CNS Flashcards

(96 cards)

1
Q

two mechanisms of brain death

A

anaerobic metabolism

deterioration of ion gradients

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2
Q

critical factor in determining neuronal cell fate

A

ATP depletion

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3
Q

if we decrease blood flow to the brain

A

we decrease washout of waste products

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4
Q

causes K+ to leave the cell and Na+, Cl+, and Ca++ to come in

A

Anoxic depolarization

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5
Q

NT important in learning/memory

A

glutamate

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6
Q

Excititatoy NT, binds with NMDA receptor to allow Ca++ to flow into cell

A

Glumamate

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7
Q

Excessive glumamate release with ____________

A

impaired membrane integrity

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8
Q

Glutamate reuptake is dependent on ____________. When repute fails glutamates now _____________.

A

ATP

Excitotoxic

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9
Q

Excess glutamate release and Open NMDA receptors leads to

A

Calcium overload

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10
Q

ca++ overload and swell in

A

cytotoxic edema and swelling

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11
Q

NMDA receptor activation and calcium overload stimulates nitrous oxide production and body cannot clear

A

reactive nitrogen species

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12
Q

lipid peroxidation causes

A

injury to the cell membrane and inflammatory response

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13
Q

formation of arachidonic acid leads to MORE free radials and inflammatory mediators

A

lipid peroxidation

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14
Q

Work- stimulates to bring in new bold flow and carry out wast products

A

metabolic vasodilation

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15
Q

influenced by pH, CO2 and O2

A

metabolic vazodilation

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16
Q

cases hyper perfusion and edema

A

impaired vasoconstriction

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17
Q

Normal ICP

A

0-15

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18
Q

can occur with vasogenic or cytotoxic (glutamate or Ca++) edema, space occupying lesions, or obstruction/excess production CSF

