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Neuro Rehab 2 > CVA - 1a Intro to CVAs > Flashcards

CVA - 1a Intro to CVAs Flashcards

1
Q

what is a CVA

A

cerebral vascular accident

sudden loss of neurologic function d/t lack of blood flow to brain

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2
Q

what is the path of a CVA in 1 word

A

vascular

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3
Q

what flag is a CVA

A

red - medical emergency
call 911!

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4
Q

what is the differential b/w CVA and TIA

A

sx of a CVA persist for >24hrs

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5
Q

what is the usual duration of TIAs

A

5min

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6
Q

what is a TIA

A

transient ischemic attack

sx are same as CVA, but resolve w/i 24hrs

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7
Q

what flag is a TIA and why

A

red - medical emergency, call 911!

can’t distinguish TIA from stroke-in-evolution

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8
Q

what is the CVA morbidity post TIA

A

50% of all CVA occur in first few days after TIA

almost 1/2 (40%) of people will have stroke w/i 5yrs after a TIA

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9
Q

what are the main sx of a CVA

A

BE FAST
Balance - loss of balance?
Eyes - visual disturbances?
Face - symmetry?
Arms - raise for 10sec?
Speech - slurred? difficulty swallowing/speaking?
Time = brain

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10
Q

what sx are more common in post circulation strokes

A

5Ds
Dizziness
Drowsiness
Dysarthria
Diplopia
Dysphasia

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11
Q

how does a higher education influence the CVAs

A

people w higher education are more aware of early stroke sx

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12
Q

where does almost 3/4 of strokes occur in the world

A

low and middle income countries

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13
Q

how does race factor into CVAs

A

black people are 50% more likely to have a stroke than white people

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14
Q

what are non modifiable risk factors for CVAs(4)

A

age
family history
african americans
sex

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15
Q

how is age a risk factor for CVAs

A

risk 2x every 10yrs after 55yo
- 70% occur in >65yo

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16
Q

why is being african american a risk factor for CVAs

A

AAs have congenital inc risk for sickle cell anemia
- inc risk factor for blood clots

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17
Q

how is sex a risk factor for CVAs

A

men > women

ovarian estrogen dec risk of stroke = dec risk in women

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18
Q

what are 5 modifiable risk factors for CVAs

A

smoking
HTN
DM type 2
CVD
SDOH

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19
Q

what is the greatest modifiable risk factor for CVAs

A

HTN

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20
Q

what are modifiable risk factors that contribute to HTN (5)

A

hypercholesterolemia
hyperlipidemia
obesity
heavy EtOH
sedentary lifestyle

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21
Q

what CVD is a significant risk for CVAs

A

a-fib
- inc risk for CVAs 5fold
- inc risk of embolus -> embolic stroke

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22
Q

what is 1 SDOH that inc risk of CVA

A

health inequities

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23
Q

what are 5 races/ethnicities that have and inc risk of CVAs

A

african americans
mexican americans
hispanics
native americans
native alaskans

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24
Q

what type of CVA is most common

A

ischemic > hemorrhagic

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25
Q

where in the meninges should be filled w CSF in a normal/healthy human

A

sub arachnoid space

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26
Q

where in the meninges are blood vessels contained in a normal/healthy human

A

arachnoid mater

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27
Q

what are 5 etiologies for an ischemic CVA

A

thrombotic
embolic
vasospasm
low perfusion
coagulopathy

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28
Q

what happens during an ischemic stroke

A

blood flow to corresponding brain territory is blocked
- leading to ischemia and infarction

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29
Q

what is infarction

A

obstruction of blood supply to brain d/t clot and causes cell death

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30
Q

what is ischemia

A

inadequate blood flow to brain, doesn’t necessarily mean cell death
- could just mean dec perfusion and oxygenation

