Neurology Flashcards
Epinephrine
α-agonist
Decreases IOP by inhibiting synthesis of aqueous humor via vasoconstriction.
Glaucoma
Mydriasis. Do not use in closed-angle glaucoma
Brimonidine
α2-agonist
Decreases IOP by decreasing inhibiting synthesis of aqueous humor
Glaucoma
Blurry vision, ocular hyperemia, foreign body sensation, ocular allergic reactions, ocular pruritis
Timolol
β-blocker
Decreases IOP by decreasing inhibiting synthesis of aqueous humor
Glaucoma
No pupillary or vision changes
Betaxolol
β-blocker
Decreases IOP by decreasing inhibiting synthesis of aqueous humor
Glaucoma
No pupillary or vision changes
Carteolol
β-blocker
Decreases IOP by decreasing inhibiting synthesis of aqueous humor
Glaucoma
No pupillary or vision changes
Acetazolamide
Decreases IOP by decreasing amount of aqueous humor production via inhibition of carbonic anhydrase
Glaucoma
No pupillary or vision changes
Pilocarpine
Direct cholinomimetic
Increases outflow of aqueous humor via contraction of ciliary muscle and opening of trabecular meshwork
Glaucoma, especially in emergencies. Very effective in opening meshwork into canal of Schlemm
Miosis and cyclospasm (contraction of ciliary muscle)
Carbachol
Direct cholinomimetic
Increases outflow of aqueous humor via contraction of ciliary muscle and opening of trabecular meshwork
Glaucoma
Miosis and cyclospasm (contraction of ciliary muscle)
Physostigmine
Indirect cholinomimetic
Increases outflow of aqueous humor via contraction of ciliary muscle and opening of trabecular meshwork
Glaucoma
Miosis and cyclospasm (contraction of ciliary muscle)
Echothiophate
Indirect cholinomimetic
Increases outflow of aqueous humor via contraction of ciliary muscle and opening of trabecular meshwork
Glaucoma
Miosis and cyclospasm (contraction of ciliary muscle)
Latanoprost (PGF2α)
Decreases IOP by Increasing outflow of aqueous humor
Glaucoma
Darkens iris color (browning)
Morphine
Opioid analgesic
Acts as opioid receptor agonist to modulate synaptic transmission. Opens K channels, closes Ca channels, leading to decreased synaptic transmission. Inhibits release of Ach, NE, 5-HT, glutamate, and substance P.
Pain, acute pulmonary edema, general anesthetic (in combination with other CNS depressants)
Addiction, respiratory depression, constipation, miosis (pinpoint pupils), additive CNS depression with other drugs. Tolerance does not develop to miosis and constipation.
Treat toxicity with naloxone or naltrexone (opioid receptor antagonist).
Fentanyl
Opioid analgesic
Acts as opioid receptor agonist to modulate synaptic transmission. Opens K channels, closes Ca channels, leading to decreased synaptic transmission. Inhibits release of Ach, NE, 5-HT, glutamate, and substance P.
Pain, acute pulmonary edema, general anesthetic (in combination with other CNS depressants)
Addiction, respiratory depression, constipation, miosis (pinpoint pupils), additive CNS depression with other drugs. Tolerance does not develop to miosis and constipation.
Treat toxicity with naloxone or naltrexone (opioid receptor antagonist).
Codeine
Opioid analgesic
Acts as opioid receptor agonist to modulate synaptic transmission. Opens K channels, closes Ca channels, leading to decreased synaptic transmission. Inhibits release of Ach, NE, 5-HT, glutamate, and substance P.
Pain, acute pulmonary edema
Addiction, respiratory depression, constipation, miosis (pinpoint pupils), additive CNS depression with other drugs. Tolerance does not develop to miosis and constipation.
Treat toxicity with naloxone or naltrexone (opioid receptor antagonist).
Methadone
Opioid analgesic
Acts as opioid receptor agonist to modulate synaptic transmission. Opens K channels, closes Ca channels, leading to decreased synaptic transmission. Inhibits release of Ach, NE, 5-HT, glutamate, and substance P.
Maintenance programs for individuals with heroin addiction
Addiction, respiratory depression, constipation, miosis (pinpoint pupils), additive CNS depression with other drugs. Tolerance does not develop to miosis and constipation.
Treat toxicity with naloxone or naltrexone (opioid receptor antagonist).
