High-yield drug classes (first half of the alphabet by system: CNS, cardiovascular, autonomic) with mechanism of action, one card per class or key drug.
50 cards · basic cards · AI-written, checked twice. Edit anything.
- SSRIs: What is their primary mechanism of action?
- Inhibit selective reuptake of serotonin at the presynaptic terminal
- SNRIs: What neurotransmitters do they block reuptake of?
- Serotonin and norepinephrine
- Tricyclic antidepressants: What is their mechanism?
- Block reuptake of norepinephrine and serotonin, plus antimuscarinic and antihistamine effects
- Monoamine oxidase inhibitors: How do they work?
- Inhibit the enzyme MAO, preventing breakdown of serotonin, norepinephrine, and dopamine
- Atypical antipsychotics: What is their mechanism?
- Block D2 dopamine receptors and 5-HT2 serotonin receptors
- Typical antipsychotics: What is their mechanism?
- Block D2 dopamine receptors, primarily in the mesolimbic pathway (antipsychotic effect); also block D2 receptors in the nigrostriatal pathway, causing extrapyramidal side effects, and in the tuberoinfundibular pathway, causing hyperprolactinemia
- Benzodiazepines: How do they enhance CNS depression?
- Potentiate GABA-A receptor function, increasing chloride channel opening
- Barbiturates: What is their mechanism?
- Enhance GABA-A receptors and also directly open chloride channels, producing CNS depression
- Amphetamines: How do they increase alertness?
- Increase release of norepinephrine and dopamine, inhibit their reuptake
- Lithium: What is its proposed mechanism in bipolar disorder?
- Inhibits inositol monophosphatase, disrupting the phosphatidylinositol cycle, reducing IP3 signaling
- Phenytoin (anticonvulsant): What is its mechanism?
- Blocks voltage-gated sodium channels, stabilizing neuronal membranes
- Opioids: How do they produce analgesia?
- Bind to mu, delta, and kappa opioid receptors, decreasing neurotransmitter release and hyperpolarizing neurons
- Acetaminophen: What is its mechanism of analgesia?
- Inhibits cyclooxygenase (COX) in the CNS and also acts on serotonergic and endocannabinoid pathways
- NSAIDs: What enzyme do they inhibit?
- Cyclooxygenase (COX-1 and COX-2), decreasing prostaglandin and thromboxane synthesis
- Alpha-1 agonists (e.g., phenylephrine): What is their effect?
- Activate alpha-1 adrenergic receptors, causing vasoconstriction and increasing blood pressure