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Neuro Pharm Flashcards

1
Q

How do you treat essential tremor (postural tremor)?

A

Beta-blockers
Primidone (anti-convulsant)
ETOH (decreases tremor amplitude)

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2
Q

How do you precipitate Wernicke-Korsakoff syndrome?

A

Giving glucose without B1 to a B1 deficient patient

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3
Q

Treat subarachnoid hemorrhage?

A

Nimodipine (Ca channel blocker)

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4
Q

What is indicated in ischemic stroke?

A

tPA within 4.5 hours

as long as paint presents within 3 hours of onset & there is no major risk of hemorrhage

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5
Q

What are some ALS therapies?

A

Riluzole (decrease presynaptic glutamate release)

Baclofen (GABA-B agnoist to dec spasticity)

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6
Q

What is contraindicated in closed (narrow angle) glaucoma?

A

Epinephrine

bc causes mydriasis

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7
Q

How do you treat Dry ARMD (nonexudative age-related macular degeneration)?

A

prevent progression– multivitamins & antioxidants

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8
Q

How do you treat Wet ARMD (exudative age-related macular degeneration)?

A

anti-VEGF injections or laser

stops choroidal neovascularization

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9
Q

How do you treat MS?

A

Beta-interferon
Natalizumab (monoclonal AB against alpha-4 integrin for cell adhesion)
Glatiramer (immune modulator)
Symptomatic Tx: 1) Baclofen (GABA-B agonist– tx spasticity), 2) Muscarinic antagonist & catheterization (neurogenic bladder), 3) Opiods (pain)

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10
Q

How do you treat Guillain-Barre?

A

Respiratory ventilator support
Plasmapheresis
IV immune globulins

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11
Q

What is the DOC for partial (focal) seizures?

A

Carbemazepine

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12
Q

How do you treat cluster HA?

A

inhaled oxygen

sumatriptan

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13
Q

How do you treat migraine?

A

Abortive– triptans

Prophylacitc– propranolol, topiramate

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14
Q

What is the general mechanism of glaucoma drugs?

A

decrease amount of aqueous humor to decrease intraocular pressure

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15
Q

Which drug classes are used to treat glaucoma?

A 
alpha-agonists
beta-blockers
diuretics
cholinomimetics
prostaglandin
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16
Q

Which alpha-agonists are used to treat glaucoma?

A

Epinepherine

Brimonidine (alpha 2)

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17
Q

What is the MOA of alpha-agonists in glaucoma?

A

decrease aqueous humor synthesis

epi does so via vasoconstriction

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18
Q

Side effects of alpha-agonists in glaucoma?

A

Mydriasis– Epi is contraindicated in closed-angle glaucoma

blurry vision, ocular hyperemia, foreign body sensation, ocular allergic rxn, ocular pruritis

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19
Q

Which beta-blockers are used in glaucoma?

A

Timolol
Betaxolol
Carteolol

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20
Q

What is the MOA of beta-blockers in glaucoma treatment?

A

Dec aqueous humor synthesis

*no pupillary or vision change S/E

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21
Q

Which diuretic is used to treat glaucoma?

A

Acetazolamide

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22
Q

What is the MOA of acetazolamide?

A

dec aqueous humor synthesis via carbonic anhydrase inhibition
*no pupillary or vision change S/E

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23
Q

Which cholinomimetics are used to treat glaucoma?

A

Direct– Pilocarpine, Carbachol

Indirect– Physostigmine, Echothiphate

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24
Q

What is the MOA of cholinomimetics in glaucoma?

A

inc outflow of humor via contraction of ciliary muscle and opening of trabecular meshwork

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25
Q

Which cholinomimetic is very effective in emergencies?

A

Pilocarpine (direct cholinomimetic)

acts quickly at opening trabecular meshwork into canal of schlemm

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26
Q

What are the side effects of cholinomimetics in glaucoma?

A

Miosis

Cyclospasm (contraction of ciliary muscle)

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27
Q

Which prostaglandin is used in glaucoma?

A

Latanoprost (PGF-2-alpha)

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28
Q

What is the MOA of prostaglandin used in glaucoma?

A

inc outflow of aqueous humor

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29
Q

What is the S/E of prostaglandin in glaucoma?

A

Darkening of the iris (browning)

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30
Q

What are the common opioid analgesics?

A 
Morphine
Fentanyl
Codeine
Heroin
Methadone
Meperidine
Dextromethorphan
Diphenoxylate
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31
Q

What is the MOA of opioid analgesics?

