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Leila's Yr 5 Pathology > Histopathology 2 - CVS disease > Flashcards

Histopathology 2 - CVS disease Flashcards

1
Q

Describe the pathogenesis of an atheromatous plaque

A

1) endothelial injury –> LDL accumulation in tunica intima
2) monocyte adhesion to endothelium
3) monocyte migration into intima –> macrophages and foam cells
4) platelet adhesion –> factor release –> smooth muscle cell recruitment, VSMCs make the fibrous cap
5) lipid accumulation

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2
Q

Earliest change seen in atherosclerotic disease

A

Fatty streak, no flow disturbance, virtually present in everyone >10 years olf

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3
Q

where do atherosclerotic plaques occur?

A

Areas of disturbed flow e.g. carotids and coronary arteries

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4
Q

Characteristics of a vulnerable atherosclerotic plaque

A

Thin fibrous cap, lots of foam cells and extracellular lipid, few smooth muscle cells

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5
Q

2 main fates of an atherosclerotic plaque

A

Rupture or obstruction

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6
Q

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

A

Low/oscillatory shear stress/turbulent = atherogenic

High laminar flow = protective

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7
Q

CAUSE OF STABLE ANGINA?

A

Atheromatous plaque causes 70% occlusion of vessel and demand > supply, this level of occlusion cannot be reversed by vasodilation

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8
Q

What is the main cause of MI?

A

90% of MI is caused by reduced blood flow due to atherosclerosis

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9
Q

What % of stenosis is needed to cause pain at rest?

A

90% stenosis

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10
Q

3 main types of angina

A

Stable, unstable, prinzmetal

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11
Q

Site of atherosclerotic plaques in IHD

A

First few cm of LAD or LCX

Entire length of rCA

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12
Q

What is angina?

A

Transient myocyte ischaemia that does not cause necrosis

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13
Q

What can be a cause of stable angina becoming unstable;e

A

Superimposed thrombus

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14
Q

What is the most common cause of death in post menopausal women?

A

IHD

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15
Q

At what point does myocardial ischaemia –> myocyte necrosis?>

A

20-30 mins

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16
Q

2 most commonly affected arteries in MI

A

LAD, RCA

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17
Q

Does HF always come after and MI?

A

NO!
Myocyte ischaemia for 60s –> loss of contractility –> HF
Ischaemia takes 20-30 mins to come on therefore you can have HF without histological changes of ischaemia

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18
Q

Histological findings of MI after 4 hours?

A

Normal histology (Takes around 6 hours for histology to show ischaemia)

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19
Q

CK-MB levels after 4 hours post MI

A

Normal

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20
Q

Histological findings of MI after 23 hours?

A

Loss of nuclei, COAGULATIVE necrotic cell death (6-24 hours)

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21
Q

Histological findings of MI after 3 days

A

Infiltration of neutrophils and then macrophages to clear up debris

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22
Q

Histological findings of MI after 10 days

A

Granulation, angiogenesis (angioblasts), collagen synthesis (myofibroblasts)

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23
Q

Histological findings 3 weeks post MI

A

Decellularising scar tissue

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24
Q

Complications of MI (DARTH VADER)

A

Death, arrhythmias, rupture (papillary muscle), tamponade, heart failure
Valvular disease, aneurysms of ventricle, Dressler’s syndrome, embolism, recurrence

25
Q

Mean time post-mI for ventricular wall rupture?

A

4-5 days

26
Q

Mean time for pericarditis post MI?

A

2-4 days

27
Q

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

A

Dressler’s syndrome

28
Q

What is believed to be the cause of sudden cardiac death?

A

Ischaemia induced electrical instability

29
Q

Features of right sided heart failure

A

Peripheral oedema and nutmeg liver

30
Q

What is the most common cause of right sided heart failure?

A

Left sided heart failure

31
Q

3 main histological changes in heart failure

A

Dilated LV
Thin and scarred heart walls
replacement of myocytes with scar tissue

32
Q

What type of necrosis in MI?

A

COAGULATIVE NECROSIS

33
Q

Causes of dilated cardiomyopathy

A

Idiopathic, alcohol, viral myocarditis, haemochromatosis, endo- hyper/hypothyroid,DM

34
Q

What is the most common cause of myocarditis?

A

Viral infection

35
Q

HCM most common cause? How is it inherited?

A

50% are inherited mutation in beta myosin heavy chain, AD

36
Q

What is HOCM?

A

Septal hypertrophy –> outflow obstruction

37
Q

Causes of restrictive cardiomyopathy?

A

Sarcoidosis, amyloidosis

38
Q

2 most commonly affected valves in rheumatic heart disease?

A

Mitral > aortic

39
Q

Most common cause of aortic stenosis?

A

Calcific aortic stenosis (calcification due to old age)

40
Q

Name 3 causes of aortic regurgitation (3 categories)

A
  1. Dilational (Marfan’s, aortic dissection, ank spond)
  2. Destructive (endocarditis)
  3. Rigidity (rheumatic heart disease, degeneration)
41
Q

2 main types of aneurysm

A

True - all layers of the wall dilate (Adventitia, media intima)
False - extravascular haematoma –> aortic dissections

42
Q

3 main causes of aneurysms

A

Marfan’s, atherosclerosis, hypertension

43
Q

Major and minor criteria of rheumatic fever (Jones)

A 
CASES
Carditis
Arthritis
Sydenhams chorea
Erythema marginatum
Subcutaneous nodules
FRAPP
Fever
Raised ESR/CRP
Arthralgia (migratory)
Prolonged PR interval 
Previous RF
44
Q

Haemopericardium on autopsy post MI - cause?

A

Cardiac rupture of ventricular wall

45
Q

VSD post MI - cause?

A

Cardiac rupture of septum

46
Q

Mitral regurgitation post MI - cause?

A

Cardiac rupture of papillary muscle

47
Q

When do arrhythmias tend to come on post MI? Which arrhythmia most common?

A

Within first 24 hours, VF v common

48
Q

What is required for the diagnosis of acute rheumatic fever?

A

group A strep infection +2 major criteria or 1 major criteria + 2 minor criteria

49
Q

Histology findings in acute rheumatic fever

A

Beady fibrous vegetations (verrucae), Aschoff bodies, Anitschkov myocytes

50
Q

Small giant cell granulomas (Acute rheumatic fever)

A

Aschoff bodies

51
Q

Regenerating myocytes (Acute rheumatic fever)

A

Anitschkov myocytes

52
Q

Treatment for acute rheumatic fever

A

Benpen

53
Q

Vegetations found on heart in rheumatic heart disease vs infective endocarditis

A

Rheumatic heart disease: small, warty vegetations (verrucae)

IE: Large irregular masses on valve cusps

54
Q

Causative organisms of acute IE

A

S.aureus, S.pyogenes

55
Q

Causative organisms of subacute IE

A

Strep. viridian’s, S.epidermidis, HACEK, Coxiella, Mycoplasma, Candida

56
Q

The murmur usually heard in IE

A

MR/AR

57
Q

Immune phenomena in IE

A

Osler’s nodes, Roth spots, haematuria due to glomerulonephritis

58
Q

Thromboembolic phenols in IE

A

Splinter haemorrhages, Janeway lesions, micro emboli

59
Q

Criteria used to diagnose IE

A

Duke’s criteria

Leila's Yr 5 Pathology (100 decks)

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