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Neruo 1 - Test 3 > Hemorrhagic CVA - Lecture 11 > Flashcards

Hemorrhagic CVA - Lecture 11 Flashcards

1
Q

most common types

A

intracerebral hemorrhage

SAH

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2
Q

intracerebral hemorrhage is d/t

A

HTN or cerebral amyloid angiopathy (CAA)

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3
Q

what is CAA

A

harmless protein deposit that occurs with natural aging

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4
Q

SAH is d/t

A

ruptured saccular aneurysm or AVM

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5
Q

what else can hemorrhagic CVA be caused by

A

hyper anticoagulation

hemorrhage from brain tumor

trauma (such as TBI)

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6
Q

incidence (age)

A

low under age of 45

dramatically increases after 65

exponential with further aging

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7
Q

incidence (gender and race)

A

men > women

black > white

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8
Q

other risk factors

A

CAA induced changes in the blood vessel of the elderly

thrombolytic therapy

long term anticoagulation use

drug and alc abuse

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9
Q

pathogenesis

A

hyalinization of blood vessels

accumulation of fats and proteinaceous material

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10
Q

hyalinization of blood vessels

A

replace of smooth muscle cells by collagen

changes to the permeability of the vessel wall

hardening and calcification of vessel wall

loss of elasticity

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11
Q

accumulation of fats and proteinaceous material

A

leading to vessel walls that are prone to leak and rupture

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12
Q

onset of ICH

A

typified by gradual and steady evolution that occurs over minutes, hours and days

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13
Q

how many cases are sudden onset (ICH)

A

30%

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14
Q

when do hemorrhagic CVA occur

A

during physical activity in the daytime

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15
Q

how do hemorrhagic CVA present

A

severe HA

vomiting

seizures

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16
Q

ICH cuase

A

bleeding from an arterial source into the brain parenchyma

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17
Q

what are ICH often referred to as

A

intraparenchymal hemorrhage

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18
Q

ICH is

A

most fatal of all CVA subtypes

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19
Q

primary ICH is

A

spontaneous bleed

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20
Q

Primary ICH d/t

A

microvascular dz associated w/ HTN and/or aging

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21
Q

proposed scenario ICH

A

rupture of microaneurysms that burst as a result of HTN

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22
Q

what are most frequently involved (primary ICH)

A

small penetrating arteries

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23
Q

secondary ICH is NOT caused by

A

HTN

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24
Q

what are secondary ICH d/t

A

trauma

impaired coagulation

tumors

toxins

25
Q

medical intervention ICH

A

lowering BP into normal range

treatment of edema

anticonvulsants

26
Q

lowering BP into normal range via

A

antihypertension meds

27
Q

treatment of edema

A

steroids

mannitol

glycerol-3

28
Q

anticonvulsants

A

if seizures are present

29
Q

what does an expanding lesion cause

A

significant increase in HTN

30
Q

why can an expanding lesion be fatal

A

compression of vital centers

31
Q

how does recovery occur

A

blood is reabsorbed before significant tissue destruction occurs

32
Q

subarachnoid hemorrhage

A

WORST HEADACHE OF LIFE

WHOL

33
Q

what is a SAH

A

hemorrhaging in the subarachnoid space

b/w arachnoid and pia mater

34
Q

SAH accounts for

A

6-8% of all CVA

35
Q

causes of SAH

A

trauma

non-traumatic causes

developmental defects

neoplasm

infection

spontaneous

36
Q

non-traumatic causes

A

aneurysms and vascular malformations

37
Q

spontaneous

A

occur in normotensive persons

38
Q

aneurysms account for

A

90% of all SAHs

39
Q

what is an aneurysm

A

abnormal distension of the blood vessels at bifurcations

caused by dz or weakening of the vessel walls

40
Q

aneurysm stimulus

A

elevated BP

41
Q

surgical interventions –>aneurysms

A

surgical clipping

endovascular coiling

42
Q

surgical clipping

A

craniotomy

“clipping” at neck

43
Q

endovascular coiling

A

catheter up femoral artery –> aorta –> aneurysm

platinum coils –> thrombotic reaction –> blocks flow and prevents rupture

44
Q

most common sites of SAH

A

anterior communicating artery

posterior communicating artery

middle cerebral artery

45
Q

dangers of SAH

A

spewing of blood, under high pressure, into brain tissue

susceptibility to re-rupture

obstruction of the SA space

blood in SA space

46
Q

what can obstruction of SA space lead to

A

hydrocephalus d/t CSF blockage

47
Q

blood in SA space

A

vasospasm

inflammatory and fibrotic responses in the meninges

48
Q

vasospasm

A

resulting in ischemic infarction of the adjacent vessels

49
Q

secondary complications often prove

A

fatal

50
Q

what do SAH cause

A

extreme elevations in ICP

fatal brain herniation

51
Q

extreme elevations in ICP d/t

A

obstruction of CSF and cerebral edema

52
Q

fatal brain herniation d/t

A

increased pressure and mass within cranial cavity

53
Q

primary sites of herniation

A

bones of the orbit and posterior fossa

54
Q

SAH can be

A

mild to severe

55
Q

mild SAH

A

often associated with stiff neck

mild HA

minimal focal neurologic signs

confusion lasting for weeks

56
Q

moderate SAH

A

mild coma

moderate to severe HA

57
Q

severe SAH

A

can be fatal

severe HA

decerebrate rigidity

deep coma

58
Q

when is there significant chances of rebleeding

A

mod/severe

Neruo 1 - Test 3 (12 decks)

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