Meperidine
Opioid analgesic
Acts as opioid receptor agonist to modulate synaptic transmission. Opens K channels, closes Ca channels, leading to decreased synaptic transmission. Inhibits release of Ach, NE, 5-HT, glutamate, and substance P.
Pain, acute pulmonary edema
Addiction, respiratory depression, constipation, miosis (pinpoint pupils), additive CNS depression with other drugs. Tolerance does not develop to miosis and constipation.
Treat toxicity with naloxone or naltrexone (opioid receptor antagonist).
Dextromethorphan
Opioid analgesic
Acts as opioid receptor agonist to modulate synaptic transmission. Opens K channels, closes Ca channels, leading to decreased synaptic transmission. Inhibits release of Ach, NE, 5-HT, glutamate, and substance P.
Cough suppressant
Addiction, respiratory depression, constipation, miosis (pinpoint pupils), additive CNS depression with other drugs. Tolerance does not develop to miosis and constipation.
Treat toxicity with naloxone or naltrexone (opioid receptor antagonist).
Diphenoxylate
Opioid analgesic
Acts as opioid receptor agonist to modulate synaptic transmission. Opens K channels, closes Ca channels, leading to decreased synaptic transmission. Inhibits release of Ach, NE, 5-HT, glutamate, and substance P.
Pain, acute pulmonary edema
Addiction, respiratory depression, constipation, miosis (pinpoint pupils), additive CNS depression with other drugs. Tolerance does not develop to miosis and constipation.
Treat toxicity with naloxone or naltrexone (opioid receptor antagonist).
Butorphanol
Mu-opiod receptor partial agonist and kappa-opioid receptor agonist. Produces analgesia.
Severe pain (migraine, labor, etc).
Less respiratory depression than full opioid agonists. Can cause opioid withdrawal symptoms if patient is also taking full opioid agonist (competition for opioid receptors).
Overdose not easily reversed.
Tramadol
Very weak opioid agonist. Also inhibits serotonin and norepinephrine reuptake.
Chronic pain.
Toxicity similar to opioids. Decreases seizure threshold. Serotonin syndrome.
Phenobarbitol
Barbituate
Facilitate GABA-A action by increased duration of Cl channel opening, thus decreasing neuron firing.
Sedate for anxiety, seizures, insomnia.
Respiratory and cardiovascular depression (can be fatal). CNS depression (exacerbated by EtOH use), dependence, drug interactions (induces CYP450). Contraindicated in porphyria.
Overdose treatment is supportive (assist respiration, maintain BP).
Pentobarbital
Barbituate
Facilitate GABA-A action by increased duration of Cl channel opening, thus decreasing neuron firing.
Sedate for anxiety, seizures, insomnia.
Respiratory and cardiovascular depression (can be fatal). CNS depression (exacerbated by EtOH use), dependence, drug interactions (induces CYP450). Contraindicated in porphyria.
Overdose treatment is supportive (assist respiration, maintain BP).
Thiopental
Barbituate
Facilitate GABA-A action by increased duration of Cl channel opening, thus decreasing neuron firing. High potency, high lipid solubility, rapid entry into brain. Decreases cerebral blood flow. Effects terminated by rapid redistribution into tissue and fat.
Induction of anesthesia, short surgical procedures.
Respiratory and cardiovascular depression (can be fatal). CNS depression (exacerbated by EtOH use), dependence, drug interactions (induces CYP450). Contraindicated in porphyria.
Overdose treatment is supportive (assist respiration, maintain BP).
Secobarbital
Barbituate
Facilitate GABA-A action by increased duration of Cl channel opening, thus decreasing neuron firing.
Sedate for anxiety, seizures, insomnia.
Respiratory and cardiovascular depression (can be fatal). CNS depression (exacerbated by EtOH use), dependence, drug interactions (induces CYP450). Contraindicated in porphyria.
Overdose treatment is supportive (assist respiration, maintain BP).
Diazepam
Benzodiazepine
Facilitate GABA-A action by increasing frequency of Cl channel opening. Decreases REM sleep. Long half-life with active metabolites.
Anxiety, spasticity, status epilepticus (first line treatment for acute), eclampsia (after magnesium sulfate), detoxification (especially alcohol withdrawal/delirium tremens), night terrors, sleepwalking, general anesthetic (amnesia, muscle relaxation), hypnotic (insomnia).
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 benzodiazpeine receptor).
Lorazepam
Benzodiazepine
Facilitate GABA-A action by increasing frequency of Cl channel opening. Decreases REM sleep. Long half-life with active metabolites.
