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A2. Respiratory system > Pathophysiology of Ischaemia and Infarction > Flashcards

Pathophysiology of Ischaemia and Infarction Flashcards

1
Q

What is meant by hypoxia?

A

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

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2
Q

What is hypoxic hypoxia?

A

(a) Low inspired O2 level
(b) Normal inspired O2 but low PaO2 – impairment of diffusion.

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3
Q

What is anaemic hypoxia?

A

•Normal inspired O2 but blood abnormal

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4
Q

What is stagnant hypoxia?

A

•Normal inspired O2 but abnormal delivery

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

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5
Q

What is cytotoxic hypoxia?

A

•Normal inspired O2 but abnormal at tissue level – Something not working with oxygen delivery to the cells

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6
Q

What are the factors afecting oxygen supply?

A
  1. Inspired O2
  2. Pulmonary function
  3. Blood constituents (haemoglobin)
  4. Blood flow (hypotension impairs supply)
  5. Integrity of vasculature (atheroma, thrombus/embolus)
  6. Tissue mechanisms – deliver oxygen to respiring organelles
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7
Q

What are the factors affecting oxygen demand?

A

Tissue itself - different tissues have different requirements – fat, bone, connective tissue have lower demand than brain and heart

Activity of tissue above baseline value

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8
Q

What are the two mechanisms for heart ischaemia?

A

Supply malfunction

Demand Malfunction

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9
Q

Describe supply issues that can cause heart ischaemia

A

Coronary artery atheroma

Cardiac failure

Pulmonary function - disease and pulmonary oedema

Anaemia

Previous MI

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10
Q

Where is the localised accumulation of lipid and fibrous tissue in atheroma?

A

In the intima of the arteries

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11
Q

What is the link between atheroma and:

  • Stable angina
  • Unstable angina
  • Thrombosis
    • Aneurysm
A

Stable angina - established atheroma in the coronary artery - pain on excertion

Unstable angina - complicated atheroma in coronary artery

Thrombosis - Ulcerated/fissured plaques - thrombosis - ischaemia and infarction

Aneurysm - Atheroma in aorta - walls of aorta become weakened and dilate

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12
Q

What are the clinical consequences of atheroma?

A

MI

Transient ischaemic attack

Cerebral infarction

Abdominal aortic aneurysm

Peripheral vascular disease

Cardiac failure

Coronary artery disease - MI - Cardiac failure

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13
Q

What are the

  • Functional
  • General
  • Biochemical
  • Cellular
  • Clinical

Effects of Ischaemia?

A

Functional - Blood/O2 supply fails to meet demands of tissue - (can be because of a reduction in supply or an increase in demand)

General

  • Acute
  • Chronic - claudication
  • Acute-on-chronic – sudden worsening of an already chronic condition

Biochemical

Results in Lactate production -

Lactate to pyruvate takes energy

Lactate can cause death of the cell

Cellular

Variable susceptibility to O2 depending on tissue type and the metabolic rate

Clinical

Dysfunction

Pain

Physical damage to specialised cells

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14
Q

What are the outcomes of Ischaemia?

A

No clinical effect

Resolution / therapeutic intervention

Infarction

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15
Q

What is meant by infarction?

A

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

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16
Q

What are the possible aetiologies for infarction?

A
  1. Thrombosis
  2. Embolism
  3. Strangulation e.g. gut
  4. Trauma - cut/ruptured vessel
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17
Q

What does the scale of damage of ischamia/infarction depend on?

A
  1. Time period
  2. Tissue/organ
  3. Pattern of blood supply (consider collateral circulation – whereby one branch can still supply cells if one is blocked)
  4. Previous disease
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18
Q

What is the mechanism of tissue breakdown caused by infarction?

A

Anaerobic metabolism - cell death - liberation of enzymes

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19
Q

What are the two types of necrosis?

A

Coagulative

Colliquitive

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20
Q

Where do you find coagulative necrosis?

A

Heart, lung (most organs)

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21
Q

What is coagulative ischaemia?

A

Typically caused by ischaemia or infarction

Architecture of the dead tissue is preserved for at least a coupls of days.

Injury denatures structural proteins and lysosomal enzymes - blocks proteolysis of damaged cells - maintains coagulated morphology.

22
Q

What is liquefactive necrosis/colliquitive necrosis?

A

Necrosis which results in a transformation of the tissue into a liquid viscous mass. Affected cell is completely digested by hydrolytic enzymes - circumscribed lesion of pus and fluid remains of necrotic tissue - debris is removed by white blood cells and a fluid space is left

23
Q

How does myocyte death occur as a result of infarction?

