Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharm > eneuro > Flashcards

eneuro Flashcards

1
Q

DOC for absence seizures

A

ethoxsuximide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

mechanism for ethosuximide

A

blocks thalamic T type Ca 2+ channels that trigger and sustain rhytmical burst discharges in thalamic neurons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

SE of ethoSUXimide

A 
EFGHIJ
ethoxsuximide causes
fatigue
GI distress
Headache
itching (and urticaria)
SJS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

epilepsy benzodiazepines

A

diazepam, lorazepam, midazolam

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

DOC for status epilepticus

A

lorazepam

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

SE of epilepsy benzodiazepines

A

sedation tolerance, dependdance, resp depression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

also for eclampsia seizures

A

benzodiazepines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

1st line for eclampsia seizures

A

mgso4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

phenobarbitol is 1st line in

A

neonates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

SE of phenobarbitol

A

sedation, tolerance, depdence, induction of p450, cardiresp depression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

phenobarbital treats which seizures

A

partial (focal), tonic-clonic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

phenotoin, fosphenytoin mechanism of action

A

blocks na+ channels; 0 order kinetics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

prophylaxis for status epilepticus

A

phenytoin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

1st line for acute status epilepticus

A

benzodiazepines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Neurologic SE of phenytoin

A

nystagmus, diplopia, ataxia, sedation, peripheral neuropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

derm se of phenytoin

A

hirsuitism, SJS, gingival hyperplasia, DRESS syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

MSK se of phenytoin

A

osteopenia, SLE-like syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

hematologic se of phenytoin

A

megaloblastic anemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

reproductive SE of phenytoin

A

teratogeniss (fetal hydantoin syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

other SE of phentyoin

A

cytochrome p450 induction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

1st line for tonic clonic seizures

A

phenytoin , valproic acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

carbamazepine first line for

A

partial seizures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

mechanism of action for carbamazzepin

A

blocks na+ channel (reduces aiblity of na channel to receover from inactivation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

SE of carbamezipne

A

dipolopia, ataxia, blood dyscrasisas (agranulocytosis aplastic anemia), liver toxicity, teratogensis, induction of cytochrone p450, SIADH, SJS; bone marrow suppression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

1st line for trigeminal neuralgia

A

carbamezepin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

episodic severe unilateral eelctrical shock like pattern distrubiton of CN5; symptoms triggered by innocus stimuli: shaving/ washing face

A

trigeminal neuralgia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

mechanism of action for valproic acid

A

na+ channel inactivation, increase Gaba concentration by inhibiting gaba transaminase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

SE of valproic acid:

A

GI distress, rare but fatal hepatoocity, pancreatitis, neural tube defects, tremor, weight gain, CI in pregnancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

1st line for myoclonic seizures

A

valproic acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

used in bipolar disorder and migraine prophylaxis

A

valproic acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

vigabatrin mechanism

A

increaese gaba by irreversibly inhibitng gaba transaminase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

se of vigabatrin

A

permanent visual loss (black box warning)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

vigabatrin treats

A

partial seizure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

gabapentin mechanism

A

primarily inhibits high voltage activated ca channels; designed as gaba analog

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

se of gabapentin

A

sedation, ataxia, confusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

also used for peripheral neuropathy, postherpetic neuralgia

A

gabapentin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

use of gabapentin

A

focal seizure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

topiramate mechanism

A

blocks na+ channels, increase gaba action

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

SE of topiramate

A

sedation , mental dulling, KIDNEY STONES, weight loss, glaucoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

topiramte also used for migraine prevention

A

true

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

topiramate treats

A

partial, tonic clonic seizures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

lamotrigine mechanism

A

blocks voltage gated na channels; inhibits release of glutamate; also effective for BPD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

SE of lamotrigine

A

SJS; also

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

lamotrigine use

A

partial, tonic clonic, absence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

levetiracetam mechanism

A

binds to synaptic vesicel protein (SV2A)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

