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Path - Histopath > Vascular and cardiac pathology > Flashcards

Vascular and cardiac pathology Flashcards

1
Q

coronary heart disease, cvd and strokes are responsible in total for what proportion of deaths?

A

1/3

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2
Q

what is atherosclerosis?

A

atheromatous deposits in the innre layer of the artery followed by fibrosis of the same

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3
Q

what is the pathophysiology of atherosclerosis?

A

endothelium of vessel damaged

Endothelial injury

Lipoprotein accumulation (LDL) (deposition off cholesteerol in core - “fatty core”)

Monocyte adhesion to endothelium
Monocyte migration into intima -> macrophages & foam cells

Platelet adhesion - stick to damaged tissue
Factor release
Smooth muscle cell recruitment

fibrous caps form on top of endothelium

endothelium proliferates

this is the formation of the plaque

-> Response to Injury Hypothesis

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4
Q

what are the Constitutional Risk Factors (impossible/hard to control) in atherosclerosis

A

Age

Gender - Postmenopausal risk increases

Genetics - most significant independent risk factor
- mendelian or multifactorial inheritance

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5
Q

what is the MOA of statins?

A

Statins inhibit HMG-CoA reductase rate limiting enzyme in liver cholesterol synthesis

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6
Q

which factors perrpetuate atheroma formation?

A

Early atheroma arises in intact endothelium

Endothelial dysfunction important – increase permeability, gene expression & adhesion

Haemodynamic disturbance -> dysfunction

Hypercholesterolaemia -> dysfunction

Inflammation -> vicious circle

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7
Q

what is the Earliest lesion in atherosclerosis ?

A

fatty streak

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8
Q

lsit some Consequences of Atheroma?

A

Stenosis
- stable angina : at approx 70% occlusion

Acute/Sudden Plaque Change

- Rupture 
- Erosion 
- Haemorrhage into plaque – increase size
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9
Q

Majority of plaques that show acute change have _____ luminal stenosis prior to acute change. they are named as ____ victims

A

only mild to moderate

“asymptomatic potential victims”

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10
Q

what are the characteristics of a Vulnerable Plaque?

A

Lots foam cells or extracellular lipid
Thin fibrous cap
Few smooth muscle cells
Clusters inflammatory cells

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11
Q

why does emotional stress increases risk of sudden death ?

A

Adrenalin increases blood pressure & causes vasoconstriction

Increases physical stress on ‘vulnerable plaques’

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12
Q

plaque rupture can lead to which things?

A

Vessel occlusion

Thrombosis

mechanism for plaque growth

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13
Q

what are the different preesentations of IHD?

A

Angina pectoris
Myocardial infarction
Chronic IHD with heart failure
Sudden cardiac death.

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14
Q

ruptures, haemorrhage and erosions of plaques lead to?

A

prothrombotic factor activation

leads to superimposed thrombus which increases occlusion

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15
Q

small plaque

vs large plaque in patient who has been suffering from angina

which is moree likely to rupture?

A

small one

just by figures - so not everyone has a stepwise progression

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16
Q

__% stenosis can lead to pain at rest

A

90%

17
Q

which vessels tend to be affected most in IHD?

A

epicardial vessels:

Plaques mainly form in first few cm of LAD or LCX
Entire length RCA

18
Q

list the types of angina and their cause?

A

Stable, Prinzmetal,Unstable

  1. Stable comes on with exertion, relieved by rest, no plaque disruption
  2. Prinzmetal Uncommon, due to artery spasm
3. Unstable angina:
Disruption of plaque
Superimposed thrombus
Possible embolisation or vasospasm
Warning of impending infarction
19
Q

what is the pathogenesis of an MI?

A 
Sudden change to plaque
Platelet aggregation
Vasospasm
Coagulation
Thrombus evolves
20
Q

what is the prognosis of MI?

A

Potentially reversible

Irreversible after 20-30 minutes

21
Q

which arteries are most implicated in MI?

A

LAD – 50%, ant wall LV, ant septum, apex

RCA - 40%, post wall LV, post septum, post RV

LCx - 20%, lat LV not apex

22
Q

after an MI what does cellular response look like?

A

After 1 day - Neutrrophils (+ loss of nuclei & striations)

After 3 days - macrophage

7days+ (1 wk+) - fibroblasts n collagen

- will still see granulation tissue, macrophages
23
Q

which factors are associated with worse prognosis in MI?

A

Age, female, DM, previous MI

24
Q

characterise a typical reperfusion injury

A

Arrhythmias common

reversible cardiac failure lasting several days - “stunned myocardium”

25
Q

List some complications of MI?

A

Contractile dysfunction – 40% infarct-> cardiogenic shock with 70% mortality rate

Arrhythmia due to myocardial irritability & conduction disturbance

Myocardial rupture - free wall most common, septum less common, papillary muscle least common.
(At mean 4-5days, range 1-10 days)

Pericarditis (Dressler syndrome) 2nd or 3rd day !!

RV infarction
Infarct extension – new necrosis adjacent to old
Infarct expansion
Mural thrombus

Chronic Ischaemic Heart Disease
Papillary muscle rupture

and more

26
Q

what is the aetiology of Sudden Cardiac Death?

A

Felt to be acute ischaemia induced electrical instability!!

Others:
Marked atherosclerosis (>75% stenosis) in one or more vessels
10% non atherosclerotic cause (long QT etc)
½ have plaque rupture

Genetic

27
Q

how does heart failure present?

A

Congestive Heart Failure (L&R)

Left sided (-> SOB, pulmonary oedema)

Right sided (-> peripheral oedema)

28
Q

list some causes of heart failure?

A 
Ischaemic heart disease
Valve disease
Hypertension
Myocarditis
Cardiomyopathy
29
Q

list some complications of heart failure?

A

Sudden Death
Arrhythmias
Systemic emboli
Pulmonary oedema with superimposed infection

30
Q

fibrosis and replacement of ventricular myocardium is sen on microscopy in which condition?

A

heart failure

31
Q

list the types of cadiomyopahty?

A

dilated, hypertrophic, restrictive

too thin, too thick, too stiff

32
Q

what is the aetiology of restrictive cardiomyopathy?

A

Idiopathic or secondary to myocardial disease eg amyloid, sarcoidosis

Normal size heart – big atria

33
Q

which cardiomyopathy has a signifficant familial component?

A

Hypertrophic (HCM):

Left ventricular hypertrophy
Familial in 50% (autosomal dominant, variable penetrance)
Beta-myosin heavy chain
Thickening of septum narrows left ventricular outflow tract

34
Q

what is the order of valve involvement in CHRONIC RHEUMATIC VALVULAR DISEASE?

A

Mitral > Aortic > Tricuspid > Pulmonic
Mitral alone 48%, Mitral + aortic 42%

a lot of thickening and fusion occurs

35
Q

what is the Commonest cause aortic stenosis?

A

Calcific aortic stenosis

Calcium deposits outflow side cusp

36
Q

list some causes of AORTIC REGURGITATION

A

rheumatic disease -causes rigidity
microbial endocarditis - causes destruction

Disease of aortic valve ring :
Marfan's Syndrome 
Dissecting aneurysm
Syphilitic aortitis 
Ankylosing spondylitis
37
Q

what are true/false aneurysms?

A

True - all layers wall

False – extravascular haematoma

38
Q

list somecauses of aneurysms?

A

Weak wall
Congenital eg Marfans
Atherosclerosis
Hypertension

Path - Histopath (21 decks)

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