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APEX > Unit 7 - Neuro - Brain > Flashcards

Unit 7 - Neuro - Brain Flashcards

1
Q

list 4 types of cells in CNS

A

astrocytes
ependymal cells
oligodendrocytes
microglia

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2
Q

what type of CNS cell is most prone to brain tumors

A

glial

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3
Q

function of dendrites

A

receive & process signal

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4
Q

function of soma

A

integrates signal

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5
Q

function of axon

A

send signal

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6
Q

function of presynaptic terminal

A

releases NTs

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7
Q

what is the “nerve glue” that supports neural function

A

glial cells

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8
Q

4 functions of glial cells

A
  • Create a healthy ionic environment
  • Modulate nerve conduction
  • Control reuptake of neurotransmitters
  • Repair neurons following neuronal
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9
Q

3 types of neurons in CNS

A
  • Multipolar
  • Pseudounipolar
  • Bipolar
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10
Q

what type of neurons are most CNS neurons

A

multipolar

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11
Q

where are pseudounipolar CNS neurons found

A

dorsal root ganglion & cranial ganglion

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12
Q

where are bipolar CNS neurons found

A

retina
ear

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13
Q

most abundant type of glial cell

A

astrocytes

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14
Q

where are ependymal cells concentrated

A

in 3rd & 4th ventricles + spinal canal

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15
Q

cells from choroid plexus, which produces CSF

A

ependymal cells

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16
Q

glial cells that form myelin sheath in CNS

A

Oligodendrocytes

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17
Q

CNS cells that act as macrophages and phagocytize neuronal debris

A

microglia

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18
Q

type of glial cell that regulates metabolic environment

A

astrocytes

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19
Q

type of glial cell that repairs neuron after neuronal injury

A

astrocytes

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20
Q

2 major structures of diencephalon

A

thalamus
hypothalamus

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21
Q

3 anatomic structures of brainstem

A

midbrain
pons
medulla oblongata

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22
Q

where is the RAS located

A

brainstem

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23
Q

4 brain areas

A

cerebral hemispheres, diencephalon, brainstem, cerebellum

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24
Q

connects 2 cerebral hemispheres

A

Corpus callosum

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25
Q

where is corpus collosum located

A

deep in longitudinal fissure

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26
Q

lobe that contains motor cortex

A

frontal

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27
Q

lobe that contains somatic sensory cortex

A

parietal

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28
Q

lobe that contains vision cortex

A

occipital

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29
Q

lobe that contains auditory cortex & speech centers

A

temporal

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30
Q

Wernicke’s area

A

understanding speech

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31
Q

Wernicke’s area

A

understanding speech

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32
Q

Broca’s area

A

motor control of speech

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33
Q

where is broca’s area

A

in frontal lobe, connected to Wernicke’s via neural pathways

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34
Q

functions of cerebral cortex

A
  • cognition, movement (precentral gyrus of frontal lobe)
  • sensation (postcentral gyrus of parietal lobe)
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35
Q

functions of hippocampus

A

memory and learning

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36
Q

functions of hippocampus

A

memory and learning

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37
Q

responsible for emotion, appetite, responds to pain and stressors

A

amygdala

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38
Q

responsible for fine control of movement

A

Basal ganglia

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39
Q

acts as a relay station that directs information to various cortical structures

A

thalamus

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40
Q

primary neurohumoral organ

A

hypothalamus

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41
Q

part of brainstem responsible for autonomic integration

A

medulla

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42
Q

3 parts of cerebellum

A
  • Archicerebellum
  • Paleocerebellum
  • Neocerebellum
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43
Q

part of cerebellum that maintains equilibrium

A

Archicerebellum

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44
Q

part of cerebellum that regulates muscle tone

A

Paleocerebellum

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45
Q

part of cerebellum that coordinates voluntary muscle movement

A

Neocerebellum

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46
Q

function of CN 3

A

oculomotor
eye movement, pupil constriction

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47
Q

CN innvervation of eye muscles

A

CN 3:
* inferior oblique (extorsion-elevation)
* superior rectus (supraduction)
* medial rectus (adduction)
* inferior rectus (infraduction)

CN 4:
* superior oblique (intorsion-depressioN)

CN 6:
* lateral rectus (abduction)

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48
Q

branches & functions of CN 5

A

V1 = opthalamic (somatic sensation to face)
V2 = maxillary (somatic sensation to anterior 2/3 tongue)
V3 = mandibular (muscles of mastication)

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49
Q

branches of facial n.