A

agonists at opioid receptors to modulate synaptic transmission
opens K channels & closes Ca channels to decrease synaptic transmission.
inhibits release of ACh, HE, 5-HT, glutamate, substance P

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32
Q

What are the opioid receptors?

A 
Mu = morphine
delta = enkephalin
kappa = dynorphin
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33
Q

Clinical use of opioid analgesics?

A 
pain
cough suppression (dextromethorphan)
diarrhea (loperamide & diphenoxylate)
acute pulmonary edema
maintenance for addicts (methadone)
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34
Q

Toxicity of opioid analgesics?

A 
Addiction
Respiratory depression
constipation
miosis (pinpoint pupils)
additive CNS depression with other drugs (esp ETOH, BZD, Barbs)
NO tolerance to miosis & constipation
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35
Q

What is the antidote to opioid OD?

A

Naloxone or Naltrexone

opioid receptor antagonists

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36
Q

What is the MOA of Butorphanol?

A

Mu-opioid receptor partial agonist

Kappa-opioid receptor agonist

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37
Q

Clinical use of Butorphanol?

A

Analgeisa for severe pain (migraine, labor, etc)

causes less respiratory depression than full opioid agonists.

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38
Q

What is the toxicity of Butorphanol?

A

opioid withdrawal symptoms if also taking full opioid agonist (competition for opioid receptors)
OD not easily reversed with Naloxone

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39
Q

What is the MOA of Tramadol?

A

Very weak opioid agonist

inhibitis serotonin & NE reuptake

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40
Q

What is the clinical use of Tramadol?

A

chronic pain

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41
Q

What is the toxicity of Tramadol?

A

similar to opioids– resp depression, miosis, constipation, etc.
decreases seizure threshold

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42
Q

Anti-epileptic drugs

A 
Phenytoin
Carbamazepine
Lamotrigine
Gabapentin
Topiramate
Phenobarbital
Valproic Acid
Ethosuximide
Benzodiazepines (Diazepam or Lorazepam)
Tiagavine
Vigabatrin
Levetiraceteam
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43
Q

1st line for tonic-clonic?

A

Phenytoin
Carbamazepine
Valproic Acid

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44
Q

1st line for Complex partial?

A

Carbamazepine

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45
Q

1st line for simple partial?

A

carbamazepine

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46
Q

1st line for absence seizure?

A

ethosuximide

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47
Q

1st line for status epilepticus?

A

Acute tx– loreazepam (or diazepam)

Prophylaxis– phenytoin

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48
Q

MOA of Phenytoin?

A

inc Na channel inactivation (use-dependent blockade)

inhibits glutamate release from excitatory presynaptic neuron

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49
Q

Use of Phenytoin?

A

tonic-clonic (also simple partial, complex partial)
status epilepticus prophylaxis
*use Fosphenytoin if parenteral

Class 1B antiarrhythmic

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50
Q

MOA of Carbamazepine?

A

Inc Na channel inactivation

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51
Q

Use of Carbamazepine?

A

1st line for simple partial, complex partial, tonic-clonic, and trigeminal neuralgia

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52
Q

MOA of Lamotrigine?

A

blocks voltage-gated NA channels

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53
Q

Use of Lamotrigine?

A

Simple partial, complex partial, tonic-clonic

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54
Q

MOA of Gabapentin?

A

GABA analog

inhibits high-voltage-activated Ca channels

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55
Q

Use of Gabapentin?

A

simple partial, complex partial, tonic-clonic

peripheral neuropathy, postherpetic neuralgia, migraine prophylaxis, bipolar disorder

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56
Q

MOA of Topiramate?

A

blocks Na channels

inc GABA action

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57
Q

Use of Topiramate?

A

simple partial, complex partial, tonic- clonic

migraine prevention

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58
Q

MOA of phenobarbital?

A

inc GABA-A Action

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59
Q

Use of Phenobarbital?

A

1st line in children w/ simple partial, complex partial, tonic-clonic

60
Q

MOA of Valproic Acid?

A

inc Na channel inactivation

inc GABA concentration

61
Q

Use of valproic acid?

A

1st line for tonic clonic

simple partial, complex partial, absence, and myoclonic seizures (can be used for all seizure types)

62
Q

MOA of Ethosuximide?

A

blocks thalamic T-type Ca channels

63
Q

Use of Ethosuximide?

A

absence seizures (1st line)

64
Q

MOA of benzodiazepines in seizures?

A

inc GABA-A action

65
Q

Use of Bezodiazepines in seizures?

A

1st line for acute status epilepticus

Use for eclampsia seizures (after 1st line MgSO4)

66
Q

MOA of Tiagabine?

