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Fa: Pharm 3 > 6. Neuro > Flashcards

6. Neuro Flashcards

1
Q

what drugs are used to lower ICP

A

-mannitol
-hypertonic saline (3%)

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2
Q

how do hyperosmotic drugs work

A

-transient increase in osmolality of plasma
-draws water from tissues (including brain) into plasma
-eliminated renally

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3
Q

what are secondary effects of hypertonic drugs

A

-diuresis
-reduction in blood volume

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4
Q

where is mannitol filtered at? what does this mean?

A

-filtered at glomerulus (not reabsorbed in PT)
-so prevents normal osmotic reabsorption of water

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5
Q

SE of mannitol

A

-hyperosmolality
-hyponatremia
-hypokalemia

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6
Q

dose of mannitol

A

0.25-0.5 g/kg
(some references say up to 1 g/kg)

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7
Q

concentration of IV bag of mannitol

A

20% mannitol in 500 mL bag
20 g/100 mL
100 g per bag

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8
Q

concentration of mannitol in vial

A

25% mannitol
25 g/ 100 mL
12.5 g/50 mL vial

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9
Q

what happens if larger initial doses of mannitol are given?

A

may lead to rebound increase in ICP

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10
Q

goal serum osmolality of mannitol

A

300-315 mOsm/L

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11
Q

when to stop mannitol

A

if 320 mOsm/L is reached

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12
Q

with mannitol, how much fluid is removed from the brain

A

100 mL

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13
Q

with mannitol, how long does it take for ICP to be decreased

A

within 30 min (max effect 1-2 hours)

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14
Q

with mannitol, how much UOP is there

A

1-2 L within 1 hour

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15
Q

with mannitol, what is the duration of hyperosmotic effect

A

about 6 hours

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16
Q

what needs to be monitored when giving mannitol

A

-serum osmolality
-UOP
-BP
-serum electrolytes
-may need tx with crystalloids and electrolyte solutions

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17
Q

what is needed to be intact to give mannitol? why?

A

-intact BBB
-if disrupted, drug may cross and cause cerebral edema and increase brain size

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18
Q

how can mannitol affect the heart

A

can cause symptomatic HF in pts with LV dysfx and poor cardiac reserve

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19
Q

when should mannitol be avoided

A

-aneurysms
-arteriovenous malformations
-intracranial hemorrhage until cranium opened

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20
Q

how is 3% sodium chloride IV administered

A

central venous catheter

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21
Q

initial dose of hypertonic saline

A

1-2 mL/kg over 5 minutes

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22
Q

target serum Na of hypertonic saline

A

145-155 mEq/L

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23
Q

target serum osmolarity of hypertonic saline

A

<320 mOsm/L

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24
Q

how often should serum Na and osmolarity be monitored while on hypertonic saline infusion

A

q6h

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25
Q

what can serum Na of 160 mEq/L cause

A

-renal injury
-pulmonary edema
-seizures
-cardiac dysfx

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26
Q

is mannitol or hypertonic saline considered a higher risk

A

hypertonic saline

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27
Q

use of loop diuretics (furosemide)

A

-sx associated with increased IV volume (pulm edema)
-can be used with mannitol and hypertonic saline for pt with CHF and nephrotic syndrome

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28
Q

what corticosteroids are used for ICP

A

dexamethasone or methylprednisolone

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29
Q

how do corticosteroids lower ICP

A

-causes upregulation of expression of proteins responsible for integrity of tight junctions btw endothelial cells constituting components of the BBB

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30
Q

what cause of ICP are corticosteroids useful for

A

-useful for ICP caused by localized vasogenic edema (brain tumor, craniotomy)
-not for head trauma

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31
Q

decadron dose for ICP

A

-10 mg IV immediately
-then 4 mg IM q6h until subsides
-may switch to PO after

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32
Q

what should be monitored with corticosteroids

A

BG for hyperglycemia

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33
Q

use of barbiturates for ICP

A

give in high doses, esp with increased ICP after acute head injury

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34
Q

use of propofol for ICP

A

-may be helpful
-use w caution for prolonged periods, esp in peds
-avoid high anion-gap metabolic acidosis

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35
Q

use of sedatives and opioids in ICP

A

-use sparingly -leads to hypoventilation -> hypercarbia -> further elevation of ICP

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36
Q

what is used for anesthetic induction for ICP

A

propofol or barbiturates (with modest hyperventilation)

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37
Q

paralytics for ICP

A

NDMR

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38
Q

use of sux for ICP

A

-can increase ICP
-may be used for RSI or diff airway though

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39
Q

during maintenance, what periods may require increased anesthetic requirements?

