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USMLE Step I Pharmacology > Neurology Pharmacology > Flashcards

Neurology Pharmacology Flashcards

1
Q

glaucoma drugs–mechanism

A
  • decrease IOP by decreasing amount of aqueous humor
    • inhibit synthesis synthesis/secretion of aqueous humor OR increase drainage
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2
Q

what are the 5 categories of glaucoma drugs?

A
  • alpha agonists
  • beta blockers
  • diuretics
  • cholinomimetrics (M3)
  • prostaglandin
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3
Q

name the alpha agonist glaucoma drugs

A
  • epinephrine (alpha 1)
  • brimonidine (alpha 2)
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4
Q

alpha agonist (glaucoma drugs)–mechanism

A
  • decrease aqueous humor synthesis via vasoconstriction
  • decrease aqeous humor synthesis
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5
Q

alpha agonist (glaucoma drugs)–toxicity

A
  • mydriasis (alpha 1)
  • blurry vision
  • ocular hyperemia
  • foreign body sensation
  • ocular allergic rxns
  • ocular pruritus
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6
Q

what is a contraindication for using epinephrine for glaucoma?

A
  • patients with closed angle glaucoma
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7
Q

name the beta blocker glaucoma drugs

A
  • timolol
  • betaxolol
  • carteolol
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8
Q

beta blocker (glaucoma drugs)–mechanism

A
  • decrease aqueous humor synthesis
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9
Q

beta blocker (glaucoma drugs)–toxicity

A
  • no pupillary or vision changes
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10
Q

name the diuretics glaucoma drugs

A
  • acetazolamide
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11
Q

diuretics (glaucoma drug)–mechanism

A
  • decrease aqueous humor synthesis by inhibition of carbonic anhydrase
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12
Q

diuretics (glaucoma drug)–toxicity

A
  • no pupillary or vision changes
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13
Q

name the 2 categories of cholinomimetics glaucoma drugs and their corresponding drugs

A
  • direct
    • pilocarpine
    • carbachol
  • indirect
    • physostigmine
    • echothiophate
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14
Q

cholinomimetics–mechanism

A
  • increase outflow of aqueous humor via contraction of ciliary muscle and opening of trabecular meshwork
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15
Q

when should pilocarpine be used and why?

A
  • pilocarpine is a cholinomimetic glaucoma drug
    • use in emergencies
    • very effective at opening meshwork into the canal of Schlemm
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16
Q

cholinomimetics–toxicity

A
  • miosis–contraction of pupillary sphincter muscles
  • cyclospasm–contraction of ciliary muscle
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17
Q

name the prostaglandin glaucoma drugs

A
  • bimatoprost
  • latanoprost (PGF 2 alpha)
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18
Q

prostaglandin (glaucoma drugs)–mechanism

A
  • increase outflow of aqueous humor
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19
Q

prostaglandin (glaucoma drugs)–toxicity

A
  • darkens color of iris (browning)
  • eyelash growth
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20
Q

name the opioid analgesics

A
  • morphine
  • fentanyl
  • codeine
  • loperamide
  • methadone
  • meperidine
  • dextromethorphan
  • diphenoxylate
  • pentazocine
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21
Q

opioid analgesics–mechanism

A
  • acts as agonists at opioid receptors to modulate synaptic transmission–open K + channels and close Ca2+ channels –> dec synaptic transmission
    • opioid receptors:
      • µ = beta endorphin
      • delta = enkephalin
      • kappa = dynorphin
  • inhibit release of ACh, norepinephrine, 5-HT, glutamine, substance P
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22
Q

opioid analgesics–use

A
  • pain
  • cough suppression (dextromethorphan)
  • diarrhea (loperamide, diphenoxylate)
  • acute pulmonary edema
  • maintenance programs for heroin addicts (methadone, buprenorphine + naloxone)
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23
Q

opioid analgesics–toxicity

A
  • addiction
  • respiratory depression
  • constipation
  • miosis
    • except meperidine which causes mydriasis
  • additive CNS depression with other drugs
  • tolerance does not develop to miosis and constipation
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24
Q

