UPPER GI

What is Peptic Ulcer Disease (PUD)?

Ulcers in the GI tract’s muscular mucosa, usually in the duodenum or stomach.

What are the 3 main causes of PUD?

H. pylori infection, NSAID use, and stress-related mucosal damage.

What are the components of mucosal protection?

Mucus, bicarbonate, microcirculation, and prostaglandins.

How do prostaglandins protect the GI mucosa?

They increase mucus, bicarbonate, and blood flow.

What is Helicobacter pylori?

An acid-labile, gram-negative rod that resides between the mucus layer and epithelial cells.

How is H. pylori transmitted?

Fecal–oral and oral–oral routes.

What is the first-line H. pylori eradication therapy?

Optimized Bismuth Quadruple Therapy: Bismuth + Metronidazole + Tetracycline + PPI.

What are alternative H. pylori regimens?

• Talicia®: Rifabutin + Amoxicillin + Omeprazole
• Voquenza DualPak®: Vonoprazan + Amoxicillin

How do NSAIDs cause ulcers?

They inhibit prostaglandin synthesis, reducing mucus and blood flow.

What population is most at risk for NSAID-induced ulcers?

Older adults or chronic NSAID users.

What is GERD?

Reflux of gastric contents into the esophagus causing symptoms or tissue injury.

What causes GERD?

Abnormal LES function or anatomy, allowing acid backflow.

What are typical GERD symptoms?

• Heartburn
• Acid regurgitation
• Belching
• Abdominal bloating
• Early satiety
• Nausea

What lifestyle modifications help GERD?

• Lose weight
• Eat small, low-fat meals
• Avoid acidic foods/caffeine
• Don’t lie down for 2–3 hours post-meal
• Quit smoking
• Elevate head of bed
• Avoid tight clothing

What is the mechanism of action of antacids?

They neutralize gastric acid directly (local action).

What is their onset and duration?

Rapid onset, short duration (20–40 min fasting, up to 3 hrs post-meal).

What are the ADRs of aluminum antacids?

Constipation, phosphate depletion, osteoporosis.

What are the ADRs of magnesium antacids?

Diarrhea, hypermagnesemia (in renal failure).

What are the ADRs of calcium carbonate?

Constipation, acid rebound, kidney stones, milk-alkali syndrome.

What are the ADRs of sodium bicarbonate?

Alkalosis, sodium overload, acid rebound.

What are common combination antacids?

• Rolaids®: Calcium carbonate + Magnesium hydroxide
• Mylanta®, Maalox®: Magnesium hydroxide + Aluminum hydroxide

How do antacids interact with other drugs?

Bind (chelate) tetracyclines, bisphosphonates; increase pH $\rightarrow$ $\downarrow$ absorption of ketoconazole, iron.

Patient counseling tips for antacid use?

• Take 1–3 hours after meals & at bedtime
• Separate from meds by 2 hours
• Shake liquids, refrigerate for taste
• Chew tablets fully
• Avoid milk/vitamins with calcium antacids

What is alginic acid (Gaviscon®)?

Forms a foam barrier that floats on stomach contents to reduce reflux; works only upright.

What is simethicone (Mylicon®, Gas-X®)?

A defoaming agent that relieves intestinal gas and bloating; no systemic effects.

What are the H2RAs?

Cimetidine, Famotidine, Nizatidine.

What is the mechanism of H2RAs?

Block H2 receptors on gastric parietal cells $\rightarrow$ $\downarrow$ histamine-mediated acid secretion.

What are the ADRs of H2RAs?

Generally mild; cimetidine causes gynecomastia, menstrual changes (antiandrogenic).

Name the PPIs.

Omeprazole, Lansoprazole, Dexlansoprazole, Esomeprazole, Rabeprazole, Pantoprazole, Vonoprazan.

What is the mechanism of PPIs?

Irreversible inhibition of the H$^{+}$/K$^{+}$ ATPase enzyme on parietal cells $\rightarrow$ $\downarrow$ 80–95% acid.

When should PPIs be taken?

20–30 minutes before the first major meal of the day.

What are the risks of long-term PPI use?

Pneumonia, osteoporosis/fractures.

What’s special about vonoprazan (Voquenza®)?

New acid-stable PPI, works day or night, with or without food.

What is sucralfate (Carafate®)?

Forms a protective barrier at ulcer sites (needs pH $<$ 4).

What are sucralfate’s uses and ADRs?

Used for mucositis, radiation proctitis, burn wounds; causes constipation.

What caution applies with sucralfate?

Use carefully in renal failure (contains aluminum).

What are common causes of nausea/vomiting?

GI, cardiac, metabolic, neurological diseases; pregnancy; drugs; infection.

Why is persistent vomiting dangerous?

Can cause dehydration, alkalosis, electrolyte loss, esophageal damage.

Name the 6 main antiemetic classes.

Anticholinergics, 5-HT3 antagonists, Dopamine antagonists, Cannabinoids, Corticosteroids, Neurokinin antagonists.

Anticholinergic examples & uses?

Scopolamine, Meclizine, Dimenhydrinate $\rightarrow$ for motion sickness/simple nausea.

5-HT3 antagonist examples & uses?

Ondansetron, Granisetron, Dolasetron, Palonosetron $\rightarrow$ chemo or acute nausea.

Dopamine antagonist examples & uses?

Promethazine, Metoclopramide $\rightarrow$ general nausea.

Cannabinoid examples & uses?

Dronabinol, Nabilone $\rightarrow$ mild/moderate nausea, low appetite.

Corticosteroid examples & uses?

Dexamethasone, Methylprednisolone $\rightarrow$ chemo/post-surgical nausea.

Neurokinin antagonist example & use?

Aprepitant (Emend®) $\rightarrow$ chemo or post-surgical nausea.