A

temporal
zygomatic
buccal
mandibular
cervical

Two Zebras Bit My Carrot

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50
Q

functions of facial nerve

A
  • facial movement (except mastication)
  • eyelid closing
  • taste to anterior 2/3 tongue
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51
Q

sensory function of CN 9

A

somatic sensation to posterior 1/3 tongue

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52
Q

CN responsible for swallowing

A

vagus

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53
Q

CN responsible for 70% of all PNS activity

A

CN 10

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54
Q

all CN are part of peripheral nervous system except:

A

CN 2

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55
Q

only CN surrounded by dura

A

CN 2

optic n.

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56
Q

what is Tic douloreaux

A

trigeminal neuralgia
generates excruciating neuropathic facial pain

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57
Q

s/s injury to facial n.

A

bell’s palsy = unilateral facial paralysis

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58
Q

locations of CSF

A
  • ventricles (L lateral, R lateral, 3rd, 4th)
  • cisterns around brain
  • subarachnoid space in brain and spinal cord
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59
Q

CSF volume

A

~150 mL

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60
Q

produces CSF

A

ependymal cells of choroid plexus in cerebral ventricles (30 mL/hr)

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61
Q

normal CSF pressure

A

5-15 mmHg

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62
Q

reabsorbs CSF

A

arachnoid villi in superior sagittal sinus

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63
Q

what is CSF absorption via arachnoid villi dependent on

A

pressure gradient between CSF and venous circulation

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64
Q

separates CSF from plasma

A

Blood brain barrier

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65
Q

causes BBB to become dysfunctional

A

sites of tumor, injury, infection, or ischemia

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66
Q

places BBB is not present

A
  • CTZ
  • posterior pituitary gland
  • pineal gland
  • choroid plexus
  • parts of hypothalamus
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67
Q

how can some drugs that can’t pass BBB cause N/V?

A

absence of BBB at CTZ

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68
Q

normal CSF flow

A

lateral ventricles - foramen of Monro - 3rd ventricle - Aqueduct of Sylvius - 4th ventricle - Foramen of Luschka - Foramen of Magendie - subarachnoid space - superior sagittal sinus (site of reabsorption)

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69
Q

composition of CSF

A
  • Isotonic with plasma, but not an ultrafiltrate of plasma
  • Osmolarity = 295 mOsm/L
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70
Q

similarities & differences in composition of CSF vs. plasma

A
  • Similarities: Na+ level, HCO3, PaCO2
  • Differences: K+, pH, glucose, protein
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71
Q

most common type of hydrocephalus

A

Obstructive

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72
Q

cause of communicating hydrocephalus

A

decreased CSF absorption by arachnoid villi (ex. intracranial hemorrhage)

or overproduction of CSF (very rare)

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73
Q

what is cerebral autoregulation

A

brain’s ability to maintain a constant cerebral blood flow over a wide range of mean arterial blood pressures

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74
Q

cerebral blood flow =

A

cerebral perfusion pressure / cerebral vascular resistance

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75
Q

normal global CBF

A

45-55 mL/100g tissue/min
or 15% CO

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76
Q

normal cortical CBF

A

75-80 mL/100g tissue/min

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77
Q

normal subcortical CBF

A

20 mL/100g tissue/min

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78
Q

CBF assoc. with evidence of ischemia

A

CBF ~ 20 mL/100g tissue/min

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79
Q

CBF assoc. with complete cortical suppression

A

CBF ~ 15 mL/100g tissue/min

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80
Q

CBF assoc. with membrane failure & cell death

A

CBF < 15 mL/100g tissue/min

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81
Q

normal CMRO2

A

3.0 – 3.8 mL/O2/100g brain tissue/min

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82
Q

5 Determinants of Cerebral Blood Flow

A
  1. Cerebral metabolic rate for oxygen
  2. Cerebral perfusion pressure
  3. PaCO2
  4. PaO2
  5. Venous pressure
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83
Q

