Psyc/Neuron Pharm Flashcards
Tricyclic antidepressants (TCAs)
“-iptyline, -ipramine” & doexpin, amoxapine (amitriptylin, nortriptylin, imipramine, desipramine, clomipramine) Blocks NET/SERT-> decreases reuptake of NE and 5HT (also blocks mACh, alpha-1, H1), requires 2-3 wks to work and 8-10 wks for max effect Use: major depression, bedwetting (imipramine), OCD (clomipramine), fibromyalgia, chronic pain (amitriptyline) Toxicity: CNS - sedation CV - orthostatic HTN (alpha 1), tachy & arrythmia (increased NE& anti ACh) ANS - dry mouth, blurred vision, constipation, urinary retention & confusion/hallucinations in elderly (anticholinergic) Tri Cs: convulsions, coma, cadiotoxicity (arrythmia), respiratory depression, hyperpyrexia (fever) Tx cardiotoxicity with NaHCO3 Ami (3rd gen) more anticholinergic Nori (2nd gen), despiramine less sedating & higher seizure threshold
Buproprion
Atypical antidepressant, smoking cessation inhibitor of NE and DA reuptake, nAChR antagonist Toxicity: Stimulant effets (tachy, insomnia) Headache Seizure in bulimc pts NO wt gain or sexual dysfxn
Mirtazapine
blocks 5HT2, 5HT3, and alpha-2 (presyn receptor normally reduces NE/5HT release) receptors Clinical use: atypical antidepressant Adverse effects: Sedation (good for depression w/ insomnia) INcreased appetitie Wt gain (good for elderly & anorexics) Dry mouth
Maprotiline
Blocks NE reuptake Clinical use: atypical antidepressant Toxicity: sedation, orthostatic HTN
Trazodone
Inhibits 5HT reuptake (and lbocks 5HT2 receptors) Clinical use: insomnia (VERY sedating), high dose for antidepressant efects Toxicity: Sedation Nausea Priapism (trazaBONE) postural hypoTN`
SSRIs
Fluoxetine, paroxetine, sertraline, citalopram (Flashbacks paralyze senior citizens) Blocks SERT, takes 4-8 wks for effect & duration long & several week washout period Use: depression, generalized anxiety disorder, panic disorder, OCD, bulimia, social phobia, PTSD Toxicity: Less than TCAs GI distress (nausea, upset) Sexual dysfunction (anorgasmia, decreased libido) SIADH Serotonin syndrome Drug combo that increases 5HT (MAO inhibitors, SNRIs, TCAs) Sx: triad of mental status change/autonomic hyperactivitiy/neurmuscular abnlalities - hyperthermia, conusion, myoclonus, flushing, diarrhea, seizure, cardiovascular collapse Tx: cyprohepatdine (5HT2 receptor antag) (stop all drugs, supporitve care)
SNRIs
Venlafaxine, duloxetine Blocks NE and 5HT reuptake Use: depression, Venlafaxine - generalized anxiety and panic, Duloxetine - diabetic PN, has a greater effect on NE Toxicity: same as SSRIs + HTN More restlessness than SSRIs Increased BP Sedation Nausea
MAO Inhibitors
Tranylcypromine, Phenelzine, Isocarboxazid, Selegiline (selective MAO B -> used for Parkinsons) = MAO Takes Pride In Shanghai Non-selective MAO inhibitor (normally deaminates catechol & 5HT , Brain - MAO A & B, Gut - MAO A) -> increase NE, 5HT, Dopamine Use: atypical depression, anxiety, hypochondriasis Toxicity: HTN crisis (esp w/ tyramine ingestion - wine & cheese) CNS stim (mood elevation) To prevent Serotonin Syndrome - contraindicated w/ SSRI, TCA, St John Wort, meperidine, dextrmethorphan
Lithium
Unknown mech - PIP cascade inhibition? Use: bipolar disorder mood stabilizer (blocks relapse and acute manic events), SIADH Toxicity: LMNOP Movement (tremor) Nephrogenic DI (polyuria - ADH antagonist) hypOthyroidism Pregnancy problems: cardiac defects - Ebstein anomoly, malformation of the great vessels Others: edema (Na+ retention), wt gain, heart block Renal clearance - most reabsorbed at PCT following Na+ reabsorption Low therapeutic index
Barbiturates
Phenobarbital, pentobarbital, thiopental, secobarbital Binds to GABA A and increases DURATION (barbiDURate) of Cl- ch opening Use: anxiety, insmonia, seizures (PHENObarbital - 1st line tx in children), induction of anesthesia (THIOpental) Toxicity: Respiratory and cardiovascular depression -> fatal! CNS depression - exacerbated with EtOH P450 inducer- many drug drug interactions (additive w/ other CNS depressants, cross tol w/ other CNS depressants, induces hepatic microsomal enzymes) Contraindicated in porphyria - induces ALA synthase Low safety margin/therapeutic index
Benzodiazepines
Diazepam, Lorazepam, Triazolam, Temazepam, Oxazepam, Midazolam, Chlordiazepoxide, Alprazolam Increase freq of GABA A Cl- channel opning, decrease REM sleep. Long t1/2 and active metabolites except: triazolam, midazolam, oxazepam -> less sedation but higher addictive potential Phase II conjugation only -> oxazepam, lorezepam -> good for elderly/liver disease Clinical use: anxiety, spasticity, detoxification from EtOH +/- delrium tremens, night terrors/sleep walking, general anesthetic (amnesia,musce realxation), hypnotic (insomnia) Lorazepam/Diazepam - status epilepticus Toxicity: Dependence, addictive CNS depression w/ EtOH Less risk of resp depression/coma than barbiturates Tx overdose: flumazenil (GABA benzo competative antagonist)
