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ACE > ACE Review - Neuro > Flashcards

ACE Review - Neuro Flashcards

1
Q

Questions

A

Answers

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2
Q

does age increase risk of stroke for non neuro cases

A

yes, 62 or older

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3
Q

do heart problems increase risk of stroke for non neuro cases

A

yes, MI within 6 months

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4
Q

do kidney problems increase risk of stroke for non neuro cases

A

yes, hx of ckd or dialysis imply pt w vascular dz

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5
Q

do pt with pulm problems increase risk of stroke for non neuro cases

A

yes, copd and smoking increases risk

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6
Q

does obesity increase risk of stroke for non neuro cases

A

actually no, bmi higher decreases risk of stroke

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7
Q

who has a higher risk of stroke for non neuro cases. akd vs dialysis pt

A

acute kidney disease pt

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8
Q

what metabolic disease predisoe pt to periop stroke

A

htn

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9
Q

in pt with sub arach hemorrhage…what 3 things predict m&M

A

degree of bleed, action to correct bleed, presence of vasospasm

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10
Q

what is the greatest predictor of vasospasm in sub arch hemorrhage

A

the degree of bleeding

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11
Q

what is pseudotumor cerebri

A

it is increased ICP secondary to decreased resorption of csf

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12
Q

what anesthestic technique is contraindicated in pseudotumor cerebri

A

non

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13
Q

can spinals be done in psuedotumor cerebri

A

actually it is one of the treatments

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14
Q

who is at increased risk for recall under general anesthesia

A

patients with long history of substance abuse, alcohol use, chronic opiod/ benzo use,

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15
Q

why dose substance abuse have increased of recall

A

their cyp450 are increased and thus metabolism of anesthetic agents

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16
Q

what kind of surgeries predispose pt to recall

A

pt who cannot tolerate low bp or high anesthetics…like cardiac or c-section

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17
Q

how does neuromusclar blocking drugs increase rate of recall

A

bc monitoring movement under ga can help us indicate low anesthesia…paralysis prevents this assessment

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18
Q

what is core temperature

A

brain temperature

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19
Q

does measureing bladder temperature over or underestimate core temp

A

it underestimates core…core could actually be colder than what bladder temp shows

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20
Q

where can u measure core temp

A

distal esoph, pa cath, tympanic, nasopharynx

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21
Q

what does general anesthesia do to the threshold of thermoregulation

A

it decreases the threshold

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22
Q

does “decreasing” threshold for thermoregulation make sense?

A

yes it does…decreasing threshold means that the temperature at which shivering and other mechs for temp maintanence is dropped to a lower temp…thus you wont shiver until you are reallllly cold

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23
Q

by how much does GA decrease the threshold for thermogenesis

A

2-3 degrees celcius

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24
Q

is agitation post op considered post op delerium

A

yes…it is a hyperactive variant

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25
Q

Is agitation required for diagnosis of delerium

A

no

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26
Q

is depression a risk factor for postop delerium

A

yes

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27
Q

what kind of surgery has the highest risk for postop delerium

A

hip surgery

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28
Q

does post op delerium increase mortality

A

yes

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29
Q

most common risk factor for post op delerium

A

pre-existing cognitive dysfuction

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30
Q

what things can be done to prevent post op delerium

A

prevent hyothermia. And avoid certain drugs

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31
Q

what is the diagnosis of delerium

A

acute onset, flux in mental status, innattention, and disorganized thinking vs abnormal behavior

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32
Q

why are the hyoactive delerium patients higher chance of mortality than the hyperactive delerium variant

A

because diagnosis is more difficult to be made in the hypoactive delerium pt…so treatment is done later

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33
Q

during craniotomy, what angle puts the patient at risk for venous air embolism

A

angle greater or equal to 15 degrees

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34
Q

how dose cvp affect risk for venous air embolism

A

when cvp is low in pressure, higher chance to get Venous air embolism

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35
Q

what is the treatment for venous air embolism

A

multiorifice central cath

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36
Q

where should the multiorifice central cath be placed to get venous air emboism

A

at the svc and atrial junction

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37
Q

for neuro case, what is the most sensitive detector for venous air embolism

A

tee

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38
Q

for neuro case, what is the 2nd most sensitive detector of venous air embolis

A

precordial doppler

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39
Q

what do you hear on stethoscope when you have a venous air emboism

A

mill whill murmur

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40
Q

what is the first line treatment for venous air embolism

A

decrease head height, flood surgical field, apply bone wax, occlude the offending vessel

