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Flashcards in Psychiatry - Pharmacology Deck (16):
1

Preferred drugs for these psychiatric conditions

  • ADHD
  • Alcohol withdrawal
  • Anxiety
  • Bipolar disorder
  • Bulimia
  • Depression

  • ADHD
    • Methylphenidate
  • Alcohol withdrawal
    • Benzodiazepines
  • Anxiety
    • SSRIs, SNRIs, buspirone
  • Bipolar disorder
    • “Mood stabilizers” (e.g., lithium, valproic acid, carbamazepine), atypical antipsychotics
  • Bulimia
    • SSRIs
  • Depression
    • SSRIs, SNRIs, TCAs, bupropion, mirtazapine (especially with insomnia)

2

Preferred drugs for these psychiatric conditions

  • Obsessive-compulsive disorder
  • Panic disorder
  • PTSD
  • Schizophrenia
  • Social phobias
  • Tourette syndrome

  • Obsessive-compulsive disorder
    • SSRIs, clomipramine
  • Panic disorder
    • SSRIs, venlafaxine, benzodiazepines
  • PTSD
    • SSRIs
  • Schizophrenia
    • Antipsychotics
  • Social phobias
    • SSRIs, β-blockers
  • Tourette syndrome
    • Antipsychotics (e.g., haloperidol, risperidone)

3

CNS stimulants

  • Examples
  • Mechanism
  • Clinical use

  • Examples
    • Methylphenidate, dextroamphetamine, methamphetamine, phentermine.
  • Mechanism
    • Increased catecholamines at the synaptic cleft, especially norepinephrine and dopamine.
  • Clinical use
    • ADHD, narcolepsy, appetite control.

4

Antipsychotics (neuroleptics)

  • Examples
  • Mechanism
  • Clinical use
  • Potency
    • High potency
    • Low potency

  • Examples
    • Haloperidol, trifluoperazine, fluphenazine, thioridazine, chlorpromazine (haloperidol + “-azines”).
  • Mechanism
    • All typical antipsychotics block dopamine D2 receptors (increased [cAMP]).
  • Clinical use
    • Schizophrenia (primarily positive symptoms), psychosis, acute mania, Tourette syndrome.
    • Chlorpromazine—Corneal deposits
    • Thioridazine—reTinal deposits
    • Haloperidol—NMS, tardive dyskinesia.
  • Potency
    • High potency
      • Trifluoperazine, Fluphenazine, Haloperidol
        • Try to Fly High
      • Neurologic side effects (EPS symptoms).
    • Low potency
      • Chlorpromazine, Thioridazine 
        • Cheating Thieves are low
      • Non-neurologic side effects (anticholinergic, antihistamine, and α1-blockade effects).

5

Antipsychotics (neuroleptics)

  • Toxicity
  • Other toxicities
    • Neuroleptic malignant syndrome (NMS)
    • Tardive dyskinesia

  • Toxicity
    • Highly lipid soluble and stored in body fat
      • Thus, very slow to be removed from body.
    • Extrapyramidal system side effects (e.g., dyskinesias).
      • Evolution of EPS side effects:
        • 4 hr acute dystonia (muscle spasm, stiffness, oculogyric crisis)
        • 4 day akathisia (restlessness)
        • 4 wk bradykinesia (parkinsonism)
        • 4 mo tardive dyskinesia
      • Treatment: benztropine or diphenhydramine.
    • Endocrine side effects (e.g., dopamine receptor antagonism --> hyperprolactinemia -->Ž galactorrhea).
    • Side effects arising from blocking muscarinic (dry mouth, constipation), α1 (hypotension), and histamine (sedation) receptors.
  • Other toxicities
    • Neuroleptic malignant syndrome (NMS)
      • Rigidity, myoglobinuria, autonomic instability, hyperpyrexia.
      • Treatment: dantrolene, D2 agonists (e.g., bromocriptine).
      • For NMS, think FEVER:
        • Fever
        • Encephalopathy
        • Vitals unstable
        • Enzymes increased
        • Rigidity of muscles
    • Tardive dyskinesia
      • Stereotypic oral-facial movements as a result of long-term antipsychotic use.
      • Potentially irreversible.

6

Atypical antipsychotics

  • Examples
  • Mechanism
  • Clinical use
  • Toxicity

  • Examples
    • Olanzapine, clozapine, quetiapine, risperidone, aripiprazole, ziprasidone.
    • It’s atypical for old closets to quietly risper from A to Z.
  • Mechanism
    • Not completely understood.
    • Varied effects on 5-HT2, dopamine, and α- and H1-receptors.
  • Clinical use
    • Schizophrenia—both positive and negative symptoms.
    • Also used for bipolar disorder, OCD, anxiety disorder, depression, mania, Tourette syndrome.
  • Toxicity
    • Fewer extrapyramidal and anticholinergic side effects than traditional antipsychotics. 
    • Olanzapine/clozapine may cause significant weight gain.
    • Clozapine may cause agranulocytosis (requires weekly WBC monitoring) and seizure.
      • Must watch clozapine clozely!
    • Risperidone may increase prolactin (causing lactation and gynecomastia) Ž--> decreased GnRH, LH, and FSH (causing irregular menstruation and fertility issues).
    • Ziprasidone may prolong the QT interval.