O2 utilization by the brain

A

60% for electrical activity
40% for cellular integrity

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84
Q

decreasing CMRO2

A

Hypothermia
Halogenated anesthetics
Propofol
Etomidate
Barbiturates

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85
Q

increasing CMRO2

A

Hyperthermia
Seizures
Ketamine
N2O

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86
Q

why do volatiles increase CBF but decrease CMRO2

A

Volatiles uncouple CBF from CRMRO2

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87
Q

improves outcomes after out-of-hospital V-fib and resuscitation

A

Mild hypothermia (32-34°C) for 12-24 hours

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88
Q

CPP =

A

MAP - ICP (or CVP, whicever is higher)

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89
Q

Brain autoregulates CBF between :

A

CPP of 50-150 mmHg or MAP 60-160 mmHg

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90
Q

Brain autoregulates CBF between :

A

CPP of 50-150 mmHg or MAP 60-160 mmHg

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91
Q

O2 utilization by the brain

A

60% for electrical activity
40% for cellular integrity

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92
Q

CMRO2 decrease with hypothermia

A

↓ by 7% for every 1°C decrease in temp

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93
Q

temp assoc with EEG suppression

A

18-20°C

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94
Q

negative effects assoc with temp > 42°C

A
  • denatures protein
  • destroys neurons
  • ↓ CBF
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95
Q

why does CPP become dependent on MAP when above upper or lower limit of autoregulation

A

veins either maximally dilated (below lower limit) or maximally constricted (above upper limit)

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96
Q

MAP to ensure CPP 50

A

MAP 55-65 mmHg if ICP is normal (5-15)

higher ICP requires higher MAP to maintain CPP

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97
Q

normal controls of cerebral autoregulation

A
  • products of local metabolism
  • myogenic mechanics
  • autonomic innervation
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98
Q

3 things that decrease effectiveness of cerebral autoregulation

A
  1. brain tumor
  2. head trauma
  3. volatiles
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99
Q

contemporary model of chronic HTN and cerebral autoregulation

A
  • Suggests plateau of curve narrows and CBF becomes more closely dependent on CPP
  • Likely a high degree of patient-to-patient variability
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100
Q

traditional model of chronic HTN and cerebral autoregulation

A
  • Chronic HTN shifts entire curve to the right
  • Brain becomes more tolerant of HTN and less tolerant of hypotension
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101
Q

at a PaCO2 of 40, global CBF is:

A

50 mL/100g brain tissue/min

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102
Q

For every 1 mmHg increase in PaCO2, CBF will increase by:

A

1-2 mL/100g brain tissue/min

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103
Q

For every 1 mmHg decrease in PaCO2, CBF will decrease by

A

1-2 mL/100g brain tissue/min

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104
Q

maximal vasodilation occurs at PaO2 of:

A

80-100 mmHg

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105
Q

Maximal vasoconstriction occurs at PaCO2 of:

A

~ 25 mmHg

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106
Q

how is cerebral vascular resistance controlled

A

The pH of the CSF & arterioles controls

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107
Q

how does respiratory acidosis affect CBF

A

increases CBF

↓ CSF pH (↑ PaCO2) = ↓ CVR = ↑ CBF

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108
Q

how does respiratory alkalosis affect CBF

A

decreases CBF
↑ CSF (↓ PaCO2) = ↑ CVR = ↓ CBF

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109
Q

how does metabolic acidosis affect CBF

A

doesn’t directly affect CBF (H+ in blood doesn’t pass BBB)

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110
Q

what causes the “steal” phenomena

A

cerebral vessels that supply ischemic/atherosclerotic vessels are maximally dilated

situations causing vasodilation dilate vessels that supply healthy brain tissue and “steal” flow from ischemic areas

