Drug Notecards Wink Wink

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Parkinson's disease drugs

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Dopamine agonists,
MAO inhibitors,
Antimuscarinics,
COMT inhibitors.

BALSA: Bromocriptine, Amantadine, Levodopa, Selegiline, Antimuscarinics

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Dopamine agonists

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L-dopa/carbidopa, bromocriptine (an ergot alkaloid and partial dopamine agonist), pramipexole, ropinirole, amantadine (enhances dopamine release)

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MAO inhibitors

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Selegiline (selective MAO type B inhibitor)

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Antimuscarinics

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Benztropine (improves tremor and rigidity but has little effect of bradykinesia)

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COMT inhibitors

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Entacapone, tolcapone (adjunct to levodopa)

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L-dopa (levodopa)/carbidopa

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Mechanism: increased level of dopamine in brain. Parkinsonism thought to be due to loss of dopaminergic neurons and excess cholinergic function. Can cross blood-brain barrier and is converted by dopa decarboxylase in the CNS to dopamine.
Toxicity: Arrhythmias from the peripheral conversion to dopamine. Carbidopa, a peripheral decarboxylase inhibitor, is given with L-dopa in order to increase the bioavailablity of L-dopa in the brain and to limit the peripheral side effects. Dyskinesias also occur.

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Selegiline (deprenyl)

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Mechanism: selectively inhibits MAO-B, thereby increasing the availability of dopamine.
Clinical Use: Adjunctive agent to L-dopa in treating Parkinson's disease
Toxicity: May enhance adverse effects of L-dopa

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Sumatriptan

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Mechanism: 5-HT₁D (okay the 1D is all supposed to be subscript but it wouldn't work for me!) agonist. Half-life less than 2 hours.
Clinical Use: Acute migraine, cluster headache attacks.
Toxicity: Chest discomfort, mild tingling (contraindicated in patients with CAD or Prinzmetal's angina)

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Epilsepsy drug toxicities

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Benzodiazepines: sedation, tolerance, dependence
Carbamazepine: diplopia, ataxia, induction of cytochrome P-450, blood dyscrasias (agranulocytosis, aplastic anemia), liver toxicity (always check LFTs! duh!)
Ethosuximide: (haha sux) GI distress, lethargy, headache, urticaria, Stevens-Johnson syndrome
Phenobarbital: Sedation, induction of cytochrome P-450, tolerance, dependence
Phenytoin
Valproic acid: GI distress, rare but fatal hepatotoxicity (measure LFTs), neural tube defects in fetus (spina bifida)
Lamotrigine: Life threatening rash (really?!??!), Stevens-Johnson syndrome
Gabapentin: sedation, movement disorders
Topiramate: sedation, mental dulling, kidney stones, weight loss

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Phenytoin

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Mechanism: use-dependent blockade of Na+ channels
Clinical Use: Grand mal seizures. Also a class IB antiarrhythmic.
Toxicity: Nystagmus, ataxia, diplopia, lethargy. Chronic use produces gingival hyperplasia in children, peripheral neuropathy, hirsutism, megaloblastic anemia (decrease vitamin B12), and malignant hyperthermia (rare); teratogenic (fetal hydantoin syndrome)

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Barbiturates

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Phenobarbital, pentobarbital, thiopental, secobarbital
Mechanism: Facilitate GABA A action by increasing duration of Cl- channel opening
Clinical Use: Sedative for anxiety, seizures, insomnia, induction of anesthesia (thiopental)
Toxicity: dependence, additive CNS depression effects with alcohol, respiratory or cardiovascular depression (can lead to death (of a sad heart :-( )), drug interactions owing to induction of liver microsomal enzymes (cytochrome P-450)
**BarbiDURATe = increased DURATion**

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Benzodiazepines

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Diazepam, lorazepam, triazolam, temazepam, oxazepam, midazolam, chlordiazepoxide
Mechanism: facilitate GABA A action by increased frequency of Cl- channel opening. Most have long half-lives and active metabolites.
Clinical Use: Anxiety, spasticity (meaning Casey), status epilepticus (diazepam), detoxification (especially alcohol withdrawal-DTs)
Toxicity: Dependence, additive CNS depression effects with alcohol. Less risk of respiratory depression and coma than with barbiturates. Treat overdose with flumazenil.
**FREnzodiazepines = increased FREquency**
**Short acting = TOM thumb = Triazolam, Oxazepam, Midazolam**

