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
Mean time post-mI for ventricular wall rupture?
4-5 days
26
Mean time for pericarditis post MI?
2-4 days
27
Pt develops chest pain relieved on leaning forward, and fevers, 2 months after admission for MI?
Dressler's syndrome
28
What is believed to be the cause of sudden cardiac death?
Ischaemia induced electrical instability
29
Features of right sided heart failure
Peripheral oedema and nutmeg liver
30
What is the most common cause of right sided heart failure?
Left sided heart failure
31
3 main histological changes in heart failure
Dilated LV Thin and scarred heart walls replacement of myocytes with scar tissue
32
What type of necrosis in MI?
COAGULATIVE NECROSIS
33
Causes of dilated cardiomyopathy
Idiopathic, alcohol, viral myocarditis, haemochromatosis, endo- hyper/hypothyroid,DM
34
What is the most common cause of myocarditis?
Viral infection
35
HCM most common cause? How is it inherited?
50% are inherited mutation in beta myosin heavy chain, AD
36
What is HOCM?
Septal hypertrophy --> outflow obstruction
37
Causes of restrictive cardiomyopathy?
Sarcoidosis, amyloidosis
38
2 most commonly affected valves in rheumatic heart disease?
Mitral > aortic
39
Most common cause of aortic stenosis?
Calcific aortic stenosis (calcification due to old age)
40
Name 3 causes of aortic regurgitation (3 categories)
1. Dilational (Marfan's, aortic dissection, ank spond) 2. Destructive (endocarditis) 3. Rigidity (rheumatic heart disease, degeneration)
41
2 main types of aneurysm
True - all layers of the wall dilate (Adventitia, media intima) False - extravascular haematoma --> aortic dissections
42
3 main causes of aneurysms
Marfan's, atherosclerosis, hypertension
43
Major and minor criteria of rheumatic fever (Jones)
``` CASES Carditis Arthritis Sydenhams chorea Erythema marginatum Subcutaneous nodules ``` ``` FRAPP Fever Raised ESR/CRP Arthralgia (migratory) Prolonged PR interval Previous RF ```
44
Haemopericardium on autopsy post MI - cause?
Cardiac rupture of ventricular wall
45
VSD post MI - cause?
Cardiac rupture of septum
46
Mitral regurgitation post MI - cause?
Cardiac rupture of papillary muscle
47
When do arrhythmias tend to come on post MI? Which arrhythmia most common?
Within first 24 hours, VF v common
48
What is required for the diagnosis of acute rheumatic fever?
group A strep infection +2 major criteria or 1 major criteria + 2 minor criteria
49
Histology findings in acute rheumatic fever
Beady fibrous vegetations (verrucae), Aschoff bodies, Anitschkov myocytes
50
Small giant cell granulomas (Acute rheumatic fever)
Aschoff bodies
51
Regenerating myocytes (Acute rheumatic fever)
Anitschkov myocytes
52
Treatment for acute rheumatic fever
Benpen
53
Vegetations found on heart in rheumatic heart disease vs infective endocarditis
Rheumatic heart disease: small, warty vegetations (verrucae) | IE: Large irregular masses on valve cusps
54
Causative organisms of acute IE
S.aureus, S.pyogenes
55
Causative organisms of subacute IE
Strep. viridian's, S.epidermidis, HACEK, Coxiella, Mycoplasma, Candida
56
The murmur usually heard in IE
MR/AR
57
Immune phenomena in IE
Osler's nodes, Roth spots, haematuria due to glomerulonephritis
58
Thromboembolic phenols in IE
Splinter haemorrhages, Janeway lesions, micro emboli
59
Criteria used to diagnose IE
Duke's criteria