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111
Q

what is the Robinhood effect

A
  • Concept of using hyperventilation to constrict cerebral vessels that supply healthy brain tissue
  • Idea is that flow will be redistributed to ischemic regions, which are maximally dilated
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112
Q

how can the Robinhood effect cause harm

A

from cerebral ischemia (not enough CBF) and shifting oxyhgb dissociation curve to the left

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113
Q

how does PaO2 < 50-60 affect CBF

A

causes cerebral vasodilation, increases CBF

114
Q

when PaO2 > _ , CBF is unaffected

A

60

115
Q

Conditions that impair venous drainage:

A
  • Jugular compression due to improper head positioning (ex. head flexion when sitting)
  • Increased intrathoracic pressure 2/2 coughing or PEEP
  • Vena cava thrombosis
  • Vena cava syndrome
116
Q

cerebral HTN

A

ICP > 20 mmHg

117
Q

S/S intracranial HTN

A
  • headache
  • N/V
  • papilledema
  • pupil dilation and non-reactivity to light
  • focal neurological deficit
  • seizure
  • coma
118
Q

Monroe-Kellie hypothesis

A

describes pressure-volume equilibrium between brain, blood, & CSF within the confines of the cranium

Increase in one component must be countered with a decrease in one or bo

119
Q

Monroe-Kellie hypothesis

A

describes pressure-volume equilibrium between brain, blood, & CSF within the confines of the cranium

Increase in one component must be countered with a decrease in one or bo

120
Q

brain causes of increased CBV

A
  • cerebral swelling
  • tumor
121
Q

blood causes of increased CBV

A
  • increased CBF
  • bleeding
122
Q

CSF causes of increased CBV

A
  • increased CSF produciton by choroid plexus
  • reduced CSF removal by arachnoid villi
  • obstruction to reabsorption
  • passage of fluid across BBB
123
Q

Cushing’s triad

A

HTN, bradycardia, irregular respirations

124
Q

what causes irregular respirations with inc ICP

A

Compression of medulla

125
Q

most common site of herniation

A

temporal uncus

126
Q

what causes fixed/dilated pupils with temporal uncus herniation

A

CN 3 originates from midbrain, crosses near tentorium

herniation applies pressure to the nerve, making it ischemic

127
Q

what is Pseudotumor Cerebri

A

idiopathic intracranial HTN

condition where ICP increases for no apparent reason (“false tumor”)

128
Q

what is papilledema

A

swelling of optic n./

129
Q

2 methods to decrease CBV

A
  1. decrease CBF
  2. increase venous outflow
130
Q

2 methods to decrease CSF

A
  1. CSF drainage
  2. drugs
131
Q

2 methods to decrease cerebellar mass

A
  1. tumor debulking
  2. diuretics
132
Q

2 methods to decrease cerebral edema

A
  1. diuretics
  2. corticosteroids
133
Q

how does hyperventilation decrease CBF

A

Mild hyperventilation (30-35) constricts vessels = ↑ CVR = ↓ CBF= ↓ ICP

134
Q

PaO2 < ____ increases risk of cerebral ischemia

A

30

135
Q

how long do the decreased CBF effects of mild hyperventilation last

A

6-20 hours

(pH of CSF equilibrates with PaCO2)

136
Q

how long do the decreased CBF effects of mild hyperventilation last

A

6-20 hours

(pH of CSF equilibrates with PaCO2)

137
Q

PaO2 < ____ greatly increases CBF and ICP

A

50-60

138
Q

drugs to avoid when trying to decrease CBF

A

vasodilators - NTG, Nipride

139
Q

positioning that facilitates venous drainage from brain

A

Head elevation > 30 °

140
Q

positioning that can increase ICP

A
  • Neck flexion or extension (can compress jugular veins)
  • Trendelenburg
141
Q

how can PEEP affect ICP

A

PEEP = ↑ intrathoracic pressure = ↓ venous drainage from brain (can ↑ ICP)

142
Q

when is CSF drainage the most useful treatment of increased ICP

A

obstruction to CSF flow (hydrocephalus)