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Antipsychotics (neuroleptics)

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Thioridazine, haloperidol, fluphenazine, chlorpromazine
Mechanism: Most block dopamine D2 receptors
Clinical Use: Schizophrenia, psychosis
Toxicity: Extrapyramidal system (EPS) side effects, sedation, endocrine side effects, and side effects from blocking muscarinic, alpha (little fishy looking symbol?) and histamine receptors.
--Neuroleptic malignant syndrome: rigidity, autonomic instability, hyperprexia (treat with dantrolene and dopamine agonists)
--Tardive dyskinesia: stereotypic oral-facial movements probably due to dopamine receptor sensitization; results of long-term antipsychotic use

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Evolution of EPS side effects

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4 h acute dystonia
4d akinesia
4wk akathisia
4 mo tardive dyskinesia (often irreversible)

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Atypical antipsychotics

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Clozapine, olanzapine, risperidone.
Mechanism: Block 5-HT2 and dopamine receptors
Clinical use: schizophrenia; useful for positive and negative symptoms.
--Olanzapine is also used for OCD, anxiety disorder, and depression
Toxicity: fewer extrapyramidal and anticholinergic side effects than other antipsychotics.
--Clozapine may cause agranulocytosis (requires weekly WBC monitoring)

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Lithium

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Mechanism: not established; possibly related to inhibition of phosphoinositol cascade
Clinical use: Mood stabilizer for bipolar affective disorder; blocks relapse and acute manic events.
Toxicity: Tremor, hypothyroidism, polyuria (ADH antagonist causing nephrogenic diabetes insipidus), teratogenesis. Narrow therapeutic window requiring close monitoring of serum levels.

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SSRIs

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Fluoxetine, sertraline, paroxetine, citalopram
Mechanism: Serotonin-specific reuptake inhibitors
Clinical use: endogenous depression
Toxicity: Fewer than TCAs. CNS stimulation - anxiety, insomnia, tremor, anorexia, nausea, vomiting.
--"Serotonin syndrome" with MAO inhibitors - hyperthermia, muscle rigidity, cardiovascular collapse

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Tricyclic antidepressants

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Imipramine, amitriptyline, desipramine, nortriptyline, clomipramine, doxepin.
Mechanism: Block reuptake of NE and serotonin
Clinical use: endogenous depression, bedwetting (imipramine), OCD (clomipramine)
Side effects: Sedation, fishy-blocking effects, atropine-like (anticholinergic) side effects (tachycardia, urinary retention). 3° TCAs (amitriptyline) have more anticholinergic effects than do 2° TCAs (nortriptyline). Desipramine is the least sedating.
Toxicity: Tri-Cs: Convulsions, Coma, Cardiotoxicity (arrhythmias); also respiratory depression, hyperpryrexia. Confusion and hallucinations in elderly.

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Heterocyclics

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2nd and 3rd generation antidepressants with varied and mixed mechanisms of action. Used in major depressive disorders.
Traxodone: Primarily inhibit serotonin reuptake.
--Toxicity: sedation, nausea, priapism, postural hypotension
Buproprion: Also used for smoking cessation. Mechanism not well known.
--Toxicity: stimulant effects (tachycardia, agitation), dry mouth, aggravation of psychosis (useful? not really)
Venlafaxine: also used in generalized anxiety disorder. Inhibits seratonin, NE, and dopamine reuptake.
--Toxicity: stimulant effects (anxiety, agitation, headache, insomnia)
Mirtazapine: fishy2 antagonist (increased release of NE and serotonin) and potent 5-HT2 receptor antagonist.
--Toxicity: sedation, increased serum cholesterol, increased appetite (bad for the giambos)
Maprotiline: blocks NE reuptake

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Monoamine oxidase (MAO) inhibitors

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Phenelzine, tranylcypromine
Mechanism: Nonselective MAO inhibition
Clinical Use: Atypical depressions (i.e. with psychotic or phobic features), anxiety, hypochondriasis
Toxicity: Hypertensive crisis with tyramine ingestion (in many foods) and meperidine; CNS stimulation. Contraindication with SSRIs or β-agonists