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41
Q

in a neurosurg pt that develops diabetes insipidus, what Is the most common lab

A

decreased urine specific gravity/hypOosmolar urine

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42
Q

what is the lab value in diabetes insipidus for Na and osmolarity

A

hypernatremia, hyperosmolar

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43
Q

how to treat diabetes insipidus

A

free water replacement slowly, vasopressin q4hrs till intranasal desmopressin can be used

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44
Q

how to decrease icp in a emergency neuro decompression case

A

increase rr to decrease co2, 1g/kg mannitol, head up,

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45
Q

can you repeat mannitol for further decrease in icp

A

most likely, serum osm increased already and wont aid any more…

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46
Q

what is risk for repeat mannitol

A

hyperkalemia

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47
Q

what is risk of further hyperventilation beyond etco25

A

this will not only decrease icp, it will put pt at risk for ischemia

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48
Q

if rr mannitol and head raise still not bring icp down, what other tx can be done to decrease icp

A

barbituate/propofol bolus, ventriculostomy

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49
Q

if pt has a lumbar drain in already for an emergency decompressive craniotomy, should you use it

A

not the best choice on multiple choice exam…it can be used, but too rapid drain may cause herniation

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50
Q

how does propofol and barbs cause decrease icp

A

since the brain is still coupled, decreasing the cmro2 will decrease o2 demand and thus decrease flow to the brain

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51
Q

what is adverse effect of prop and thiopental (barb) usage

A

it may decrease bp, aka map, aka cerebral perfusion pressure

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52
Q

what can be used other than prop or thiopental

A

etomidate which also decreases icp

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53
Q

what adverse effect dose using etomidate cause

A

it can actually cause hypertension and adrenal suppression

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54
Q

does GBS have decreased or hyper reflexia at dtr

A

decreased dtr

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55
Q

do gbs patients present with fever?

A

no…this is uncommon…fever usually means another diagnosis and not gbs

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56
Q

what is gbs

A

guillan barre syndrome - a autoimmune polyradiculopathy

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57
Q

how does gbs present

A

after 3 weeks of infxn, has symmetrical rapid progressive neuropathy/weakness

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58
Q

what are 2 common manifestations of gbs

A

decreased dtr and facial weakness

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59
Q

what labwork is done to test for gbs

A

csf shows high protien and normal wbc aka not infectious

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60
Q

how long does gbs last

A

days …up to 4 weeks

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61
Q

when do you see evelated protien in gbs pt

A

it may show up 2 weeks after onset of weakness

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62
Q

what usually precedes gbs weakness

A

diarrhea or uri

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63
Q

besides virus, what other things might cause onset of gbs

A

vaccinations for influenza, hepatitis, polio, and rabies

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64
Q

what is the most common symptom other than weakness found in gbs pts

A

pain!!! Occurs in 89% of pts

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65
Q

what is the cause for pain of gbs during the acute phase

A

the inflammation of nerves

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66
Q

what is the cause for pain of gbs during the late phase

A

regeneration of sensory nerves

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67
Q

pain treatment for gbs associated pain

A

carbamazepine, corticosteriods, gabapentin, opiods

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68
Q

does bowel constipation and urine incontinence present with gbs pt

A

no

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69
Q

what are the 3 phases of gbs

A

acute, plateau, recovery

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70
Q

what is the acute phase

A

weakness, ascending, bilateral, symmetrical, rapidly progressive

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71
Q

when is acute phase the max weakness

A

at 2 weeks

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72
Q

how long can acute phase last

A

4 weeks

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73
Q

what is the plateau phase

A

the pt has unchanged variables

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74
Q

how long does plateau last

A

several weeks to several months

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75
Q

how long does recovery last

A

depends on severity of weakness, variable, but is usually several months

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76
Q

what factors put pt at risk for not being able to walk or walk without assistance s/p gbs event

