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Cardiovascular System > Pathology of Ischaemia and Infarction > Flashcards

Pathology of Ischaemia and Infarction Flashcards

(50 cards)

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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

Study These Flashcards
A

Acute

Chronic

22
Q

Biochemical effects of ischaemia

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A

Anaerobic metabolism

cell death

23
Q

Cellular effects of ischaemia

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A

Different tissues have different O2 requirements

High metabolic are more susceptible

24
Q

Clinical effects of ischaemia (3)

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A

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

25
Outcomes of Ischaemia (3)
a) No clinical effect b) Resolution versus therapeutic intervention c) Infarction
26
What is Infarction
Ischaemic necrosis within a tissue/organ in living body produced by occlusion of either the arterial supply or venous drainage
27
Cessation of blood supply can be caused by (4)
1. Thrombosis 2. Embolism 3. Strangulation e.g. gut 4. Trauma- cut/ruptured vessel
28
What is the scale of damage of ischaemia/infarction dependent on (4)
1. Time period 2. Tissue/organ 3. Pattern of blood supply 4. Previous disease
29
How does infarction lead to the break down of tissues
Anaerobic metabolism leads to cell death with liberates the enzymes and causes the breakdown of tissues
30
What is coagulative necrosis and where does it occur
. heart and lung- semi-solid debris due to the presence of protein fibres
31
What is colliquative necrosis and where does it occur
brain- characterized by the digestion of dead cells to form a viscous liquid mass.
32
What does coronary arterial obstruction cause
Myocardial dysfunction and myocyte death
33
Events that follow myocardial ischaemia
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
Appearance of infarcts less than 24 hours (2)
 No change on visual inspection |  A few hours to 12 hours post insult, see swollen mitochondria on electron microscopy
35
Appearance of infarct 24-48 hours (3)
 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
Appearance of infarcts 72 hours (3)
 Macroscopically: pale infarct- yellow/white and red periphery  Red infarct- little change  Microscopically: Chronic inflammation; macrophages remove debris granulation tissue  fibrosis
37
End result of infarcts (3)
 Scar replaces area of tissue damage  Shape depends on territory of occluded vessel  Reperfusion injury
38
Name Reparative Processes (6)
* Cell death * Acute inflammation * Macrophage phagocytosis of dead cells * Granulation tissue * Collagen deposition (fibrosis) * Scar formation
39
MI 4-12 hours
Early coagulation necrosis, oedema, haemorrhage
40
MI 12-24 hours
ongoing coagulation necrosis, myocyte changes, early neutrophilic infiltrate
41
1-3 days MI
Coagulation necrosis, loss of nuclei and striations, brisk neutrophilic infiltrate
42
3-7 days MI
Disintegration of dead myofibres, dying neutrophil, early phagocytosis
43
7-10 days MI
well developed phagocytosis, granulation tissue at margins
44
10-14 days MI
well established granulation tissue with new blood vessels and collagen deposition
45
2-8 weeks
Increased collagen deposition, decreased cellularity
46
>2months
Dense collagenous scar
47
Transmural Infarctions
Ischemic necrosis affects full thickness of the myocardium
48
Subendocardial infarction
Ischemic necrosis mostly limited to a zone of myocardium under the endocardial lining of the heart
49
What infarction correlates with NSTEMI
Subendocardial infarction
50
What are the histological features of transmural and subendocardial infarction like
They are the same | the repair time in subendocardial is slightly shortened

Cardiovascular System (42 decks)

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