A

during stimulating periods (incision, dural opening, mayfield pin placement, closure)

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40
Q

what can be used during emergence

A

precedex -> used during asleep and awake cranis

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41
Q

fluid management for maintenance of anesthesia

A

IV fluid iso-osmolar (LR or 0.9% NaCl) maintain euvolemia

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42
Q

what to avoid in fluids

A

dextrose containing solution, can cause CNS ischemia and neuronal injury

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43
Q

during crani, what to give during pinning

A

-opioids: fent 50-100 mcg or remi 25-50 mcg
-prop: 20-50 mg
-esmolol: 0.25-0.5 mg
-lidocaine: 1 mg/kg

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44
Q

anesthetic depth during pre-incision prep for crani

A

light sedation (lines, positioning, skin prep, draping)

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45
Q

anesthetic management during incision, raising scalp, and bone flaps

A

-raise anesthetic level
-brain relaxation (shrinkage) may be needed prior to dural opening (mannitol, 3% NaCl)

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46
Q

anesthetic management when opening dura during crani

A

deep level of anesthesia (very painful, lots of pain fibers)

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47
Q

anesthetic management during intracranial procedure part of crani

A

lighter level due to brain tissue has no pain receptors (depends on procedure)

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48
Q

anesthetic management during wound closure of crani

A

-painful, but not as bad as incision
-opioids, acetaminophen, antihypertensives

49
Q

premedication for cranis

A

versed 1-2 mg (in 0.5 mg increments)

50
Q

SE of using propofol for induction for crani

A

-autoregulation and CO2 responsiveness maintained
-reduction in CBF and ICP
-may cause hypotension

51
Q

SE of using methohexital for induction for crani

A

-activates seizure foci
-less hypotension than prop

52
Q

SE of using etomidate for induction for crani

A

-does not decrease BP or CO
-preserves CO responsiveness
-single dose inhibits adrenal steroid production up to 24 hour AVOID!!!!!!!!!!!!!!!!!!!!!!!!!

53
Q

SE of using ketamine for induction for crani

A

-conflicting data on cerebral physiology AVOIDDDD or use with caution!!!

54
Q

for RSI and diff intubation, what NMB agents to give

A

-give sux for induction
-add in defasciculating dose of NDMR for ICP

55
Q

defasciculating of the NMBs

A

roc: 2 mg
cisatracurium: 1.5 mg
vec: 0.3 mg
sux: 1.5 - 2 mg/kg

56
Q

if elevated ICP, what should be used for maintenance

A

IV technique (prop, opioids, precedex) not volatile agents

57
Q

which opioid should be avoided with ICP? why?

A

morphine -> histamine release

58
Q

glycemic control during crani

A

110-150 g/dL treat if >180

59
Q

BP goal during emergence

A

-SBP <160 (can cause postop intracranial hemorrhage)
-avoid hypotension (can cause cerebral hypoperfusion and ischemia)

60
Q

use of long acting opioids (like dilaudid) during emergence of crani

A

avoid

61
Q

dosing for labetalol

A

initial dose 0.2 mg/kg, then 0.4, 0.8, 1.6 q10 min

62
Q

max dose for labetalol

A

do not exceed 200 mg/dose (max dose repeated up to 3 times)

63
Q

how to give esmolol during crani

A

continuous infusion otherwise rebound HTN

64
Q

how to give nicardipine during crani

A

need continuous infusion or combination with longer acting agent

65
Q

how to tx hypotension during organ retrieval

A

-avoid vasoconstrictors!
-inotropes are preferred!

66
Q

for organ retrieval, what are first and second line for inotropes

A

first: dobutamine, dopamine
second: low dose epi

67
Q

management of heart retreival

A

minimize / avoid catecholamines

68
Q

risks of catecholamines during heart retrieval

A

-catecholamine induced cardiomyopathy
-ECG abnormalities and dysrhythmias

69
Q

how to tx diabetes insipidus during organ retrieval

A

inotropic support with vasopressin (0.04-0.1 units/h)
or
desmopressin (1-4 mcg)

70
Q

what is a seizure

A

transient alteration of behavior due to disordered, synchronous, and rhythmic firing of populations of brain neurons

71
Q

what is epilepsy

A

a disorder of brain fx with periodic and unpredictable occurrence of seizures

72
Q

drug classes to tx seizures / epilepsy

A

-antiepileptic drugs (AEDs)
-antiseizure drugs
-anticonvulsants (basically, all the same thing)

73
Q

MOA of antiseizure drugs

A

-modulation of Na+, K+, Ca+ channels
-enhance GABA transmission
-modulation of synaptic release through actions of synaptic vesicle protein SV2A (leviteracetam) or Ca channels containing alpha 2 delta subunit
-diminishing glutamate R (AMPA)

74
Q

what do antiseizure drugs do to Na+ channels

A

prolongation of the inactivated state of voltage gated Na+ channels

75
Q

what do antiseizure drugs do to K+ channels

A

positive modulation of K channels

76
Q

what do antiseizure drugs do to Ca+ channels

A

inhibition of Ca channels

77
Q

how do antiseizure drugs affect GABA

A

-enhance GABA transmission through actions on GABA R, modulation of GABA metabolism, and inhibition of GABA reuptake

