How does sucralfate work? Why must it be given on an empty stomach? When should it NOT be co-dosed with PPIs?
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Answer
Sucralfate: sucrose sulfate-aluminum compound Mechanism: Requires acidic environment to polymerize → binds directly to ulcer base, forms protective gel, ↑mucus & bicarbonate Dosing: On empty stomach (1 hr before/2 hrs after meals) — needs acid to activate Key: Do NOT give simultaneously with PPIs or H₂ blockers (acid suppression inhibits activation)
LO 4 — Misoprostol
What is misoprostol? How does it prevent NSAID-induced ulcers? What is the critical absolute contraindication?
For motion sickness: mechanism of scopolamine (patch) vs. dimenhydrinate. Which is better for long trips?
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Answer
Scopolamine (hyoscine): M₁ muscarinic antagonist → transdermal patch (sustained release, 72 hrs) • Ideal for long trips; ↓central effects • Side effect: dry mouth, blurred vision
Dimenhydrinate (Dramamine): H₁ antihistamine → oral; faster onset but shorter duration • Side effect: sedation (useful, also undesired)
Choice: Scopolamine for prophylaxis; Dramamine for acute use
LO 7 — ORS & SGLT1
Why is ORS (oral rehydration solution) so effective? What is the SGLT1 co-transporter mechanism?
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Answer
SGLT1 co-transport: Glucose + Na⁺ compete for same transporter on enterocyte apical membrane → active transport into cell → water follows osmotically
ORS formula: ~75 mmol/L Na⁺, ~65 mmol/L Cl⁻, ~20 mmol/L K⁺, ~25 mmol/L glucose (1:1 glucose:Na⁺ ratio is key)
Impact: Saved millions from cholera/infectious diarrhea. Simple, cheap, effective.
LO 7 — Diphenoxylate vs. Loperamide
Both are μ-opioid antidiarrheals. Why is diphenoxylate combined with atropine? How does loperamide differ?
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Answer
Diphenoxylate + atropine (Lomotil): μ-opioid agonist; atropine added to discourage abuse (anticholinergic side effects at high doses)
Loperamide (Imodium): μ-opioid agonist; peripheral only — does NOT cross BBB at therapeutic doses → no euphoria, minimal abuse potential, available OTC
CONTRAINDICATION for both: Infectious diarrhea (C. diff, shigella, Salmonella) — risk of toxic megacolon
LO 8 — Laxatives by Mechanism
Name four laxative classes, one drug per class, onset time, and mechanism.
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Answer
Bulk-forming: Psyllium, methylcellulose → water retention; 1–3 days Osmotic/saline: Magnesium citrate, lactulose, PEG → osmotic water draw; hours to overnight Stimulant/irritant: Senna, bisacodyl → myenteric nerve stimulation; hours (abuse potential) Stool softener: Docusate → ↑water penetration of stool; days
LO 8 — Lactulose & Hepatic Encephalopathy
Why is lactulose used in hepatic encephalopathy, not just as a laxative? What is the mechanism?
Why unique: Peripherally active (does NOT cross BBB) → blocks μ receptors in GI tract (reversing opioid-induced constipation) WITHOUT antagonizing opioid analgesia in CNS
Use: Palliative care patients on opioids; allows adequate pain control without severe constipation
LO 9 — 5-ASA Drugs
What is mesalamine (5-ASA)? What role in IBD? How does sulfasalazine differ?
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Answer
Mesalamine (5-aminosalicylic acid): Anti-inflammatory; ↓prostaglandins & leukotrienes Uses: UC first-line induction & maintenance (topical enema form ↑efficacy); less effective in Crohn's
Sulfasalazine: 5-ASA + sulfapyridine (carrier); requires colonic bacteria for activation • Older agent; GI side effects common • Sulfa allergy? Use mesalamine instead
LO 9 — Steroids in IBD
Why are corticosteroids used in IBD? Which steroid (budesonide vs. prednisone) is preferred for Crohn's and why?