Buspirone
Mech: Stimulates 5HT1A receptors Clinical use: generalized anxiety disorder (“I’m always anxious if the BUS will be ON time so I take BUSpirONe) Does not interact w/ EtOH (vs barbiturates & benzos)
Nonbenzodiazpene hypnotics
Zopidem (Ambien), zalepon, eszopiclone Mech: BZ1 subtype GABA receptor, effects reversed by flumazenil. Short duration (rapid metabolism), modest day after psychomotor depression (vs benzos w/ carry over hangover), few amnesia effects, lower dependence risk Clinical use: insomnia Toxicity: Ataxia Headaches Confusion
Addiction Tx: Disulfuram Naltrexone Acamprosate Buprenorphine Methadone Naloxone + buprenorphine
Disulfuram Inhibits acetylaldehyde DH -> build up acetylaldehyde -> headache, nausea, vomiting w/ EtOH use Naltrexone Opioid receptor antagonist -> blocks endogenous opioids and reduces impulsive use Acamprosate NMDA antagonist, GABA agonist -> restores excitaiton/inhibition altered by chronic EtOH -> increases abstinence Buprenoprhine Parital opioid agonist -> for opioid w/ drawal (good for hospital setting) Methadone Full opiate agonist, long acting -> maintenace therapy, blocks withdrawal but not craving (good for >1 yr dep) Naloxone+buprenorphine partial agonist, long acting w/ fewer w/drawal sx than methadone, buprenorphine slowly GI absorbed & naloxone – not active when taken orally so w/drawal sx only w/ injection (thus oral naloxone has lower abuse potential)
Anitpsychotics
Haloperidol + “azines” (trifluoperazine, fluphenazine, thioridazine, chlorpromazine) Mechanism: block D2 receptors (-> increase CAMP) Clinical uses: schizophrenia (positive sx), psychosis, acute mania, Tourettes Potency: high = Try to Fly High (Trifluoperazine, Fluphenazine, Haloperidol) -> neurologic side effects (EPS) low = Cheating Thieves are low (Chlorpromazine, Thioridazine) - > nonneurologica side effets (anticholinergic, antihistamine, alpha1 blockade side effects) Toxicity: Slow to be removed - highly lipid soluble/stored in body fat EPS extrapyramidal side effects 4 hr acute dystonia - muscle spasm, stiffness, oculogyric crisis 4 day akathisia - restlessness 4 wk bradykinesia - Parkinsonism sx 4 mo tardive dyskinesia - orofacial mvmnts from long-term antipsychotic use often reversible Endocrine side effects (D receptor antagonist): hyperprl -> galactorrhea Muscarinic block (dry mouth, constipation) Alpha 1 block (hypoTN) Histamine block (sedation) Neuroleptic malignant syndrome: FEVER (fever, encephalopathy, vitals unstable - autonomic instab, elevated enzymes, rigidity of muscles) -> Tx: dantrolene (muscle relax) + D2 agonist (bromocriptine) Chlorpromazine - Corneal deposits Thioridazine - reTinal deposits Haloperidol - NMS, tardive dyskinesia
Atypical antipsychotics
Olanzapine, clozapine, quetiapine, risperidone, aripiprazole, ziprasidone - its ATYPICAL for OLd CLOSets to QUIETly RISPER from A to Z Mechanism: not sure, varied on 5HT2, DA, alpha, H1 receptors Clinical use: schizophrenia (both positive/negative sx), also used for biopolar disorder, OCD, anxiety, depression, mania, Tourettes syndrome Toxicity: fewer EPS and anticholinergic side effects * Olanzapine/Clozapine - sig wt gain * Clozapine - agranulocytosis (weekly WBC monitoring) & seizure * Ziprasidone - prolong QT interval
Sumatriptan
“SUMo wrestler TRIPs ANd falls onyour HEAD” Mech: 5HT1B /!D agonist -> inhibits CN V nerve activation, prevents vasoactive peptide release, induces vasoconstriciton t1/2 ~ Use: acute migraine, culster HEADache attacks Toxicity: coronary vasospasm (contraindicated in CAD or Pinzmetals angina), mild tingling
Memantine
Mech: NMDA antagonist, prevent excitotoxicity (by increased Ca2+ that kills cell) Use: AD Toxicity: dizziness, confusion, hallucinations (dirty drug binds to many receptors)
Donepezil, galantamine, rivastigmine
Mech: ACHase inhibitors Uses: AD Toxicity: nuasea, dizziness, insomnia
Selegiline
Mech: Selectively inhibts MAO-B (pref metab DA over NE/5HT) Uses: Adjunct to LDOPA in PD treatment Toxicity: May enhance toxicities of LDOPA
Glaucoma drug - Epi/Bimonidine
alpha 2 agonists - decrease aq humour synthesis and decrease synthesis via vasoconstriction
Side Effects: mydriasis, blurry vision, ocular hyperemia, foregin body sensation, ocular alllergic reactions, ocular pruritis
Do NOT use in closed angle glaucoma
Glaucoma - Timolol, bextalol, carteolol
Beta blockers: decrease aq humour synthesis
No side effects
Glaucoma - acetazolamide
Carbonic anhydrase inhibitor - decrease aq humour synthesis
No side effects
Glaucoma - Direct & Indirect cholinmimetics
Increase outflow of aq humour -> contraction of ciliary muscle and opening of trabecular meshwork
Pilocarpine used in emergencies - very effective in opening meswhrok into cnala of Schlemme
Side effects: miosis, cyclospasm (constrict ciliary muscle)