opioid analgesics–antidote

A
  • naloxone
  • naltrexone
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25
Q

pentazocine–mechanism

A
  • kappa-opioid receptor agonist
  • µ-opioid receptor antagonist
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26
Q

pentazocine–use

A
  • analgesia for moderate to severe pain
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27
Q

pentazocine–toxicity

A
  • can cause opiod withdrawal symptoms if patient is also taking full opioid antagonist
    • b/c competition for opioid receptors
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28
Q

butorphanol–mechanism

A
  • kappa opiod receptor agonist
  • µ opioid receptor partial agonist
  • produces analgesia
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29
Q

butorphanol–use

A
  • severe pain
    • migraine
    • labor
  • causes less respiratory depression than full opioid agonists
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30
Q

butorphanol–toxicity

A
  • can cause opioid withdrawal symptoms if patient is also taking full opioid agonist
    • competition for opioid receptors
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31
Q

butorphanol–antidote

A
  • overdose not easily reversed with naloxone
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32
Q

tramadol–mechanism

A
  • very weak opioid agonist
  • inhibits 5-HT and norepinephrine reuptake
    • works on multiple neurotransmitters
      • “tram it all” in with tramadol
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33
Q

tramadol–use

A
  • chronic pain
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34
Q

tramadol–toxicity

A
  • similar to opioids
  • decreases seizure threshold
  • serotonin syndrome
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35
Q

ethosuximide–use

A
  • first line for generalized absence (petit mal) seizures
    • Sucks to have Silent (absence) Seizures
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36
Q

ethosuximide–side effects

A
  • DI
  • fatigue
  • headache
  • urticaria
  • Stevens-Johnson syndrome
  • EFGHIJ–Ethosuximide causes fatigue, GI distress, Headache, Itching, and Stevens Johnson syndrome
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37
Q

ethosuximide–mechanism

A
  • blocks thalamic T type Ca2+ channels
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38
Q

name the benzodiazepines

A
  • diazepam
  • lorazepam
  • midazolam
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39
Q

benzodiazepines–use

A
  • generalized static epilepticus
  • first line for acute
  • also for eclampsia seizures
    • first line for eclampsia seizures is MgSO4
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40
Q

benzodiazepines–mechanism

A
  • increase GABAA action
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41
Q

benzodiazepines–side effects

A
  • sedation
  • tolerance
  • dependence
  • respiratory depression
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42
Q

phenobarbital–use

A
  • simple partial (focal) seizures
  • complex partial (focal) seizures
  • generalized tonic clonic seizures (grand mal)
  • first line in neonates
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43
Q

phenobarbital–mechanism

A
  • increase GABAA action
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44
Q

phenobarbital–side effects

A
  • sedation
  • tolerance
  • dependence
  • induction of cytochrome P 450
  • cardiorespiratory depression
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45
Q

phenytoin, fosphenytoin–use

A
  • simple partial (focal) seizures
  • complex partial (focal) seizures
  • first line generalized tonic clonic (grand mal) seizures
  • generalized static epilepticus
    • first line for prophylaxis
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46
Q

phenytoin, fosphenytoin–mechanism

A
  • blocks Na+ channels
  • zero order kinetics
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47
Q

phenytoin, fosphenytoin–side effects

A
  • neurologic
    • nystagmus
    • diplopia
    • ataxia
    • sedation
    • peripheral neuropathy
  • dermatologic
    • hersutism
    • Stevens Johnson syndrome
    • gingival hyperplasia
    • DRESS syndrome
  • musculoskeletal
    • osteopenia
    • SLE-like syndrome
  • hematologic
    • megaloblastic anemia
  • reproductive
    • teratogenesis–fetal hydantoin syndrome
  • other
    • cytochrome P 450 induction
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48
Q

carbamazepine–use

A
  • first line for simple partial (focal) seizures
  • first line for complex partial (focal) seizures
  • generalized tonic clonic (grand mal) seizures
  • first line for trigeminal neuralgia
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49
Q

