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CR3 > Chest Pain & Breathlessness > Flashcards

Chest Pain & Breathlessness Flashcards

1
Q

IHD Syndromes

A

MI
Angina (stable and unstable)
Sudden cardiac death

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2
Q

Most common cause of IHD

A

Atheroma of coronary arteries

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3
Q

Causes of IHD

A

Atheroma of coronary arteries
Coronary artery Vasculitis
Coronary artery vasospasm

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4
Q

RF for IHD

A 
Male
Old
FH
Hyperlipidaemia
Hypertension
Diabetes Mellitus
Smoking
Obesity
Stress
Lack of exercise
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5
Q

Stage 1 of atherosclerosis

A

Blood flow forms eddies

Loose platelet aggregation

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6
Q

Stage 2 of atherosclerosis

A 
Arterial wall injury at platelet reaction sites
Loosened injured endothelium
Low grade inflammation
Oedema
Ruptured internal elastic membrane
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7
Q

Stage 3 of atherosclerosis

A

Smooth muscle cells proliferate and produce collagen

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8
Q

Stage 4 of atherosclerosis

A

Blood lipids leak into vessel wall
Smooth muscle cells take up fat and store as droplets
Macrophages take up released fat droplets by phagocytosis
Collagen fibres form

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9
Q

Stage 5 of atherosclerosis

A

Collagen increases

Cellularity decreases

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10
Q

Stage 6 of atherosclerosis

A

Acellular plaque with abundant collagen

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11
Q

Stage 7 of atherosclerosis

A

Necrotic centre and calcified

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12
Q

Stage 8 of atherosclerosis

A

Calcified necrotic area becomes gruel like
Cholesterol crystals form
Vasa vasorum vessels grow into intima

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13
Q

Complications of atherosclerosis

A 
Ulceration
Fissuring
Haemorrhage
Thrombosis
Aneurysm
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14
Q

Stage 9 of atherosclerosis

A

Risk of massive thrombus formation as exposure of collagen, coagulation and blood flow
Plaque suddenly ruptures

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15
Q

Stage 10 of atherosclerosis

A

Eddies downstream form plaque stenosis

Platelets thrombus formed = may grow and occlude lumen

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16
Q

Acute MI Types

A

Transmural

Subendocardial

17
Q

Transmural Infarction

A
  • involving whole thickness of ventricular wall

- underlying lesion is atheromatous plaque undergone fissuring and occlusive thrombosis

18
Q

Subendocardial infarction

A
  • inner third or half of myocardium

- from generalised underperfusion of myocardium

19
Q

MI in L. coronary artery

A

Massive anterolateral MI

20
Q

MI in LAD

A

Anteroseptal MI

21
Q

MI in L circumflex

A

Lateral MI

22
Q

MI in RCA

A

Posterior MI

23
Q

0-12hrs MI appearance

A

No changes

24
Q

12-24hrs MI appearance

A
  • pale blotchy discolouration

- bright eosinophilia of muscle fibres

25
Q

24-72hrs MI appearance

A
  • soft, pale, yellow
  • loss of nuclei striations
  • heavy interstitial neutrophil infiltrate
26
Q

3-10d MI appearance

A
  • soft yellow/brown
  • hyperaemic border
  • replacement of infarcted area with granulation tissue
27
Q

weeks- months appearance

A
  • white fibrous scar

- collagenous scar tissue

28
Q

ST MI complications

A
  • L ventricular failure
  • cardiac dysrhythmias
  • ventricular wall rupture
  • papillary muscle infarction
  • mural thrombus
  • fibrinous pericarditis
  • DVT -> PE
29
Q

LT MI complications

A
  • intractable L. ventricular failure
  • ventricular aneurysm
  • Dressler’s syndrome
  • recurrent MI
30
Q

What do effects of PE depends on?

A
  • size of occluded vessel
  • number of emboli
  • adequacy of bronchial blood supply
31
Q

Define large PE

A
  • large embolus coils within 1 pulmonary artery
  • saddle embolus blocks both pulmonary artery
    = circulatory collapse
32
Q

Define medium sized PE

A
  • dural blood supply protects lungs from pulmonary artery obstruction
33
Q

How does a pulmonary infarction occur?

A

multiple emboli combined with poor bronchial blood supply

34
Q

Pathogenesis of atheroma

A
  • encrustation (platelets form thrombi over injured endothelium)
  • inhibition (inflammation = plasma filtration)
  • Reaction to injury (increased permeability and SM accumulation
  • Monoclonal hypothesis (SM cells)

CR3 (30 decks)

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