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31
Q

what is mortality rate of ischemic CVAs

A

low

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32
Q

what is a thrombus

A

blood clot commonly caused by atherosclerotic plaques in cerebral blood vessels

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33
Q

what is an embolus

A

travelling clot from outside cerebral circulation

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34
Q

what is a common origin of an embolus and why

A

heart
- d/t afib

35
Q

what result does an embolic stroke has on disability

A

results in greater disability
- clots tend to be bigger
- get to smaller vessels of brain
- more ischemia and dec O2 perfusion bc bigger blockage

36
Q

what are 3 reasons for low perfusion leading to an ischemic stroke

A

cardiac failure
HoTN
blood loss

37
Q

how can atherosclerotic plaques lead to a thrombus

A

atherosclerosis
- artery wall thickens d/t chronic inflammation and WBCs -> dec elasticity of artery walls

plaque formation = accumulation of lipids, fibrin, calcium deposits on walls
-> narrowing of walls -> dec blood flow

38
Q

what could global low perfusion indicate

A

anoxic brain injury

39
Q

what are vasospasms

A

blood vessels continuously contract

40
Q

what are 3 etiologies for vasospasms in the brain

A

SE to drugs
SE from hemorrhagic stroke
Raynauds dz

41
Q

what is coagulopathy as it relates to causing an ischemic stroke

A

RBCs get sticky and block blood flow

42
Q

what role does HTN play in the etiology of ischemic strokes

A

HTN damages arterial linings
HTN can push thru build up of cells and lipids large enough to block blood flow

43
Q

how quickly can cell death happen in the brain

A

w/i 5-6min

44
Q

describe the ischemic stroke pathophysiological process after there is a lack of blood flow

A
  1. lack of blood flow = loss of O2 and glucose
  2. neuronal cell death in ischemic core w/i minutes
  3. ischemic cascade = impaired energy production and further neural damage/death
  4. ischemic penumbra forms in areas adjacent to ischemic core
  5. cerebral edema leads to inc ICP (frequent cause of death in large strokes)
45
Q

describe the ischemic cascade in detail

A
  1. changes in neural cell permeability
  2. release of excess transmitters
  3. inability of brain cells to produce energy
  4. influx of Na+ and output of K+
  5. open Ca- channels and allow influx of Ca-
  6. RESULTS IN FREE RADICAL DAMAGED CELLS
46
Q

describe the movement of fluid in ischemic strokes and a possible result

A

movement of fluid from blood into brain tissues and redistribution of CSF on ipsilateral side
- bc of edema from one side to other, can have midline shift

47
Q

what is a hemorrhagic CVA

A

rupture of blood vessel -> bleeding into extravascular spaces of brain

48
Q

what occurs after the initial bleeding in a hemorrhagic CVA (3)

A

edema
ischemia
infarction

49
Q

when do you see edema in hemorrhagic strokes and what is the accompanying risk w edema

A

get edema/swelling if bleed into area that is restricted by skull

risk factor for brainstem herniation (life threatening)

50
Q

what happens to the blood cells once they bleed out of the broken vessel in a hemorrhagic stroke

A

blood is a neurotoxin
- blood cells die, swell, and burst -> releasing toxins that further damage brain cells in areas surrounding the hematoma

51
Q

infarction and necrosis in hemorrhagic vs ischemic strokes

A

much more infarction (tissue death) and necrosis in hemorrhagic
- in ischemic, blood reperfusion is possible

52
Q

mortality of hemorrhagic CVAs

A

higher than ischemic

53
Q

what are 2 types of hemorrhagic strokes

A

intracerebral hemorrhage (ICH)
subarachnoid hemorrhage (SAH)

54
Q

what is an intracerebral hemorrhage (ICH)

A

rupture of cerebral blood vessel w bleeding into brain

55
Q

what is a subarachnoid hemorrage (SAH)

A

rupture of vessel on brain surface w bleeding into subarachnoid space

56
Q

what is the problem w SAH and what does this result in

A

not much space b/w pia and arachnoid, and dura maters
- causes swelling throughout whole brain and can be very damaging

57
Q

what is the most common cause of a SAH

A

aneurysm (80% of time)

