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Pathophysiology Spring 16 > CNS > Flashcards

CNS Flashcards

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
Q

papilledema

A

edema of the optic disc r/t increased ICP

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26
Q

protrusion of brain through an opening on the supporting dura of the brain

A

herneation

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27
Q

herniation of tentorum cerebeli

A

transtentorial herniation

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28
Q

herniation around falx cerebri

A

subfalcine herniation

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29
Q

dependent on the reticular activating system (RAS)

A

Level of conciousness

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30
Q

responsible for sleep wake transitions and arousal

A

RAS

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31
Q

Pupil reflex, change in size, shape and reactivity

A

CN II and III

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32
Q

Eye movements controlled by

A

CN 3,4,6

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33
Q

oculovestibular reflex:

rotate head side to side

normally turn eyes to opposite direction of head rotation

A

Dolls eyes maneuver

Positive if eyes do not rotate in the opposite directions

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34
Q

oculovestibular reflex:

inject cold water into ear

A

cold calorics

tonic deviation of both eyes toward the irrigated side

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35
Q

wisp of cotton touches cornea to illicit a blink response

absent in severely impaired brain function

A

corneal reflex

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36
Q

Hypothermia used to

A

decrease brain metabolism, decreases workload and save 02 for the cells that need it

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37
Q

Why do we want CPP >60?

A

Proper oxygenation and CLEARANCE of waste products

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38
Q

fever, seizures, agitation and pain

A

increase brain metabolism

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39
Q

focal TBI

A

Coup - primary area of insult

40
Q

Polar

A

Conta coup, acceleration/deceleraton

41
Q

Diffuse

A

global axonal injuy to brain, movement of brain in scull “shearing”

42
Q

above dura mater

43
Q

below dura and above arachnoid space

44
Q

below arachnoid space

A

subarachnoid

45
Q

alteration or loss of consciousness without any evidence of brain damage on CT

A

Concussion

46
Q

necrosis, laceration or bruising

47
Q

collection of blood

A

Intercranial hematoma

48
Q

arterial

lucid interval

A

epidural hematoma

49
Q

bridging veins

symptoms 2-10 days later,

A

subdural hematoma

50
Q

bridging veins

rupture of cerebral aneurism, AVM

A

subarachnoid hematoma

51
Q

blood spreads throughout CSF causing meningeal irritation, hydrocephalus, headache, vasospasms and ischemia

A

subarachnoid hematoma

52
Q

Why do we want to maintain normal PaCO2

A

to keep blood supply normal and not increase ICP

53
Q

sudden onset of neurologic dysfunction that leads to area of brain infarction

54
Q

Most common form of stroke

55
Q

Sudden occlusion of cerebral artery SECONDARY to thrombus formation or emboli

A

ischemic stroke

56
Q

atherosclerosis and coagulopathies

A

thrombotic stroke

57
Q

cardiac dysfunction or dysrhythmias

A

embolic stroke

58
Q

contralateral hemiplegia, hemisensory loss, contralateral visual field blindness

A

Ischemic stroke

59
Q

Aim of early thrombolytic therapy

A

salvaging penumbra

60
Q

if neurologic deficits completely resolve

61
Q

TIA warning sign for

A

thrombotic disease that may carry a risk for ischemic stroke-

62
Q

preventative for thrombolytic (ischemic) stroke

A

ASA, carotid endarterectomy, angioplasty if 70% occluded

63
Q

brain parenchyma (functional tissue of brain)

A

hemorrhagic stroke

64
Q

secondary to chronic HTN

A

hemorrhagic stroke

65
Q

morbidity and mortality much hight

A

hemorrhagic stroke

66
Q

Tx for Hemmorhagic stroke

A

CV stabilization, BP management, keep mildly hypertensive at first

67
Q

Tx for ischemic stroke

A

thrombolytics, andticoagulants, antiplatelet, enarterectomy, angioplasty, stents

68
Q

total blindnes to right eye

A

d/t complete vision of right optic nerve

69
Q

bipolar hemianopia

A

midline chiasmal lesion

70
Q

right nasal hemianopia

A

lesion of right peichiasmal area

71
Q

left homonymous hemianopia

A

lesion or pressure on right optic tract

72
Q

brain damage to DOMINANT cerebral hemisphere

73
Q

poor articulation and sparse vocabulary

A

Broca’a Aphasia

74
Q

impaired AUDITORY comprehension and speech that is fluent but dost make sense

A

Wernike Aphasia

75
Q

Most common cause of subarachnoid hemorrhage

A

cerebral aneurisms and AVM’s

76
Q

Marfans

A

week medial layer of artery

77
Q

four key points with aneurisms

A
  1. weakened MEDIAL layer of artery- commonly congenital
  2. happens at areas of BIFURCATION
  3. Sudden/ severe HA
  4. Meningisus Triad
78
Q

Meninngismus Triad

A

Photophobia, NV, Stiff neck

79
Q

most commonly found in circle of willis

A

saccular / berry aneurisms

80
Q

vasospasm managed by keeping blood volume and pressure at NORMAL TO HIGH levels

Ca++ Channel Blockers

81
Q

Failure of capillary system to develop

arterial blood shunted

venous system progressively enlarges r/t high pressure

SEIURES/ nerologic dysfunction

82
Q

surgical removal, gamma knife, streotactic radiosurgery, irradiation, glue embolism

83
Q

commonly associated with bacterial infections

A

meningitis

84
Q

usually viral

A

encephalitis

85
Q

nasopharynx entry point

A

meningitis

86
Q

secondary problem = accumulation of neutrophils and degranulation

A

Meningitis -

87
Q

destroys brain tissue, bacteria, nerves and blood vessels

A

NEUTROPHILS degranulation

88
Q

LP - neutrophils, LOW glucose, bacteria, protein ELEVATED

A

Meningitis

89
Q

NEUTROPHILS cause vasculitis and clotting leading to cerebral infarcts

A

meningitis

90
Q

respiratory tracts, GI tract, inoculation by insects and animal bites such as rabies

A

entry point fro encephalitis

91
Q

attacks arachnid membrane and CSF

A

encephalitis

92
Q

CYTOKINES and MACROPHAGES cause vascular and tissue injury cells and blood vessels

A

encephalitis

93
Q

pus with neutrophils and pyogenic bacteria

A

brain abcess

94
Q

infected core of NEUTROPHIL and TISSUE DEBRIS

A

brain abcess

95
Q

PERIFOCAL edema with proliferation of ASTROCYTES

A

brain abcess

96
Q

LIQIFIED core and fibrous gliosis(dark ring)

A

brain abcess

Pathophysiology Spring 16 (9 decks)

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