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First Aid > Neurology - Pharmacology > Flashcards

Neurology - Pharmacology Flashcards

1
Q

Glaucoma drugs

A
  • Decrease IOP via decreased amount of aqueous humor
  • Inhibit synthesis/secretion or increase drainage
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2
Q

Epinephrine

  • Type of drug
  • Mechanism
  • Side effects
A
  • Type of drug
    • Glaucoma drug: α-agonist
  • Mechanism
    • Decreases aqueous humor synthesis via vasoconstriction
  • Side effects
    • Mydriasis
    • Do not use in closed-angle glaucoma
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3
Q

Brimonidine

  • Type of drug
  • Mechanism
  • Side effects
A
  • Type of drug
    • Glaucoma drug: α-agonist
  • Mechanism
    • Decreases aqueous humor synthesis
  • Side effects
    • Blurry vision
    • Ocular hyperemia
    • Foreign body sensation
    • Ocular allergic reactions
    • Ocular pruritus
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4
Q

Timolol, betaxolol, carteolol

  • Type of drug
  • Mechanism
  • Side effects
A
  • Type of drug
    • Glaucoma drugs: β-blockers
  • Mechanism
    • Decrease aqueous humor synthesis
  • Side effects
    • No pupillary or vision changes
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5
Q

Acetazolamide

  • Type of drug
  • Mechanism
  • Side effects
A
  • Type of drug
    • Glaucoma drug: Diuretic
  • Mechanism
    • Decreases aqueous humor synthesis via inhibition of carbonic anhydrase
  • Side effects
    • No pupillary or vision changes
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6
Q

Pilocarpine, carbachol

  • Type of drug
  • Mechanism
  • Side effects
A
  • Type of drug
    • Glaucoma drugs: Direct cholinomimetics
  • Mechanism
    • Increase outflow of aqueous humor via contraction of ciliary muscle and opening of trabecular meshwork
  • Side effects
    • Miosis and cyclospasm (contraction of ciliary muscle)
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7
Q

Physostigmine, echothiophate

  • Type of drug
  • Mechanism
  • Side effects
A
  • Type of drug
    • Glaucoma drugs: Indirect cholinomimetics
  • Mechanism
    • Use pilocarpine in emergencies
    • Very effective at opening meshwork into canal of Schlemm
  • Side effects
    • Miosis and cyclospasm (contraction of ciliary muscle)
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8
Q

Latanoprost

  • Type of drug
  • Mechanism
  • Side effects
A
  • Type of drug
    • Glaucoma drug: Prostaglandin (PGF2α)
  • Mechanism
    • Increases outflow of aqueous humor
  • Side effects
    • Darkens color of iris (browning)
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9
Q

Opioid analgesics

  • Examples
  • Mechanism
  • Clinical use
  • Toxicity
A
  • Examples
    • Morphine, fentanyl, codeine, loperamide, methadone, meperidine, dextromethorphan, diphenoxylate.
  • Mechanism
    • Act as agonists at opioid receptors (mu = morphine, delta = enkephalin, kappa = dynorphin) to modulate synaptic transmission
    • Open K+ channels, close Ca2+ channels –>Ž decreased synaptic transmission.
    • Inhibit release of ACh, norepinephrine, 5-HT, glutamate, substance P.
  • Clinical use
    • Pain, cough suppression (dextromethorphan), diarrhea (loperamide and diphenoxylate), acute pulmonary edema, maintenance programs for heroin addicts (methadone).
  • Toxicity
    • Addiction, respiratory depression, constipation, miosis (pinpoint pupils), additive CNS depression with other drugs.
    • Tolerance does not develop to miosis and constipation.
    • Toxicity treated with naloxone or naltrexone (opioid receptor antagonist).
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10
Q