carbamazepine–mechanism

A
  • blocks Na+ channels
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50
Q

carbamazepine–side effects

A
  • diplopia
  • ataxia
  • blood dyscrasias
    • agranulocytosis
    • aplastic anemia
  • liver toxicity
  • teratogenesis
  • induction of cytochrome P-450
  • SIADH
  • Stevens Johnson Syndrome
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51
Q

valproic acid–use

A
  • simple partial (focal) seizures
  • complex partial (focal) seizures
  • first line for generalized tonic clonic (grand mal) seizures
  • generalized absence seizures
  • also used for myoclonic seizures, bipolar disorder, migraine prophylaxis
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52
Q

valproic acid–mechanism

A
  • increase Na+ channel inactivation
  • increase GABA concentration by inhibiting GABA transaminase
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53
Q

valproic acid–side effects

A
  • GI distress
  • rare but fetal hepatotoxicity (measure LFTs)
  • pancreatitis
  • neural tube defects
  • tremor
  • weight gain
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54
Q

what is a contraindication for valproic acid?

A
  • pregnancy
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55
Q

vigabatrin–use

A
  • simple partial (focal) seizures
  • complex partial (focal) seizures
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56
Q

vigabatrin–mechanism

A
  • increase GABA by irreversibly inhibiting GABA transaminase
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57
Q

gabapentin–use

A
  • simple partial (focal) seizures
  • complex partial (focal) seizures
  • also used for peripheral neuropathy, postherpetic neuralgia
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58
Q

gabapentin–mechanism

A
  • primarily inhibits high voltage activated Ca2+ channels
  • designed as a GABA analog
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59
Q

gabapentin–side effects

A
  • sedation
  • ataxia
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60
Q

topiramate–use

A
  • simple partial (focal) seizures
  • complex partial (focal) seizures
  • generalized tonic clonic (grand mal) seizures
  • also used for migraine prevention
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61
Q

lamotrigine–use

A
  • simple partial (focal) seizures
  • complex partial (focal) seizures
  • generalized tonic clonic (grand mal) seizures
  • generalized absence (petit mal) seizures
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62
Q

lamotrigine–mechanism

A
  • blocks voltage gated Na+ channels
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63
Q

lamotrigine–side effects

A
  • Stevens Johnson syndrome
    • must be titrated slowly
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64
Q

levetiracetam–use

A
  • simple partial (focal) seizures
  • complex partial (focal) seizures
  • generalized tonic clonic (grand mal) seizures
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65
Q

levetiracetam–mechanism

A
  • unknown
    • may modulate GABA and glutamate release
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66
Q

tiagabine–use

A
  • simple partial (focal) seizures
  • complex partial (focal) seizures
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67
Q

tiagabine–mechanism

A
  • increase GABA by inhibiting reuptake
68
Q

name the barbiturates

A
  • phenobarbital
  • pentobarbital
  • thiopental
  • secobarbital
69
Q

barbiturates–mechanism

A
  • facilitate GABAA action by increasing duration of Cl- channel opening
    • so decreases neuron firing
      • barbidurates increase duration
70
Q

what is a contraindication for barbiturate use?

A
  • porphyria
71
Q

barbiturates–use

A
  • sedative for anxiety
  • seizures
  • insomnia
  • induction of anesthesia (thiopental)
72
Q

barbiturates–toxicity

A
  • respiratory and cardiovascular depression–can be fatal
  • CNS depression–can be exacerbated by alcohol use
  • dependence
  • drug interactions–induces cytochrome P-450
73
Q

barbiturates–antidote

A
  • overdose treatment is supportive
    • assist respiration
    • maintain BP
74
Q

name the benzodiazepines

A
  • diazepam
  • lorazepam
  • triazolam
  • temazepam
  • oxazepam
  • midazolam
  • chlordiazepoxide
  • alprazolam
75
Q