143
Q

drugs that decrease CSF production

A

Acetazolamide & furosemide

144
Q

where does arterial bleeding in the brain most commonly occur

A

subarachnoid space
(between arachnoid and pia mater)

145
Q

where does venous bleeding in the brain usually occur

A

subdural space
between dura and arachnoid mater

146
Q

what forms myelin sheath in PNS

A

Schwann cells

147
Q

3 meningeal layers covering brain and spinal cord

A
  1. dura mater
  2. arachnoid mater
  3. pia mater
148
Q

3 meningeal layers covering brain and spinal cord

A
  1. dura mater
  2. arachnoid mater
  3. pia mater
149
Q

glial cells that increase neuronal conduction velocity

A

oligodendrocytes

150
Q

CN most likely to be compressed by pituitary tumor

A

CN 2

151
Q

where is CSF produced

A

choroid plexus

152
Q
A
153
Q

fixed/dilated pupil suggests herniation of:

A

temporal uncus

154
Q

main blood supply to brain’s posterior circulation

A

basilar artery (only 1)

155
Q

gives rise to paired posterior communicating arteries

A

basilar artery

156
Q

gives rise to paired vertebral arteries

A

subclavian arteries

157
Q

gives rise to paired middle cerebral arteries

A

internal carotids

158
Q

anticonvulsant that is excreted unchanged by kidneys

A

gabapentin

159
Q

methods to decrease cerebral mass with increased ICP

A

tumor debulking
evacuation of hematoma
mannitol

160
Q

how do loop diuretics decrease cerebral edema

A

inducing diuresis and increasing rate of CSF production

161
Q

how do osmotic diuretics reduce cerebral edema

A

by increasing serum osmolarity and “pulling” water across BBB

0.25-1 g/kg mannitol

162
Q

dose of mannitol to decrease cerebral edema

A

0.25-1 g/kg

163
Q

how does 3% NaCl affect cerebral edema

A

high tonicity decreases cerebral edema by “pulling” water across BBB

164
Q

downside of using mannitol for decreasing cerebral edema

A

transiently increases blood volume
can increase ICP and stress failing heart

165
Q

use of steroids in cerebral edema

A

decadron & methylpred decrease cerebral edema from mass lesions & spinal cord injuries
should NOT be used with TBI or funcitonal pituitary adenoma

166
Q

methods to decrease CBV

A
  • propofol
  • hyperventilation
  • maintain neck neutrality
  • HOB elevated
167
Q

methods to derease CSF

A

VP shunt
acetelazomide
interventricular drain

168
Q

decreased cerebral mass/edema

A

corticosteroids
debulking
mannitol

169
Q

what med should be used to support CPP with increased ICP

A

phenylephrine

170
Q

why should dextrose solutions be avoidd

A
171
Q

why should dextrose solutions be avoided in cases of increased ICP/head injury

A

in the setting of cerebral ischemia, excess glucose in brain is converted to lactic acid & worsens outcomes

172
Q
A
173
Q

supplies anterior circulation to the brain

A

internal carotids

174
Q

where do internal carotids enter skull

A

foramen lacerum

175
Q

anterior cerebral circulation flow

A

Aorta - carotid - internal carotid - circle of Willis - cerebral hemispheres

176
Q

what supplies posterior cerebral circulation

A

vertebral arteries

177
Q

main supply of posterior cerebral circulation

A

basilar artery (only 1)

178
Q

posterior cerebral circulation flow

A

aorta - subclavian a. - vertebral a. - basilar a - posterior fossa structures and cervical spinal cord

179
Q

primary function of circle of Willis

A

provide redundancy of blood flow in the brain

180
Q

how does venous blood from cerebral cortex & cerebellum drain

A

via superior sagittal sinus & dural sinuses

181
Q

how does venous blood from basal brain structures drain

A

via inferior sagittal sinus, the vein of Galen, and straight sinuses

182
Q

where do venous cerebral pathways converge

A

confluence of sinuses

183
Q

how does venous blood exit the brain

A

all exits via paired jugular veins

184
Q

Most common type of CVA

A

ischemic

185
Q

most likely cause of ischemic CVA

A

cardio-embolic event like A-fib

186
Q

A person who exhibits a sudden change in neurologic function or progressive change in neuro status is most likely experiencing a ?