Butorphanol

  • Mechanism
  • Clinical use
  • Toxicity
A
  • Mechanism
    • Mu-opioid receptor partial agonist and kappa-opioid receptor agonist; produces analgesia.
  • Clinical use
    • Severe pain (migraine, labor, etc.).
    • Causes less respiratory depression than full opioid agonists.
  • Toxicity
    • Can cause opioid withdrawal symptoms if patient is also taking full opioid agonist (competition for opioid receptors).
    • Overdose not easily reversed with naloxone.
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11
Q

Tramadol

  • Mechanism
  • Clinical use
  • Toxicity
A
  • Mechanism
    • Very weak opioid agonist
    • Also inhibits serotonin and norepinephrine reuptake
    • Works on multiple neurotransmitters
      • “Tram it all” in with tramadol
  • Clinical use
    • Chronic pain.
  • Toxicity
    • Similar to opioids.
      • Addiction, respiratory depression, constipation, miosis (pinpoint pupils), additive CNS depression with other drugs.
      • Tolerance does not develop to miosis and constipation.
      • Toxicity treated with naloxone or naltrexone (opioid receptor antagonist).
    • Decreases seizure threshold.
    • Serotonin syndrome.
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12
Q

Ethosuximide

  • Type of drug
  • Partial (focal)
    • Simple?
    • Complex?
  • Generalized
    • Tonic-clonic?
    • Absence?
    • Status Epileptics?
  • Mechanism
  • Side effects
  • Notes
A
  • Type of drug
    • Epilepsy drug
  • Partial (focal)
    • Simple? N
    • Complex? N
  • Generalized
    • Tonic-clonic? N
    • Absence? Y (1st line)
    • Status Epileptics? N
  • Mechanism
    • Blocks thalamic T-type Ca2+ channels
  • Side effects
    • GI, fatigue, headache, urticaria, Steven-Johnson syndrome.
    • EFGHIJ—Ethosuximide causes Fatigue, GI distress, Headache, Itching, and Stevens-Johnson syndrome
  • Notes
    • Sucks to have Silent (absence) Seizures
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13
Q

Benzodiazepines (diazepam, lorazepam)

  • Type of drug
  • Partial (focal)
    • Simple?
    • Complex?
  • Generalized
    • Tonic-clonic?
    • Absence?
    • Status Epileptics?
  • Mechanism
  • Side effects
  • Notes
A
  • Type of drug
    • Epilepsy drug
  • Partial (focal)
    • Simple? N
    • Complex? N
  • Generalized
    • Tonic-clonic? N
    • Absence? N
    • Status Epileptics? Y (1st line for acute)
  • Mechanism
    • Increases GABAA action
  • Side effects
    • Sedation, tolerance, dependence, respiratory depression
  • Notes
    • Also for eclampsia seizures (1st line is MgSO4)
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14
Q

Phenytoin

  • Type of drug
  • Partial (focal)
    • Simple?
    • Complex?
  • Generalized
    • Tonic-clonic?
    • Absence?
    • Status Epileptics?
  • Mechanism
  • Side effects
  • Notes
A
  • Type of drug
    • Epilepsy drug
  • Partial (focal)
    • Simple? Y
    • Complex? Y
  • Generalized
    • Tonic-clonic? Y (1st line)
    • Absence? N
    • Status Epileptics? Y (1st line for prophylaxis)
  • Mechanism
    • Increases Na+ channel inactivation
    • Zero-order kinetics
  • Side effects
    • Nystagmus, diplopia, ataxia, sedation, gingival hyperplasia, hirsutism, peripheral neuropathy, megaloblastic anemia, teratogenesis (fetal hydantoin syndrome) SLE-like syndrome, induction of cytochrome P-450, lymphadenopathy, Stevens-Johnson syndrome, osteopenia
  • Notes
    • Fosphenytoin for parenteral use
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15
Q

