Vascular and cardiac pathology

Question 1

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

Answer 1

1/3

Question 2

what is atherosclerosis?

Answer 2

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

Question 3

what is the pathophysiology of atherosclerosis?

Answer 3

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

Question 4

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

Answer 4

Age

Gender - Postmenopausal risk increases

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

Question 5

what is the MOA of statins?

Answer 5

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

Question 6

which factors perrpetuate atheroma formation?

Answer 6

Early atheroma arises in intact endothelium

Endothelial dysfunction important – increase permeability, gene expression & adhesion

Haemodynamic disturbance -> dysfunction

Hypercholesterolaemia -> dysfunction

Inflammation -> vicious circle

Question 7

what is the Earliest lesion in atherosclerosis ?

Answer 7

fatty streak

Question 8

lsit some Consequences of Atheroma?

Answer 8

Stenosis
- stable angina : at approx 70% occlusion

Acute/Sudden Plaque Change

- Rupture 
- Erosion 
- Haemorrhage into plaque – increase size

Question 9

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

Answer 9

only mild to moderate

“asymptomatic potential victims”

Question 10

what are the characteristics of a Vulnerable Plaque?

Answer 10

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

Question 11

why does emotional stress increases risk of sudden death ?

Answer 11

Adrenalin increases blood pressure & causes vasoconstriction

Increases physical stress on ‘vulnerable plaques’

Question 12

plaque rupture can lead to which things?

Answer 12

Vessel occlusion

Thrombosis

mechanism for plaque growth

Question 13

what are the different preesentations of IHD?

Answer 13

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

Question 14

ruptures, haemorrhage and erosions of plaques lead to?

Answer 14

prothrombotic factor activation

leads to superimposed thrombus which increases occlusion

Question 15

small plaque

vs large plaque in patient who has been suffering from angina

which is moree likely to rupture?

Answer 15

small one

just by figures - so not everyone has a stepwise progression

Question 16

__% stenosis can lead to pain at rest

Answer 16

90%

Question 17

which vessels tend to be affected most in IHD?

Answer 17

epicardial vessels:

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

Question 18

list the types of angina and their cause?

Answer 18

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

Question 19

what is the pathogenesis of an MI?

Answer 19

Sudden change to plaque
Platelet aggregation
Vasospasm
Coagulation
Thrombus evolves

Question 20

what is the prognosis of MI?

Answer 20

Potentially reversible

Irreversible after 20-30 minutes

Question 21

which arteries are most implicated in MI?

Answer 21

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

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

LCx - 20%, lat LV not apex

Question 22

after an MI what does cellular response look like?

Answer 22

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

After 3 days - macrophage

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

- will still see granulation tissue, macrophages

Question 23

which factors are associated with worse prognosis in MI?

Answer 23

Age, female, DM, previous MI

Question 24

characterise a typical reperfusion injury

Answer 24

Arrhythmias common

reversible cardiac failure lasting several days - “stunned myocardium”

Question 25

List some complications of MI?

Answer 25

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

Question 26

what is the aetiology of Sudden Cardiac Death?

Answer 26

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

Question 27

how does heart failure present?

Answer 27

Congestive Heart Failure (L&R) Left sided (-> SOB, pulmonary oedema) Right sided (-> peripheral oedema)

Question 28

list some causes of heart failure?

Answer 28

``` Ischaemic heart disease Valve disease Hypertension Myocarditis Cardiomyopathy ```

Question 29

list some complications of heart failure?

Answer 29

Sudden Death Arrhythmias Systemic emboli Pulmonary oedema with superimposed infection

Question 30

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

Answer 30

heart failure

Question 31

list the types of cadiomyopahty?

Answer 31

dilated, hypertrophic, restrictive too thin, too thick, too stiff

Question 32

what is the aetiology of restrictive cardiomyopathy?

Answer 32

Idiopathic or secondary to myocardial disease eg amyloid, sarcoidosis Normal size heart – big atria

Question 33

which cardiomyopathy has a signifficant familial component?

Answer 33

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

Question 34

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

Answer 34

Mitral > Aortic > Tricuspid > Pulmonic Mitral alone 48%, Mitral + aortic 42% a lot of thickening and fusion occurs

Question 35

what is the Commonest cause aortic stenosis?

Answer 35

Calcific aortic stenosis Calcium deposits outflow side cusp

Question 36

list some causes of AORTIC REGURGITATION

Answer 36

rheumatic disease -causes rigidity microbial endocarditis - causes destruction ``` Disease of aortic valve ring : Marfan's Syndrome Dissecting aneurysm Syphilitic aortitis Ankylosing spondylitis ```

Question 37

what are true/false aneurysms?

Answer 37

True - all layers wall | False – extravascular haematoma

Question 38

list somecauses of aneurysms?

Answer 38

Weak wall Congenital eg Marfans Atherosclerosis Hypertension