A

CVA

187
Q

what is a TIA

A

focal neuro deficit that spontaneously resolves within 24 hours

warning sign of cerebrovascular disease, impending stroke

188
Q

what is a TIA

A

focal neuro deficit that spontaneously resolves within 24 hours

warning sign of cerebrovascular disease, impending stroke

189
Q

ischemic stroke risk factors

A
  • HTN (most important)
  • smoking
  • DM
  • HLD
  • excessive ETOH
  • ↑ homocysteine level
190
Q

treatment for stroke symptoms after hemorrhage ruled out

A
  • 1st line: aspirin
  • IV thrombolytic within 4.5 hours of stmprom onset
191
Q

when should patients undergo embolectomy

A

pts with large vessel occlusion should undergo within 6 hours

192
Q

target BP after ischemic CVA

A

under 185/110

193
Q

purpose of fluid replacement with CVA

A

supports BP, CO, CPP, & improves CBF by ↓ viscosity

194
Q

why is blood sugar control important in CVA pts

A

during cerebral hypoxia, glucose is converted to lactic acid
cerebral acidosis destroys brain tisue

195
Q

most common cause of subarachnoid bleeding

A

aneurysm rupture

most from circle of Willis

196
Q

most common cause of subarachnoid bleeding

A

aneurysm rupture

most from circle of Willis

197
Q

transmural pressure =

A

MAP - ICP

198
Q

Most common sign of SAH

A

intense headache often described as “worst headache of my life”

Other s/s: focal neuro deficits, N/V, photophobia, fever, LOC ~50% of the time

199
Q

Most common sign of SAH

A

intense headache often described as “worst headache of my life”

Other s/s: focal neuro deficits, N/V, photophobia, fever, LOC ~50% of the time

200
Q

Most common sign of SAH

A

intense headache often described as “worst headache of my life”

Other s/s: focal neuro deficits, N/V, photophobia, fever, LOC ~50% of the time

201
Q

what causes meningismus in hemorrhagic stroke patients

A

blood spreads and irritates meninges

202
Q

Morbidity of hemorrhagic stroke results from:

A
  • obstructive hydrocephalus
  • rebleeding
  • vasospasm
203
Q

surgical options for hemorrhagic stroke

A

aneurysm clipping or endovascular coiling

204
Q

general intraop SBP goal in aneurysm clipping or endovascular coiling

A

120-150 mmHg

205
Q

when should surgical repair of hemorrhagic stroke take place

A

24-48 hours following initial bleed

Intervention at this time makes triple H therapy safer

206
Q

what should you do if aneurysm ruptures during coiling procedure and heparin has been given

A

immediately reverse with 1mg protamine for every 100 u heparin

207
Q

why is controlled hypotension not needed when clamp is used for hemorrhagic stroke

A

↓ transmural pressure and risk of rupture & eliminates need

High/normal BP required to perfuse collateral circulation

208
Q

why is controlled hypotension not needed when clamp is used for hemorrhagic stroke

A

↓ transmural pressure and risk of rupture & eliminates need

High/normal BP required to perfuse collateral circulation

209
Q

why is controlled hypotension not needed when clamp is used for hemorrhagic stroke

A

↓ transmural pressure and risk of rupture & eliminates need

High/normal BP required to perfuse collateral circulation

210
Q

Most significant drawback of controlled hypotension for cerebral aneurysm clipping

