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This deck focuses on Adverse Reactions, giving you a quick way to review the definitions, rules, and examples that matter most for NAPLEX.
Study Adverse Reactions in NAPLEX with focused flashcards that help you recognize the idea, recall the key rule, and apply it in practice-style prompts.
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What is an adverse effect caused by off-target pharmacology at therapeutic doses called?
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Side effect. Side effects occur from unintended activation of non-primary targets at normal doses, differing from toxicities or hypersensitivities.
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This deck focuses on Adverse Reactions, giving you a quick way to review the definitions, rules, and examples that matter most for NAPLEX.
Work through these flashcards in short sessions. Try to answer each prompt before flipping the card, then revisit any cards you miss until the explanation feels automatic.
Answer: Side effect. Side effects occur from unintended activation of non-primary targets at normal doses, differing from toxicities or hypersensitivities.
Answer: Pruritus (pseudoallergy). Opioids directly stimulate mast cell histamine release, causing itch without involving adaptive immune responses or IgE.
Answer: Unpredictable, non–dose-related reaction due to host factors. Idiosyncratic reactions depend on genetic or unique patient factors, making them unpredictable and not linked to drug dose or pharmacology.
Answer: ADR implies causal relationship; adverse event does not. ADRs require evidence of causality between the drug and the reaction, whereas adverse events are any unfavorable occurrences without proven drug linkage.
Answer: Dose-related, predictable, related to pharmacology. Type A reactions stem from exaggerated pharmacological effects, making them foreseeable and often preventable by dose adjustment.
Answer: Type A. Type A reactions account for the majority of ADRs due to their basis in known pharmacological actions and dose dependency.
Answer: Noxious, unintended response at doses normally used in humans. The WHO definition emphasizes harmful, unintended effects occurring at standard therapeutic doses, distinguishing ADRs from other drug-related issues.
Answer: Toxicity. Toxicity results from supratherapeutic levels overwhelming normal physiological tolerances, often due to overdose or impaired clearance.
Answer: Risk of serious or life-threatening adverse effects. Black box warnings highlight critical risks identified in post-marketing surveillance or clinical trials to alert prescribers and patients.
Answer: Type A adverse drug reaction. Aminoglycoside toxicities are extensions of their antibacterial mechanism, accumulating in ears and kidneys with higher doses.
Answer: Intramuscular epinephrine. Epinephrine rapidly counteracts vasodilation and bronchoconstriction in anaphylaxis by stimulating alpha and beta adrenergic receptors.
Answer: DRESS (drug reaction with eosinophilia and systemic symptoms). DRESS is a delayed hypersensitivity reaction involving T-cell activation, leading to multi-organ inflammation after prolonged drug exposure.
Answer: Clindamycin. Clindamycin potently disrupts gut flora, promoting C. difficile overgrowth and toxin production leading to pseudomembranous colitis.
Answer: Vancomycin infusion reaction (red man syndrome). Rapid vancomycin infusion causes histamine release from mast cells, resulting in flushing, pruritus, and hemodynamic changes.
Answer: Stevens-Johnson syndrome/toxic epidermal necrolysis. SJS/TEN results from cytotoxic T-cell responses causing keratinocyte apoptosis and widespread skin and mucosal detachment.
Answer: Fluoroquinolones. Fluoroquinolones disrupt tendon matrix integrity via metalloproteinase upregulation, increasing rupture risk especially in vulnerable populations.
Answer: Acute, life-threatening systemic hypersensitivity reaction. Anaphylaxis involves rapid IgE-mediated mast cell degranulation, causing widespread histamine release and systemic symptoms.
Answer: ACE inhibitors. ACE inhibitors increase bradykinin levels by inhibiting its degradation, triggering vascular permeability and angioedema.
Answer: Withdrawal reaction. Withdrawal occurs when the body adapts to chronic drug presence, leading to symptoms upon cessation due to disrupted homeostasis.
Answer: Malignant hyperthermia. Succinylcholine triggers uncontrolled calcium release in genetically susceptible muscle cells, leading to hypermetabolism and hyperthermia.
Answer: Rebound phenomenon. Rebound involves hyperactivation of suppressed pathways after drug removal, causing symptoms to exceed pre-treatment levels.
Answer: Immune-mediated reaction requiring prior sensitization. Allergic reactions involve immune system activation after initial exposure, leading to hypersensitivity upon re-exposure.
Answer: Type B. Type B reactions, being idiosyncratic or allergic, often lead to severe outcomes necessitating complete drug avoidance in affected individuals.
Answer: ACE inhibitor–associated cough. Lisinopril inhibits ACE, elevating bradykinin which irritates airways and induces non-productive cough in susceptible patients.
Answer: Not dose-related, unpredictable, often immune-mediated. Type B reactions arise from individual hypersensitivity or immunological responses, rendering them hard to predict and unrelated to dose.