58
Q

what does it mean if a SAH is caused by trauma

A

this is a TBI not a stroke
- not vascular in nature, secondary to trauma

59
Q

why are both ICH and SAH dangerous in nature

A

both can cause brainstem herniation and cell death
- blood accumulates and presses on surrounding tissues
- restriction of blood flow to areas

60
Q

what is a subdural hematoma/hemorrhage (SDH)

A

bleeding usually caused by head trauma b/w dura and arachnoid layers
- TBI not a stroke

61
Q

what are 4 causes of hemorrhagic stroke

A

HTN
cocaine use
aneurysm
arteriovenous malformation (AVM)

trauma - but TBI not a stroke

62
Q

how can HTN lead to a hemorrhagic stroke

A

overstretching internal elastic membrane of blood vessels
-> aneurysm -> stroke

63
Q

how can cocaine use lead to a hemorrhagic stroke

A

vasoconstriction -> HTN -> overstretching internal elastic membrane of blood vessels
-> aneurysm -> stroke

64
Q

what is an aneurysm

A

bulge in wall of blood vessel, that over time can weaken wall and burst

can be congenital or d/t atherosclerosis

65
Q

what is an arteriovenous malformation (AVM)

A

abnormal connection of blood vessels
tangle of blood vessels in brain that bypasses normal brain tissues and directly diverts blood from arteries to veins

66
Q

do AVM change? how?

A

don’t grow or change much
- vessels might grow, dilate, or shrink d/t clots

67
Q

what will AVMs most likely lead to

A

ICH
- bleeding caused by weakened vessels that burst d/t high pressure of blood flow in arteries

68
Q

how can AVMs be dx

A

CAT scan
MRI
cerebral angiogram

69
Q

treatment for AVMS?

A

typically treated if accessible and not too large

if can’t be treated:
- avoid activities that elevate BP
- avoid blood thinners

70
Q

etiology of AVMs

A

congenital

71
Q

how common are each of the etiologies of non-traumatic ICHs

A

HTN = aneurysm
AVM (less than either)

72
Q

what is the MAIN difference in sx b/w SAH and ICH

A

SAH will come in saying worst HA of their life
- “thunderclap headache”

73
Q

what are the 3 main different sx of SAH compared to ICH

A

thunderclap HA
diplopia
stiff neck, LBP

74
Q

why do you see stiff neck and LBP in SAH

A

accumulation of blood in CSF
-> meningeal irritation that travels down SC

75
Q

how is ICP impacted in ICH vs SAH

A

elevated ICP in both

76
Q

describe 7 sx seen in ICH

A

severe HA
difficulty speaking
confusion
impaired vision
large pupils
n/v, sz
LOC

77
Q

describe 8 sx seen in SAH

A

*thunderclap HA
facial/eye pain
*diplopia
impaired peripheral vision
confused, difficulty to arouse
restless
*stiff neck, LBP
vomitting, dizziness

78
Q

edema in ischemic vs hemorrhagic strokes

A

edema local in ischemic
- global in hemorrhagic

79
Q

what is the pathophys of a hemorrhagic stroke

A
  1. release of blood causes destruction of brain tissue
  2. toxins in released blood cause edema in response to inflammatory brain processes from these cellular changes
  3. inc ICP from added volume of blood being released
  4. severe edema restricts blood flow to remote areas and leads to global anoxia
  5. greater risk of brainstem herniation and death
80
Q

how can SAH lead to hydrocephalus

A

blood enters CSF pathway or the CSF pathway is obstructed
-> potentially blocking sites of CSF absorption -> restricts CSF flow -> hydrocephalus

81
Q

what is hydrocephalus

A

abnormal accumulation of CSF w/i cavities in brain -> pressure inc -> ventricles enlarge -> inc ICP

82
Q

what is a consideration of blood in the CSF other than causing a secondary sequelae of hydrocephalus

A

blood in CSF irritates meninges -> LE pain

83
Q

what are 2 concerns with hydrocephalus

A

can lead to herniation and death

84
Q

treatment for hydrocephalus

A

EVDs - tube placed into ventricles to drain some of fluid and dec ICP

Neuro Rehab 2 (48 decks)

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