benzodiazepines–mechanism

A
  • facilitate GABAA action by in frequency of Cl- channel opening
    • “frenzodiazepines increase frequency”
    • benzos, barbs, and alcohol all bind the GABAA receptor, which is a ligand gated Cl- channel
  • decrease REM sleep
  • most have long half lives and acive metabolites
    • exceptions: ATOM: Alprazolam, Triazolam, Oxazepam, Midazolam–short acting
      • higher addictive potential
76
Q

benzodiazepines–use

A
  • anxiety
  • spasticity
  • status epilepticus (lorazepam and diazepam)
  • eclampsia
  • detoxification–especially alcohol withdrawal (DTs)
  • night terrors
  • sleepwalking
  • general anesthetic–amnesia, muscle relaxation
  • hypnotic–insomnia
77
Q

benzodiazepines–toxicity

A
  • dependence
  • additive CNS depression effects with alcohol
  • less risk of respiratory depression and coma than with barbiturates
78
Q

benzodiazepines–antidone

A
  • treat overdose with flumazenil–competitive antagonist at GABA benzodiazepine receptor
    • can precipitate seizures by causing acute benzodiazepine withdrawal
79
Q

name the non-benzodiazepine hypnotics

A
  • Zolpidem
  • Zalepon
  • esZopiclone
    • “All ZZZs put you to sleep”
80
Q

non-benzodiazepine hypnotics–mechanism

A
  • act via the BZ1 subtype of the GABA receptor
    • sleep cycle less affected as compared with benzodiazepine hypnotics
81
Q

non-benzodiazepine hypnotics–antidote

A
  • flumazenil
82
Q

non-benzodiazepine hypnotics–use

A
  • insomnia
83
Q

non-benzodiazepine hypnotics–toxicity

A
  • ataxia
  • headaches
  • confusion
  • decreased dependence risk than benzodiazepines
84
Q

why do non-benzodiazepine hypnotics have a short duration?

A
  • b/c of rapid metabolism by liver enzymes
85
Q

how are non-benzodiazepine hypnotics different than older sedative hypnotics?

A
  • they have only modest day-after psychomotor depression
  • have few amnestic effects
86
Q

what is important about CNS drugs?

A
  • must be lipid soluble (cross the blood brain barrier) OR be actively transported
87
Q

what is true about anesthetics with decreased solubility in blood?

A
  • rapid induction
  • rapid recovery times
88
Q

what is true about anesthetics with increased solubility in lipids?

A
  • increased potency = 1/MAC
    • MAC = Minimal Alveolar Concentration (of inhaled anesthetic) required ot prevent 50% of subjects from moving in response to noxious stimulus (ie. skin incision)
      • examples:
        • nitrous oxide (N2O) has dec blood and lipid solubility, and thus fast induction and low potency
        • halothan has increased lipid and blood solubility, and thus high potency and slow induction
89
Q

name the inhaled anesthetics

A
  • desflurane
  • halothane
  • enflurane
  • isoflurane
  • secoflurane
  • methoxyflurane
  • N2O
90
Q

inhaled anesthetics–mechanism

A
  • mechanism unknown
91
Q

inhaled anesthetics–side effects

A
  • myocardial depression
  • respiratory depression
  • nausea/emesis
  • increased cerebral blood flow
    • decreased cerebral metabolic demand
92
Q

inhaled anesthetics–toxicity

A
  • hepatotoxicity (halothane)
  • nephrotoxicity (methoxyflurane)
  • proconvulsant (enflurane)
  • expansion of trapped gas in a body cavity (N2O)
  • malignant hyperthermia
93
Q

explain malignant hyperthermia

A
  • rare, life threatening condition in which inhaled anesthetics or succinylcholine induce fever and severe muscle contractions
  • susceptibility inherited as autosomal dominant with variable penetrance
  • mutations in voltage sensitive ryanodine receptor cause increased Ca2+ release from sarcoplasmic reticulum
  • treatment: dantrolene–ryanodine receptor antagonist
94
Q

name the intravenous anesthetics

A
  • barbiturates
    • THiopental
  • benzodiazepines
    • Midazolam
  • arylcyclohexylamines
    • Ketamine
  • Propofol
  • Opioids
    • “The Mighty King Proposes Foolishly to Oprah.”
95
Q