Anxiety, spasticity, status epilepticus (first line treatment for acute), eclampsia (after magnesium sulfate), detoxification (especially alcohol withdrawal/delirium tremens), night terrors, sleepwalking, general anesthetic (amnesia, muscle relaxation), hypnotic (insomnia).
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 benzodiazpeine receptor).
Triazolam
Benzodiazepine
Facilitate GABA-A action by increasing frequency of Cl channel opening. Decreases REM sleep. Short acting, higher addictive potential.
Anxiety, spasticity, detoxification (especially alcohol withdrawal/delirium tremens), night terrors, sleepwalking, general anesthetic (amnesia, muscle relaxation), hypnotic (insomnia).
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 benzodiazpeine receptor).
Temazepam
Benzodiazepine
Facilitate GABA-A action by increasing frequency of Cl channel opening. Decreases REM sleep. Long half-life with active metabolites.
Anxiety, spasticity, detoxification (especially alcohol withdrawal/delirium tremens), night terrors, sleepwalking, general anesthetic (amnesia, muscle relaxation), hypnotic (insomnia).
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 benzodiazpeine receptor).
Oxazepam
Benzodiazepine
Facilitate GABA-A action by increasing frequency of Cl channel opening. Decreases REM sleep. Short acting, higher addictive potential.
Anxiety, spasticity, detoxification (especially alcohol withdrawal/delirium tremens), night terrors, sleepwalking, general anesthetic (amnesia, muscle relaxation), hypnotic (insomnia).
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 benzodiazpeine receptor).
Midazolam
Benzodiazepine
Facilitate GABA-A action by increasing frequency of Cl channel opening. Decreases REM sleep. Short acting, higher addictive potential.
Anxiety, spasticity, detoxification (especially alcohol withdrawal/delirium tremens), night terrors, sleepwalking, general anesthetic (amnesia, muscle relaxation), hypnotic (insomnia). Used adjunctively with gaseous anesthetics and narcotics.
Dependence, additive CNS depression effects with alcohol. Less risk of respiratory depression and coma than with barbiturates. May cause severe postoperative respiratory depression, hypotension, and anterograde amnesia.
Treat overdose with flumazenil (competitive antagonist at GABA benzodiazpeine receptor).
Chlordiazepoxide
Benzodiazepine
Facilitate GABA-A action by increasing frequency of Cl channel opening. Decreases REM sleep. Long half-life with active metabolites.
Anxiety, spasticity, detoxification (especially alcohol withdrawal/delirium tremens), night terrors, sleepwalking, general anesthetic (amnesia, muscle relaxation), hypnotic (insomnia).
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 benzodiazpeine receptor).
Alprazolam
Benzodiazepine
Facilitate GABA-A action by increasing frequency of Cl channel opening. Decreases REM sleep. Long half-life with active metabolites.
Anxiety, spasticity, detoxification (especially alcohol withdrawal/delirium tremens), night terrors, sleepwalking, general anesthetic (amnesia, muscle relaxation), hypnotic (insomnia).
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 benzodiazpeine receptor).
Zolpidem (Ambien)
Non-benzodiazepine hypnotic
Act via BZ1 subtype of the GABA receptor.
Insomnia.
Ataxia, headaches, confusion. Short duration of action because of rapid metabolism by liver enzymes. Unlike older sedative-hypnotics, cause only modest day-after psychomotor depression and few amnestic effects. Less dependence risk than benzodiazepines.
Effects reversed by flumazenil.
Zaleplon
Non-benzodiazepine hypnotic
Act via BZ1 subtype of the GABA receptor.
Insomnia.
Ataxia, headaches, confusion. Short duration of action because of rapid metabolism by liver enzymes. Unlike older sedative-hypnotics, cause only modest day-after psychomotor depression and few amnestic effects. Less dependence risk than benzodiazepines.
Effects reversed by flumazenil.
Eszopiclone
Non-benzodiazepine hypnotic
Act via BZ1 subtype of the GABA receptor.
Insomnia.
Ataxia, headaches, confusion. Short duration of action because of rapid metabolism by liver enzymes. Unlike older sedative-hypnotics, cause only modest day-after psychomotor depression and few amnestic effects. Less dependence risk than benzodiazepines.
Effects reversed by flumazenil.
Halothane
Inhaled anesthetic.
Unknown mechanism.
Myocardial depression, respiratory depression, nausea/emesis, increased cerebral blood flow (decreased cerebral metabolic demand).
Hepatotoxicity, malignant hyperthermia.