Quiz 3 - Module 5 Flashcards

1
Q

Main vessels of cerebral circulation and the general areas of the brain they feed

A

internal carotid –> common carotid –> ACA, MCA
basilar artery –> vertebral –> PCA

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2
Q

Vessels involved in epidural bleed + S/S

A

arterial

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3
Q

Vessels involved in subdural bleed + S/S

A

venous

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4
Q

Vessels involved in subarachnoid bleed + S/S

A

arterial

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5
Q

Circle of Willis + collateral circulation

A

where pca, aca, mca join at the base of brain
protects against ischemia

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6
Q

CPP

A

CPP = MAP - ICP

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7
Q

Determinants of ICP

A

brain volume 80%
CSF 10%
blood 10%

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8
Q

Normal ICP

A

<10 mmHg
(some sources state 5-15)

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9
Q

Cerebral autoregulation

A

ability of cerebral blood vessels to vasodilate/vasoconstrict to maintain metabolic demand
vasoconstriction when BP too high
vasodilation when acidosis, hypercapnia, hyperglycemia, temperature

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10
Q

RAS function

A

level of consciouss
circadian rhythm
sleep-wake cycle

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11
Q

AEIOUTIPS

A

acidosis, alcohol
epilepsy, encephalitis, electrolytes, hepatic encephalopathy
infection
overdose
uremia, underdose
trauma, tumor, temperature
insulin (hypo or hyperglycemia)
psychosis, poisoning
stroke (ischemic/hemorrhage), seizure, syncope

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12
Q

A&P cerebrum

A

frontal lobe (executive function, memory, problem-solving, personality)
parietal (somatosensation)
temporal (listening/comprehension, memory)
occipital (vision

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13
Q

A&P brainstem

A

pons
midbrain
medulla

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14
Q

A&P cerebellum

A

muscle coordination/balance

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15
Q

Layers of meninges

A

dura mater
arachnoid mater
pia mater

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16
Q

Epidural space

A

between dura and skull

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17
Q

Subarachnoid space

A

between dura and arachnoid mater
where CSF circulates

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18
Q

Where is CSF produced?

A

in the ventricles
chondroid plexus

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19
Q

S/S encephalitis

A

focal neurologic deficit (slurred speech, blurry vision, muscle weakness)
fever
headache
N/V
neck stiffness

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20
Q

S/S meningitis

A

triad: fever >38, stiff neck, altered LOC usually sudden onset (<24 hours)

other S/S: headache, nausea/vomiting, vision changes
**usually DOES NOT have neurological deficits)

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21
Q

Differential diagnoses

A

meningitis
stroke (ischemic or hemorrhage)
traumatic intracranial hemorrhage
concussion
overdose
alcohol intoxication

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22
Q

Normal pupil size

A

2-6 mm

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23
Q

Which cranial nerves does extraocular movement test

A

3, 4, 6

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24
Q

Cushings triad

A

late sign of impending brain herniation

irregular resps
bradycardia
widened pulse pressure (elevated SBP)

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25
Q

Decorticate positioning

A

abduction of arm at shoulder
elbows flex inwards
legs extended

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26
Q

Decerebrate positioning

A

extended, adducted, internal rotation of arm
wrists pointed outwards
legs extended
feet plantar flexed

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27
Q

Subdural hematoma

A

between dura mater + arachnoid mater
venous bleed

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28
Q

Epidural hematoma

A

between dura + skull
arterial bleed

29
Q

Frontal lobe

A

personality
emotions/arousal
intelligence
concentration, executive function, problem solving
self awareness
voluntary movement
speak/write
behavior control

30
Q

Where is broca’s area located

A

in the frontal cortex
damage –> expressive aphasia

31
Q

Where is wernicke’s area located

A

in the temporal lobe
damage –> comprehension aphasia

32
Q

S/S of stroke

A

facial droop
slurred speech
arm drift
hemiparesis
loss of sensation to one side of body
sudden trouble seeing/blurred vision/loss of sight

33
Q

S/S of increased ICP

A

headache
N/V
altered LOC

34
Q

S/S of impending brain herniation

A

pupillary asymmetry
unilateral/bilateral fixed + dilated pupils
decorticate/decerebrate positioning
respiratory depression

35
Q

Normal CPP

A

60-80

min 60 needed to maintain cerebral perfusion

36
Q

At what map does cerebral autoregulation fail?

A

map <60 or >150

37
Q

Target MAP for ICP

A

90

38
Q

Normal ICP

A

5-15
max <20

39
Q

How does fever affect metabolism?

A

an increase of one degree increases O2 demand by 6-10%

40
Q

ICP components

A

brain 80%
blood 10%
CSF 10%

brain can compensate for increased ICP by causing cerebral vasoconstriction and increasing CSF absorption

41
Q

S/S of increased ICP

A

change in LOC
loss of detail/orientation
forgetfulness
restlessness (hypercapnia, acidosis, hypoxia)
sudden quietness
pupillary changes (sluggish, fixed + dilated = BAD)
motor changes

42
Q

How long does it take for brain cells to die without perfusion?