A

inhibits GABA reuptake

67
Q

Use of Tiagabine?

A

simple & complex partial seizures

68
Q

MOA of Vigabatrin?

A

irreversibly inhibits GABA transaminase to increase GABA

69
Q

Use of Vigabatrin?

A

simple & complex partial seizures

70
Q

MOA of Levetiracetam?

A

unknown

may modulate GABA and Glutamate release

71
Q

Use of Levetiracetam?

A

simple & complex partial

tonic-clonic

72
Q

Toxicity of benzodiazepines?

A

sedation
tolerance
dependence
induction of cytochrome p450

73
Q

Toxicity of Carbamazepine?

A 
Blood Dyscrasias (agranulocytosis & aplastic anemia)
Stevens-Johnson syndrome
Diplopia, Ataxia
liver toxicity
teratogenesis
induction of cytochrome p450
SIADH (dec Na)
74
Q

Toxicity of Ethosuximide?

A

GI distress, fatigue, aggression
HA, uritcaria
Stevens-Johnson syndrome
may worsen generalized tonic-clonic seizures

75
Q

Toxicity of Phenobarbital?

A

sedation
tolerance
dependence
induction of cytochrome p450

76
Q

Toxicity of Phenytoin?

A 
Gingival hyperplasia
Hirsutism/ Hypertrichosis
Teratogenesis (fetal hydantoin syndrome & inc risk of cleft palate)
Nystagmus & Diplopia (will develop tolerance)
megaloblastic anemia (dec folate absorption)
SLE-like syndrome
Ataxia
Sedation
induction of p450
lymphadenopathy
peripheral neuropathy
Stevens-Johnson syndrome
77
Q

Toxicity of Valproic Acid?

A

Hepatotoxicty (rare but fatal– measure LFTs)
Neural tube defects (spina bifida)– Contra in pregnancy
GI distress
tremor, weight gain

78
Q

Toxicity of Lamotrigine?

A

Stevens-Johnson syndrome

increase dosage slowly

79
Q

Toxicity of Gabapentin?

A

Sedation

Ataxia

80
Q

Toxicity of Topiramate

A

Weight loss = decreases appetite
Sedation
Kidney stones
Mental dulling

81
Q

What are common barbiturates?

A

Phenobarbital
Pentobarbital
Thiopental
Secobarbital

82
Q

What is the MOA of barbiturates?

A

facilitate GABA-A action by increasing DURATION of Cl channel opening thus decreasing neuron firing)

*BARBI (barbituates) likes it longer, BEN (benzodiazepines) wants it more often

83
Q

What condition are barbiturates contraindicated in?

A

Porphyria

84
Q

Clinical use of barbiturates?

A

sedative

anxiety, seizures, insomnia, induction of anaesthesia– thiopental

85
Q

Toxicity of Barbiturates?

A

Respiratory and cardiovascular depression (may be fatal)
CNS depression (exacerbated with BZD & ETOH use)
dependence
drug interactions (induces p450)

86
Q

Antidote for Barbiturate OD?

A

supportive– respiratory assistance & BP maintenance

87
Q

What are common Benzodiazepines?

A 
Diazepam
Lorazepam
Triazolam
Temazepam
Oxazepam
Midazolam
Chlordiazepoxide
Alprazolam
88
Q

What is the MOA of Benzodiazepines?

A

facilitate GABA-A action by increasing the FREQUENCY of Cl channel opening
dec REM sleep
most have long-half lives

*Barbi likes it longer, Ben wants it more frequently

89
Q

Short-half life benzodiazepines?

A

Triazolam
Oxazepam
Midazolam

*higher addictive potential

90
Q

Clinical use of Benzodiazepines?

A

anxiety, spasticity, status epilepticus, detoxification (ETOH withdrawal/DT’s), night terros, sleepwalking, general anethetic, hypnotic.

91
Q

Toxicity of Benzodiazepines?

A

Dependence
additive CNS depression effects w/ ETOH & Barbs
Less coma & resp depression risk than Barbs

92
Q

Antidone for OD?

A

Flumazenil

competitive antagonist at GABA benzodiazepine receptor

93
Q

Nonbenzodiazepine Hypnotics

A

Zolpidem, Zaleplon, Eszopiclone

94
Q

MOA of non-benzo hypnotics?

A

act via BZ-1 subtype of GABA receptor

95
Q

clinical use of non-benzo hypnotics?

A

insomnia

96
Q

Toxicity of non-benzo hyponotics?

