LO 1

ON EXAM — parietal cell targets (H+/K+-ATPase, H2R, M3R), H2 blockers vs PPIs (potency/onset), P-CABs, side effects of long-term PPI (hypomagnesemia, B12/Ca2+, C. diff risk)

Parietal cell inputs — what stimulates acid secretion? (3 pathways)

Pathway 1 — _______ cell releases histamine → H2 receptor

Pathway 2 — Parasympathetic (vagus) releases _______ → M3 receptor

Pathway 3 — _______ cells release gastrin → CCK-B receptor

Drug classes targeting acid — name mechanism + 1 example

Drug Class	MOA	Example	Speed
Antacids
H2 receptor blockers
PPIs (proton pump inhibitors)
P-CABs

H2 blockers vs PPIs — key differences

H2 blocker: reversible or irreversible block?

PPI: reversible or irreversible block?

Which is more potent (reduces acid more)?

Which has faster onset?

Name 2 H2 blockers

Name 3 PPIs

PPI side effects — chronic use complications (fill 4)

Electrolyte — causes seizures/arrhythmias if low

Vitamin deficiency — intrinsic factor needed for absorption

Mineral deficiency — reduced absorption in alkaline stomach

What does PPI-induced achlorhydria increase risk of?

LO 2

ON EXAM — quadruple vs triple therapy regimens, which antibiotics, bismuth role, why combination (resistance + PPI dual role), eradication testing (test timing + method)

H. pylori basics — survival + pathogenesis

What enzyme does H. pylori produce to survive gastric acid?

This enzyme converts urea into _______ and _______, the second of which buffers local acid

Untreated H. pylori → chronic gastritis + risk of what 2 serious sequelae?

H. pylori diagnosis — methods

Test	Mechanism / What It Detects	Invasive?
Urea breath test
Stool antigen
CLO test (biopsy)
Serology (IgG)

Quadruple therapy regimen — name all 4 drugs + duration

MNEMONIC ALERT: Quadruple = 2 ABX + PPI + Bismuth. This is the current standard.

Component	Drug Name(s)	Duration
Antibiotic #1
Antibiotic #2
Acid suppression
Antimicrobial coating

Why PPI is essential in the regimen (2 reasons)

Reason 1 — treatment goal (healing)

Reason 2 — antibiotic efficacy (pH-dependent)

Post-treatment monitoring — eradication testing

Test for eradication how many weeks after completing antibiotics?

Which test to use (2 acceptable methods)

Why NOT use serology (IgG) for follow-up?

LO 3

ON EXAM — antacid choice (Mg/Ca/Al side effects), stepwise GERD treatment (lifestyle → antacid → H2 → PPI), LES physiology, PPIs > H2 for erosive disease

Individual antacids — GI side effects mnemonic

Antacid	Side Effect(s)	Mnemonic / Tip
Magnesium hydroxide
Aluminum hydroxide
Calcium carbonate
Sodium bicarbonate
Mg + Al 50/50 combo

GERD stepwise treatment algorithm

Step-wise GERD therapy: empiric treatment first, escalate if inadequate response or if erosive disease confirmed.

Step 1 (initial) — non-pharmacologic

Step 2 (mild symptoms) — which drug class?

Step 3 (moderate or persistent) — which drug class?

Step 4 (erosive disease confirmed) — which drug preferred?

LES and acid reflux mechanics

What is the LES and what keeps it normally closed?

What hormones/drugs RELAX the LES (promote reflux)?

What is the pathophysiology of Barrett's esophagus?

LO 5 · LO 6

ON EXAM — 5-HT3 antagonists (chemo nausea), 5-HT4 agonists (prokinetics), muscarinic antagonists (motion sickness), metoclopramide (TARDIVE DYSKINESIA risk, D2 block), chemotherapy-induced nausea mechanism

Vomiting reflex anatomy — CTZ and NTS

CTZ = chemoreceptor trigger zone; where is it located?

Is CTZ inside or outside the blood-brain barrier?

NTS = nucleus tractus solitarius; what does it do?

Name 3 inputs to the vomiting center that can trigger nausea

Antiemetic drugs — class, MOA, clinical use

Drug / Class	MOA	Best For / Indication
Ondansetron (Zofran)
Granisetron
Metoclopramide (Reglan)
Prochlorperazine (Compazine)
Scopolamine
Diphenhydramine (Benadryl)

5-HT3 antagonists vs 5-HT4 agonists — comparison

5-HT3 antagonist examples (2)

5-HT3 use — what type of nausea?

5-HT4 agonist examples (2)

5-HT4 use — what GI problem does it treat?

Metoclopramide — MOA + major side effect concern

Metoclopramide blocks which dopamine receptor?

What is the serious long-term neurological side effect?