A

rapid onsent, age greater than 60, prolong plateau, and hx of vent dependancy

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77
Q

what are indications to intubate gbs pt

A

pna, weak resp muscles, inable to handle secretions (aspiration risk)

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78
Q

what is recommended to follow for pt with gbs daily

A

daily assessment of vital capacity

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79
Q

what is the vital capacity when we need to intubate gbs pt

A

vital capacity less than 15cc/kg

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80
Q

do steriods help gbs

A

iv steriods have not shown aid and oral steriods had shown actual worsening of pt outcome

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81
Q

does interferon beta 1 alpha treat gbs

A

no, that is for multiple sclerosis pt

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82
Q

what are 2 effective treatments of gbs pt

A

plasma exchange and IVIG

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83
Q

is plasma exchange same as exchange transfusion

A

no they are not the same

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84
Q

how is plasma exchange helpful for gbs

A

it has decreased the need for vent assistance, decrease time to walk, and decrease disabilities

85
Q

during pregnancy, is there a increase in prevalence of intracranial pathology

A

no, for most tumors, av malformation, it is the same between pregnant and non pregnant patients

86
Q

what has an increase in growth response during pregnancy for intracranial lesions

A

meningiomas…they grow in response to elevated estrogen and progesterone levels

87
Q

what is the concern for intracranial mass during pregnancy

A

must handle intracranial hypertension and seizures

88
Q

can mannitol and lasix be used for neuro surge for intracranial lesions in pregnant patients

A

yes…but only at certain doses 0.2g/kg to 0.5g/kg

89
Q

what can mannitol cause the fetus

A

hyperosmolarity in the baby

90
Q

what does hyperosm of mannitol given in pregos to the baby

A

hyperosm will cause decrease in fetal lung fluid, decrease fetal urine flow, and over all dehydration

91
Q

main complication of intracranial mass in prego

A

seizure that can lead to death. These pt must have anticonvulsant meds

92
Q

what is concern of anticonvulant given to pregos

A

levels are altered 2ndry to hepatic metabolism, protien and blood volume changes

93
Q

xxxxxxxxxxxxxxxxxxxxxxxxxx

A

xxxxxxxxxxxxxxxxxxxxxxxxxx

94
Q

What is the cause for neurogenic pulmonary edema

A

Increased intracranial pressure

95
Q

How does increased intracranial pressure cause neurogenic pulmonary edema

A

The brain ischemia Promotes increase catecholamines to increase cerebral perfusion pressure

96
Q

What is the result of increasing catecholamines in NPE

A

There is a constriction of the pulmonary vasculature and systemic vasculature

97
Q

What happens to cardiac output

A

Decrease because there is a decrease in left ventricle contractility

98
Q

How often does NPE happen in neurotrauma

A

20%

99
Q

When does nPE occur

A

First few hours

100
Q

What are the causes of. NPE

A

Increased capillary permeability because of inflammatory factors when the blood brain barrier is dismantled, decreased left ventricle outflow, increased pulmonary vascular resistance

101
Q

How do you treat NPE

A

Decrease ICP

102
Q

How can you decrease ICP

A

Evacuate hematoma, Decompressive craniotomy, ventricular drain, hyperosmolar treatment

103
Q

If a patient is tachycardic and hypertensive can use a beta blocker in NPE

A

It is not recommended

104
Q

His permissive hypercapnia suggested and NPE

A

Is contraindicated because elevated CO2 will cause increase in cerebral bloodflow thus increased ICP

105
Q

Where should the multiorifice cath be placed

A

At the junction of the svc and atrium

106
Q

What is the EKG sign of correct cvc placement

A

Biphasic p waves

107
Q

can pa02 influence cerebral blood flow

A

yes

108
Q

at what values does pao2 influence cerebral blood flow

A

pa02 of 60 or less

109
Q

what does pao2 of 60or less do to cerebral blood flow

A

it increases cerebreal blood flow

110
Q

what does hypothermia do to cerebral blood flow

A

decrease cbf

111
Q

what does chronic hypertension do to cerebral blood flow

A

it shifts the cerebral autoregulation curve to the right

112
Q

cerebral blood flow…what increases cbf…hyper or hypoxemia

A

hypoxemia

113
Q

cerebral blood flow…at what PaO2 doese cbf increase

A

PaO2 less than 60

114
Q

Mannitol. What happens with rapid infusion.