A

decreased CPP

211
Q

major cause of M&M in pts who have suffered SAH

A

Cerebral vasospasm

212
Q

what causes cerebral vasospasm after SAH

A

delayed contraction of cerebral arteries

Positive correlation between amount of blood on CT & incidence of spasm

213
Q

when is cerebral vasospasm most likely to occur with SAH

A

4-9 days after bleed

214
Q

methods to monitor for cerebral vasospasm after SAH

A

Frequent neuro checks and daily transcranial Dopplers

215
Q

Most common presentation of cerebral vasospasm

A

new neuro deficit, AMS

216
Q

Gold standard for cerebral vasospasm diagnosis

A

cerebral angiography

217
Q

BP goal for cerebral vasospasm treatment

A

increase MAP 20-30 mmHg above baseline

218
Q

Triple H Therapy

A
  • hypervolemia
  • HTN
  • hemodilution to Hct 27-32%
219
Q

only CCB to ↓ M&M from vasospasm

A

nimodipine

↑ collateral blood flow

220
Q

only CCB to ↓ M&M from vasospasm

A

nimodipine

↑ collateral blood flow

221
Q

treatment of medically-refractory cerebral vasospasm

A
  • intra-arterial vasodilators (verapamil, nicardipine), papaverine, milrinone
  • balloon angioplasty
222
Q

most common cause of hyponatremia with SAH

A

Cerebral Salt Wasting Syndrome

not SIADH

223
Q

most common cause of hyponatremia with SAH

A

Cerebral Salt Wasting Syndrome

not SIADH

224
Q

treatment for Cerebral Salt Wasting Syndrome

A

isotonic crystalloids

225
Q

Head CT probably not required if minor trauma +

A
  • No physical evidence of trauma above clavicles
  • No headache
  • No N/V
  • No neuro deficit
  • No impaired short-term memory
  • No intoxication
  • No seizures
  • Age < 60 years
226
Q

GCS: motor response

A

1 = no motor response
2 = abnormal extension to pain
3 = abnormal flexion to pain
4 = withdrawal to pain
5 = localizes pain
6 = obeys commands

227
Q

GCS: verbal Response

A

1 = no verbal response
2 = incomprehensible sounds
3 = inappropriate words
4 = confused
5 = oriented

228
Q

GCS: eye opening

A

1 = no eye opening
2 = eye opening to pain/pressure
3 = eye opening to sound
4 = opens spontaneously

229
Q

GCS: pupil reactivity

A

-2 = both NR to light
-1 = one NR to light
0 =PERRL

230
Q

how can warfarin be reversed

A
  • FFP
  • prothrombin complex concentrate
  • recombinant factor 7a
231
Q

how can Clopidogrel/aspirin be reversed

A
  • platelet transfusion
  • recombinant factor 7a
232
Q

CPP goal for TBI

A

> 70

233
Q

fluids to avoid in TBI

A
  • dextrose fluids
  • hypotonic solutions
  • albumin
234
Q

inhaled anesthetic to avoid with TBI

A

N2O

235
Q

sz activity localized to particular cortical region

A

Partial seizure

236
Q

Generalized seizure

A

activity affects both hemispheres

237
Q

Jacksonian march

A

partial seizure progresses to generalized seizure

238
Q

phases of grand mal sz

A

Tonic phase = whole body rigidity
Clonic phase = repetitive jerking motions

239
Q

types of seizures assoc with respiratory arrest

A

grand mal
status epilepticus

240
Q

Acute treatment of grand mal sz

A

propofol, diazepam, thiopental

241
Q

Surgical treatment of grand mal sz

A

vagal nerve stim, foci resection

242
Q

sz linked to particular cortical region

A

focal cortical

usually no LOC

243
Q

sz linked to particular cortical region

A

focal cortical

usually no LOC

244
Q

sz with temporary loss of awareness (remains awake)

A

Absence (Petit Mal)

245
Q

sz assoc. with temporary loss of consciousness & postural tone

A

Akinetic

246
Q

Status Epilepticus

A

Seizure activity > 30 min or 2 grand mal seizures without regaining consciousness in between

247
Q

treatment of Status Epilepticus

A

phenobarbital, thiopental, phenytoin, benzos, propofol, GA

248
Q

in adults, epilepsy usually results from 1 of what 2 things

A

1) structural brain lesion: tumor, head trauma, cerebrovascular event
2) metabolic cause: hypoglycemia, drug toxicity, withdrawal, infection

249
Q

how do inhaled anesthetics affect EEG activity

A

tend to ↓ EEG activity (dose-dependent) but all have been implicated in producing seizures (very rare)