barbiturates (thiopental) as IV anesthetic–mechanism

A
  • high potency
  • high lipid solubility
  • rapid entry into brain
  • effect terminated by rapid reditribution into tissue and fat
96
Q

barbiturates (thiopental) as IV anesthetic–use

A
  • used for induction of anesthesia
  • short surgical procedures
97
Q

barbiturates (thiopental) as IV anesthetic–toxicity

A
  • decreased cerebral blood flow
98
Q

benzodiazepines (midazolam) as IV anesthetic–use

A
  • used for endoscopy
  • used adjunctively with gaseous anesthetics and narcotics
99
Q

benzodiazepines (midazolam) as IV anesthetic–toxicity

A
  • may cause severe post op respiratory depression
  • decrease BP
    • treat overdose with flumazenil
  • anterograde amnesia
100
Q

arylcyclohexylamines (ketamine) as IV anesthetic–mechanism

A
  • PCP analogs that act as dissociative anesthetics
  • block NMDA receptors
  • cardiovascular stimulants
101
Q

arylcyclohexylamines (ketamine) as IV anesthetic–toxicity

A
  • disorientation
  • hallucination
  • bad dreams
  • increased cerebral blood flow
102
Q

propofol as IV anesthetic–use

A
  • sedation in ICU
  • rapid anesthesia
  • short procedures
103
Q

propofol as IV anesthetic–mechanism

A
  • potentiates GABAA
104
Q

benefits of using propofol as IV anesthetic

A
  • less post op nausea than thiopental
105
Q

opioids as IV anesthetic–use

A
  • morphine, fentanyl used with other CNS depressants during general anesthesia
106
Q

name the local anesthetics that are esters

A
  • procaine
  • cocaine
  • tetracaine
  • benzocaine
107
Q

name the local anesthetics that are amides

A
  • lIdocaIne
  • mepIvacaIne
  • bupIvacaIne
    • amIdes have 2 I’s
108
Q

local anesthetics–mechanism

A
  • block Na+ channels by binding to specific receptors on inner portion of channel
    • tertiary amine local anesthetics penetrate membrane in uncharged form, then bind to ion channels as charged form
109
Q

where are local anesthetics most effective?

A

rapidly firing neurons

110
Q

why would local anesthetics be administered with vasoconstrictors, particularly epinephrine?

A
  • to enhance local action
    • causes decreased bleeding, increased anesthesia by decreasing systemic concentration
111
Q

alkaline anesthetics in infected (acidic) tissue

A
  • in infected (acidic) tissue, alkaline anesthetics are charged and cannot penetrate membrane effectively
    • you would need more anesthetic
112
Q

what is the order of the nerve blockade with local anesthetics?

A
  • small diameter fibers > large diameter fibers
  • myelinated fibers > unmyelinated fibers
    • overall size factor predominates over myelination, so:
      • small myelinated fibers > small unmyelinated fibers > large myelinated fibers > large unmyelinated fibers
113
Q

what is the order of loss with local anesthetics?

A
  1. pain
  2. temperature
  3. touch
  4. pressure
114
Q

local anesthetics–use

A
  • minor surgical procedures
  • spinal anesthesia
  • if allergic to esters, give amides
115
Q

local anesthetics–toxicity

A
  • CNS excitation
  • severe cardiovascular toxicity (bupivacaine)
  • hypertension
  • hypotension
  • arrhythmias (cocaine)
  • methemoglobinemia (benzocaine)
116
Q

neuromuscular blocking drugs–use

A
  • muscle paralysis in surgery
  • mechanical ventilation
117
Q

neuromuscular blocking drugs–mechanism

A
  • selective for motor (vs autonomic) nicotinic receptors
118
Q

name the depolarizing neuromuscular blocking drugs

A
  • succinylcholine
119
Q

succinylcholine–mechanism

A
  • (depolarizing neuromuscular blocking drug)
  • strong ACh receptor agonist
  • produces sustained depolarization
  • prevents muscle contraction
120
Q