A

Transient increase in icp

115
Q

Mannitol. What happens with slow infusion,

A

Decrease in ICP and improved brain oxygen delivery and blood flow

116
Q

Mannitol. When should it be stopped

A

When serum osm is greater than 310 or when Na is greater than 150.

117
Q

Mannitol. What is lost in mannitol diuresis

A

Na K and Mg

118
Q

venous air emolism. what are the most sensitive tests for this

A

tee is the most…but almost as equal is precordial doppler

119
Q

venous air embolism. what is the most neuro surgery to get it

A

posterior fossa tumor excision

120
Q

venous air embolism. what happens to fractiion expired nitrogen

A

increase

121
Q

venous air embolism. what happens to PaO2

A

decrease

122
Q

venous air embolism. what happens to etco2

A

decrease

123
Q

venous air embolism. what happens to pulmonary artery pressure,

A

increase

124
Q

venous air embolism. what happens to paco2

A

increase…builds up in blood bc cant vent out

125
Q

venous air embolism. what happens to cvp

A

increase

126
Q

venous air embolism. what should be first done

A

drop head, flood field, apply pressure to jugular viens

127
Q

venous air embolism. how should volume be resuscitated

A

it should increase to apply cvp pressure to improve cardiac output forward flow

128
Q

venous air embolism. what position is supposedly suppose to help

A

durants left lateral decubitus position

129
Q

venous air embolism. what is durants position suppose to do

A

it is suppose to decrease right ventricular outflow obstruction

130
Q

venous air embolism. a paradoxial vae occurs…why

A

bc there is some form of vsd or asd

131
Q

venous air embolism. what to do to treat paradoxical vae

A

use hyperbaric oxygen

132
Q

cerebral blood flow. what is dexemetomidines effect on cbf on normal autoregulatoin pressures

A

at increasing doses, it decreases cbf and decreases cmro2

133
Q

cerebral blood flow. what is esmolol effect on cbf at normal autoregulatoin pressures

A

no effect

134
Q

cerebral blood flow. what is epinephrine effect on cbf at normal autoregulation pressures

A

it increases cbf

135
Q

cerebral blood flow. what is phenylephrine effect on cbf at normal autoregulation pressures

A

no effect

136
Q

icp. what is the gold standard for monitoring icp

A

intraventricular drain catheter

137
Q

icp. what are the benefits of an intraventric cath

A

it can be rezeroed while in place and can be a mode of therapy for elevated icp

138
Q

icp. what are the disadvantages of intraventric cath

A

highest rate of infection, difficult placement, risk for damaging paranchyma

139
Q

icp. what is a subarachoid bolt

A

it is a bolt that sits outside of the brain in the subarachnoid space

140
Q

icp. what is the advantage of the subarachnoid bolt

A

less infection risk and less risk to damage brain paranchyma

141
Q

icp. what is the disadvantage of a subarachnoid bolt

A

it may not be as accurate as brain matter may occlude the lumen

142
Q

neuromonitoring. lumbar surgery. what kind of monitoring is more common

A

SSEP…bc lumbar surgery is mainly @ cauda equina level…and SSEP is enough to monitor both sensory and motor…bc if ssep is affected…motor most likey is affected too…there is no anterior spinal chord for surgery to affect seperately.