78
Q

which antiseizure drugs rely on renal elimination

A

-gabapentin
-levetiracetam

79
Q

which antiseizure drugs induce CYP enzymes

A

-phenytoin
-carbamazepine

80
Q

how do the antiseizure drugs of phenytoin and carbamazepine affect NMBs

A

-cause relative resistance to NMBs due to accelerated clearance of these drugs
- so need to give more NMBs

81
Q

metabolism of phenytoin

A

-capacity limited (based on liver)

82
Q

how do small changes of dosing in phenytoin affect the total concentration

A

small changes in dose lead to larger magnitude change in concentration (can easily lead to toxic concentration)

83
Q

what dose of phenytoin exceeds the maximal clearance of the liver

A

300 mg/day

84
Q

therapeutic range of phenytoin

A

10-20 mg/dL (free 1-2 mg/dL)

85
Q

how to manage antiseizure drugs and surgery

A

continue antiseizure med periop

86
Q

what are parenteral antiseizure drugs

A

-levetiracetam
-phenytoin and fosphenytoin
-valproate
-phenobarbital

87
Q

dose of carbamazepine

A

2-4 times / daily

88
Q

dose of valproic acide

A

1-3 times /daily

89
Q

dose of phenytoin

A

1-2 times / daily

90
Q

dose of levetiracetam

A

2 times / daily

91
Q

which anesthetic drugs can induce seizures

A

-methohexital
-etomidate
-meperidine (metabolite normeperidine can cause seizures)
-laudanosine (metabolite of atracurium and cisatracurium)

92
Q

what drugs can cause epileptiform EEG activity in pts w/o epilepsy but also suppress such activity

A

-alfentanil
-ketamine
-enflurane
-isoflurane
-sevo

93
Q

causes of seizures in a periop pt

A

-drug and alc withdrawal
-acute neurologic injury
-intracranial and cerebrovascular surgery
-periop stroke (ischemic or hemorrhagic)
-CNS tumors
-metabolic derangements (hyponatremia, hypocalcemia, sepsis, hypoglycemia)

94
Q

if seizure pt is hypoglycemic, what should you give

A

50 mL 50% glucose

95
Q

drugs used to tx motor seizures

A

-fosphenytoin
-levetiracetam
-valproic acid
-propofol
-benzos

96
Q

what is fosphenytoin

A

water soluble prodrug for IV or IM administration (better tolerated than phenytoin)

97
Q

loading dose of fosphenytoin

A

15-20 phenytoin equivalents (PE) / kg infused at a rate of 150 mg/min

98
Q

how to dose of phenytoin

A

15-20 mg/kg IV limited loading dose rate of 50 mg/min

99
Q

SE of phenytoin

A

-hypotension
-asystole, widened QRS, prolonged QT, arrhythmias

100
Q

how can phenytoin NOT be administered

A

IM

101
Q

what can happen with extravasation or intraarterial injection of phenytoin

A

-“purple glove syndrome”
-skin necrosis
-compartment syndrome
-gangrene

102
Q

dosing of levetiracetam

A

2000-3000 mg IV over 15 min

103
Q

what is status epilepticus

A

continuous or intermittent seizures for more than 5 min w/o recovery or consciousness -after 5 min, less likely to spontaneously terminate -more likely to cause neuronal damage

104
Q

first and second line tx for status epilepticus

A

first: benzos second: antiseizure drug

105
Q

onset of benzos for status epilepticus

A

fast

106
Q

DOA of benzos for status epilepticus

A

short lived

107
Q

onset of diazepam to tx status epilepticus

A

2 min

108
Q

DOA of diazepam for status epilepticus

A

15-60 min

109
Q

adult dose of diazepam for status epilepticus

A

5-10 mg or 0.15-0.25 mg/kg (no faster than 5 mg/min)
-repeat in 5 min if seizure persists

110
Q

onset of lorazepam for status epilepticus

A

3 min (slightly slower than diazepam)

111
Q

DOA of lorazepam for status epilepticus

A

12-24 hr (longer than diazepam)

112
Q

adult dose of lorazepam for status epilepticus

A

2-4 mg or up to 0.1 mg/kg

113
Q

adult dose of midazolam for status epilepticus

A

0.1-0.2 mg/kg up to 4 mg q5min until seizure controlled

114
Q

sedation drugs to avoid epileptiform activity

A

-thiopental
-opioids
-benzos

115
Q

maintenance drugs to avoid epileptiform activity

A

-iso
-des
-sevo
-prop

116
Q

agents to avoid during electrocorticography

A

-benzos
-volatile agents
-barbiturates
-prop

117
Q

agents that are okay to use during electrocorticography

A

-opioids
-nitrous oxide
-droperidol
-diphenhydramine
-precedex

118
Q

agents that enhance electrocorticography

A

-high dose short acting opioids
-methohexital
-etomidate

119
Q

drugs that may be epileptogenic

A

-ketamine, enflurane, etomidate, opioids
-methohexital
- metabolites (meperidine, atracurium)
-sevo (dose concentration related)

Fa: Pharm 3 (10 decks)

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