Medical autopsy - cardiovascular Flashcards

1
Q

what causes myocardial ischaemia?

A

coronary atherosclerosis (90%)

coronary emboli

obstruction small myocardial vessels

decreased blood pressure (shock)

vasospasm

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2
Q

how can myocardial ischaemia present? (4)

A

MI

angina

chronic IHD with heart failure

sudden cardiac death

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3
Q

types of angina

A

stable (perfusion/demand imbalance, relieved by rest)

prinzmetal (artery spasm)

unstable (disruption or change in plaque)

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4
Q

(usual) steps of MI

A
  1. sudden change in plaque
  2. activated platelets and mediators
  3. coagulation cascade leading to thrombus
  4. vessel occlusion and myocyte necrosis (irreversible damage after 20-30min)
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5
Q

progress of myocardial necrosis

A
  1. subendocardial (=NSTEMI)
  2. extends to epicardium
  3. full thickness necrosis (=STEMI)
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6
Q

distribution of coronary arteries

A

LAD: apex, ant LV, ant 2/3 of septum

LCx: lateral LV

RCA: RV, post LV, post 1/3 of septum

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7
Q

MI at 0-4 hrs

A

gross: none
histo: wavy myocytes

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8
Q

MI at 4-24 hrs

A

gross: dark mottling
histo: necrosis, oedema, haemorrhage, contraction bands, eosinophilic

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9
Q

MI at 1-3 days

A

gross: yellow centre
histo: neutrophils, loss of nuclei

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10
Q

MI at 3-7 days

A

gross: yellow centre, hyperaemic rim
histo: phagocytosis by macrophages

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11
Q

MI at 7+ days

A

gross: yellow tan (turning to grey white scar by 2 months)
histo: granulation tissue (turning to collagen scar by 2 months)

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12
Q

reperfusion histo

A

haemorrhage (due to bleeding by injured blood vessels)

contraction bands (due to calcium through membranes of dead cells)

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13
Q

possible consequences of MI (6)

A

contractile dysfunction

arrythmia

rupture (usu with haemopericardium and tamponade)

pericarditis (Dressler syndrome)

thrombus/aneurysm

chronic IHD

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14
Q

what causes chronic IHD and what does it look like?

A

usually after MI due to hypertrophied unaffected myocardium

large heavy hearts, with CAD and healed infarcts

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15
Q

causes of sudden cardiac death

A

fatal arrythmia (acute MI is most common trigger)

congenital/structural

valve disease

myocarditis

hereditary arrythmia

dilated or hypertrophic cardiomyopathy

drugs/metabloic/meds

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16
Q

definition of hypertension

A

diastolic >90, systolic >140

17
Q

causes of hypertension

A

essential (>90%)

renal eg RAS

endocrine (eg phaeo)

CV (eg increased cardiac output)

neuro (eg psychogenic)

18
Q

consequences of hypertension

A

atherosclerosis

cardiac hypertrophy/heart failure

multi-infarct dementia

aortic dissection

CVA

renal failure

19
Q

formula for blood pressure

A

BP = cardiac output x vascular resistance

CO: blood volume, sodium etc

VR: constriction vs dilatation

20
Q

vascular changes in hypertension

A
  1. hyaline arteriosclerosis: diffuse impairment of renal blood supply with glomerular scarring (=nephrosclerosis)
  2. hyperplastic arteriosclerosis (onion skinning): due to malignant hypertension
21
Q

heart changes in hypertension

A

pressure overload with ventricular hypertrophy

L side: >2cm thick, >500g (micro: thick myocytes and interstitial fibrosis)

R side (cor pulmonale): acute dilatation and chronic thickening

22
Q

brain changes in hypertension

A

lacunar infarcts (sclerosis of small vessels)

slit haemorrhages (rupture of small vessels)

hypertensive encephalopathy: raised ICP (acute), multiinfarct dementia (chronic)

massive bleed (assoc with sclerosis)

23
Q

what is valve stenosis and what causes it?

A

= failure to open completely, leading to pressure overload

caused by:

rheumatic heart disease (AV or MV)

calcific aortic stenosis

calcification of congenitally deformed valve (AV)

24
Q

features of rheumatic heart disease

A

(immune disease after Strep throat)

macro: thick leaflets, fusion of commisures, thick and fused tendinous cords
micro: Aschoff bodies (inflammatory cell collections)

25
Q

what is valve insufficency and what causes it?

A

failure to close completely, leading to volume overload

lots of causes:

esp aortic dilatation in htn and aging

and mitral valve prolapse in myxomatous degeneration

also: Marfans, rh arthritis, infective endocarditis

26
Q

heart valve vegetations

A

rheumatic heart disease –.-.-.-.-.–

infective endocarditis —<0>—

non-bacterial thrombotic endocarditis –o–o–o–

Libman-Sachs endocarditis (SLE) –0-o-.-0-o–

27
Q

potential problems with artificial valves (4)

A

thrombus

infection

dysfunction

anticoag-related bleeding

28
Q

causes of myocarditis

A

viral infection (most common): cocksackie, CMV, HIV

other infection: trypanosoma (Chagas disease), toxo, Lyme, diphtheria

non-infectious:

hypersensitivity (esp drugs)

SLE, rh fever and other immune

sarcoidosis

transplant rejection

29
Q

pathological features of myocarditis

A

gross: normal or dilated, mottled

micro:

usu lymphocytic inflammation

heals by progressive fibrosis

eosinophils in hypersensitivity types

giant cell variant (unknown cause)

30
Q

causes of aortic aneurysm (6)

A

connective tissue disease (Marfans, Ehlers-Danlos etc)

collagen degradation in atherosclerosis

cystic medial degeneration (due to htn)

trauma

vasculitis

infection

31
Q

consequences of aortic aneurysm (3)

A

rupture

obstruction/embolism

compression of adjacent structure (eg ureter)

32
Q

what is aortic dissection and what causes it?

A

=blood-filled channel in media (may or may not be assoc with aneurysm)

usually hypertensive (esp men in 40s-60s)

also: CTD, iatrogenic, pregnancy

33
Q

types of aortic dissection

A

type A: starts at proximal aortic (DeBakey II to arch vessels, DeBakey I past arch vessels)

type B: starts distal to arch vessels

34
Q

how does aortic dissection cause death?

A
  1. rupture

or 2. retrograde involvement of aortic valve (tamponande, infarct, valve insufficiency ect)

35
Q

What is HCM?

A

hypertrophic cardiomyopathy:

structural disorder caused by point mutations in sarcomere proteins

causes hypertrophy and myocyte disarray

AD: 50% chance of inheritance