Risk is highest if used > _______ months at high dose

LO 7 · LO 8

ON EXAM — laxative onset categories (bulk/osmotic/stimulant timing), diphenoxylate vs loperamide, when to AVOID antidiarrheals (toxin-mediated/invasive), ORS rationale (glucose-sodium coupling)

Laxative classification by onset — name drugs in each category

Laxative Type	Onset	MOA	Example Drug(s)
Bulk
Osmotic
Stimulant
Stool softener

Antidiarrheals — drugs + mechanism

Diphenoxylate (Lomotil) — MOA + concern

Loperamide (Imodium) — MOA + difference from diphenoxylate

Bismuth subsalicylate (Pepto-Bismol) — MOA

When to AVOID antidiarrheals — contraindications

CRITICAL: Never give antidiarrheals in inflammatory diarrhea (toxin-mediated or invasive). They worsen outcomes by trapping toxins/bacteria.

Condition: C. difficile toxin-mediated diarrhea → why avoid diphenoxylate/loperamide?

Condition: Shigella or EAEC invasive diarrhea → why avoid?

General rule: avoid antidiarrheals if _______ and _______ are present

Diarrhea management — ORS and fluid/electrolyte rationale

ORS contains what 2 key components that work synergistically?

Mechanism: how does this combo reduce stool losses?

Why is ORS preferred over plain water?

LO 9

ON EXAM — 5-ASA location (colon-targeted for UC), anti-TNF biologics (infliximab/adalimumab both GI+systemic), anti-IL-23 (risankizumab), Crohn's vs UC drug choice, steroid role (acute flare only)

IBD classification — Crohn's vs UC key differences

Feature	Crohn's Disease	Ulcerative Colitis
Location(s)
Depth of inflammation
Complications (fistula/stricture?)

5-ASA compounds — drugs + mechanism

What does 5-ASA stand for?

Mesalamine (Asacol) — how is it formulated for colon delivery?

Sulfasalazine — what is it + why useful?

Role of 5-ASA in Crohn's vs UC: which is better indicated?

Biologic agents — anti-TNF and anti-IL-23

Drug	Target / MOA	GI + Systemic Effect?	Crohn's / UC?
Infliximab (Remicade)
Adalimumab (Humira)
Risankizumab

Steroids in IBD — role and limitations

When are systemic steroids (prednisone) used in IBD?

Why are steroids NOT used for maintenance therapy?

What is budesonide and when is it used?

Practice Questions

Q1: Acid suppression mechanism

A 38-year-old man with erosive GERD is started on omeprazole. Which of the following best describes the mechanism of this drug?

A) Reversible blockade of H₂ histamine receptors on parietal cells
B) Irreversible blockade of the H⁺/K⁺-ATPase (proton pump) in parietal cell canaliculus
C) Neutralization of existing gastric acid via alkaline ions
D) Inhibition of gastrin release from G cells
E) Competitive blockade of H⁺/K⁺-ATPase (reversible)

Correct Answer: B

Omeprazole is a proton pump inhibitor (PPI) that irreversibly blockades the H⁺/K⁺-ATPase. This is the final common pathway for acid secretion, making PPIs the most potent acid suppressors. They are activated in the acidic canalicular space and bind irreversibly to the pump. A is H₂ blockers (reversible). C is antacids. D is not a mechanism of any major acid-suppressive drug. E describes P-CABs, which are newer.

Q2: H. pylori eradication regimen

A 45-year-old woman is diagnosed with H. pylori by urea breath test and presents with a peptic ulcer. She is prescribed quadruple therapy. Which of the following is the correct combination?

A) Amoxicillin + Clarithromycin + PPI
B) Metronidazole + Tetracycline + PPI + Bismuth subsalicylate
C) Levofloxacin + Clarithromycin + H₂ blocker
D) Amoxicillin + Doxycycline + PPI + Antacid
E) Triple therapy is sufficient; quadruple is not standard

Correct Answer: B

Quadruple therapy (the current standard per Medical Letter) consists of: Metronidazole + Tetracycline + PPI + Bismuth subsalicylate for 7–14 days. The PPI reduces acid (heals ulcer) AND improves antibiotic efficacy. Bismuth has intrinsic antimicrobial activity. A is older triple therapy (falling out of favor). C uses wrong drugs. D mixes different agents. E is incorrect; quadruple is now preferred due to clarithromycin resistance.

Q3: Antacid side effects

A patient is given aluminum hydroxide for 2 weeks to treat GERD symptoms. Which side effect would you expect?

