Medical autopsy - cardiovascular Flashcards

(35 cards)

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
what is valve insufficency and what causes it?
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
heart valve vegetations
rheumatic heart disease --.-.-.-.-.-- infective endocarditis ---\<0\>--- non-bacterial thrombotic endocarditis --o--o--o-- Libman-Sachs endocarditis (SLE) --0-o-.-0-o--
27
potential problems with artificial valves (4)
thrombus infection dysfunction anticoag-related bleeding
28
causes of myocarditis
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
pathological features of myocarditis
gross: normal or dilated, mottled micro: usu lymphocytic inflammation heals by progressive fibrosis eosinophils in hypersensitivity types giant cell variant (unknown cause)
30
causes of aortic aneurysm (6)
connective tissue disease (Marfans, Ehlers-Danlos etc) collagen degradation in atherosclerosis cystic medial degeneration (due to htn) trauma vasculitis infection
31
consequences of aortic aneurysm (3)
rupture obstruction/embolism compression of adjacent structure (eg ureter)
32
what is aortic dissection and what causes it?
=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
types of aortic dissection
type A: starts at proximal aortic (DeBakey **II** to arch vessels, DeBakey **I** past arch vessels) type B: starts distal to arch vessels
34
how does aortic dissection cause death?
1. rupture or 2. retrograde involvement of aortic valve (tamponande, infarct, valve insufficiency ect)
35
What is HCM?
hypertrophic cardiomyopathy: structural disorder caused by point mutations in sarcomere proteins causes hypertrophy and myocyte disarray AD: 50% chance of inheritance