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Answer
Role: INDUCTION only (not maintenance) — potent anti-inflammatory
Budesonide: Preferred for ileocecal Crohn's • High first-pass hepatic metabolism (↓systemic side effects) • Topical action in terminal ileum/colon
Prednisone: Systemic steroid for severe UC/Crohn's; more systemic side effects
What are vedolizumab and ustekinumab? How do their mechanisms differ from anti-TNF drugs?
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Answer
Vedolizumab: Anti-integrin α4β7 (gut-selective) → blocks lymphocyte homing to GI mucosa; effective in UC + Crohn's
Ustekinumab: Anti-IL-12/23 (blocks cytokine signaling) → effective in moderate-severe Crohn's
Advantage vs. anti-TNF: Gut-selective (vedolizumab) or different immune pathway (ustekinumab) → potentially fewer systemic infections
FIB 01 — LO 1
PPIs irreversibly inhibit the ___________ on parietal cells. Gastrin stimulates this enzyme via the ___________ receptor, while histamine acts on the ___________ receptor.
FIB 02 — LO 1
___________ is a CYP450 inhibitor and antiandrogen side effect risk. The safer H₂ blockers include ___________, famotidine, and nizatidine.
FIB 03 — LO 1
Three major PPI adverse effects are ___________ infection risk, malabsorption of ___________ and ___________, and increased hip fracture risk.
FIB 04 — LO 2
H. pylori quadruple therapy is abbreviated PBMT: ___________ + Bismuth + ___________ + Tetracycline. An alternative triple therapy uses PPI + Clarithromycin + ___________.
FIB 05 — LO 3
GERD stepwise therapy: lifestyle modification → ___________ → PPIs → ___________. Common GERD triggers include fatty meals, caffeine, ___________, and alcohol.
FIB 06 — LO 4
Sucralfate requires ___________ environment to polymerize and should be given on ___________ stomach. It must NOT be co-dosed simultaneously with ___________ or H₂ blockers.
FIB 07 — LO 4
Misoprostol is a ___________ analog that ↑mucus and ↓acid. CRITICAL: it is absolutely contraindicated in ___________ because it is teratogenic and ___________.
FIB 08 — LO 5–6
Motion sickness involves the ___________ inputs that use H₁ and M₁ receptors; treat with ___________ (H₁ blocker) or ___________ patch (M₁ blocker). Chemo nausea uses D₂/5-HT₃ → treat with ___________ (5-HT₃ antagonist).
FIB 09 — LO 7
___________ (Imodium) is a μ-opioid that does NOT cross the BBB at therapeutic doses → no euphoria/abuse potential. Both antidiarrheals are contraindicated in ___________ infections due to risk of toxic megacolon.
FIB 10 — LO 8–9
In UC, ___________ (5-ASA) is first-line both for induction and maintenance. For IBD, ___________ (anti-TNF-α, chimeric) requires ___________ screening before starting due to reactivation risk.
Instructions: Drag and drop the items into the correct order, then click "Check Order." Use "Show Answer" if you get stuck.
Drill 1 — GERD Stepwise Management: First → Last
Arrange the four therapeutic tiers in order of escalation.
Test Trap Mode: Each statement is either TRUE or FALSE as written. Many are designed to catch common exam errors. Click T or F — then read the explanation carefully.
Trap 01 — LO 1
"PPIs are reversible inhibitors of the H⁺/K⁺ ATPase, while H₂ blockers are irreversible."
FALSE. This is REVERSED! PPIs bind IRREVERSIBLY to the proton pump — accounts for their sustained effect and why they're tapered. H₂ blockers bind REVERSIBLY to the H₂ receptor. Once you learn which is which, remember: PPI = Persistent (irreversible).
Trap 02 — LO 1
"Cimetidine is preferred over other H₂ blockers because it has no drug interactions or hormonal side effects."
FALSE. Cimetidine is actually the WORST choice for routine use! It inhibits CYP450 (↑drug interactions) AND causes antiandrogen effects (gynecomastia, impotence). Ranitidine, famotidine, and nizatidine are safer alternatives with minimal CYP450 interactions.
Trap 03 — LO 1
"Sucralfate should be taken simultaneously with PPIs for maximal acid suppression and mucosal protection."
