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53 Cards in this Set
- Front
- Back
Glaucoma dugs (6 types)
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Alpha agonists: Epinephrine, brimonidine
Beta blockers: timolol, betaxolol, carteolol Diuretics: Azetazolamide Direct Cholinomimetics: pilocarpine, carbachol Indirect Cholinomimetics: physostigmine, echothiophate Prostaglandin: Latanoprost |
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Mechanism of Opioid Analgesics
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Act as agonists at opioid receptors (mu = morphine, delta = enkephalin, kappa = dynorphin) to modulate synaptic transmission—open K+ channels, close Ca2+ channels --> decreased synaptic transmission. Inhibit release of ACh, norepinephrine, 5-HT, glutamate, substance P.
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Toxicity of opioid analgesics
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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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dextromethorphan
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opioid analgesics for cough suppression
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loperamide
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opioid analgesics for diarrhea
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diphenoxylate
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opioid analgesics for diarrhea
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Butorphanol (mech, clinical use, fox)
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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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Tramadol
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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. Decreases seizure threshold. Serotonin syndrome. |
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First line for absence
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Ethosuximide
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First line for acute status epilepticus
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Benzodiazepines
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First line for status epilepticus prophylaxis
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Phenytoin
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Valproic acid uses
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first line for tonic-clonic. Used in simple, complex and absence
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Carbamazepine uses
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first line for simple, complex, tonic-clonic
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Seizure drugs that cause Steven-Johnson
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Ethosuximide, Phenytoin, Carbamazepine, Lamotrigine
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Ethosuximide MOA
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blocks thalamic t-stype Ca2+ channels
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Benzo MOA
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Facilitate GABA-A action by increasing frequency of
Cl- channel opening. Decrease REM sleep. Most have long half-lives and active metabolites |
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Which seizure meds inactivate sodium channels?
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Phenytoin, cabamazepine, valproic acid,
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Which seizure meds increase GABA
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benzos, valproic acid, phenobarbital, topiramate, tiagabine, vigabatrin
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secobarbital
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Barbiturate
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Phenobarbital
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Barbiturate
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pentobarbital
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Barbiturate
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thiopental Uses and details
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Barbiturate. induction of anesthesia.
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. |
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Barbiturates MOA, Clinical Use and Tox
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MECHANISM: Facilitate GABA-A action by duration of Cl- channel opening, thus neuron firing. Contraindicated in porphyria.
CLINICAL USE: Sedative for anxiety, seizures, insomnia. 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). |
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Short acting benzos
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triazolam, oxazepam, and midazolam
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Zolpidem
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Nonbenzodiazepine hypnotic
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Zaleplon
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Nonbenzodiazepine hypnotic
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eszopiclone
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Nonbenzodiazepine hypnotic
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Nonbenzodiazepine hypnotic MOA, Clinical use and fox
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MECHANISM: Act via the BZ1 subtype of the GABA receptor.
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. Decreased dependence risk than benzodiazepines. |
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How to reverse effects of Nonbenzodiazepine hypnotic
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flumazenil
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endoscopy sedative
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Midazolam
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Succinylcholine MOA and use
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Depolarizing neuromuscular junction blocker used for muscle paralysis in surgery. Strong ACh receptor agonist; produces sustained depolarization and prevents muscle contraction.
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Non depolarizing neuromuscular blockers
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Tubocurarine, atracurium, mivacurium, pancuronium, vecuronium, rocuronium
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Dantrolene Use and MOA
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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). |
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Bromocriptine
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Ergot dopamine agonist for parkinsons
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pramipexole
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non-ergot dopamine agonist for parkinsons
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ropinirole
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non-ergot dopamine agonist for parkinsons
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Amantadine
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Increase dopamine release; also
used as an antiviral against influenza A and rubella; toxicity = ataxia |
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l-dopa/carbidopa MOA and tox
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MOA: increase 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. Tox: Arrhythmias from increased peripheral formation of catecholamines. Long-term use can lead to dyskinesia following administration (on-off phenomenon), akinesia between doses. |
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Selegiline MOA, Clinical use, tox
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MECHANISM: Selectively inhibits MAO-B, which preferentially metabolizes dopamine over norepinephrine and 5-HT, thereby the availability of dopamine.
CLINICAL USE: Adjunctive agent to l-dopa in treatment of Parkinson disease. TOXICITY: May enhance adverse effects of l-dopa. |
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Memantine MOA Clinical use and tox
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MECHANISM: NMDA receptor antagonist; helps prevent excitotoxicity (mediated by Ca2+).
USE: Alzheimer TOXICITY: Dizziness, confusion, hallucinations. |
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Donepezil
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MECHANISM: AChE inhibitors.
USE: Alzheimers TOXICITY: Nausea, dizziness, insomnia. |
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Galantamine,
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MECHANISM: AChE inhibitors.
USE: Alzheimers TOXICITY: Nausea, dizziness, insomnia. |
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Rivastigmine
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MECHANISM: AChE inhibitors.
USE: Alzheimers TOXICITY: Nausea, dizziness, insomnia. |
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Tetrabenazine
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MOA: inhibit vesicular monoamine transporter (VMAT); limit dopamine vesicle packaging and release.
USE: huntington |
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Reserpine
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MOA: inhibit vesicular monoamine transporter (VMAT); limit dopamine vesicle packaging and release.
USE: huntington |
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Haloperidol
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dopamine receptor antagonist.
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Sumatriptan
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MECHANISM: 5-HT1B/1D agonist. Inhibits trigeminal nerve activation; prevents vasoactive peptide release;
induces vasoconstriction. Half-life < 2 hours. USE: Acute migraine, cluster headache attacks. TOX: Coronary vasospasm (contraindicated in patients with CAD or Prinzmetal angina), mild tingling. |
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Halothane MOA, use, tox
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Inhaled anesthetic
MECHANISM: Mechanism unknown. EFFECTS: 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). |
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methoxyflurane MOA, use, tox
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Inhaled anesthetic
MECHANISM: Mechanism unknown. EFFECTS: Myocardial depression, respiratory depression, nausea/emesis, increased cerebral blood flow (decreased cerebral metabolic demand). TOXICITY: nephrotoxicity |
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enflurane MOA, use, tox
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Inhaled anesthetic
MECHANISM: Mechanism unknown. EFFECTS: Myocardial depression, respiratory depression, nausea/emesis, increased cerebral blood flow (decreased cerebral metabolic demand). TOXICITY: proconvulsant |
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Inhaled anesthetics
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Halothane, enflurane, isoflurane, sevoflurane, methoxyflurane, nitrous oxide.
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Clinical use of Benzos
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Anxiety, spasticity, status epilepticus (lorazepam and diazepam), detoxification (especially alcohol withdrawal–DTs), night terrors, sleepwalking, general anesthetic (amnesia, muscle relaxation), hypnotic (insomnia).
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Tox of benzos
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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). |