Carbamazepine

  • Type of drug
  • Partial (focal)
    • Simple?
    • Complex?
  • Generalized
    • Tonic-clonic?
    • Absence?
    • Status Epileptics?
  • Mechanism
  • Side effects
  • Notes
A
  • Type of drug
    • Epilepsy drug
  • Partial (focal)
    • Simple? Y (1st line)
    • Complex? Y (1st line)
  • Generalized
    • Tonic-clonic? Y (1st line)
    • Absence? N
    • Status Epileptics? N
  • Mechanism
    • Increases Na+ channel inactivation
  • Side effects
    • Diplopia, ataxia, blood dyscrasias (agranulocytosis, aplastic anemia), liver toxicity, teratogenesis, induction of cytochrome P-450, SIADH, Stevens-Johnson syndrome
  • Notes
    • 1st line for trigeminal neuralgia
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16
Q

Valproic acid

  • Type of drug
  • Partial (focal)
    • Simple?
    • Complex?
  • Generalized
    • Tonic-clonic?
    • Absence?
    • Status Epileptics?
  • Mechanism
  • Side effects
  • Notes
A
  • Type of drug
    • Epilepsy drug
  • Partial (focal)
    • Simple? Y
    • Complex? Y
  • Generalized
    • Tonic-clonic? Y (1st line)
    • Absence? Y
    • Status Epileptics? N
  • Mechanism
    • Increases Na+ channel inactivation
    • Increases GABA concentration by inhibiting GABA transaminase
  • Side effects
    • GI, distress, rare but fatal hepatotoxicity (measure LFTs), neural tube defects in fetus (spina bifida), tremor, weight gain, contraindicated in pregnancy
  • Notes
    • Also used for myoclonic seizures, bipolar disorder
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17
Q

Gabapentin

  • Type of drug
  • Partial (focal)
    • Simple?
    • Complex?
  • Generalized
    • Tonic-clonic?
    • Absence?
    • Status Epileptics?
  • Mechanism
  • Side effects
  • Notes
A
  • Type of drug
    • Epilepsy drug
  • Partial (focal)
    • Simple? Y
    • Complex? Y
  • Generalized
    • Tonic-clonic? Y
    • Absence? N
    • Status Epileptics? N
  • Mechanism
    • Primarily inhibits high-voltage-activated Ca2+ channels
    • Designed as GABA analog
  • Side effects
    • Sedation, ataxia
  • Notes
    • Also used for peripheral neuropathy, postherpetic neuralgia, migraine prophylaxis, bipolar disorder
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18
Q

Phenobarbital

  • Type of drug
  • Partial (focal)
    • Simple?
    • Complex?
  • Generalized
    • Tonic-clonic?
    • Absence?
    • Status Epileptics?
  • Mechanism
  • Side effects
  • Notes
A
  • Type of drug
    • Epilepsy drug
  • Partial (focal)
    • Simple? Y
    • Complex? Y
  • Generalized
    • Tonic-clonic? Y
    • Absence? N
    • Status Epileptics? N
  • Mechanism
    • Increases GABAA action
  • Side effects
    • Sedation, tolerance, dependence, induction of cytochrome P-450, cardiorespiratory depression
  • Notes
    • 1st line in neonates
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19
Q

Topiramate

  • Type of drug
  • Partial (focal)
    • Simple?
    • Complex?
  • Generalized
    • Tonic-clonic?
    • Absence?
    • Status Epileptics?
  • Mechanism
  • Side effects
  • Notes
A
  • Type of drug
    • Epilepsy drug
  • Partial (focal)
    • Simple? Y
    • Complex? Y
  • Generalized
    • Tonic-clonic? Y
    • Absence? N
    • Status Epileptics? N
  • Mechanism
    • Blocks Na+ channels
    • Increases GABA action
  • Side effects
    • Sedation, mental dulling, kidney stones, weight loss
  • Notes
    • Also used for migraine prevention
20
Q

