Psychiatry - Pharmacology Flashcards
1
Q
Preferred drugs for these psychiatric conditions
- ADHD
- Alcohol withdrawal
- Anxiety
- Bipolar disorder
- Bulimia
- Depression
A
- 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
Q
Preferred drugs for these psychiatric conditions
- Obsessive-compulsive disorder
- Panic disorder
- PTSD
- Schizophrenia
- Social phobias
- Tourette syndrome
A
- 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
Q
CNS stimulants
- Examples
- Mechanism
- Clinical use
A
- Examples
- Methylphenidate, dextroamphetamine, methamphetamine, phentermine.
- Mechanism
- Increased catecholamines at the synaptic cleft, especially norepinephrine and dopamine.
- Clinical use
- ADHD, narcolepsy, appetite control.
4
Q
Antipsychotics (neuroleptics)
- Examples
- Mechanism
- Clinical use
- Potency
- High potency
- Low potency
A
- 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).
-
Trifluoperazine, Fluphenazine, Haloperidol
-
Low potency
-
Chlorpromazine, Thioridazine
- Cheating Thieves are low
- Non-neurologic side effects (anticholinergic, antihistamine, and α1-blockade effects).
-
Chlorpromazine, Thioridazine
-
High potency
5
Q
Antipsychotics (neuroleptics)
- Toxicity
- Other toxicities
- Neuroleptic malignant syndrome (NMS)
- Tardive dyskinesia
A
- 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.
- Evolution of EPS side effects:
- Endocrine side effects (e.g., dopamine receptor antagonism –> hyperprolactinemia –> galactorrhea).
- Side effects arising from blocking muscarinic (dry mouth, constipation), α1 (hypotension), and histamine (sedation) receptors.
- Highly lipid soluble and stored in body fat
- 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.
-
Neuroleptic malignant syndrome (NMS)
6
Q
Atypical antipsychotics
- Examples
- Mechanism
- Clinical use
- Toxicity
A
- 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) –> decreased GnRH, LH, and FSH (causing irregular menstruation and fertility issues).
- Ziprasidone may prolong the QT interval.
7
Q
Lithium
- Mechanism
- Clinical use
- Toxicity
A
- 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
Q
Buspirone
- Mechanism
- Clinical use
A
- 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
Q
Antidepressants (518)
A
10
Q
SSRIs
- Examples
- Mechanism
- Clinical use
- Toxicity
- Treatment for toxicity
A
- 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
Q
SNRIs
- Examples
- Mechanism
- Clinical use
- Toxicity
A
- 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
Q
Tricyclic antidepressants
- Examples
- Mechanism
- Clinical use
- Toxicity
- Treatment for toxicity
A
- 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
Q
Monoamine oxidase (MAO) inhibitors
- Examples
- Mechanism
- Clinical use
- Toxicity
A
- 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
Q
Bupropion
- Type of drug
- Mechanism
- Clinical use
- Toxicity
A
- 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
Q
Mirtazapine
- Type of drug
- Mechanism
- Toxicity
A
- 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.