depolarizing neuromuscular blocking drugs–reversal of blockade

A
  • phase I–prolonged depolarization
    • no antidote
    • block potentiated by cholinesterase inhibitors
  • phase 2–repolarized but blocked; ACh receptors are available but desensitized
    • may be reversed with cholinesterase inhibitors
121
Q

depolarizing neuromuscular blocking drugs–complications

A
  • hypercalcemia
  • hyperkalemia
  • malignant hyperthermia
122
Q

name the nondepolarizing neuromuscular blocking drugs

A
  • tubocurarine
  • atracurium
  • mivacurium
  • pancoronium
  • vecuronium
  • rocuronium
123
Q

nondepolarizing neuromuscular blocking drugs–mechanism

A
  • competitive antagonists
  • compete with ACh for receptors
124
Q

nondepolarizing neuromuscular blocking drugs–reversal of blockade

A
  • neostigmine–must be given with atropine to prevent muscarinic effects such as bradycardia
  • endrophonium
  • other cholinesterase inhibitors
125
Q

dantrolene–mechanism

A
  • prevents release of Ca2+ from the sarcoplasmic reticulum of skeletal muscle by binding to the ryanodine receptor
126
Q

dantrolene–use

A
  • malignant hyperthermia
  • neuroleptic malignant syndrome–a toxicity of antipsychotic drugs
127
Q

baclofen–mechanism

A
  • activates GABAB receptors at spinal cord level
    • which induces skeletal muscle relaxation
128
Q

baclofen–use

A
  • muscle spasms
    • ie. acute low back pain
129
Q

cyclobenzaprine–mechanism

A
  • centrally acting skeletal muscle relaxant
  • structurally related to TCAs
    • similar anticholinergic side effects
130
Q

cyclobenzaprine–use

A
  • muscle spasms
131
Q

what is the cause of Parkinson disease?

A
  • loss of dopiminergic neurons
  • excess cholinergic activity
132
Q

what are the 5 Parkinson disease drugs?

A
  • Bromocriptine
  • Amantidine
  • Levodopa (with carbidopa)
  • Selegiline (and COMT inhibitors)
  • Antimuscarinics
    • “BALSA”
133
Q

what are 5 strategies used for Parkinson disease drugs?

A
  1. dopamine agonists
  2. increase dopamine availability
  3. increase L-dopa availability
  4. prevent dopamine breakdown
  5. curb excess cholinergic activity
134
Q

name the Parkinson disease drugs that are dopamine agonists

A
  • Ergot–Bromocriptine
  • Non-Ergot (preferred)–pramipexole, ropinirole
135
Q

Parkinson disease drugs that increase dopamine availability

A
  • Amantidine
    • increase dopamine release and decrease dopamine reuptake
136
Q

amantidine–toxicity

A
  • (Parkinson disease drug that inc dopamine availability)
  • ataxia
  • livedo reticularis
137
Q

name the Parkinson disease drugs that increase L-DOPA availability

A
  • Levodopa/cardidopa
  • Entacarpone
  • tolcapone
138
Q

Parkinson disease drugs that increase L-DOPA availability–mechanism

A
  • agents prevent peripheral (pre-BBB) L-dopa degradation –> increase L-DOPA entering CNS –> increase central L-DOPA availabilie for conversion to dopamine
139
Q

Entacapone, Tolcapone–mechanism

A
  • (Parkinson disease drugs that increase L-DOPA availability)
  • prevent peripheral L-dopa degradation to 3-O-methyldopa (3-OMD) by inhibiting COMT
140
Q

name the Parkinson disease drugs that prevent dopamine breakdown

A
  • agents act centrally (post BBB) to inhibit breakdown of dopamine
  • Selegiline
  • Tolcapone
141
Q

Selegiline–mechanism

A
  • (Parkinson disease drugs that prevent dopamine breakdown)
  • blocks conversion of dopamine into DOPAC by selectively inhibiting MAO-B
142
Q

Tolcapone–mechanism

A
  • (Parkinson disease drugs that prevent dopamine breakdown)
  • blocks conversion of dopamine to 3-OMD by inhibiting central COMT
143
Q

name the Parkinson disease drugs that curb excess cholinergic activity and what is the mechanism?

