Key Psychotropic Medications

Why This Matters

Understanding psychotropic medications is essential for grasping how biological interventions target the underlying neurochemistry of mental disorders. You're being tested on more than just drug names—exams focus on mechanisms of action, neurotransmitter systems, therapeutic applications, and side effect profiles. These medications represent the practical application of everything you've learned about brain chemistry, and questions often ask you to connect a drug class to its target neurotransmitter or explain why certain medications work for specific disorders.

The key to mastering this content is recognizing patterns: medications that boost serotonin treat different conditions than those targeting dopamine, and the receptor systems involved predict both therapeutic effects and side effects. Don't just memorize brand names—know which neurotransmitter each drug class affects, what disorders it treats, and what risks come with it. That's what separates a 3 from a 5 on medication-related questions.

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Serotonin-Targeting Antidepressants

These medications primarily increase serotonin availability in the synaptic cleft, making them first-line treatments for depression and anxiety. By blocking reuptake transporters, they allow serotonin to remain active longer, gradually improving mood regulation.

Selective Serotonin Reuptake Inhibitors (SSRIs)

• First-line treatment for depression and anxiety—includes fluoxetine (Prozac) and sertraline (Zoloft), the most commonly prescribed antidepressants today
• Mechanism blocks serotonin reuptake only—this selectivity produces fewer side effects than older antidepressants that affect multiple neurotransmitter systems
• Therapeutic lag of 2-4 weeks—patients must be monitored during this period, as suicide risk may temporarily increase before mood improves

Serotonin-Norepinephrine Reuptake Inhibitors (SNRIs)

• Dual-action on serotonin AND norepinephrine—examples include venlafaxine (Effexor) and duloxetine (Cymbalta), offering broader neurochemical effects
• Effective for treatment-resistant depression—often prescribed when SSRIs alone don't produce adequate response
• Additional benefit for chronic pain conditions—the norepinephrine component helps explain efficacy for fibromyalgia and neuropathic pain

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Older Antidepressant Classes

Before SSRIs revolutionized treatment, these medications were the primary options for depression. They remain clinically relevant but carry greater risks due to their broader neurochemical effects.

Tricyclic Antidepressants (TCAs)

• Block reuptake of both serotonin and norepinephrine—examples include amitriptyline and nortriptyline, now considered second-line treatments
• Significant anticholinergic side effects—causes dry mouth, constipation, sedation, and weight gain due to effects on acetylcholine receptors
• Dangerous in overdose—cardiac toxicity makes TCAs a concern for suicidal patients, explaining why SSRIs largely replaced them

Monoamine Oxidase Inhibitors (MAOIs)

• Inhibit the enzyme that breaks down monoamines—phenelzine (Nardil) and tranylcypromine (Parnate) increase serotonin, norepinephrine, AND dopamine levels
• Requires strict dietary restrictions—tyramine in aged cheeses, wine, and cured meats can trigger hypertensive crisis, a potentially fatal spike in blood pressure
• Reserved for atypical or treatment-resistant depression—rarely first-line due to dangerous food and drug interactions

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GABA-Enhancing Medications

These drugs work by potentiating the inhibitory neurotransmitter GABA, producing calming, sedative, and anxiolytic effects. By increasing chloride ion flow into neurons, they reduce neural excitability.

Benzodiazepines

• Enhance GABA-A receptor activity—examples include diazepam (Valium) and lorazepam (Ativan), producing rapid anxiolytic and sedative effects
• High risk of dependence and tolerance—long-term use leads to physical dependence, and abrupt discontinuation can cause dangerous withdrawal seizures
• Fast-acting but short-term solution—effective for acute anxiety and panic but not recommended as maintenance therapy

Hypnotics (Sleep Medications)

• Target GABA receptors to promote sleep—zolpidem (Ambien) and eszopiclone (Lunesta) are non-benzodiazepine hypnotics with more selective receptor binding
• Risk of complex sleep behaviors—patients may sleepwalk, sleep-eat, or even sleep-drive without memory of the event
• Short-term use only recommended—tolerance develops quickly, and dependence potential requires careful prescribing

Buspirone (Non-Benzodiazepine Anxiolytic)

• Partial agonist at serotonin 5-HT1A receptors—works differently than benzodiazepines, with no sedation, dependence risk, or withdrawal syndrome
• Requires 2-4 weeks for therapeutic effect—cannot be used for acute anxiety relief like benzodiazepines
• Preferred for generalized anxiety disorder—safer long-term option for patients with substance abuse history

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Dopamine-Targeting Medications

Dopamine plays a central role in psychosis, reward, and attention. These medications either block dopamine (for psychosis) or enhance it (for ADHD), demonstrating how the same neurotransmitter system requires opposite interventions for different disorders.

Typical (First-Generation) Antipsychotics

• Block dopamine D2 receptors—haloperidol and chlorpromazine reduce positive symptoms of schizophrenia like hallucinations and delusions
• High risk of extrapyramidal symptoms (EPS)—includes dystonia, akathisia, parkinsonism, and potentially irreversible tardive dyskinesia
• Dopamine hypothesis support—effectiveness of D2 blockers provided early evidence that schizophrenia involves dopamine dysregulation

Atypical (Second-Generation) Antipsychotics

• Block both dopamine AND serotonin receptors—risperidone, olanzapine, and quetiapine offer broader receptor profiles
• Lower EPS risk but metabolic concerns—weight gain, diabetes risk, and metabolic syndrome require regular monitoring
• First-line for schizophrenia today—better side effect profile makes them preferred over typical antipsychotics

Stimulants (for ADHD)

• Increase dopamine and norepinephrine in prefrontal cortex—methylphenidate (Ritalin) and amphetamine salts (Adderall) improve focus and impulse control
• Paradoxical calming effect in ADHD—stimulating underactive prefrontal regions actually reduces hyperactivity
• Schedule II controlled substances—high abuse potential requires careful monitoring, especially in adolescents and young adults

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Mood Stabilizers

These medications prevent the extreme highs and lows of bipolar disorder rather than simply treating one mood state. Their mechanisms vary, but all help regulate neural excitability and mood cycling.

Lithium

• Gold standard for bipolar disorder—the oldest and most studied mood stabilizer, particularly effective for preventing manic episodes
• Narrow therapeutic index—blood levels must be monitored regularly because toxic levels are close to therapeutic levels
• Side effects include thyroid and kidney dysfunction—long-term use requires monitoring of thyroid function and renal status

Anticonvulsant Mood Stabilizers

• Originally developed for epilepsy—valproate (Depakote) and lamotrigine (Lamictal) stabilize neural membranes and regulate ion channels
• Valproate effective for acute mania—also useful for rapid-cycling bipolar disorder
• Lamotrigine prevents depressive episodes—particularly valuable since bipolar depression is harder to treat than mania

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Quick Reference Table

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Self-Check Questions

1. Both SSRIs and SNRIs block serotonin reuptake—what additional mechanism do SNRIs have, and how does this affect their clinical applications?

2. A patient needs long-term anxiety treatment but has a history of substance abuse. Compare benzodiazepines and buspirone—which would you recommend and why?

3. Explain why typical antipsychotics cause extrapyramidal symptoms while atypical antipsychotics have lower EPS risk but higher metabolic risk.

4. An FRQ describes a patient with bipolar disorder who experiences more depressive episodes than manic episodes. Which mood stabilizer would be most appropriate, and what's your reasoning?

5. Compare the mechanisms and safety profiles of TCAs and SSRIs—why have SSRIs largely replaced TCAs as first-line antidepressants?