Lamotrigine

  • Type of drug
  • Partial (focal)
    • Simple?
    • Complex?
  • Generalized
    • Tonic-clonic?
    • Absence?
    • Status Epileptics?
  • Mechanism
  • Side effects
A
  • Type of drug
    • Epilepsy drug
  • Partial (focal)
    • Simple? Y
    • Complex? Y
  • Generalized
    • Tonic-clonic? Y
    • Absence? Y
    • Status Epileptics? N
  • Mechanism
    • Blocks voltage-gated Na+ channels
  • Side effects
    • Stevens-Johnson syndrome (must be titrated slowly)
21
Q

Levetiracetam

  • Type of drug
  • Partial (focal)
    • Simple?
    • Complex?
  • Generalized
    • Tonic-clonic?
    • Absence?
    • Status Epileptics?
  • Mechanism
A
  • Type of drug
    • Epilepsy drug
  • Partial (focal)
    • Simple? Y
    • Complex? Y
  • Generalized
    • Tonic-clonic? Y
    • Absence? N
    • Status Epileptics? N
  • Mechanism
    • Unknown
    • May modulate GABA and glutamate release
22
Q

Tiagabine

  • Type of drug
  • Partial (focal)
    • Simple?
    • Complex?
  • Generalized
    • Tonic-clonic?
    • Absence?
    • Status Epileptics?
  • Mechanism
A
  • Type of drug
    • Epilepsy drug
  • Partial (focal)
    • Simple? Y
    • Complex? Y
  • Generalized
    • Tonic-clonic? N
    • Absence? N
    • Status Epileptics? N
  • Mechanism
    • Increases GABA by inhibiting re-uptake
23
Q

Vigabatrin

  • Type of drug
  • Partial (focal)
    • Simple?
    • Complex?
  • Generalized
    • Tonic-clonic?
    • Absence?
    • Status Epileptics?
  • Mechanism
A
  • Type of drug
    • Epilepsy drug
  • Partial (focal)
    • Simple? Y
    • Complex? Y
  • Generalized
    • Tonic-clonic? N
    • Absence? N
    • Status Epileptics? N
  • Mechanism
    • Increases GABA by irreversibly inhibiting GABA transaminase
24
Q

Stevens-Johnson syndrome

A
  • Prodrome of malaise and fever followed by rapid onset of erythematous/purpuric macules (oral, ocular, genital).
  • Skin lesions progress to epidermal necrosis and sloughing.
25
Q

Barbiturates

  • Examples
  • Mechanism
  • Clinical use
  • Toxicity
A
  • Examples
    • Phenobarbital, pentobarbital, thiopental, secobarbital.
  • Mechanism
    • Facilitate GABAA action by increasing duration of Cl- channel opening, thus decreasing neuron firing
      • Barbidurates increase duration
    • Contraindicated in porphyria.
  • Clinical use
    • Sedative for anxiety, seizures, insomnia, induction of anesthesia (thiopental).
  • Toxicity
    • Respiratory and cardiovascular depression (can be fatal)
      • CNS depression (can be exacerbated by EtOH use)
      • Dependence
      • Drug interactions (induces cytochrome P-450).
    • Overdose treatment is supportive (assist respiration and maintain BP).
26
Q

Benzodiazepines

  • Examples
  • Mechanism
  • Clinical use
  • Toxicity
A
  • Examples
    • Diazepam, lorazepam, triazolam, temazepam, oxazepam, midazolam, chlordiazepoxide, alprazolam.
  • Mechanism
    • Facilitate GABAA action by increasing frequency of Cl- channel opening. 
      • “Frenzodiazepines” increase frequency
    • Decrease REM sleep.
    • Most have long half-lives and active metabolites
      • Exceptions: triazolam, oxazepam, and midazolam are short acting –>Ž higher addictive potential
    • Benzos, barbs, and EtOH all bind the GABAA receptor, which is a ligand-gated Cl- channel.
  • Clinical use
    • Anxiety, spasticity, status epilepticus (lorazepam and diazepam), detoxification (especially alcohol withdrawal–DTs), night terrors, sleepwalking, general anesthetic (amnesia, muscle relaxation), hypnotic (insomnia).
  • Toxicity
    • Dependence, additive CNS depression effects with alcohol.
    • Less risk of respiratory depression and coma than with barbiturates.
    • Treat overdose with flumazenil (competitive antagonist at GABA benzodiazepine receptor).
27
Q