143
Q

neuromonitoring. what is more sensitive to volatiles

A

MEP is more sensitive to volatiles

144
Q

neuromonitoring. how does volatile sensitivity help select between modes of neuromonitoring

A

since MEP are more sensitive to volatiles…SSEP is better used to monitor and not worry about false positives caused by anesthesia…so at lumber sites…SSEP is good enough to monitor both sensory and inferred motors

145
Q

neuromonitoring. at what level of the spinal chord is it best to monitor ssep and mep seperately

A

at or above L1 level

146
Q

neuromonitoring. what do volatiles do to ssep

A

decrease amplitude and increased latentcy

147
Q

neuromonitoring. what is latentcy

A

it is the time from stimulus to response in neuromonitoring

148
Q

neuromonitoring. between mep and ssep, when is tiva more recommended

A

if MEP is used, it highly rec that TIVA is used bc only MAC of 0.25 is recommended when MEP is monitored

149
Q

neuromonitoring. what is more sensitive to hypoperfusion. mep or ssep

A

there are more MEP synapses compared to SSEP and hypoperfusion and hypoxia affects MEPS the most

150
Q

neuromonitoring. what the goal hg when spinal cord surgery is done and MEP is being monitored

A

attempt to keep Hg above 10

151
Q

subarachnoid hemorrhage. what is the diagnostic test of choice

A

ct head non contrast

152
Q

subarachnoid hemorrhage. what are the risk factors for older patients

A

smoking, hypertension, etoh abuse

153
Q

subarachnoid hemorhage. what are the risk factors for young patients

A

cocaine abuse

154
Q

subarachnoid hemorrhage. what increases the chances of ct scan detecting the sah

A

the greater the symptoms, the greater likely hood of detecting sah

155
Q

subarachnoid hemorrhage. what is the next step after ct scan is ordered

A

consult neurosurgery service

156
Q

subarachnoid hemorrhage. what is the next step after ct scan is ordered and neurosurg notified..

A

ct arteriogram for confirm diagnosis and treatment

157
Q

subarachnoid hemorrhage. what is the greatest risk for these pt

A

rebleeding

158
Q

subarachnoid hemorrhage. what are risk factors rebleeding

A

pt w/ small vessel disease: uncontrolled htn, renal disease, atrial fib, heart failure, cad

159
Q

subarachnoid hemorrhage. what about the initial hemorrhage puts the pt at increased risk for rebleeding

A

increase time to treatment, increased size of initial hemorrhage, posterior circulation locaiton of previosu hemorrhage,

160
Q

suarachnoid hemorrhage. what percent of pt will rebleed if no intervention is done

A

4% of patients

161
Q

subarachnoid hemorrhage. what symptoms can tell you that there is intracranial hypertension

A

hypertension with bradycardai, altered mentation, posturing

162
Q

subarachnoid hemorrhage. what interventions can u do during acute increase in intracranial htn

A

mannitol, lasix, acute brief hyperventilation,

163
Q

subarachnoid hemorrhage. what neuroprotection can u do

A

glucose control and anticonvulsants

164
Q

subarachnoid hemorrhage. what is prefered, tiva vs volatile anesthetics

A

tiva, bc volatiles increase cbf and thus increase intracranial htn

165
Q

subarachnoid hemorrhage. how is bp maintained

A

normotension is prefered. during temp aneurysm clip, moderate htn can be used.

166
Q

subarachnoid hemorrhage. what do wide swings in bp mean

A

possibly rebleeding.

167
Q

subarachnoid hemorrhage. should u use hypothermia

A

as of now no data to support decrease in mortality

168
Q

Neuro monitoring. What are considered changes in amplitude or latentcy

A

50 percent decrease in amplitude or 30 percent increase in latentcy

169
Q

Neuro monitoring. Does nitrous oxides cause change in neuromonitoring

A

Yes.

170
Q

Neuro monitoring. Do narcotics affect neuromonitoring.

A

No u dumb fuck. That’s why we use it in tiva

171
Q

Neuromonitoring. Does ketamine cause any effect

A

It increases amplitude. And possible at low doses helps with interpretation of monitoring

172
Q

Icp. Of barbiturate mannitol and hyperventilate. What is the best at lowering icp.

A

Mannitol

173
Q

Icp. Mannitol. How fast should it be given.

A

Within 30 minutes.

174
Q

Icp. Mannitol. When do u see its effects.

A

15 minutes.

175
Q

Icp. Mannitol. When is its peak effect.

A

1 hour

176
Q

Icp. Mannitol. How long does it last.

