5.1 pcol ahahah
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100 Terms
A: Second-generation H1 blockers
Q: Class of antihistamines that cause minimal sedation and have less CNS penetration.
A: Cetirizine, loratadine, fexofenadine
Q: Examples of second-generation H1 blockers.
A: Non-sedating / minimal sedation
Q: Sedation profile of second-generation H1 blockers.
A: Low CNS penetration
Q: Ability of second-generation H1 blockers to cross the blood–brain barrier.
A: Once daily
Q: Dosing frequency typical of second-generation H1 blockers.
A: Cetirizine
Q: Second-generation H1 blocker with the fastest onset of action.
A: Mild sedation
Q: Sedative effect that may still occur with cetirizine.
A: Urticaria (hives)
Q: Allergic skin condition strongly relieved by cetirizine.
A: Renal failure
Q: Condition requiring dose adjustment when using cetirizine.
A: Alcohol
Q: Substance that should be avoided with cetirizine due to additive sedation.
A: Levocetirizine
Q: Active isomer of cetirizine.
A: More potent
Q: Comparative potency of levocetirizine versus cetirizine.
A: Fewer side effects
Q: Side-effect profile of levocetirizine compared with cetirizine.
A: Renal function
Q: Organ function requiring dose adjustment for levocetirizine.
A: Loratadine
Q: Second-generation H1 blocker that is a prodrug.
A: Desloratadine
Q: Active metabolite of loratadine.
A: Non-sedating
Q: Sedation profile of loratadine.
A: CYP3A4 inhibitors
Q: Drug class that can interact with loratadine.
A: Severe liver disease
Q: Condition in which loratadine should be avoided.
A: Desloratadine
Q: Second-generation H1 blocker that is the active metabolite with less variability.
A: Non-sedating
Q: Sedation profile of desloratadine.
A: Allergic rhinitis
Q: Allergic condition strongly relieved by desloratadine.
A: Hepatic elimination
Q: Elimination pathway of desloratadine requiring caution.
A: Fexofenadine
Q: Second-generation H1 blocker with the safest cardiovascular profile.
A: Fexofenadine
Q: Least sedating second-generation H1 blocker.
A: Hepatic metabolism
Q: Metabolic pathway that fexofenadine does NOT use.
A: Renal elimination
Q: Main route of elimination of fexofenadine.
A: Fruit juice
Q: Beverage that decreases absorption of fexofenadine.
A: Aluminum/magnesium antacids
Q: Type of antacids that reduce the effect of fexofenadine.
A: Mast cell stabilizers
Q: Class of drugs that prevent histamine release by inhibiting mast cell degranulation.
A: Cromolyn sodium
Q: Mast cell stabilizer commonly used for asthma prophylaxis.
A: Nedocromil
Q: Mast cell stabilizer similar to cromolyn used in allergic asthma.
A: Prevention of mast cell degranulation
Q: Main mechanism of action of cromolyn sodium and nedocromil.
A: Asthma prophylaxis
Q: Primary clinical use of mast cell stabilizers in respiratory disease.
A: Epinephrine
Q: Drug that acts as a physiologic antagonist to histamine.
A: Anaphylaxis
Q: Clinical condition in which epinephrine is the drug of choice to counteract histamine effects.
A: Physiologic antagonist to histamine
Q: Overall pharmacologic role of epinephrine in histamine-mediated reactions.
A: H2 blockers
Q: Drug class that competitively blocks H2 receptors on gastric parietal cells.
A: Decreased gastric acid secretion
Q: Primary gastric effect of H2 blockers.
A: Decreased basal acid output
Q: Effect of H2 blockers on nighttime acid secretion.
A: Decreased acid secretion
Q: Effect of H2 blockers on food-stimulated acid secretion.
A: Decreased acid secretion
Q: Effect of H2 blockers on gastrin-stimulated acid secretion.
A: Decreased acid secretion
Q: Effect of H2 blockers on vagal-stimulated acid secretion.
A: Pepsin
Q: Digestive enzyme production reduced by H2 blockers.
A: Gastric emptying
Q: Gastric function NOT affected by H2 blockers.
A: Histamine release
Q: Process that H2 blockers do NOT inhibit (they only block receptor action).