Nonbenzodiazepine hypnotics

  • Examples
  • Mechanism
  • Clinical use
  • Toxicity
A
  • Examples
    • Zolpidem (Ambien), Zaleplon, esZopiclone.
    • “All ZZZs put you to sleep.”
  • Mechanism
    • Act via the BZ1 subtype of the GABA receptor.
    • Effects reversed by flumazenil.
  • Clinical use
    • Insomnia.
  • Toxicity
    • Ataxia, headaches, confusion.
    • Short duration because of rapid metabolism by liver enzymes.
    • Unlike older sedative-hypnotics, cause only modest day-after psychomotor depression and few amnestic effects. 
    • Decrease dependence risk than benzodiazepines.
28
Q

Anesthetics—general principles

  • CNS drug solubility
  • MAC
  • Examples
    • N2O
    • Halothane
A
  • CNS drug solubility
    • CNS drugs must be lipid soluble (cross the blood-brain barrier) or be actively transported.
    • Drugs with decreased solubility in blood = rapid induction and recovery times.
    • Drugs with increased solubility in lipids = increased potency = 1 / MAC
  • MAC
    • MAC = Minimal Alveolar Concentration (of inhaled anesthetic) required to prevent 50% of subjects from moving in response to noxious stimulus (e.g., skin incision).
  • Examples
    • N2O has decreased blood and lipid solubility, and thus fast induction and low potency.
    • Halothane, in contrast, has increased lipid and blood solubility, and thus high potency and slow induction.
29
Q

Inhaled anesthetics

  • Examples
  • Mechanism
  • Clinical use
  • Toxicity
A
  • Examples
    • Halothane, enflurane, isoflurane, sevoflurane, methoxyflurane, nitrous oxide.
  • Mechanism
    • Mechanism unknown.
  • Clinical use
    • Myocardial depression, respiratory depression, nausea/emesis, increased cerebral blood flow (decreased cerebral metabolic demand).
  • Toxicity
    • Hepatotoxicity (halothane), nephrotoxicity (methoxyflurane), proconvulsant (enflurane), expansion of trapped gas in a body cavity (nitrous oxide).
    • Can cause malignant hyperthermia—rare, life-threatening hereditary condition in which inhaled anesthetics (except nitrous oxide) and succinylcholine induce fever and severe muscle contractions.
    • Treatment: dantrolene.
30
Q

Intravenous anesthetics

A
  • B. B. King on OPIOIDS PROPOses FOOLishly.
  • Barbiturates
  • Benzodiazepines
  • Arylcyclohexylamines (Ketamine)
  • Opioids
  • Propofol
31
Q

Barbiturates

A
  • Intravenous anesthetics
  • Thiopental—high potency, high lipid solubility, rapid entry into brain.
  • Used for induction of anesthesia and short surgical procedures.
  • Effect terminated by rapid redistribution into tissue (i.e., skeletal muscle) and fat. 
  • Decreased cerebral blood flow.
32
Q

Benzodiazepines

A
  • Intravenous anesthetics
  • Midazolam most common drug used for endoscopy
  • Used adjunctively with gaseous anesthetics and narcotics.
  • May cause severe postoperative respiratory depression, decreased BP (treat overdose with flumazenil), and anterograde amnesia.
33
Q

Arylcyclohexylamines (Ketamine)

A
  • Intravenous anesthetics
  • PCP analogs that act as dissociative anesthetics.
  • Block NMDA receptors.
  • Cardiovascular stimulants.
  • Cause disorientation, hallucination, and bad dreams. 
  • Increased cerebral blood flow.
34
Q

Opioids

A
  • Intravenous anesthetics
  • Morphine, fentanyl used with other CNS depressants during general anesthesia.
35
Q

