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psychopharm exam 2
| Term | Definition |
|---|---|
| Dopamine Pathway | Mediates pleasure, reward, and motivation. Decreased dopamine transmission contributes to anhedonia and lack of interest in MDD. |
| Norepinephrine System | Regulates alertness, energy, attention, and arousal. Deficiency leads to fatigue and cognitive dulling. |
| Serotonin Network | Controls mood, anxiety, sleep cycles, and appetite regulation. Central target for most antidepressant medications. |
| SSRIs (Selective Serotonin Reuptake Inhibitors) | Mechanism: Block serotonin reuptake at presynaptic terminals, increasing synaptic serotonin availability. Examples: Fluoxetine, sertraline, escitalopram, paroxetine, citalopram, fluvoxamine Clinical use: First-line treatment for MDD, anxiety disord |
| SNRIs (Serotonin-Norepinephrine Reuptake Inhibitors) | Mechanism: Dual inhibition of both serotonin and norepinephrine reuptake Examples: Venlafaxine, duloxetine, desvenlafaxine Clinical use: MDD with fatigue, chronic pain syndromes, treatment resistant depression Caution: Venlafaxine may elevate blood |
| NDRIs (Norepinephrine-Dopamine Reuptake Inhibitors) | Mechanism: Inhibits reuptake of norepinephrine and dopamine without affecting serotonin Example: Bupropion (Wellbutrin, Zyban) Clinical use: MDD with low energy, smoking cessation (FDA-approved), ADHD (off-label) Key consideration: Lower sexual side e |
| SARIs (Serotonin Antagonist/Reuptake Inhibitors) | Mechanism: Blocks serotonin 5-HT2 receptors while weakly inhibiting serotonin reuptake Example: Trazodone Clinical use: Depression with insomnia, low-dose sleep aid Unique risk: Priapism (persistent painful erection requiring emergency intervention) |
| TCAs (Tricyclic Antidepressants) | Mechanism: Block reuptake of serotonin and norepinephrine; also block histamine, acetylcholine, and alpha-adrenergic receptors Examples: Amitriptyline, nortriptyline, imipramine Clinical use: Treatment-resistant depression, chronic pain, migraine prophy |
| MAOIs (Monoamine Oxidase Inhibitors) | Mechanism: Inhibit MAO enzymes that break down serotonin, norepinephrine, and dopamine Example: Phenelzine Clinical use: Atypical depression, treatment-resistant cases Critical warning: Avoid tyramine-containing foods (aged cheese, cured meats, wine) |
| Common Side Effects by Class | SSRIs/SNRIs: Sexual dysfunction (delayed orgasm, decreased libido), GI upset, initial anxiety/activation, hyponatremia (especially in elderly), weight gain (long-term), discontinuation syndrome Bupropion: Insomnia, anxiety, seizure risk at high doses (>4 |
| Pregnancy and Lactation | Safest option: Sertraline is generally considered safest during pregnancy with most evidence for safety Avoid: Paroxetine (associated with cardiac defects), MAOIs Risk-benefit analysis: Untreated maternal depression poses significant risks; treatment de |
| Geriatric Considerations | Start low, go slow: Use lower initial doses and slower titration Hyponatremia risk: SSRIs, particularly sertraline, may cause SIADH and hyponatremia in older adults4monitor sodium levels Fall risk: TCAs and sedating antidepressants increase fall risk du |
| Drug Interactions | Serotonin syndrome: Avoid combining SSRIs with MAOIs, tramadol, linezolid, or other serotonergic agents. Symptoms include confusion, tremors, sweating, hyperreflexia, agitation, and hyperthermia. NSAIDs + SSRIs: NSAIDs (ibuprofen, naproxen) can increase |
| When to Switch Antidepressants | Inadequate response after adequate trial (4-6 weeks at therapeutic dose) Intolerable side effects Persistent fatigue and lack of motivation (consider SSRI to SNRI switch) Sexual dysfunction (switch to bupropion or mirtazapine) Weight gain concerns |
| Augmentation Approaches | Augmentation involves adding a second agent to boost the effectiveness of a partially effective antidepressant. Evidence-based augmentation strategies include: Bupropion: Lower sexual side effects; adds norepinephrine and dopamine activity; often used |
| Adequate Trial | 4-6 weeks at therapeutic dose |
| Implement Strategy | Cross-taper or add augmenting agent |
| Assess Response | Partial? Consider augmentation. None? Consider switch |
| Monitor and Adjust | Reassess efficacy and tolerability |
| Mesolimbic Pathway | Function: Reward, pleasure, motivation, emotional regulation Clinical significance: Excess dopamine transmission in this pathway is associated with positive symptoms of psychosis (hallucinations, delusions). Antipsychotic blockade of D2 receptors here |
| Nigrostriatal Pathway | Function: Motor control and movement coordination Clinical significance: D2 blockade in this pathway produces extrapyramidal symptoms (EPS) including parkinsonism, dystonia, and akathisia. Long-term blockade increases risk of tardive dyskinesia. |
| Mesocortical Pathway | Function: Executive function, working memory, attention, emotional processing Clinical significance: Reduced dopamine activity contributes to negative symptoms (flat affect, amotivation) and cognitive deficits in schizophrenia. Excessive D2 blockade h |
| Tuberoinfundibular Pathway | Function: Prolactin regulation Clinical significance: D2 blockade removes dopamine's inhibitory effect on prolactin, leading to hyperprolactinemia. This causes galactorrhea, amenorrhea, sexual dysfunction, and potential bone density loss. |
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