A

6 hours.

177
Q

Icp. Mannitol. How should it be monitored.

A

Keep the serum osmolarity 300-320

178
Q

Icp. Mannitol. What happens when serum osm. Gets above 340

A

Hypovolemia and electrolyte disturbance bc excess diuresis

179
Q

Awake craniotomy. What is the kind of sedation preferred for this case.

A

Moderate sedation. With propofol.

180
Q

Awake craniotomy. When should sedation be stopped.

A

30 minutes before cortical mapping so it does not interfere with the mapping.

181
Q

Awake craniotomy. What helps awake approach be successful

A

Local anesthestics to provide comfort.

182
Q

ect. what is a good duration of seizure activity to help improve depression

A

greater than 25 seconds

183
Q

ect. what is the first hemodynamic change

A

bradycardia because of parasympathetic discharge.

184
Q

ect. what is the danger for bradycardia

A

in some cases, parasympathetic overtone is so great you get asystole

185
Q

ect. what is given prophylactically to prevent the parasympathetic discahrge

A

glycopyrroalte

186
Q

ect. does glycopyrrolate affect the seizure

A

no

187
Q

ect. what can be done if pt in previous ect does not reach long enough seizure duration

A

give iv caffeine or theophylline

188
Q

ect. what about anesthesia ventilation and oxygenation can effect the duration of seizure

A

hypercapnea and hypoxemia may decrease the duration of seizure

189
Q

ect. how should you treat the second hemodynamic effect of ect

A

sympathetic discharge (tachycardia and htn) should be treated with labetalol

190
Q

autonomic hyper-reflexia. when the bladder is stimulated…what is the afferent limb

A

the dorsal collumns, spinothalamic track, and a massive sympathetic discharge

191
Q

autonomic hyper-reflexia. what happens normally if the spinal cord is intact and you get the afferent signals

A

the sympathetic discharge would cause htn and the carotid barorecptors would see this and send out vagal responses and inhibitory signals to ablate the sympathetic vasoconstriction

192
Q

autonomic hyer-reflexia. what are the bp above and below the transection

A

hypo above, hyper below

193
Q

autonomic hyper-reflexia. what is the treatment

A

nitroglycerine to bring down the bp below the transection. so that that strong vagal response will no persist and cause asystole

194
Q

autonomic hyper-reflexia. what is the catecholeamine causing the htn

A

noreepi

195
Q

subarachnoid hemorrhage. what is the most common cause of death after first bleeding event

A

vasospasm

196
Q

subarachnoid hemorrhage. what is triple h therapy

A

hypertension, hypervolemia, hemodilution

197
Q

subarachnoid hemorrhage. what is the goal of hypervolemia

A

get cvp above 8 or wedge pressure of 15 or greater

198
Q

subarachnoid hemorrhage. triple h. what is the mechanism of hypervolemia

A

it increases cardiac output

199
Q

subarachnoid hemorrhage. triple h. what is the goal for hemodilution.

A

to keep the hematocrit around 30.

200
Q

subarachnoid hemorrhage. triple h. when should hypertension be induced.

A

when hypervolemia and hemodilution is reached

201
Q

subarachnoid hemorrhage. vasosopasm. what are risk factors for vasospasm after a bleeding event

A

previous big bleeding, history htn, old, hydrocephalus, female, smoker

202
Q

subarachnoid hemorrhage. when can vasosopasm happen

A

up to 14 days out

203
Q

subarachnoid hemorrhage. how urgent is it to operate on vasospasm

A

emergency

204
Q

subarachnoid hemorrhage. how is diagnosed

A

frequent neuro exam. cerebral angiogram, transcranial doppler

205
Q

guillain-barre. what is the moa

A

viral infection. (cmv, gbs) or bacterial infection. antigens mimic myelin sheath, autoimmune attack schwan cells. ascending paralysis

206
Q

gulillan-barre. can you use succ

A

contraindicated

207
Q

gullian-barre. can you use nondepol mm block

A

not contraindicated, but may be more sensitive

208
Q

gullian-barre. are epidurals contraindicated

A

no

ACE (18 decks)

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