250
Q

S/S seizures under GA

A

↑ HR, HTN, ↑ EtCO2

251
Q

IV anesthetic that can induce sz

A

ketamine

252
Q

EEG effects. of etomidate

A

commonly causes myoclonus - not assoc. with ↑ EEG activity in pts without epilepsy

253
Q

meds useful for cortical mapping in pts with sz disorders (increase EEG activity)

A
  1. methohexital
  2. etomidate
  3. alfentanil
254
Q

first-line agent for control of sz activity

A

propofol

255
Q

anticonvulsants assoc with NDNMB resistance

A
  • phenytoin
  • Carbamazepine
256
Q

anticonvulsant that undergoes zero order kinetics

A

Phenytoin

257
Q

SEs of phenytoin

A
  • dysrhythmias/hypotension (if IV rate > 50 mcg/min)
  • gingival hyperplasia
  • aplastic anemia, cerebellar-vestibular dysfunction (nystagmus, ataxia)
  • SJS
  • birth defects
258
Q

anticonvulsant assoc with purple glove syndrome

A

phenytoin

259
Q

anticonvulsant that slows phenytoin metabolism

A

valproic acid

260
Q

SEs of Valproic Acid

A
  • hepatotoxicity
  • thrombocytopenia
  • displaces phenytoin from plasma proteins
261
Q

SEs of Valproic Acid

A
  • hepatotoxicity
  • thrombocytopenia
  • displaces phenytoin from plasma proteins
262
Q

MOA of carbamazepine, phenytoin, and valproic acid

A

block voltage-gated Na+ channels
membrane stabilizer

263
Q

anticonvulsant useful for trigeminal neuralgia

A

Carbamazepine

264
Q

SEs of Carbamazepine

A
  • aplastic anemia
  • thrombocytopenia
  • liver dysfunction
  • leukopenia
  • hyponatremia (ADH-like effect)
265
Q

MOA of gabapentin

A

inhibition of alpha-2 delta subunit of voltage-gated Ca2+ channels in CNS

decreased excitatory NT release

Chemical analogue of GABA, NOT GABA agonist

266
Q

SEs of gabapentinoids

A

dizziness, somnolence

267
Q

why should gabapentin be tapered off

A

Abrupt withdrawal can produce sz if patient has hx sz

taper for at least 1 week

268
Q

why should gabapentin be tapered off

A

Abrupt withdrawal can produce sz if patient has hx sz

taper for at least 1 week

269
Q

why should gabapentin be tapered off

A

Abrupt withdrawal can produce sz if patient has hx sz

taper for at least 1 week

270
Q

most common cause of dementia in pts > 65

A

Alzheimer’s Disease

271
Q

key findings in alzheimers

A

beta amyloid rich plaques & neurofibrillary tangles in the brain

272
Q

consequences of amyloid plaque formation in Alzheimers

A
  • dysfunctional synaptic transmission (most noticeable with ACh)
  • apoptosis
273
Q

class of drugs used to treat Alzheimer’s & AIs of use

A

cholinesterase inhibitors
increase duration of succs (questionable significance)

274
Q

patho of Parkinson’s

A

dopaminergic neurons in basal ganglia destroyed

decreased dopamine + normal ACh = relative ACh increase

275
Q

what is suppressed vs overactive in parkinsons

A

corticospinal motor system suppressed
extrapyramidal motor system overactive

276
Q

what drugs increase extrapyramidal s/s in pt with parkinsons

A

dopamine antagonists
* Reglan
* haldol
* droperidol
* promethazine

277
Q

most common cause of POVL

A

ION

278
Q

patho of ION

A

optic nerve ischemia

likely r/t venous congestion

279
Q

procedural risk factors for ION

A
  • prone
  • wilson frame
  • long duration
  • large blood loss
  • low ratio colloid:crystalloid
  • hypotension
280
Q

pt risk factors for ION

A
  • male
  • obese
  • DM
  • HTN
  • smoking
  • old age
  • atherosclerosis

APEX (54 decks)

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