A

ataxia, HA, confusion
rapid metab by liver enzymes = short duration of action
few amnestic events and modest day-after psychomotor depression
lower dependence risk than BZDs

97
Q

Anesthetic drugs with low solubility in blood

A

rapid induction and recovery times

lower potency

98
Q

Anesthetic drugs with high solubility in lipids

A

high potency = 1/ MAC

MAC = minimal alveolar concentration at which 50% of the population is anesthetized. varies with age

99
Q

Inhaled anesthetics

A 
halothane
enflurane
isoflurane
secoflurane
methoxyflurane
nitrous oxide
100
Q

Effects of inhaled anesthetics?

A

unknown MOA

myocardial depression, respiratory depression, nausea/ emesis, inc cerebral blood flow (dec cerebral metabolic demand)

101
Q

Toxicity of inhaled anesthetics?

A

Hepatotoxicity (halothane)
nephrotoxicity (methoxyflurane)
proconvulsant (enflurane)
malignant hyperthermia (all but nitrous oxide– rare & life-threatening, inherited susceptibility)
expansion of trapped gas in body cavity (Nitrous oxide)

102
Q

IV anesthetics?

A 
Barbiturates (Thiopental)
Benzodiazepines (Midazolam)
Arylcyclohexylamines (ketamine-- PCP analogs)
Opioids (morphine & fentayl)
Propofol
103
Q

Thiopental

A

barbiturate anesthetic
high potency– high lipid solubility & rapid entry into brain
used for induction of anesthesia & short surgical procedures
effects terminated by rapid redistribution into tissue & fat
decreased cerebral blood flow

104
Q

Midazolam

A

most common drug used in endoscopy
used adjunctively with gas anesthetics & narcotics
may cause severe post-op respiratory depression, dec BP (tx OD w/ Flumazenil) and amnesia

105
Q

Ketamine/ PCP analogs

A 
dissociative anesthetics
block NMDA receptors
Cardiovascular stimulants
cause disorientation, hallucination, and bad dreams
inc cerebral blood flow
106
Q

Morphine & Fentanyl

A

used with other CNS depressants in general anesthesia

107
Q

Propofol

A 
sedation in ICU
rapid induction of anesthesia
short procedure anesthesia
less post-op nausea than thiopental
potentiates GABA-A
108
Q

Local anesthetics

A

2 classes:

1) esters— procaine, cocaine, tetracaine
2) amides— lidocaine, mepivacaine, bupivacaine (all have 2 I’s in name)

*if ester allergy, give amide

109
Q

MOA of local anesthetics

A

blocks Na channels by dividing into specific receptors on inner portion of channel
preferentially bind to activated Na channels– so most effective in rapidly firing neurons
tertiary amine local anesthetics penetrate membrane in uncharged form, then bind to ion channels as charged form

110
Q

Order of nerve blockade in local anesthetics?

A

small-diameter fibers > large-diameter fibers
myelinated fibers > nonmyelinated fibers
*size predominates over myelination status
sm myelinated > sm unmyelinated > lg myelinated > lg unmyelinated

111
Q

Order of loss of sensations in local anesthetic?

A

1) pain
2) temperature
3) touch
4) pressure

112
Q

What happens when you give local anesthetic at an infected tissue?

A

infected tissue is acidic
anesthetic is alkaline and charged (therefore cannot penetrate membrane as effectively)
*must give more anesthetic at infected tissues

113
Q

What can you combine with local anesthetics to enhance local action?

A

vasoconstrictors (epinephrine)

decreases bleeding, increases anesthesia locally by decreasing systemic concentration

114
Q

Clinical use of local anesthetics?

A

Minor surgical procedures

Spinal anesthesia

115
Q

Toxicity of local anesthetics?

A

CNS excitation
severe cardiovascular toxicity (bupivacaine)
hypertension, hypotension & arrhythmias (cocaine)

116
Q

What are neuromuscular blockade drugs used for?

A

muscle paralysis in surgery or mechanical ventilation

selective for motor nicotinic receptor (not autonomic)

117
Q

What are the two types of neuromuscular blockade drugs?

A

Depolarizing (succinylcholine)

Nondepolarizing (Tubocurarine, etc)

118
Q

What is the common depolarizing NM blocking drug?

A

Succinylcholine

strong Ach receptor agonist

119
Q

What is the MOA of succinylcholine?

A

produces sustained depolarization and prevents muscle contraction

120
Q

How does blockade reversal occur in succinylcholine?

A

2 phases:
Phase I– prolonged deloparization.
no antidone. block potentiated by cholinesterase inhibitors.
Phase II– repolarized but blocked (ACh receptors are available but desensitized)
antidote = neostigmine (cholinesterase inhibitors)

121
Q

Complication of succinylcholine?