SE of levetiracetam

A

fatigue, drowsiness, headache, neuropsychiatric symptoms (personality changes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

use of levetiracetam

A

partial, tonic clonic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

tiagabine use

A

partial

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

tiagabine mechaism

A

increase gaba by inhibiting reuptake

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Juvenile mycolonus epilepsy treated with

A

valproic acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

DRESS SYDNROME

A

phenytoin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

2-8 weekks after use of anticonvulsants, allopurinol, sulfonamides, antiboitics. pt’s get fever, generalized lymphadenopathy facial edema, diffuse morbiliform skin rash that progress to a confluent erythema w follicular accentaution; internal organ dysfucntion. lab studies: eosinophilia, atypical lymphocytes

A

dress sydnrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

thiopental is a

A

barbiturate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

name the barbiturates

A

phenobarbital, pentobarbital, thiopental, secobarbital

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

mechanism of barbiturates

A

faciliate GABAa action by increasing duration of CL- channel opening, thus decrease neuron firing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

contraindicated in porphyria

A

barbiturates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

induction of anesthesia caused by which barbiutrate

A

thiopental

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

barbiturates use

A

sedative for anxiety, seizures, insomnia, induction of anesthesia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

name the benzodiazepines

A

diazepam, lorazepam, traizolam, temazepam , oxazepam, midazolam, chlordiazepoxide, alprazolam

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

mechanism of benzodiazepines

A

facilitate GABAa action by increaseing frequency of CL- channel opening. Decreases rem sleep

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

benzodiazepines have short or long half lives

A

long half lives and active metabolites mostly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

exceptiosn to long halv lives and active metabolites

A 
ATOM
alprazolam
triazolam
oxazepam
midazolam
63
Q

midazolam is a

A

benzodiazepine

64
Q

ATOM have higher or lower addictive potential

A

higher; bc shorter acting : alprazolam, triazolam, oxazepam, midazolam

65
Q

allosterically modulates binding of gaba

A

benzodiazpeines

66
Q

which benzodiazepines are metabolized outside the liver

A

oxazepam temazepam, lorazepam

OTL (outside the liver)

67
Q

use of benzodiazepines

A

anxiety, spasticity, status epilepticus (lorazepam, diazepam), eclampsia, detoxification (esp alcohol withdrawll), night terrors, general anesthetic (amnesia, muscle relaxation), hypnotic (insomnia

68
Q

seizures assoc w alcohol withdrawl treated with

A

diazepam and chlordiazepoxide

69
Q

oxazepam, temazepan, and lorazepam have or dont have active metabolites

A

do not have active metabolites

70
Q

treat benzo overdose with

A

flumazenil (competitive antagnoist at gaba benzo receptor)

71
Q

SE of benzo

A

depedence, additive Cns depression effects w alcohol; less risk of resp depressoin and coma than barbiutrates

72
Q

nonbenzodiazepine hypnotics

A

zolpidem, zaleplon, eszopiclone

73
Q

zolpidem, zaleplon, eszopiclone mechanism

A

acts via bz1 subtype of gaba receptor; effects reversed by flumazenil. sleep cycle less affected as compared w benzodiazepines hypnoitcs

74
Q

use of zolpidem, zaleplon, eszoplicone

A

insomnia

75
Q

SE of zolpidem, zaleplon, eszoplicone

A

ataxia, headaches, confusion. short duration because of rapid metabolism by liver enzymes; only modest day after psychomotor depression and few amnestic effects

76
Q

less dependence risk than benzodiazepines

A

zolpidem zalpelon, eszopiclone

77
Q

SE in older adults: increase risk of falls and confusion

A

zolpidem, zaleplon, eszoplicone

78
Q

phenytoin metabolis is dose dependdnet

A

yes

79
Q

orexin (hypocretin) receptor antagnoist

A

suvorexant

80
Q

suvorexant use

A

insomnia

81
Q

se of suvorexant

A

cns depression, headache, dizziness, abnormal dreams, upper resp tract infection

82
Q

CI of suvorexant

A

patients with narcolepsy, liver disease. strong cyp3a4 inhibirtors

83
Q

suvorexant has low physical dependence

A

true

84
Q

melatonin receptor agonist, binds MT1 and MT2 in suprachiasmatic nucelus

A

ramelteon

85
Q

se of ramelteon

A

dizziness, fatigue, nausea, headache

86
Q

5Ht 1b/1d agonist

A

sumatriptan

87
Q

inhibit trigeminal nerve activation; prevent vasoactive peptide release; induce vasoconstriction