Propofol

A
  • Intravenous anesthetic
  • Used for sedation in ICU, rapid anesthesia induction, and short procedures.
  • Less postoperative nausea than thiopental.
  • Potentiates GABAA.
36
Q

Local anesthetics

  • Examples
  • Mechanism
  • Principle
  • Clinical use
  • Toxicity
A
  • Examples
    • Esters—procaine, cocaine, tetracaine.
    • Amides—lIdocaIne, mepIvacaIne, bupIvacaIne
      • AmIdes have 2 I’s in name
  • Mechanism
    • Block Na+ channels by binding to specific receptors on inner portion of channel.
    • Preferentially bind to activated Na+ channels, so most effective in rapidly firing neurons.
    • 3° amine local anesthetics penetrate membrane in uncharged form, then bind to ion channels as charged form.
  • Principle
    • Can be given with vasoconstrictors (usually epinephrine) to enhance local action
      • Decrease bleeding, increase anesthesia by decreasing systemic concentration.
    • In infected (acidic) tissue, alkaline anesthetics are charged and cannot penetrate membrane effectively –>Ž need more anesthetic.
    • Order of nerve blockade: small-diameter fibers > large diameter.
      • Myelinated fibers > unmyelinated fibers.
      • Overall, size factor predominates over myelination such that small myelinated fibers > small unmyelinated fibers > large myelinated fibers > large unmyelinated fibers.
    • Order of loss: (1) pain, (2) temperature, (3) touch, (4) pressure.
  • Clinical use
    • Minor surgical procedures, spinal anesthesia.
    • If allergic to esters, give amides.
  • Toxicity
    • CNS excitation, severe cardiovascular toxicity (bupivacaine), hypertension, hypotension, and arrhythmias (cocaine).
37
Q

Neuromuscular blocking drugs

  • Clinical use
  • Depolarizing
    • Succinylcholine
    • Reversal of blockade
      • Phase I
      • Phase II
    • Complications
  • Nondepolarizing
    • Tubocurarine, atracurium, mivacurium, pancuronium, vecuronium, rocuronium
    • Reversal of blockade
A
  • Clinical use
    • Used for muscle paralysis in surgery or mechanical ventilation.
    • Selective for motor (vs. autonomic) nicotinic receptor.
  • Depolarizing
    • Succinylcholine
      • Strong ACh receptor agonist
      • Produces sustained depolarization and prevents muscle contraction.
    • Reversal of blockade
      • Phase I
        • Prolonged depolarization
        • No antidote.
        • Block potentiated by cholinesterase inhibitors.
      • Phase II
        • Repolarized but blocked
        • ACh receptors are available, but desensitized
        • Antidote consists of cholinesterase inhibitors.
    • Complications include hypercalcemia, hyperkalemia, and malignant hyperthermia.
  • Nondepolarizing
    • Tubocurarine, atracurium, mivacurium, pancuronium, vecuronium, rocuronium
      • Competitive antagonists
      • Compete with ACh for receptors.
    • Reversal of blockade
      • Neostigmine (must be given with atropine to prevent muscarinic effects such as bradycardia), edrophonium, and other cholinesterase inhibitors.
38
Q

Dantrolene

  • Mechanism
  • Clinical use
A
  • Mechanism
    • Prevents the release of Ca2+ from the sarcoplasmic reticulum of skeletal muscle.
  • Clinical use
    • Used to treat malignant hyperthermia and neuroleptic malignant syndrome (a toxicity of antipsychotic drugs).
39
Q

