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Pathology > Hi - Cardiovascular > Flashcards

Hi - Cardiovascular Flashcards

1
Q

Describe the pathogenesis of an atherosclerotic plaque

A
  • ENDOTHELIAL injury –> endothelial dysfunction (increased permeability and adhesion)
  • LDL enters intima and is oxidised
  • MACROPHAGES enter intima + take up ox-LDL –> FOAM CELLS!
  • Foam cells die –> necrotic core
  • Attracts even more white cells
  • VSMCs form fibrous cap
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2
Q

3 main components of a plaque

A
  • Lipid core - necrotic
  • Fibrous cap with collagen and ECM
  • Cells - VSMCs, foam cells,
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3
Q

Which part of the aorta is more commonly affected by atherosclerosis - thoracic or abdominal?

A

ABdominal

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4
Q

What kinda flow through vessels is atherogenic? What kinda flow protects against atherogenesis

A

Atherogenic = Turbulent, oscillatory shear stress
Protective = High laminar flow

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5
Q

4 outcomes of atheromatous plaques?
i.e. what can happen to them eventually which has subsequent v bad results

A
  1. Obstruction (70% occlusion –> stable angina)
  2. Rupture (exposes pro-thrombotic contents)
  3. Erode(exposes pro-thrombotic contents)
  4. Haemorrhage into plaque
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6
Q

RFs for atherosclerosis ? split them into 2 categories

A

Non-modifiable: age, gender, family Hx
Modifiable: cholesterol, HTN, obesity, T2DM, smoking

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7
Q

Cause of stable angina

A

Atheromatous plaque causes 70% occlusion of a vessel, + myocyte demand exceeds supply.

This level of occlusion cannot be reversed by vasodilatation

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8
Q

3 types of angina

A

stable
unstable
Prinzmetal

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9
Q

Describe the pathogenesis of myocardial infarction

A

Myocyte necrosis due to acute ischemia as a result of a sudden event - eg plaque rupture + thrombosis or vasospasm

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10
Q

At what point does myocyte ischaemia–> myocyte necrosis

A

after 20-40 mins of ischemia

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11
Q

How can psychological stress –> MI?

A

Adrenaline release –> vasoconstriction –> physical stress on atheromatous plaque –> plaque rupture etc etc

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12
Q

Does HF always come after and MI?

A

No!
Myocardial ischemia for 1 minute leads to reduced myocyte contractility –> HF
However, myocytes don’t die until >20 mins of ischemia

Thus HF can precede myocardial infarction

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13
Q

3 most common complications of Mi

A
  • Contractile dysfunction (–> shock)
  • Arrhythmia
  • Cardiac rupture of ventricular wall(–> haemopericardium)
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14
Q

A patient develops mitral regurgitation after an MI. How has this happened?

A

Papillary muscle dysfunction/necrosis/rupture due to LV infarct

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15
Q

Mean time post-MI for ventricular wall rupture?

A

4-5 days

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16
Q

2 Most commonly affected arteries in MI?

A

LAD
RCA

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17
Q

Mean time post-MI for arrhythmia

A

within 24 hours

18
Q

Mean time post-MI for ventricular aneurysm?

A

> 4 weeks

19
Q

Mean time post-MI for pericarditis?

A

2-4 days

20
Q

Pt develops chest pain relieved on leaning forward, and fevers, 2 months after admission for MI?

A

Dresslers syndrome

21
Q

Histological findings of MI after 4 hours?

A

Normal histology

22
Q

Histological findings of MI after 23 hours?

A

Loss of nuclei, necrotic cell death

23
Q

Histological findings of MI after 3 days

A

Infiltration of neutrophils, then macrophages

24
Q

Histological findings of MI after 10 days

A

NEW BLOOD VESSELS (angioblasts)
Collagen synthesis

25
Q

Histological findings of MI after 3 weeks

A

Decellularising scar tissue

26
Q

3 main pathological features of heart failure

A
  1. dilated LV
  2. Thin and scarred heart walls
  3. Replacement of myocytes with scar tissue
27
Q

3 types of cardiomyopathy

A

Dilated
Hypertrophic
Restrictive

28
Q

Causes of DCM

A

Idiopathic
Alcohol
Endocrine - hypo/hyperthryoid, DM
Viral myocarditis

29
Q

Causes of restrictive cardiomyopathy

A

Sarcoidosis
Amyloidosis

30
Q

What does the heart look like in restrictive cardiomyopathy?

A

Overall heart size = normal
Atria = large

31
Q

HCM - what is the most common cause? how is it inherited?

A

Autosomal dominant inheritance of a mutation in the
BETA MYOSIN HEAVY CHAIN gene

32
Q

what is HOCM

A

Septal hypertrophy –> outflow obstruction

33
Q

2 Most commonly affected valve in rheumatic heart disesase

A
  1. mitral
  2. aortic
34
Q

List causes of aortic regurgitation (n.b. there are 3 categories)

A
  1. dilatation (Marfan’s, Ank Spon, dissecting aneurysm)
  2. destruction (endocarditis)
  3. rigidity (rheumatic fever, degeneration)
35
Q

Most common cause of aortic stenosis

A

calcification (old age)

36
Q

Aneurysms - name 2 types

A

True = involves all wall layers
False = extravascular haematoma

37
Q

3 causes of aneurysms

A

Congenital (Marfan’s)
Atherosclerosis
HTN

38
Q

Major criteria of acute rheumatic fever

A

Carditis
Arthritis
Sydenham’s chorea
Erythema marginatum
Subcutaneous nodules

39
Q

3 histological features of acute rheumatic fever

A

Vegetations
Aschoff bodies
Anitschkov myocytes

40
Q

Cause of acute rheumatic fever

A

Group A strep

Pathology (87 decks)

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