

33
Q

Events that follow myocardial ischaemia

A
  1. Anaerobic metabolism - seconds
  2. ATP depletion
  3. Loss of myocardial contractility- <2 minutes
  4. Heart failure
  5. Ultrastructural changes- a few minutes
  6. Myocyte necrosis- 20-40 minutes
  7. Injury to microvasculature >1 hour
34
Q

Appearance of infarcts less than 24 hours (2)

A

 No change on visual inspection

 A few hours to 12 hours post insult, see swollen mitochondria on electron microscopy

35
Q

Appearance of infarct 24-48 hours (3)

A

 Pale infarcts e.g. myocardium, kidney, spleen- solid tissue
 Red infarcts in lung and liver- Loose tissues, previously congested tissue; second/continuing blood supply, venous occlusion
 Microscopically: acute inflammation initially at edge of infarct; loss of specialised cell features

36
Q

Appearance of infarcts 72 hours (3)

A

 Macroscopically: pale infarct- yellow/white and red periphery
 Red infarct- little change
 Microscopically: Chronic inflammation; macrophages remove debris granulation tissue  fibrosis

37
Q

End result of infarcts (3)

A

 Scar replaces area of tissue damage
 Shape depends on territory of occluded vessel
 Reperfusion injury

38
Q

Name Reparative Processes (6)

A
  • Cell death
  • Acute inflammation
  • Macrophage phagocytosis of dead cells
  • Granulation tissue
  • Collagen deposition (fibrosis)
  • Scar formation
39
Q

MI 4-12 hours

A

Early coagulation necrosis, oedema, haemorrhage

40
Q

MI 12-24 hours

A

ongoing coagulation necrosis, myocyte changes, early neutrophilic infiltrate

41
Q

1-3 days MI

A

Coagulation necrosis, loss of nuclei and striations, brisk neutrophilic infiltrate

42
Q

3-7 days MI

A

Disintegration of dead myofibres, dying neutrophil, early phagocytosis

43
Q

7-10 days MI

A

well developed phagocytosis, granulation tissue at margins

44
Q

10-14 days MI

A

well established granulation tissue with new blood vessels and collagen deposition

45
Q

2-8 weeks

A

Increased collagen deposition, decreased cellularity

46
Q

> 2months

A

Dense collagenous scar

47
Q

Transmural Infarctions

A

Ischemic necrosis affects full thickness of the myocardium

48
Q

Subendocardial infarction

A

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

49
Q

What infarction correlates with NSTEMI

A

Subendocardial infarction

50
Q

What are the histological features of transmural and subendocardial infarction like

A

They are the same

the repair time in subendocardial is slightly shortened

Cardiovascular System (42 decks)

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