Cerebrovascular disease (stroke) + valve diseases Flashcards

1
Q

stroke/cerebrovascular disease - def, types

A

any abnormality of the brain due to vascular pathology
- ischemic (decreased perfusion): global(hypoxia/tension), focal (embolic, thrombotic)
- heamorrhagic (bleed):aneurysm, intra-cerebral

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2
Q

embolic infarct

A

usually caused by mobilisation of a thrombus (air, fat, fuild).
emboli can travel to multiple sites eg: multifocal lessons in circle of willis.
most enter through MCA
has some re-perfusion if the embolus breaks down (after infarction)

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3
Q

sources of thromboembolism

A

heart: LA, LV, heart valves, structural defects
associated with atrial fibrillation

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4
Q

outcome of cerebrovascular occlusion

A

infarction
- penumbra (outer, reversible area of necrosis) can be re-perfused which can prevent damage to that area, hence limit neuro deficits (only within 3hours)
swelling/edema
- from reaction to things the necrotic brain tisseu releases (increased vascular leakiness)
- can cause herniation in coming days

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5
Q

forms of valvular diseases

A

congenital - bicuspid aortic valve
degenerative - calcific aortic stenosis, mitrala valve prolapse
immunological - RHD
infective - IE

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6
Q

valve stenosis

A

impaired opening, obstructs BF

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7
Q

valvular regurgitation/incompetence

A

impaired closing, causing back-flow into original chamber

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8
Q

congenital VHD - bicuspid aortic valve

A

congenital disease where valve only has 2 leaflets instead of 3.
causes increased load on the leaflets so more prone to degenerative calcification = stenosis.

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9
Q

degenerative VHD - calcific aortic valve stenosis

A

calcification of leaflets (which removes suplicity of valves) as a response
valves become rigid = stenosis and regurgitation
leads to systolic murmur and maybe also a diastolic murmur
eventual LV hypertrophy
same risk factors as atheroslceorsis: HTN, dyslypidemia, increases with age and mechanical load

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10
Q

immunological VHD: Rheumatic heard disease (2phases)

A

acute
- pancarditis (myo, endo(valves), peri)

chronic
- residual chronic valvular deformities (from acute) = valve dysfunction

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11
Q

acute rheumatic fever - cause

A

from strep infection in the throat.
strep contins M protein.
body produces cross reactive antibodies for the M proteins
CD4+ T cells specific to strep peptide also attack self = cytokine production + activates macrophages
high recurrence frequency

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12
Q

acute rheumatic heart disease - pancarditis

A

from RH fever

  • soft, flabby, chamber dilation, cardiac failure, affected contractibility.
    peri
  • sterile fibrinous inflammation exudate = pericardial effusion
    endo
  • inflammation of valves (extension of layer) along lines of closure + chordae tendineae
  • focal ulceration = sterile platelet thrombi (verrucae)
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13
Q

acute rheumatic heart disease outcomes

A

fibrinoid necrosis heals via fibrosis
scarring in pan-cardiac tissues = thick leaflets
repeated RF = compiled damage (scarred leaflets lose function = stenosis and/or regurgitation

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14
Q

chronic rheumatic heart disease - effects

A

usually mitral valve involved
fusion of commisures = button hole appearance
thickenned + distorted valve leaflets
thickenned + fused + shortenned chrondae tendineae
= valve dysfunction (stenosis + regurgitation, heart failure)
increases the risk of thrombosis and infection of valves (IE, non sterile)

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15
Q

infective VHD - infective endocarditis (cause, effect)

A

from bactereamia - infection via blood (needle user, trauma, dental, IV..) which stick to vegetation
heart valve colonisation by infective organism
produces vegetation (large friable infective)
destroys valve
can embolise
acute or subacute

usually in left valves but in right for IV drug users

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