A
  • Benztropine
    • Antimuscarinic
      • improves tremor and rigidity but has little effect on bradykinesia in Parkinson disease
        • “Park your Mercedes Benz”
144
Q

Levodopa (L-dopa)/Carbidopa–mechanism

A
  • increase level of dopamine in the brain
  • converted by dopa decarboxylase in the CNS to dopamine
145
Q

how is L-dopa (levodopa)/carbidopa different than dopamine?

A
  • L-dopa can cross blood brain barrier and is converted by dopa decarboxylase in the CNS to dopamine
146
Q

why is carbidopa administered with L-dopa?

A
  • carbidopa is a peripheral DOPA decarboxylase inhibitor
    • given with L-dopa to increase the bioavailability of L-dopa in the brain and to limit peripheral side effects (like nausea and vomiting)
147
Q

L-dopa (levodopa)/Carbidopa–use

A

Parkinson disease

148
Q

L-dopa (levodopa)/Carbidopa–toxicity

A
  • arrhythmias from increase peripheral formation of catecholamines
149
Q

L-dopa (levodopa)/Carbidopa–what can come about as a result of long term use?

A
  • dyskinesia following administration (“on off” phenomenon
  • akinesia b/w doses
150
Q

selegiline, rasagiline–mechanism

A
  • selectively inhibit MAO-B (metabolize dopamine) –> increase dopamine availability
151
Q

selegiline, rasagiline–use

A
  • adjunctive agent to L-dopa in treatment of Parkinson disease
152
Q

name the 5 Alzheimer drugs

A
  • Memantine
  • Donepezil
  • galantamine
  • rivastigmine
  • tacrine
153
Q

Memantine–mechanism

A
  • (Alzheimer drug)
  • NMDA receptor antagonist
  • helps prevent excitotoxicity
    • mediated by Ca2+
154
Q

memantine–toxicity

A
  • (Alzheimer drug)
  • dizziness
  • confusion
  • hallucination
155
Q

donepezil, galantamine, rivastigmine, tacrine–mechanism

A
  • (Alzheimer drug)
  • AChE inhibitors
156
Q

donepezil, galantamine, rivastigmine, tacrine–toxicity

A
  • (Alzheimer drug)
  • nausea
  • dizziness
  • insomnia
157
Q

name the 3 drugs that can be used to treat Huntington disease

A
  • tetrabenazine
  • reserpine
  • Haloperidol
158
Q

Tetrabenazine and reserpine–mechanism

A
  • (Huntington dz drug)
  • inhibit vesicular monoamine transporter (VMAT) –> dec dopamine vesicle packaging and release
159
Q

Haloperidol–mechanism

A
  • (Huntington dz drug)
  • D2 receptor antagonist
160
Q

riluzole–mechanism and use

A
  • tx for ALS
  • modestly increases survival by decreasing glutamate excitotoxicity via an unclear mechanism
    • “For Lou Gehrig dz, give rilouzole”
161
Q

name the Triptan and what is the mechanism?

A
  • Sumatriptan
    • 5-HT1B/1D agonists
    • inhibit trigeminal nerve activation
    • prevent vasoactive peptide release
    • induce vasoconstriction
      • “A SUMo wrestler TRIPs ANd falls on your head”
162
Q

sumatriptan–use

A
  • (Triptan)
  • acute migrain
  • cluster headache attacks
    • “A SUMo wrestler TRIPs ANd falls on your head​”
163
Q

sumatriptan–toxicity

A
  • (Triptan)
  • coronary vasospasm
  • mild paresthesia
164
Q

what is a contraindication of sumatriptan?

A
  • patients with CAD or Prinzmetal angina
165
Q
A

USMLE Step I Pharmacology (17 decks)

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