7

Lithium

  • Mechanism
  • Clinical use
  • Toxicity

  • Mechanism
    • Not established
    • Possibly related to inhibition of phosphoinositol cascade.
  • Clinical use
    • Mood stabilizer for bipolar disorder
    • Blocks relapse and acute manic events.
    • Also SIADH.
  • Toxicity
    • Tremor, sedation, edema, heart block, hypothyroidism, polyuria (ADH antagonist causing nephrogenic diabetes insipidus), teratogenesis.
    • Fetal cardiac defects include Ebstein anomaly and malformation of the great vessels.
    • Narrow therapeutic window requires close monitoring of serum levels.
    • Almost exclusively excreted by the kidneys
      • Most is reabsorbed at the proximal convoluted tubules following Na+ reabsorption.
    • Lithium side effects (LMNOP)
      • Movement (tremor)
      • Nephrogenic diabetes insipidus
      • HypOthyroidism
      • Pregnancy problems

8

Buspirone

  • Mechanism
  • Clinical use

  • Mechanism
    • Stimulates 5-HT1A receptors.
  • Clinical use
    • Generalized anxiety disorder.
    • Does not cause sedation, addiction, or tolerance.
    • Takes 1–2 weeks to take effect.
    • Does not interact with alcohol (vs. barbiturates, benzodiazepines).
    • I’m always anxious if the bus will be on time, so I take buspirone.

9

Antidepressants (518)

10

SSRIs

  • Examples
  • Mechanism
  • Clinical use
  • Toxicity
  • Treatment for toxicity

  • Examples
    • Fluoxetine, paroxetine, sertraline, citalopram.
    • Flashbacks paralyze senior citizens.
  • Mechanism
    • 5-HT–specific reuptake inhibitors.
    • It normally takes 4–8 weeks for antidepressants to have an effect.
  • Clinical use
    • Depression, generalized anxiety disorder, panic disorder, OCD, bulimia, social phobias, PTSD.
  • Toxicity
    • Fewer than TCAs.
    • GI distress, sexual dysfunction (anorgasmia and decreased libido). 
    • Serotonin syndrome with any drug that increases 5-HT (e.g., MAO inhibitors, SNRIs, TCAs)—hyperthermia, confusion, myoclonus, cardiovascular collapse, flushing, diarrhea, seizures.
  • Treatment for toxicity
    • Cyproheptadine (5-HT2 receptor antagonist).

11

SNRIs

  • Examples
  • Mechanism
  • Clinical use
  • Toxicity

  • Examples
    • Venlafaxine, duloxetine.
  • Mechanism
    • Inhibit 5-HT and norepinephrine reuptake.
  • Clinical use
    • Depression.
    • Venlafaxine is also used in generalized anxiety and panic disorders
    • Duloxetine is also indicated for diabetic peripheral neuropathy.
  • Toxicity
    • Increased BP most common
    • Also stimulant effects, sedation, nausea.

12

Tricyclic antidepressants

  • Examples
  • Mechanism
  • Clinical use
  • Toxicity
  • Treatment for toxicity

  • Examples
    • Amitriptyline, nortriptyline, imipramine, desipramine, clomipramine, doxepin, amoxapine (all TCAs end in -iptyline or -ipramine except doxepin and amoxapine).
  • Mechanism
    • Block reuptake of norepinephrine and 5-HT.
  • Clinical use
    • Major depression, OCD (clomipramine), fibromyalgia.
  • Toxicity
    • Sedation, α1-blocking effects including postural hypotension, and atropine-like (anticholinergic) side effects (tachycardia, urinary retention, dry mouth).
    • 3° TCAs (amitriptyline) have more anticholinergic effects than 2° TCAs (nortriptyline) have.
    • Desipramine is less sedating, but has a higher seizure incidence.
    • Tri-C’s: Convulsions, Coma, Cardiotoxicity (arrhythmias)
    • Also respiratory depression, hyperpyrexia.
    • Confusion and hallucinations in elderly due to anticholinergic side effects (use nortriptyline).
  • Treatment for toxicity
    • NaHCO3 for cardiovascular toxicity.

13

Monoamine oxidase (MAO) inhibitors

  • Examples
  • Mechanism
  • Clinical use
  • Toxicity

  • Examples
    • Tranylcypromine, Phenelzine, Isocarboxazid, Selegiline (selective MAO-B inhibitor).
    • MAO Takes Pride In Shanghai
  • Mechanism
    • Nonselective MAO inhibition increases levels of amine neurotransmitters (norepinephrine, 5-HT, dopamine).
  • Clinical use
    • Atypical depression, anxiety, hypochondriasis.
  • Toxicity
    • Hypertensive crisis (most notably with ingestion of tyramine, which is found in many foods such as wine and cheese)
    • CNS stimulation.
    • Contraindicated with SSRIs, TCAs, St. John’s wort, meperidine, and dextromethorphan (to prevent serotonin syndrome).

14

Bupropion

  • Type of drug
  • Mechanism
  • Clinical use
  • Toxicity

  • Type of drug
    • Atypical antidepressant
  • Mechanism
    • Increases norepinephrine and dopamine via unknown mechanism
  • Clinical use
    • Also used for smoking cessation. 
  • Toxicity
    • Stimulant effects (tachycardia, insomnia), headache, seizure in bulimic patients.
    • No sexual side effects.

15

Mirtazapine

  • Type of drug
  • Mechanism
  • Toxicity

  • Type of drug
    • Atypical antidepressant
  • Mechanism
    • α2-antagonist (increases release of norepinephrine and 5-HT) and potent 5-HT2 and 5-HT3 receptor antagonist.
  • Toxicity
    • Sedation (which may be desirable in depressed patients with insomnia), increased appetite, weight gain (which may be desirable in elderly or anorexic patients), dry mouth.

16

Trazodone

  • Type of drug
  • Mechanism
  • Clinical use
  • Toxicity

  • Type of drug
    • Atypical antidepressant
  • Mechanism
    • Primarily blocks 5-HT2 and α1-adrenergic receptors.
  • Clinical use
    • Used primarily for insomnia, as high doses are needed for antidepressant effects.
  • Toxicity
    • Sedation, nausea, priapism, postural hypotension.
    • Called trazobone due to male-specific side effects.

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