CVA 2 Flashcards

1
Q

intercerebral hemorrhage

A

bleeding in brain parenchyma

typically 2/2 HTN (poorly controlled, microaneurysm)

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2
Q

how do ICHs injure brain

A

direct pressure of expanding clot and irritation of tissue

increased ICP and herniation

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3
Q

where do ICH typically occur (5)

A
basal ganglia
pons
thalamus
cerebellum
cerebrum
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4
Q

s/s ICH

A

occur without warning and with routine activity

worsen over minutes to hrs

HA, vomiting, LOC, focal deficit, behavior change

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5
Q

ICH diagnosis

A

Non contrast CT

new blood = white, old blood = gray

NO LP bc elevated ICP/herniation risk

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6
Q

ICH tx

A

no effective tx - ICU, neuro checks

manage BP (nicardipine), cent support (HOB 30), eve resale of anticoagulation, seizure prophylaxis, DVT prophylaxis

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7
Q

HTN control in ICH

A

nicardipine is DOC

optimal range = 160/90, MAP 110

AVOID NITROPRUSSIDE

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8
Q

reversal agents

A

vitamin K IV, Praxbind, prothrombin complex

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9
Q

clinical course ICH

A

deteriorating LOC in 24-48hrs

high risk of herniation 2/2 vasogenic edema

high risk fo seizures

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10
Q

specific measure to reduce ICP

A

mannitol/hypertonic saline
hypothermia
hyperventillation
decompressive craniotomy

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11
Q

ICH prevention

A

HTN goal management (<130/80)

smoking cessation, limited alcohol, exercise, healthy weight

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12
Q

SAH

A

blood bt Pia and arachnoid mater

secondary to trauma or spontaneous

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13
Q

SAH clinical picture

A

sudden, severe headache

“worst HA I’ve ver had”

symptoms being following strenuous activity

+/- n/v, LOC, meningeal signs

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14
Q

SAH diagnostics

A

non-contrast CT – may miss

follow up LP to observe for blood in CSF

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15
Q

LP findings in SAH

A

done if high clinical suspicion but negative imaging

Xanthrochromia in all 4 viles

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16
Q

CTA SAH would show

A

extrvasion of contrast

dye will be out of the vessel and into CSF

17
Q

SAH management

A

hospitalize

periodic re-eval with CT

bed/bowel regime to decrease ICP

HA pain magnet, BP management, prevention of vasospasm, statins

18
Q

vasospasm prevention

A

Nimodipine(Nimotop) non-DHP CCB

IV then PO

19
Q

SAH diagnostics AVM

A

bilateral carotid and vetetnral angiography to evaluate for aneurysm

clipping nad cooling done to prevent re bleeding

20
Q

SAH complications

A

hydrocephalus, hyponatremia, rebreeding

21
Q

family history and SAH

A

first degree relatives have increased risk of lifetime SAH

22
Q

AV malformation

A

congenital malformed communication between arteries and veins

70% will bleed, and cerebral ones do before age 40

23
Q

AV malformation rules

A

small (<2/5) more likely to bleed than >5

AVMs are likely to rebelled

cerebral AVMS are often associated with aneurysm

24
Q

AVM symptom

A

HA, seizures, focal neuro deficits in unruptured AV

25
Q

types of aneurysms

A

fusiform
mycotic
saccular

occur at vessel bifurcation

26
Q

fusiform aneurysm

A

LARGE arteries, caused by arteriosclerosis

typically in older, vertebrobasilar system

not easily accessible to surgeon

27
Q

fusiform aneurysm symptoms due to

A

compression of brain or cranial nerves by thrombosis or take off vessel

28
Q

mycotic aneurysm

A

septic emboli lodge within peripheral cerebral vessel

2/2 infective endocarditis and abscess rupture

typically have >1 aneurysm`\

29
Q

saccular aneurysm

A

small round berry out poaching (typically in circle of willis)

heomdynamicaly induced by degenerative vascular injury

MC In women, MC type of aneurysm

30
Q

diseases associated with saccular aneurysm

A

PCKD

marfans/CT disorders

coarctation of aorta

familial tendency

HTN, hyperlipidemia, smoking

31
Q

highest risk of rupture saccular aneurysm

A

found in posterior circulation

increased size

32
Q

s/s of saccular aneurysm

A

asymptomatic until rupture

small working leaks produce HA, nausea, meningeal signs hrs/weeks before rupture

33
Q

aneurysm study of choice

A

cerebral angiography gold stnd

excludes multiplicity

34
Q

tx aneurysm goal

A

prevention of further hemorrhage

surgical clipping, coil