A

sumatriptan

88
Q

use of sumatriptan

A

acute migraine, cluster headache attacks

89
Q

se of sumatriptan

A

coronary vasopasm (CI in pt’s with CAD or prinzmental angina), mild paraestheia, serotoni syndomre

90
Q

PRopranolol can treat what

A

essentail tremor (bilateral rhytmic hand tremor that worsens during fine motor activity (intention tremor))

91
Q

BB, antidepressentsa, and anticonvulsants for prophaylxis of

A

migraine

92
Q

capsaicin mechaism

A

excessive activation of trpu1 (transmembrane cation channel) causes buildup of intracellular ca2+ resulting in long-lasting dysfunction of nociceptive nerve fibers (defunctionalization). also causes depletion of substanec P

93
Q

capsaicin use

A

post herpetic neuralgia.

94
Q

dopamine agonists include

A

bromocriptine, pramipexole, ropinirole

95
Q

ergot derived

A

bromocriptine

96
Q

increases dopamine release and decreases dopamine reuptake

A

amantidine

97
Q

SE of amantadine

A

ataxia, livedo reticularis, dry mouth, blurring of vision, vissual changes

98
Q

agents that prevent peripheral L dopa degradation; increases L dopa entering cns; increase central l dopa available for conversion to dopamine

A

Levodopa (L-dopa)/carbidopa, entacapone, tolcapone

99
Q

blocks peripheral conversion of L-dopa to dopamine by inhibiting DOPA decarboxylase

A

carbidopa

100
Q

Reduces side effects of peripheral L-DOPA conversion into dopamine

A

carbidopa

101
Q

peirpheral se of dopamine

A

nausea vomiting

102
Q

prevent periphreal L dopa degradation to 3-O-methyldopa (3-OMD) by inhibiting COMT

A

entecapone , tolcapone: treats wearing off periods

103
Q

central COMT inhibtor

A

tolcapone

104
Q

blocks conversion of dopamine into DOPAC by selectively inhibiting Mao-b

A

selegiline

105
Q

blocks conversion of dopamine to 3-metoxytyramine (3-MT) by inhibiting central COMT

A

tolcapone

106
Q

curb excess cholinergic activity in parkinson’s

A

benztropine, trihexyphenidyl

107
Q

benztropine, trihexyphenidyl are what type of drugs

A

antimuscarinic

108
Q

they improve tremor and rigidty but little effect on bradykinesia

A

benztropine, triheyxphenydily

109
Q

pergolide

A

dopamine agonist : D2 receptor

110
Q

central effects of dopaine

A

anxiety, agitation, insomnia, confusion ,delusions, hallucinations.

111
Q

SE of levodopa/carbidopa

A

arrythmias from increase periperal formation of catecholamines; long term use: on off period

112
Q

drugs used in huntington disease

A

tetrabenazine, reserpine, haloperidol

113
Q

MOA for tetrabenzine and reserpine

A

inhibit VMAT: decrease dopamine vesicle packaging and release

114
Q

Haloperidol moa

A

d2 receptor antagnoist

115
Q

For LOU gehrig disasese, give

A

riLOUzole

116
Q

riluzole

A

treatment for ALS; modestly increase surivial by decrease glutamate excitotoxicity

117
Q

alzheimer disease drugs

A

memantine, donepezil, galantamine, rivastigmine, tacrine

118
Q

alzheimre drug that is an nmda receptor antagonist; helps prevent excitotoxicity (mediated by ca2+