A

hypercalcemia
hyperkalemia
malignant hyperthermia

122
Q

Common Non-depolarizing NM blocking drugs?

A 
Tubocurarine
Atracurium
Mivacurium
Pancuronium
Vecuronium
Rocuronium
123
Q

MOA of non-depolarizing NM blocking drugs?

A

competitive antagonists– compete with ACh for receptors

124
Q

Reversal of blockade by non-depolarizing NM blocking drugs?

A

neostigmine & edrophonium

cholinesterase inhibitors

125
Q

MOA of Dantrolene?

A

prevents Ca release from sarcoplasmic reticulum of skeletal muscle

126
Q

Clinical use of Dantrolene?

A

Treats malignant hyperthermia
(rare, but life-threatening S/E of succinylcholine & inhalation anesthetics– except N2O.
Neuroleptic Malignant Syndrome (toxicity of antipsychotic drugs)

127
Q

General Parkinson’s Disease Drug strategies:

A

dopamine agonists
increase dopamine release
prevent dopamine breakdown
curb excess cholinergic activity

128
Q

Dopamine agonists used in Parkinsons?

A

Bromocriptine* (ergot)
pramipexole
ropinirole (non-ergot)
(non-ergots are preferred)

129
Q

Agents that Increase Dopamine release in Parkinsons?

A

Amantadine* (inc dopa release & also antiviral against influenza A & rubella)
L-dopa/Carbidopa* (converted to dopamine in CNS)

130
Q

Agents that prevent Dopa breakdown in parkinsons?

A

Selegiline* (selective MAO-B inhibitor)

Entacapone, Tolcapone (COMT inhibitors– prevent L-Dopa degradation = inc dopamine availability)

131
Q

Agents that curb excess cholinergic activity in Parkinsons?

A

Benzotropine
(antimuscarininc that improves tremor & rigidity but has little effect on bradykinesia)

*PARK your mercedes-BENZ here.

132
Q

Typical regimen in Parkinson’s Disease?

A 
Bromocriptine
Amantadine
Levodopa (+ Carbidopa)
Selegiline
Antimuscarinics

*BALSA

133
Q

Toxicity associated with Amantadine?

A

ataxia

134
Q

MOA of Levodopa/Carbidopa?

A

increases level of dopamine in the brain
unlike dopa, L-dopa can cross BBB and is converted by dopa decarboxylase in CNS to dopamine.
Carbidopa = peripheral decarboxylase inhibitor
given with L-dopa to increase brain bioavailability and limit peripheral side effects

135
Q

Toxicity of Levodopa/Carbidopa?

A

Arrhythmias– bc inc peripheral formation of catecholamines

Long term use = dyskinesia following administration & akinesia between doses

136
Q

MOA of selegiline?

A

Selective inhibits MAO-B (which preferentially metabolizes dopamine over NE & 5-HT) = increase availability of dopamine

137
Q

Toxicity of selegiline?

A

may enhance adverse effects of L-dopa (arrhythmia & dyskinesia with long term use)

138
Q

Alzheimer’s Drugs

A

Memantine

Donepezil, Galantamine, Rivastigmine

139
Q

MOA of Memantine?

A

un-competitive NMDA receptor antagonist

helps prevent excitotoxicity (mediated by Ca & glutamate)

140
Q

Toxicity of Memantine?

A

Dizzyness
Confusion
Hallucination

141
Q

MOA of Dopepezil, Galantamine & Rivastigmine?

A

Acetylcholinesterase inhibitors = keep ACh levels up

142
Q

Toxicity of Acetylcholinesterase inhibitors in Alzheimer’s dz?

A

Nausea, diarrhea

dizziness, insomnia, urinary incontinence

143
Q

Huntington’s Treatment?

A

Tetrabenazine & Reserpine = inhibit VMAT (limit dopamine vesicle packaging & release)
Haloperidol- dopamine receptor antagonist

144
Q

Sumatripin MOA

A 
5-HT (1B/1D) agonist
inhibits trigeminal nerve activation
prevents vasoactive peptide release
induces vasoconstriction
half-life < 2 hrs
145
Q

Clinical use of Sumatriptin?

A

Cluster HA attack

Acute Migraine

146
Q

Toxicity of Sumatripin?

A 
coronary vasospasm (CONTRA in CAD or Prinzmetal's Angina)
mild tingling
147
Q

What is the MOA of alpha methyl tyrosine?

A

Inhibits tyrosine hydroxylase decreasing conversion of tyrosine to DOPA thereby inhibiting the rate-limiting step in catecholamine synthesis

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