A) Diarrhea and hypermagnesemia
B) Constipation and phosphate depletion
C) Hypercalcemia and bloating
D) Hypomagnesemia and loose stools
E) Metabolic alkalosis and muscle weakness

Correct Answer: B

Aluminum hydroxide causes CONSTIPATION (not diarrhea) and binds phosphate in the gut, leading to phosphate depletion. Magnesium hydroxide does the opposite (diarrhea). Remember: "Mg = Must Go" (diarrhea), "Al = All Locked Up" (constipation).

Q4: 5-HT3 antagonists and chemotherapy nausea

A 52-year-old woman receiving chemotherapy for breast cancer develops severe nausea. She is prescribed ondansetron IV before her next infusion. What is the mechanism of this drug?

A) Dopamine antagonist at the CTZ
B) Blocks 5-HT3 receptors, preventing vagal afferent signaling from GI to vomiting center
C) M1 muscarinic receptor antagonist (motion sickness pathway)
D) Increases gastric motility via 5-HT4 agonism
E) Reduces intracranial pressure in the CTZ

Correct Answer: B

Ondansetron (and other setrons like granisetron) are selective 5-HT3 receptor antagonists. They block 5-HT3 receptors on vagal afferent neurons, preventing the transmission of chemotherapy-induced nausea signals to the vomiting center. A is metoclopramide. C is scopolamine/antihistamines. D is cisapride/prucalopride (prokinetics). E is not a mechanism of any antiemetic.

Q5: Metoclopramide safety concern

A 40-year-old man with gastroparesis is treated with metoclopramide for 18 months at standard doses. He begins to develop involuntary orofacial movements. Which adverse effect is this consistent with?

A) Extrapyramidal side effects (acute dystonia)
B) Neuroleptic malignant syndrome
C) Tardive dyskinesia
D) Parkinsonism (tremor)
E) Akathisia

Correct Answer: C

Tardive dyskinesia (involuntary dyskinetic movements, especially orofacial) is a serious long-term risk of metoclopramide (a D2 blocker), especially with prolonged use (>3 months) at higher doses. This is an FDA black box warning. A/B/D/E are other dopamine antagonist side effects but occur acutely. The 18-month duration and specific presentation point to tardive dyskinesia.

Q6: Laxative onset classification

An elderly patient with constipation needs immediate bowel evacuation for a colonoscopy tomorrow morning. Which laxative has the fastest onset (hours)?

A) Psyllium husk (Metamucil)
B) Magnesium citrate (osmotic)
C) Docusate (stool softener)
D) Bisacodyl (stimulant)
E) Mineral oil

Correct Answer: B

Osmotic laxatives like magnesium citrate work within 2–3 hours by drawing water into the intestinal lumen. This makes them ideal for rapid bowel evacuation (prep). A (bulk) takes 12–24 hours. C (softener) is very slow. D (stimulant) takes 6–12 hours. E (mineral oil) takes 6–8 hours.

Q7: Antidiarrheal contraindication

A 35-year-old man presents with acute bloody diarrhea, fever, and positive stool culture for Shigella. He requests medication to stop the diarrhea. What is the best recommendation?

A) Prescribe loperamide (Imodium) to reduce symptoms
B) Prescribe diphenoxylate with atropine (Lomotil)
C) Avoid antidiarrheals; they worsen invasive bacterial infections by trapping organisms and toxins
D) Give bismuth subsalicylate for symptom relief
E) Both A and B are acceptable first-line treatments

Correct Answer: C

Antidiarrheals (loperamide, diphenoxylate) are CONTRAINDICATED in invasive bacterial diarrhea (Shigella, EAEC, Salmonella, Campylobacter) and toxin-mediated diarrhea (C. difficile, Enterotoxigenic E. coli) because they trap organisms/toxins in the gut, prolonging infection and worsening complications. Supportive care with ORS is preferred. D (bismuth) is less problematic but still used cautiously.

Q8: IBD drug choice — anti-TNF vs anti-IL-23

A 28-year-old woman is diagnosed with moderate Crohn's disease and is started on anti-TNF biologic therapy with infliximab. Which of the following best describes infliximab's role in IBD?

A) It blocks IL-23 signaling, preventing Th17 differentiation
B) It is a monoclonal antibody that binds TNF-α, preventing its interaction with TNFR1 and TNFR2, reducing pro-inflammatory cascade
C) It inhibits 5-HT4 receptors to reduce intestinal motility
D) It replaces missing 5-ASA at mucosal sites
E) It repairs the intestinal barrier by blocking zonula occludens proteins

Correct Answer: B

Infliximab is a chimeric monoclonal antibody against TNF-α. It binds TNF and prevents its interaction with tumor necrosis factor receptors, reducing the pro-inflammatory Th1/Th17 response in both GI and systemic sites. A describes anti-IL-23 agents like risankizumab (newer, also effective). C is antiemetic/prokinetic. D and E are not mechanisms of biologics.

GI Pharmacology — Active Recall