A

•Coronary arterial obstruction leads to a decreased blood flow to region of myocardium. Results in ischaemia, rapid myocardial dysfunction and myocyte death

24
Q

What happens within seconds of myocardial ischaemia?

A

•Anaerobic metabolism, onset of ATP depletion

25
Q

What happens in under two minutes of myocardial ischaemia?

A

•Loss of myocardial contractility (heart failure)

26
Q

What happens within a few minutes of myocardial ischaemia?

A

•Ultrastructural changes (myofibrillar relaxation, glycogen depletion, cell and mitochondrial swelling) ?reversible

27
Q

How long does it take for ischaemia to cause irreversible damage to the heart?

A

20-30 minutes

  • Myocyte necrosis (disruption of integrity of sarcolemmal membrane leading to the leakage of intracellular macromolecules: blood tests) - Troponin?
  • Injury to the microvasculature - over 1 hour
28
Q

What do areas of infarction look like less than 24 hours after insult?

A
  • No change on visual inspection
  • A few hours to 12 hours post insult, see swollen mitochondria on Electron Microscopy
29
Q

What organs do you see a plae infarct between 24 and 48 hours?

A

•Myocardium, spleen, kidney, solid tissues

30
Q

What organs show a red infarct?

A

Lung and the liver

Loose tissues, previously congested tissue; second/continuing blood supply, venous occlusion

31
Q

What can you see microscopically between 24 and 48 hours after infarction?

A

•Acute inflammation initially at edge of infarct; loss of specialised cell features

32
Q

What changes do you see in a pale and a red infarct about 72 hours after infarction?

A

Pale - yellow/white and red rim periphery

Red infarct - little change

•Microscopically: chronic inflammation; macrophages remove debris; granulation tissue; fibrosis

33
Q

What is the end result of infarction?

A
  • Scar replaces area of tissue damage
  • Shape depends on territory of occluded vessel
  • Reperfusion Injury – damage when blood supply is restored – after period of ischaemia – inflammation and damage from free radicals
34
Q

What is the reparative process of myocardial infarction?

A
  • Cell death
  • Acute inflammation
  • Macrophage phagocytosis of dead cells
  • Granulation tissue – new vessel formation
  • Collagen deposition (fibrosis)
  • Scar formation
35
Q

What happens after 4-12 hours of myocardial infarction?

A

•Early coagulation necrosis, oedema, haemorrhage

36
Q

What happens 12-24 hours after myocardial infarction?

A

•Ongoing coagulation necrosis, myocyte changes, early neutrophilic infiltrate

37
Q

What happens 1-3 days after myocardial infarction?

A

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

38
Q

What happens between 3-7 days of myocardial infarction?

A

•Disintegration of dead myofibres, dying neutrophils, early phagocytosis

39
Q

What happens during 7-10 days of myocardial infarction?

A

•Well developed phagocytosis, granulation tissue at margins (red rim if pale infarct)

40
Q

What happens between days 10-14 of myocardial infarction?

A

Well established granulation tissue with new blood vessels and collagen

41
Q

What happens during weeks 2- 8 after myocardial infarction?

A

•Increased collagen deposition, decreased cellularity

42
Q

What happens over 2 months of myocardial infarction?

A

•Dense collagenous scar

43
Q

What is meant by a transmural infarction?

A

ischaemic necrosis affects full thickness of the myocardium

44
Q

What is meant by a subendocardial infarction?

A

•ischaemic necrosis mostly limited to a zone of myocardium under the endocardial lining of the heart – just under the endocardial surface

45
Q

What are the histological features of transmural and subendocardial infarction?

A

•Histological features are the same

(repair time - granulation tissue stage followed by fibrosis - in subendocardial infarct possibly slightly shortened compared to transmural infarct)

46
Q

How are acute infarcts clasified?

A

•according to whether there is elevation of the ST segment on the ECG

47
Q

What are the features of a NSTEMI?

A

(non st elevating myocardial infarction)

no ST segment elevation but a significantly elevated serum troponin level

48
Q

What does a non-stemi correlate with?

A

subendocardial infarct

49
Q

What do the effects of infarction depend?

A

Site

Size of infarct

Death and dysfunction (pain)

Contribution of previous disease and infarction

50
Q

What are the complications of myocardial infarction?

A
  • Immediate; early; late
  • Sudden death; arrhythmias; angina; cardiac failure; cardiac rupture - ventricular wall, septum, papillary muscle; reinfarction; pericarditis; pulmonary embolism secondary to DVT; papillary muscle dysfunction - necrosis/rupture leads to mitral incompetence; mural thrombosis; ventricular aneurysm; Dressler’s syndrome

A2. Respiratory system (77 decks)

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