A: Cimetidine
Q: Least potent H2 blocker.
A: High lipophilicity
Q: Property of cimetidine that allows it to cross the BBB and placenta.
A: Cytochrome P450
Q: Enzyme system strongly inhibited by cimetidine.
A: Anti-androgenic effects
Q: Unique hormonal adverse effect group caused by cimetidine.
A: Gynecomastia
Q: Breast enlargement in males caused by cimetidine.
A: Impotence
Q: Sexual dysfunction caused by cimetidine.
A: Galactorrhea
Q: Milk secretion caused by cimetidine.
A: Elderly
Q: Population in which cimetidine should be avoided due to confusion risk.
A: Polypharmacy patients
Q: Patient group in whom cimetidine is risky due to drug interactions.
A: Renal impairment
Q: Organ impairment requiring dose adjustment for cimetidine.
A: Not preferred
Q: Pregnancy recommendation for cimetidine.
A: Ranitidine
Q: H2 blocker that is 5–10× more potent than cimetidine.
A: Minimal inhibition
Q: Effect of ranitidine on CYP450 enzymes.
A: Fewer endocrine effects
Q: Endocrine side-effect profile of ranitidine compared with cimetidine.
A: Shorter onset
Q: Onset of action of ranitidine compared with famotidine.
A: Carcinogenic impurity contamination
Q: Reason ranitidine is avoided for chronic use.
A: Renal dose adjustment
Q: Renal consideration when prescribing ranitidine.
A: No longer first-line therapy
Q: Current therapeutic status of ranitidine.
A: Famotidine
Q: Most potent H2 blocker.
A: Famotidine
Q: H2 blocker with the longest duration of action.
A: No inhibition
Q: Effect of famotidine on CYP450 enzymes.
A: None
Q: Endocrine side-effect profile of famotidine.
A: Safe
Q: Safety of famotidine for long-term use.
A: Minimal
Q: CNS side-effect profile of famotidine.
A: Renal failure
Q: Dose adjustment requirement for famotidine.
A: Very safe
Q: Safety of famotidine in pregnancy and elderly.
A: Nizatidine
Q: H2 blocker with similar potency to ranitidine.
A: Nearly 100%
Q: Oral bioavailability of nizatidine.
A: Minimal
Q: Drug interaction profile of nizatidine.
A: None
Q: Endocrine effect profile of nizatidine.Q: Endocrine effect profile of nizatidine.
A: Does not undergo first-pass metabolism
Q: Metabolic feature of nizatidine regarding first-pass metabolism.
A: Renal dose adjustment
Q: Dose adjustment requirement for nizatidine.
A: Generally safe
Q: Overall safety profile of nizatidine.
A: Famotidine
Q: H2 blocker with the strongest acid-suppressing potency.Q: H2 blocker with the strongest acid-suppressing potency.
A: Nizatidine and ranitidine
Q: H2 blockers with intermediate potency.
A: Cimetidine
Q: Weakest H2 blocker in terms of potency.
A: About 1 hour
Q: Approximate onset time of action of H2 blockers.
A: Nocturnal (nighttime) acid secretion
Q: Time period when H2 blockers achieve their greatest acid suppression.
A: 6–12 hours
Q: Usual duration of action of H2 blockers.
A: Famotidine
Q: H2 blocker with the longest duration of action.
A: Renal excretion
Q: Main route of elimination of H2 blockers.
A: Kidney disease (renal impairment)
Q: Organ dysfunction requiring dose adjustment for all H2 blockers.
A: Elderly
Q: Population at risk of confusion with H2 blockers, especially cimetidine.
A: Famotidine
Q: H2 blocker considered safest in pregnancy.
A: Patients on multiple drugs (polypharmacy)
Q: Patient group in whom cimetidine should be avoided due to drug interactions.
A: Acute gastrointestinal bleeding
Q: GI condition in which PPIs are preferred over H2 blockers.
A: Acid prophylaxis to reduce aspiration risk
Q: Pre-operative indication for IV ranitidine or famotidine.
A: Reduce gastric acidity and aspiration risk
Q: Clinical goal of giving IV H2 blockers before surgery.
A: Proton pump inhibitors (PPIs)
Q: Drug class preferred over H2 blockers for acute GI bleeding.
Note 
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