A

memantine

119
Q

SE of memantine

A

dizziness, confusion, hallucinations

120
Q

alzheimer drug that is ache inhibtior

A

donepezil, galantamine, rivastigmine, tacrine

121
Q

se of donepezil, galantamine, rivastigmine, tacrine

A

nausae, dizziness, insomina

122
Q

anesttheics drugs with decreaes solubility will have

A

rapid induction and recovery times

123
Q

Higher soluiblity in lipids (anesthetic drugs)

A

higher potency

124
Q

MAC decreases with (increase or decrease age)

A

increased age

125
Q

inhaled anesthetics include

A

desflurane, halothane, enflurane, isoflurane, sevolfurane, methoxyflurane, N20

126
Q

inhaled anesthetics are metabolzied by

A

cytocrhone p450

127
Q

effects of inhaled anesthteics

A

Myocardial depression, resp despression, nauea/emesis, increase cerebral blood flow (decrease cerebral demand), decrease renal funciton, decraesehepatic blood flow

128
Q

which inhaled anestheic causes hepatotoxciity

A

halothane

129
Q

which inhaled anestehtic causes nephrotoxcity

A

methoxyflurane

130
Q

which inhalend anesthetic is a proconvuslant

A

enflurane, epileptogenic

131
Q

expansion of trapped gas in a body cavity is caused by which anesthetic

A

n2o

132
Q

INtravenous anestehtics

A 
TMKPO: The mighty king proposes to opra
barbiturates (thiopental)
benzodiazepines (midazolam
arylcyclohexylamines (ketamine)
propofol
opioids
133
Q

barbiturates IV anesthteic

A

thiopental

134
Q

thiopential has high potency which means

A

high lipid soluiblity, rapid entry into brain

135
Q

thiopental effect

A

use for induction of anestehsia and short surgical procedures. effect terminated by rapid redistribution into tissue and fat. decreases cerebral blood flow

136
Q

beenzodiazepines drug iv anesthetic

A

midazolam

137
Q

midazolam used for

A

endoscopy; used adjunctively w gaseous anestehtics and narcotics

138
Q

se of midazolam

A

severe postop resp depression, decrease BP, anterograde amnesi

139
Q

PCP analgo used as dissociative amnesia

A

ketamine: blocks nmda receptors; cv stimulants

140
Q

ketamine se:

A

disorientation, hallucination, unplesant dreasm. increase cerebralblood flow : and ICP

141
Q

propofol:

A

used for sedation for ICU, rapid anestheisa induction, short procedures. less postop nausea than thiopental. potentiates gabAa

142
Q

SE of propfol

A

hypotension: vasodilation. rapidly cleared from plasma and prefernetially distrubted to organs receiving high blood flow (brain) = rapid onset. Redistrubted to organs receiving less blood flow. bc site of action in brain: redistribution accts for rapid termination of drug

143
Q

local anesthetics esters

A

procaine, cocaine, tetracaine, benzocaine

144
Q

local anesthetics amides

A

lidocaine, mepivacaine, bupivacaine

145
Q

local anesthteics mechanism of action

A

block na+ channels by binding to specific receptors on inner portion of channel. most effective in rapidly firing neurons.

146
Q

tertiray amine local anesthteics penetrate membrane in

A

uncharged form, then bind to ion channels as charged form

147
Q

given with vasocnostnrictors to enahcne local action

A

local anestheics

148
Q

why are local anesttheics given w vasocnostrictors

A

decrease bleeding, increases anesthesia by decreasing sysetmic concentration

149
Q

in acidic tissue: what is effect of alkaline anesthetics

A

they are charged and cannot penetrate membrane effectively ; thus need more anesthetic

150
Q

order of nerve blockade in local anesthteics

A

small diamter fibers > large diameter fibers; myelinated fibers> unmyelinated fibers. overall size predominates over myelinsation
small myelinated ifbers > small unmyelinated fibers
order of loss: pain temp touch pressure

151
Q

SE of local anesttheics

A

CNS excitaiton, htn, hypotension

152
Q

bupivacaine SE

A

cV toxicity

153
Q

cocaine SE

A

arrhtymias

154
Q

se of benzocaine

A

methemoglobinemia

Pharm (13 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions