GI pharm – Antacids (highest yield points)

a) Cimetidine, Ranitidine, Famotidine

– Don’t confuse with second-generation H1 blockers (e.g., loratadine), which are used for allergies. H2 blockers are “idine”; the second-gen H1 blockers are “adine.”

USMLE wants you to know H2 blockers are competitive and reversible, whereas proton pump inhibitors are non-competitive and irreversible.

If the USMLE asks which drug is more efficacious, choose the proton pump inhibitor.

First-line treatment of H. pylori is CAP –> Clarithromycin, Amoxicillin, Proton pump inhibitor (e.g., omeprazole).

After CAP is used for 7-10 days, a urea breath test is performed 4 weeks later to see if the H. pylori has been eradicated. If not, then assume resistance to the antibiotics. Next best step in management = substitute out the clarithromycin and amoxicillin for metronidazole, tetracycline, and bismuth.

In other words, use CAP; if doesn’t work, use metronidazole, tetracycline, bismuth, and a PPI as the second-line quad combo.

H2 blockers can rarely be used in place of the PPI for H. pylori treatment, but that is rare and will not be tested.

a) Low pH of the stomach is needed for sucralfate to work (coats ulcers). PPIs can decrease the effectiveness of sucralfate.

b) Coats ulcers / binds to base of ulcers, thereby decreasing pain.

PPIs will increase serum gastrin levels.

Normally, low pH of stomach acid negatively feeds back on gastrin secretion.

Gastrin functions to stimulate acid production from parietal cells directly.

It also binds to G receptors on enterochromaffin-like cells, inducing them to secrete histamine, which in turn binds to H2 receptors on parietal cells.

PPIs can be used to treat Zollinger-Ellison syndrome (gastrinoma of the pancreas) as an alternative to surgery.

a) Trial of PPIs or H2 blockers.

b) Metoclopramide, followed by erythromycin; wrong answer = omeprazole (PPI).

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GERD vs diabetic gastroparesis

• Diagnosis of GERD is done with 2-week trial of PPIs or H2-blockers. PPIs are classically chosen for the 2-week trial, but one of the 2CK NBME Qs has trial of H2 blockers as an answer (and PPIs not listed). Both are correct answers. If you’re forced to choose between the two, however, choose the PPI, as mentioned above.
  • 55M + burning sensation in throat after meals past three months + otherwise healthy and no cardiovascular issues; next best step in pharmacologic therapy? –> answer = trial of PPIs or H2 blockers.
• Don’t confuse with diabetic gastroparesis, which can present like GERD, but in someone who has bad diabetes. USMLE will slam you on this.
  • 55M + burning sensation in throat after meals past three months + T2DM + HbA1c of 9.6 + lack of pinpoint discrimination up to the ankles; next best step in pharmacologic therapy? –> answer = metoclopramide; wrong answer = omeprazole.
  • If the patient has poor glycemic control and neuropathy, the latter extends to the nerves innervating the GI tract as well –> can present as diarrhea/constipation or GERD-like symptoms.
  • First step is endoscopy to rule out physical obstruction. If negative, then do gastric-emptying scintigraphy (scintigraphic gastric-emptying assay) to confirm delayed gastric emptying. First step in treatment is smaller meals. If insufficient, start using metoclopramide (D2 antagonist), which is a pro-kinetic agent (stimulates peristalsis) and anti-emetic; after metoclopramide, can also use erythromycin (macrolide antibiotic that is also a motilin-receptor agonist).
  • Bottom line is:
    • GERD-like Sx in someone without diabetes, answer = GERD; do trial of PPIs or H2 blocker.
    • GERD-like Sx in someone with bad diabetes; answer = diabetic gastroparesis; do metoclopramide, followed by erythromycin.

a) Coats ulcers to decrease pain.

b) Ulcers; also used for H. pylori second-line quad therapy for this reason (soothes ulcers).

c) Sucralfate

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Bismuth, Sucralfate

• Both coat ulcers / bind to base of ulcers, thereby decreasing pain.
• Bismuth used in second-line quad therapy for H. pylori (metronidazole, tetracycline, bismuth, and a PPI); first-line is CAP (Clarithromycin, Amoxicillin, PPI).
• Sucralfate requires low pH of stomach acid for activation; PPIs ↓ effectiveness of sucralfate.

Aluminum

• Antacid
• Causes constipation –> “Aluminimum amount of feces.”

a) Antacid

b) Causes diarrhea.

• Milk of magnesia can actually be used to treat constipation (i.e., the side-effect of diarrhea is advantageous).

a) Antacid

b)

1) Can cause milk-alkali syndrome –> patient takes too many Tums –> causes hypercalcemia + metabolic alkalosis –> increased risk of calcium phosphate kidney stones.

2) Can cause rebound acid hyper-secretion.

a) Prostaglandin E1 analogue

b) ↑ production of gastric mucous and bicarbonate; ↓ acid production.

c) Used for NSAID-induced peptic ulcers (NSAIDs normally inhibit COX, the enzyme that synthesizes prostaglandins).

Calcium carbonate

• Antacid
• Can cause milk-alkali syndrome –> patient takes too many Tums –> causes hypercalcemia + metabolic alkalosis –> increased risk of calcium phosphate kidney stones.
• Can cause rebound acid hyper-secretion.

Misoprostol

• Prostaglandin E1 analogue
• ↑ production of gastric mucous and bicarbonate; ↓ acid production.
• Used for NSAID-induced gastric ulcers (NSAIDs normally inhibit COX, the enzyme that synthesizes prostaglandins).

a)

Aluminum

• Antacid
• Causes constipation –> “Aluminimum amount of feces.”

b)

Magnesium (Milk of magnesia)

• Antacid
• Causes diarrhea.
• Milk of magnesia can actually be used to treat constipation (i.e., the side-effect of diarrhea is advantageous).

c)

Calcium carbonate

• Antacid
• Can cause milk-alkali syndrome –> patient takes too many Tums –> causes hypercalcemia + metabolic alkalosis –> increased risk of calcium phosphate kidney stones.
• Can cause rebound acid hyper-secretion.