A

4-6 minutes

43
Q

Types of cerebral edema

A

vasogenic
cytotoxic
interstitialV

44
Q

Vasogenic edema

A

caused by inflammation + disruption of blood brain barrier
vasodilation + increased vascular permeability = fluid + proteins move into tissue

45
Q

Cytotoxic edema

A

damage to cells/loss of ATP
malfunction of Na/K pump
increase in intracellular sodium = water moves in = intracellular edema

46
Q

Factors causing increased ICP

A

hypercapnia
hypoxia
acidosis
hyperglycemia
temperature
loss of autoregulation (MAP <60 or >150)
impaired venous outflow (neck flexion)
anemia

47
Q

Interventions for ICP

A

airway –> intubate if necessary
ATP –> adequate glucose (NG feed, SLP ax for dysphagia)
blood pressure –> maintain adequate MAP (IV fluids, pressors, inotropes, beta blockers)
cervical collar –> if c-spine injury suspected (can inhibit venous outflow)
calm environment –> decrease stress/stimuli
gastric decompression –> improve intraabdo/intrathoracic pressure to promote breathing
dim the lights
HOB 30 degrees, neck in neutral alignment, avoid flexion
therapeutic hyperventilation (blow off CO2 to prevent acidosis)
hypertonic IV fluids (mannitol)
avoid hyperthermia
avoid hip flexion –> increases ICP by changing intraabdo pressure
surgical –> resection, CSF drainage with catheter
IV steroids –> for brain tumors
hypertonic normal saline
barbiturate coma –> refractory ICP
sedation = decrease O2 demand
neuromuscular blocking agents = decrease peripheral O2 consumption

48
Q

Adverse fx of mannitol

A

hyperglycemia
decreased hematocrit + blood viscosity
dehydration
fluid overload
hypo/hyper natremia or kalemia
can cross BBB –> vasogenic edema

49
Q

Jugular vein anatomy

A

does not have veins
fluid moves from areas of high to low pressure
drainage facilitated by gravity

50
Q

Interstitial edema

A

CSF leaks from ventricles into interstitial tissue
*occurs in meningitis

51
Q

Anticoagulant reversal agents:

A

warfarin: PCC (blood infusion), Vitamin K
DOAC: none in canada
heparin/LWMH: protamine sulfate

52
Q

Hypoxia

A

poor oxygenation of tissue with normal blood flow
low arterial oxygen content

53
Q

Ischemia

A

decreased/interrupted blood flow –> poor oxygenation

54
Q

Water shed areas

A

areas of the brain that lie between border zones
not supplied by major arteries
vulnerable to ischemia

55
Q

Etiology of vasogenic edema

A

vasogenic edema = disrupted BBB
hemorrhage
brain injury
infection

56
Q

Etiology of cytotoxic edema

A

cytotoxic edema = intracellular swelling
hypoosmotic state (hyponatremia, water intoxication)
failure of Na/K pump (ischemia, low ATP)

57
Q

LOC continuum

A

alert
confusion
lethargy
obtunded
stupor
coma

58
Q

Hydrocephalus

A

increase in ventricles d/t increase in CSF
1) overproduction of CSF
2) impaired reabsorption
3) obstruction

59
Q

Traumatic Brain Injury

A

caused by a/d forces
brain makes contact with skull –> damage to tissue, hematoma, contusions

60
Q

Brain contusion

A

bruising of brain surface
lacerations
tearing of brain tissue

61
Q

Brain hematoma

A

vascular injury/bleeding
location can be:
epidural (arterial)
subdural
subarachnoid (intracerebral)

62
Q

Concussion

A

transient neurological dysfunction caused by mechanical injury to brain
may have temporary loss of consciousness or amnesia
brain imaging negative
usually recovers within 24 hours
side fx can last months

63
Q

Types of stroke

A

ischemic (>80%)
hemorrhagic (AV malformation, ruptured aneurysm, spontaneous bleed)

64
Q

Ischemic stroke treatment

A

tPA within 3 hours
thrombectomy

65
Q

Contraindications to tPA

A

BP >185/110
bleeding RF (genetic dx, low platelets, prolonged clotting times)
>3 hours
hx of stroke/head injury within last 3 months
hx of recent GI/GU bleed in last 21 days
hemorrhagic stroke
oral anticoagulants
major surgery last 14 days
active internal bleed

66
Q

Medications that increase ICP + catecholaminse

A

nifedipine
nitric oxide
nitroprusside

67
Q

Medications to treat BP in ICP

A

beta-blockers
a-receptor antagonists

68
Q

VAN (stroke sequelae)

A

vision (hemiparesis)
aphasia
neglect (touch pt bilaterally, they cannot detect sensation on one side)

69
Q

How quickly should you drop BP during a stroke

A

15-25% in first 24 hours