FALSE. Sucralfate requires an acidic environment to polymerize and bind the ulcer base. If you co-dose with PPIs/H₂ blockers, the acid is suppressed → sucralfate CANNOT activate → no benefit! Give sucralfate 1 hr before or 2 hrs after acid suppressants.
Trap 04 — LO 4
"Misoprostol is an excellent choice for NSAID-induced ulcer prevention in pregnant patients."
FALSE. Misoprostol is ABSOLUTELY CONTRAINDICATED in pregnancy — it is teratogenic AND abortifacient. Use only in post-menopausal women or those on reliable contraception. Best choice for NSAID ulcer prevention is switching to a COX-2 inhibitor or adding a PPI instead.
Trap 05 — LO 5–6
"Ondansetron (5-HT₃ antagonist) is the best first-line antiemetic for motion sickness."
FALSE. Ondansetron works for CHEMO & POSTOP nausea (D₂/5-HT₃ sources). Motion sickness involves VESTIBULAR pathways (H₁ & M₁ receptors), so use dimenhydrinate (H₁ antagonist) or scopolamine (M₁ antagonist) instead. Wrong drug, wrong pathway.
Trap 06 — LO 6
"Metoclopramide has no risk of neurologic side effects when used long-term, making it ideal for chronic gastric dysmotility."
FALSE. Metoclopramide causes TARDIVE DYSKINESIA (irreversible involuntary movements), extrapyramidal symptoms, and parkinsonism — especially with long-term use. Black box warning for neurologic toxicity. Avoid chronic use; reserve for acute, short-term nausea only.
Trap 07 — LO 7
"Loperamide (Imodium) readily crosses the blood-brain barrier and has significant abuse potential at standard doses."
FALSE. Loperamide is a PERIPHERAL μ-opioid — does NOT cross the BBB at therapeutic doses. No euphoria, minimal abuse potential, safe for OTC. (Diphenoxylate has atropine added to deter abuse because it CAN cause CNS effects at high doses.) This is the key difference.
Trap 08 — LO 9
"5-ASA drugs are most effective for treating moderate-to-severe Crohn's disease and should be first-line induction therapy."
FALSE. 5-ASA is FIRST-LINE for UC (mild-moderate induction & maintenance), but LESS effective in Crohn's. For moderate-severe Crohn's → use corticosteroids (induction) + biologics (TNF inhibitors preferred). 5-ASA plays a role in UC, not Crohn's first-line therapy.
Prevent straining; prevent constipation from opioids
Peripherally-acting μ-antagonist
Methylnaltrexone
Hours
Block μ-opioid in GI tract (NOT CNS)
Opioid-induced constipation (preserves analgesia)
IBD First-Line Agents by Disease & Severity
Disease Type
Severity
First-Line Induction
Maintenance
UC (ulcerative colitis)
Mild–moderate
5-ASA (oral ± topical enema)
5-ASA long-term
UC (ulcerative colitis)
Moderate–severe
Systemic corticosteroids (prednisone)
5-ASA + immunomodulator (azathioprine, 6-MP)
UC (refractory)
Severe
Infliximab or adalimumab (anti-TNF); vedolizumab (anti-integrin)
Continue biologic
Crohn's (localized)
Mild–moderate
Budesonide (ileocecal) OR systemic steroid
Maintenance agent (see below)
Crohn's (pan-intestinal)
Moderate–severe
Infliximab OR adalimumab (anti-TNF); other biologics
Continue biologic + immunomodulator
Key Principle: 5-ASA is FIRST-LINE in UC; less effective in Crohn's. Steroids for INDUCTION only — taper after remission. Biologics for moderate-severe disease & maintenance. Anti-TNF-α is preferred in Crohn's (transmural disease); consider vedolizumab or ustekinumab for TNF inhibitor failure.
H. pylori Eradication: Quadruple therapy (PPI + Bismuth + Metronidazole + Tetracycline × 10–14 days) is preferred. Alternative: triple therapy (PPI + Clarithromycin + Amoxicillin). Always confirm eradication with urea breath test or stool antigen 4+ weeks post-treatment.