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53 Cards in this Set

  • Front
  • Back
Glaucoma dugs (6 types)
Alpha agonists: Epinephrine, brimonidine
Beta blockers: timolol, betaxolol, carteolol
Diuretics: Azetazolamide
Direct Cholinomimetics: pilocarpine, carbachol
Indirect Cholinomimetics: physostigmine, echothiophate
Prostaglandin: Latanoprost
Mechanism of Opioid Analgesics
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.
Toxicity of opioid analgesics
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).
dextromethorphan
opioid analgesics for cough suppression
loperamide
opioid analgesics for diarrhea
diphenoxylate
opioid analgesics for diarrhea
Butorphanol (mech, clinical use, fox)
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.
Tramadol
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.
First line for absence
Ethosuximide
First line for acute status epilepticus
Benzodiazepines
First line for status epilepticus prophylaxis
Phenytoin
Valproic acid uses
first line for tonic-clonic. Used in simple, complex and absence
Carbamazepine uses
first line for simple, complex, tonic-clonic
Seizure drugs that cause Steven-Johnson
Ethosuximide, Phenytoin, Carbamazepine, Lamotrigine
Ethosuximide MOA
blocks thalamic t-stype Ca2+ channels
Benzo MOA
Facilitate GABA-A action by increasing frequency of
Cl- channel opening. Decrease REM sleep. Most
have long half-lives and active metabolites
Which seizure meds inactivate sodium channels?
Phenytoin, cabamazepine, valproic acid,
Which seizure meds increase GABA
benzos, valproic acid, phenobarbital, topiramate, tiagabine, vigabatrin
secobarbital
Barbiturate
Phenobarbital
Barbiturate
pentobarbital
Barbiturate
thiopental Uses and details
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.
Barbiturates MOA, Clinical Use and Tox
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).
Short acting benzos
triazolam, oxazepam, and midazolam
Zolpidem
Nonbenzodiazepine hypnotic
Zaleplon
Nonbenzodiazepine hypnotic
eszopiclone
Nonbenzodiazepine hypnotic
Nonbenzodiazepine hypnotic MOA, Clinical use and fox
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.
How to reverse effects of Nonbenzodiazepine hypnotic
flumazenil
endoscopy sedative
Midazolam
Succinylcholine MOA and use
Depolarizing neuromuscular junction blocker used for muscle paralysis in surgery. Strong ACh receptor agonist; produces sustained depolarization and prevents muscle contraction.
Non depolarizing neuromuscular blockers
Tubocurarine, atracurium, mivacurium, pancuronium, vecuronium, rocuronium
Dantrolene Use and MOA
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).
Bromocriptine
Ergot dopamine agonist for parkinsons
pramipexole
non-ergot dopamine agonist for parkinsons
ropinirole
non-ergot dopamine agonist for parkinsons
Amantadine
Increase dopamine release; also
used as an antiviral against influenza A and
rubella; toxicity = ataxia
l-dopa/carbidopa MOA and tox
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.
Selegiline MOA, Clinical use, tox
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.
Memantine MOA Clinical use and tox
MECHANISM: NMDA receptor antagonist; helps prevent excitotoxicity (mediated by Ca2+).
USE: Alzheimer
TOXICITY: Dizziness, confusion, hallucinations.
Donepezil
MECHANISM: AChE inhibitors.
USE: Alzheimers
TOXICITY: Nausea, dizziness, insomnia.
Galantamine,
MECHANISM: AChE inhibitors.
USE: Alzheimers
TOXICITY: Nausea, dizziness, insomnia.
Rivastigmine
MECHANISM: AChE inhibitors.
USE: Alzheimers
TOXICITY: Nausea, dizziness, insomnia.
ƒTetrabenazine
ƒƒ
MOA: inhibit vesicular monoamine transporter (VMAT); limit dopamine vesicle packaging and release.
USE: huntington
Reserpine
MOA: inhibit vesicular monoamine transporter (VMAT); limit dopamine vesicle packaging and release.
USE: huntington
Haloperidol
dopamine receptor antagonist.
Sumatriptan
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.
Halothane MOA, use, tox
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).
methoxyflurane MOA, use, tox
Inhaled anesthetic
MECHANISM: Mechanism unknown.
EFFECTS: Myocardial depression, respiratory depression, nausea/emesis, increased cerebral blood flow (decreased cerebral metabolic demand).
TOXICITY: nephrotoxicity
enflurane MOA, use, tox
Inhaled anesthetic
MECHANISM: Mechanism unknown.
EFFECTS: Myocardial depression, respiratory depression, nausea/emesis, increased cerebral blood flow (decreased cerebral metabolic demand).
TOXICITY: proconvulsant
Inhaled anesthetics
Halothane, enflurane, isoflurane, sevoflurane, methoxyflurane, nitrous oxide.
Clinical use of Benzos
Anxiety, spasticity, status epilepticus (lorazepam and diazepam), detoxification (especially alcohol withdrawal–DTs), night terrors, sleepwalking, general anesthetic (amnesia, muscle relaxation), hypnotic (insomnia).
Tox of benzos
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).