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CVS Pathology > Pathology of Ischaemia and Infarction > Flashcards

Pathology of Ischaemia and Infarction Flashcards

1
Q

What does the heart need to function?

A

Oxygen

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2
Q

Definition of ischaemia

A

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

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3
Q

Types of hypoxia

A

Hypoxic
Anaemia
Stagnant
Cytotoxic

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4
Q

What is hypoxic hypoxia?

A

Low inspired O2 level
or
Normal inspired O2 but low PaO2

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5
Q

What is anaemic hypoxia?

A

Normal inspired O2 but blood abnormal

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6
Q

What is stagnant hypoxia?

A

Normal inspired O2 but abnormal delivery

  • local e.g. occlusion of vessel
  • systemic e.g. shock
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7
Q

What is cytotoxic hypoxia?

A

Normal inspired O2 but abnormal at tissue level

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8
Q

When does infarction occur?

A

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

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9
Q

Definition of atheroma/atherosclerosis

A

Localised accumulation of lipid and fibrous tissue in intima of arteries

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10
Q

What does an established atheroma in coronary artery result in?

A

Stable angina

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11
Q

What does complicated atheroma in coronary artery result in?

A

Unstable angina

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12
Q

What does ulcerated / fissured plaques result in?

A

Thrombosis leading to ischaemia / infarction

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13
Q

What does atheroma in the aorta result in?

A

Aneurysm

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14
Q

What does stable angina result in?

A

Ischaemic pain in heart on exertion

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15
Q

What does unstable angina result in?

A

Ischaemia pain in heart on rest

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16
Q

A change in the vessel wall can lead to what?

A

Thrombosis

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17
Q

Effects of ischaemia

A

Blood/O2 supply fails to meet demand due to decreased supply
Anaerobic metabolism
- L lactate reversibly converted to pyruvate via LDH - which can be converted to acetyl CoA and CO2
Dysfunction, pain, physical damage

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18
Q

What type of cells are affected the most in ischaemia?

A

Specialised cells

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19
Q

Clinical consequences of ischaemia

A 
MI
TIA
Stroke
AAA
Peripheral vascular disease
Cardia failure
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20
Q

What is another name for stroke?

A

Cerebral infarction

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21
Q

Factors affecting O2 supply

A 
Inspired O2
Pulmonary function 
Blood constituents eg. haemoglobin 
Blood flow
Integrity of vasculature e.g. atheroma, embolis / tumour
Tissue mechanisms
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22
Q

Factors affecting oxygen demand

A

Tissue - different ones have different O2 requirements

Activity of tissue above baseline value

23
Q

Supply issues in ischaemic heart disease

A 
Coronary artery atheroma
Cardiac failure 
Pulmonary function, other disease or pulmonary oedema (LVF)
Anaemia
Previous MI
24
Q

Demand issues in ischaemic heart disease

A

Heart has high intrinsic demand

Exertion/stress

25
Q

Possible causes of infarction

A

Thrombosis
Embolism
Strangulation e.g. gut
Trauma - cut/ruptured vessel

26
Q

Scale of damage of ischaemia/infarction depends on…..

A

Time period
Tissue / organ
Pattern of blood supply
Previous disease (decreased reserve)

27
Q

What does anaerobic metabolism lead to?

A

Cell death which leads to liberation of enzymes which leads to breakdown of tissue

28
Q

Types of necrosis

A

Coagulative e.g. heart, lung

Colliquitive e.g. brain

29
Q

Which is the most common type of necrosis?

A

Coagulative

30
Q

Pathology of myocardial ischaemia

A
  1. Anaerobic metabolism - onset of ATP depletion (seconds)
  2. Loss of myocardial contractility (leads to HF) - < 2 mins
  3. Ultrastructural changes (few mins) - possibly reversible
    Severe ischaemia is in in 20 - 30 mins - this causes irreversible damage
  4. Myocyte necrosis (20 - 40 mins)
  5. Injury to the microvasculature > 1 hour
31
Q

Appearance of infarct less than 24 hours

A

No change on visual inspection

A few hours to 12 hours post insult (swollen mitochrondia)

32
Q

Appearance of infarct 24 - 48 hours

A

Pale - myocardium, solid tissues, spleen etc
Red infarct - lung, liver etc
Microscopically - acute inflammation initially at edge of infarct, loss of specialised cell features

33
Q

Appearance of infarct at 72 hours onwards

A

Pale infarct - yellow / white in periphery
Red infarct - little change
Microscopically
- chronic inflammation
- macrophages remove debris
- granulation tissue and new vessel formation
- fibrosis - new tissue is laid down

34
Q

End results of infarct

A

Scar replaces area of tissue damage

35
Q

Shape of the scar after an infarct depends on what?

A

Territory of occluded vessel

36
Q

What is the scar called after an infarct?

A

Reperfusion injury

37
Q

Definition of transmural infarction

A

Ischaemic necrosis affects full thickness of the myocardium

38
Q

Definition of subendocardial infarction

A

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

39
Q

What are acute infarcts classified according to?

A

Whether there is elevation of the ST segment on the ECG

40
Q

What does it mean if there is no ST segment elevation but significantly elevated troponin level?

A

N-STEMI

41
Q

Complications of MI

A 
Sudden death 
Arrythmias
Angina
Cardiac failure
Cardiac rupture - ventricular wall 
Septum 
Papillary muscle
Reinfarction 
Pericarditis
PE 2ndry to DVT
Papillary muscle dysfunction - necrosis / rupture - mitral incompetence 
Mural thrombosis 
Ventricular aneurysm 
Dresslers syndrome
42
Q

What is dresslers syndrome?

A

Immune system response after damage to heart tissue or to the pericardium

43
Q

MI reparative process

A 
Cell death 
Acute inflammation 
Macrophage phagocytosis of dead cells
Granulation tissue
Collagen deposition (fibrosis)
Scar formation
44
Q

MI 4 - 12 hours

A

Early coagulation necrosis
Oedema
Haemorrhage

45
Q

MI 12 - 24 hours

A

Ongoing coagulation necrosis
Myocyte changes
Early neutrophilic infiltrate

46
Q

MI 1 - 3 days

A

Coagulation necrosis
Loss of nuclei and striations
Brisk neutrophilic infiltrate

47
Q

MI 3 - 7 days

A

Disintegration of dead myofibres
Dying neutrophils
Early phagocytosis

48
Q

MI 7 - 10 days

A

Well developed phagocytosis

Granulation tissue at margins - red rim with pale infarct

49
Q

MI 10 - 14 days

A

Well established granulation tissue with new blood vessels and collagen deposition

50
Q

MI 2-8 weeks

A

Increased collagen deposition

Decreased cellularity

51
Q

MI > 2 months

A

Dense collagenous scar

52
Q

What does an ASD allow?

A

A paradoxical stroke - where an embolism from peripheral veins may bypass the pulmonary circulation

53
Q

What murmur would be heard with an ASD?

A

Systolic Murmur
Radiating through to the back
Fixed S2 splitting

CVS Pathology (19 decks)

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