Parkinson disease drugs

  • Parkinsonism is due to…
  • Strategies
    • Dopamine agonists
    • Increase dopamine
    • Prevent dopamine breakdown
    • Curb excess cholinergic activity
A
  • Parkinsonism is due to…
    • Loss of dopaminergic neurons and excess cholinergic activity.
  • Strategies
    • Dopamine agonists
      • Bromocriptine (ergot), pramipexole, ropinirole (non-ergot)
      • Non-ergots are preferred
    • Increase dopamine
      • Amantadine
        • May increase dopamine release
        • Also used as an antiviral against influenza A and rubella
        • Toxicity = ataxia
      • L-dopa/carbidopa
        • Converted to dopamine in CNS
    • Prevent dopamine breakdown
      • Selegiline
        • Selective MAO type B inhibitor
      • Entacapone, tolcapone
        • COMT inhibitors
        • Prevent l-dopa degradation –>Ž increased dopamine availability
    • Curb excess cholinergic activity
      • Benztropine
        • Antimuscarinic
        • Improves tremor and rigidity but has little effect on bradykinesia
  • Mnemonics
    • BALSA:
      • Bromocriptine
      • Amantadine
      • Levodopa (with carbidopa)
      • Selegiline (and COMT inhibitors)
      • Antimuscarinics
      • For essential or familial tremors, use a β-blocker (e.g., propranolol).
    • Park your Mercedes-_Benz_.
40
Q

L-dopa (levodopa)/carbidopa

  • Mechanism
  • Clinical use
  • Toxicity
A
  • Mechanism
    • Increased level of dopamine in brain.
    • Unlike dopamine, L-dopa can cross blood-brain barrier and is converted by dopa decarboxylase in the CNS to dopamine.
    • Carbidopa, a peripheral decarboxylase inhibitor, is given with L-dopa to increase the bioavailability of L-dopa in the brain and to limit peripheral
      side effects.
  • Clinical use
    • Parkinson disease.
  • Toxicity
    • Arrhythmias from increased peripheral formation of catecholamines.
    • Long-term use can lead to dyskinesia following administration (“on-off” phenomenon), akinesia between doses.
41
Q

Selegiline

  • Mechanism
  • Clinical use
  • Toxicity
A
  • Mechanism
    • Selectively inhibits MAO-B, which preferentially metabolizes dopamine over norepinephrine and 5-HT, thereby increasing the availability of dopamine.
  • Clinical use
    • Adjunctive agent to l-dopa in treatment of Parkinson disease.
  • Toxicity
    • May enhance adverse effects of L-dopa.
42
Q

Memantine

  • Mechanism
  • Clinical use
  • Toxicity
A
  • Mechanism
    • NMDA receptor antagonist
    • Helps prevent excitotoxicity (mediated by Ca2+).
  • Clinical use
    • Alzheimer’s
  • Toxicity
    • Dizziness, confusion, hallucinations.
43
Q

Donepezil, galantamine, rivastigmine

  • Mechanism
  • Clinical use
  • Toxicity
A
  • Mechanism
    • AChE inhibitors.
  • Clinical use
    • Alzheimer’s
  • Toxicity
    • Nausea, dizziness, insomnia.
44
Q

Huntington drugs

  • Neurotransmitter changes in Huntington disease
  • Treatments
A
  • Neurotransmitter changes in Huntington disease
    • Decreased GABA
    • Decreased ACh
    • Increased dopamine.
  • Treatments
    • Tetrabenazine and reserpine
      • Inhibit vesicular monoamine transporter (VMAT)
      • Limit dopamine vesicle packaging and release.
    • ƒƒHaloperidol
      • Dopamine receptor antagonist.
45
Q

Sumatriptan

  • Mechanism
  • Clinical use
  • Toxicity
A
  • Mechanism
    • 5-HT1B/1D agonist.
    • Inhibits trigeminal nerve activation
    • Prevents vasoactive peptide release
    • Induces vasoconstriction.
    • Half-life < 2 hours.
  • Clinical use
    • Acute migraine, cluster headache attacks.
    • A SUMo wrestler TRIPs ANd falls on your head.
  • Toxicity
    • Coronary vasospasm (contraindicated in patients with CAD or Prinzmetal angina), mild tingling.

First Aid (92 decks)

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