A

increased ICP

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19
Q

cytotoxic edema

A

increased brain TISSUE volume

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20
Q

Vasogenic Edema

A

Increased brain TISSUE volume

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21
Q

Ischemia and Necrosis

A

Increased brain TISSUE volume

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22
Q

obstructive and non-obstructie hydrocephalus

A

Increase CSF volume

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23
Q

Acidosis

A

Increased BLOOD volume

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24
Q

High arterial PaCO2

A

Increased BLOOD volume

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25
papilledema
edema of the optic disc r/t increased ICP
26
protrusion of brain through an opening on the supporting dura of the brain
herneation
27
herniation of tentorum cerebeli
transtentorial herniation
28
herniation around falx cerebri
subfalcine herniation
29
dependent on the reticular activating system (RAS)
Level of conciousness
30
responsible for sleep wake transitions and arousal
RAS
31
Pupil reflex, change in size, shape and reactivity
CN II and III
32
Eye movements controlled by
CN 3,4,6
33
oculovestibular reflex: rotate head side to side normally turn eyes to opposite direction of head rotation
Dolls eyes maneuver Positive if eyes do not rotate in the opposite directions
34
oculovestibular reflex: inject cold water into ear
cold calorics tonic deviation of both eyes toward the irrigated side
35
wisp of cotton touches cornea to illicit a blink response absent in severely impaired brain function
corneal reflex
36
Hypothermia used to
decrease brain metabolism, decreases workload and save 02 for the cells that need it
37
Why do we want CPP >60?
Proper oxygenation and CLEARANCE of waste products
38
fever, seizures, agitation and pain
increase brain metabolism
39
focal TBI
Coup - primary area of insult
40
Polar
Conta coup, acceleration/deceleraton
41
Diffuse
global axonal injuy to brain, movement of brain in scull "shearing"
42
above dura mater
epidural
43
below dura and above arachnoid space
subdural
44
below arachnoid space
subarachnoid
45
alteration or loss of consciousness without any evidence of brain damage on CT
Concussion
46
necrosis, laceration or bruising
Contusion
47
collection of blood
Intercranial hematoma
48
arterial lucid interval
epidural hematoma
49
bridging veins symptoms 2-10 days later,
subdural hematoma
50
bridging veins rupture of cerebral aneurism, AVM
subarachnoid hematoma
51
blood spreads throughout CSF causing meningeal irritation, hydrocephalus, headache, vasospasms and ischemia
subarachnoid hematoma
52
Why do we want to maintain normal PaCO2
to keep blood supply normal and not increase ICP
53
sudden onset of neurologic dysfunction that leads to area of brain infarction
Stroke
54
Most common form of stroke
Ischemic
55
Sudden occlusion of cerebral artery SECONDARY to thrombus formation or emboli
ischemic stroke
56
atherosclerosis and coagulopathies
thrombotic stroke
57
cardiac dysfunction or dysrhythmias
embolic stroke
58
contralateral hemiplegia, hemisensory loss, contralateral visual field blindness
Ischemic stroke
59
Aim of early thrombolytic therapy
salvaging penumbra
60
if neurologic deficits completely resolve
TIA
61
TIA warning sign for
thrombotic disease that may carry a risk for ischemic stroke-
62
preventative for thrombolytic (ischemic) stroke
ASA, carotid endarterectomy, angioplasty if 70% occluded
63
brain parenchyma (functional tissue of brain)
hemorrhagic stroke
64
secondary to chronic HTN
hemorrhagic stroke
65
morbidity and mortality much hight
hemorrhagic stroke
66
Tx for Hemmorhagic stroke
CV stabilization, BP management, keep mildly hypertensive at first
67
Tx for ischemic stroke
thrombolytics, andticoagulants, antiplatelet, enarterectomy, angioplasty, stents
68
total blindnes to right eye
d/t complete vision of right optic nerve
69
bipolar hemianopia
midline chiasmal lesion
70
right nasal hemianopia
lesion of right peichiasmal area
71
left homonymous hemianopia
lesion or pressure on right optic tract
72
brain damage to DOMINANT cerebral hemisphere
Aphasia
73
poor articulation and sparse vocabulary
Broca'a Aphasia
74
impaired AUDITORY comprehension and speech that is fluent but dost make sense
Wernike Aphasia
75
Most common cause of subarachnoid hemorrhage
cerebral aneurisms and AVM's
76
Marfans
week medial layer of artery
77
four key points with aneurisms
1. weakened MEDIAL layer of artery- commonly congenital 2. happens at areas of BIFURCATION 3. Sudden/ severe HA 4. Meningisus Triad
78
Meninngismus Triad
Photophobia, NV, Stiff neck
79
most commonly found in circle of willis
saccular / berry aneurisms
80
vasospasm managed by keeping blood volume and pressure at NORMAL TO HIGH levels Ca++ Channel Blockers
Aneurisms
81
Failure of capillary system to develop arterial blood shunted venous system progressively enlarges r/t high pressure SEIURES/ nerologic dysfunction
AVM
82
surgical removal, gamma knife, streotactic radiosurgery, irradiation, glue embolism
AVM
83
commonly associated with bacterial infections
meningitis
84
usually viral
encephalitis
85
nasopharynx entry point
meningitis
86
secondary problem = accumulation of neutrophils and degranulation
Meningitis -
87
destroys brain tissue, bacteria, nerves and blood vessels
NEUTROPHILS degranulation
88
LP - neutrophils, LOW glucose, bacteria, protein ELEVATED
Meningitis
89
NEUTROPHILS cause vasculitis and clotting leading to cerebral infarcts
meningitis
90
respiratory tracts, GI tract, inoculation by insects and animal bites such as rabies
entry point fro encephalitis
91
attacks arachnid membrane and CSF
encephalitis
92
CYTOKINES and MACROPHAGES cause vascular and tissue injury cells and blood vessels
encephalitis
93
pus with neutrophils and pyogenic bacteria
brain abcess
94
infected core of NEUTROPHIL and TISSUE DEBRIS
brain abcess
95
PERIFOCAL edema with proliferation of ASTROCYTES
brain abcess
96
LIQIFIED core and fibrous gliosis(dark ring)
brain abcess