GIT 1

Question 1

What is the formal definition of Peptic Ulcer Disease (PUD)?

Answer 1

A break in the mucosal lining of the stomach and/or duodenum greater than 5mm in diameter

Question 2

What is the core pathophysiological concept of PUD?

Answer 2

An imbalance where Aggressive Factors overwhelm the Protective Factors of the GI mucosa.

Question 3

List the five major Aggressive Factors in PUD.

Answer 3

1. H. pylori infection 2. HCl acid 3. Pepsin 4. NSAIDs 5. Cigarette smoking.

Question 4

List the five major Protective Factors in PUD.

Answer 4

1. Mucus & bicarbonate secretions 2. Endogenous Prostaglandins (PGE2 , PGI2) 3. Mucosal blood flow 4. Cell-cell tight junctions 5. Rapid cell proliferation.

Question 5

What is the prevalence of H. pylori in Duodenal Ulcers (DU) and Gastric Ulcers (GU)?

Answer 5

Found in almost all (90%) Duodenal Ulcers and 70-80% of Gastric Ulcers.

Question 6

What are the two significant long-term risks associated with H. pylori infection?

Answer 6

1. Gastric Adenocarcinoma 2. Gastric MALT Lymphoma.

Question 7

List the key risk factors for developing an NSAID-induced ulcer.

Answer 7

1. Age >75 years (risk doubles) 2. Past history of PUD or GI bleeding 3. Cardiac failure 4. Prolonged NSAID use 5. Concurrent steroid use.

Question 8

Name the three primary neurohumoral stimuli that trigger acid secretion from parietal cells.

Answer 8

1. Gastrin 2. Histamine 3. Acetylcholine.

Question 9

What are the four main goals of drug therapy for Peptic Ulcer Disease (PUD)?

Answer 9

1. Immediate symptom relief 2. Healing the ulcer lesion 3. Eradication of H. pylori 4. Avoidance of precipitants (e.g.NSAIDS)

Question 10

Drug therapy for PUD targets three main areas. What are they?

Answer 10

1. Reduction of gastric acid secretion 2. Neutralization of gastric acid 3. Increasing mucosal protection.

Question 11

Name the four main drug classes used to reduce gastric acid secretion.

Answer 11

1. Proton Pump Inhibitors (PPIs) 2. H2 Receptor Blockers 3. Muscarinic Receptor Blockers (obsolete) 4. Prostaglandin Analogues (indirectly).

Question 12

What is the mnemonic for the common Proton Pump Inhibitors (PPIs)?

Answer 12

RELO: Rabeprazole , Esomeprazole, Lansoprazole, Omeprazole.

Question 13

Why are PPIs considered the first-line and most efficacious drugs for acid suppression?

Answer 13

They inhibit over 95% of daily acid secretion by irreversibly blocking the final step of acid production.

Question 14

Describe the Mechanism of Action (MOA) of Proton Pump Inhibitors (PPIs).

Answer 14

They bind covalently and irreversibly to the H+/K+-ATPase (proton pump) on parietal cells inactivating it and inhibiting acid secretion.

Question 15

What is a critical pharmacokinetic property of PPIs regarding their administration?

Answer 15

They are best absorbed in an acidic environment. Absorption is delayed by food so they must be taken 30-60 minutes BEFORE a meal.

Question 16

Name two major types of Drug-Drug Interactions for PPIs.

Answer 16

1. By raising gastric pH, they reduce absorption of drugs like Ketoconazole. 2. They inhibit CYP450, reducing metabolism of drugs like Warfarin, Phenytoin, and Benzodiazepines.

Question 17

List common and long-term side effects of PPI use.

Answer 17

Common: Flatulence headache, diarrhea, nausea. Long-term: Hypochlorhydria leading to nutrient deficiencies (Iron, Calcium, B12) and increased risk of enteric infections (e.g., C. diff).

Question 18

What are the four main H2 Receptor Antagonists?

Answer 18

Ranitidine , Cimetidine, Nizatidine, Famotidine.

Question 19

What is the Mechanism of Action (MOA) of H2 Receptor Blockers?

Answer 19

They selectively and reversibly block H2 receptors on parietal cells , inhibiting histamine-stimulated acid secretion. They also reduce acid secretion stimulated by gastrin and ACh.

Question 20

Compare the key differences between Cimetidine and Ranitidine.

Answer 20

Cimetidine: Inhibits CYP450 (many interactions) , causes anti-androgenic effects (gynecomastia), crosses BBB. Ranitidine: Minimal interactions, fewer side effects, more potent, does not cross BBB.

Question 21

Which H2 blocker has the highest oral bioavailability and which has the lowest?

Answer 21

Highest: Nizatidine (>90%). Lowest: Famotidine (40%).

Question 22

Why is Cimetidine contraindicated in pregnancy?

Answer 22

Because it crosses the placenta and can enter breast milk.

Question 23

How do Antacid drugs work?

Answer 23

They are basic substances that chemically neutralize gastric HCl acid , forming salt and water, thereby raising the gastric pH.

Question 24

Differentiate between Systemic and Non-Systemic Antacids.

Answer 24

Systemic (e.g. ., Sodium Bicarbonate): Absorbed, can cause systemic alkalosis. Non-Systemic (e.g., Al(OH)3, Mg(OH)2): Not absorbed, act locally in the GI tract.

Question 25

What is the major side effect of Aluminum hydroxide and Magnesium hydroxide?

Answer 25

Aluminum hydroxide: Constipation. Magnesium hydroxide: Diarrhea. (They are often combined to mitigate these effects).

Question 26

What is the role of Alginate in antacid preparations (e.g.Gaviscon

Answer 26

It forms a viscous 'raft' that floats on gastric contents, creating a physical barrier against reflux into the esophagus.

Question 27

How do antacids cause drug interactions?

Answer 27

By raising gastric pH , they reduce the absorption of drugs that require an acidic environment, such as Ciprofloxacin, Tetracycline, Iron, and H2 blockers.

Question 28

What is the primary clinical use of the Prostaglandin analogue Misoprostol?

Answer 28

Cytoprotection against NSAID-induced ulcers , especially in high-risk patients.

Question 29

What is the MOA of Misoprostol?

Answer 29

1. Inhibits adenylyl cyclase -> lowers cAMP -> inhibits proton pump (reducing acid). 2. Increases mucus , bicarbonate secretion, and mucosal blood flow.

Question 30

Why is Misoprostol absolutely contraindicated in pregnancy?

Answer 30

It causes uterine contractions , leading to lower abdominal pain, vaginal spotting, and miscarriage.

Question 31

How does Bismuth Subcitrate work as an ulcer protective drug?

Answer 31

1. Forms a protective coat over the ulcer. 2. Enhances local prostaglandin synthesis. 3. Stimulates bicarbonate & mucus. 4. Has a direct toxic effect on H. pylori.

Question 32

What is a characteristic , harmless side effect of Bismuth Subcitrate?,

Answer 32

,Darkening of the tongue, teeth, and feces.

Question 33

How does Sucralfate work?

Answer 33

It polymerizes in an acidic environment (pH <4) to form a viscous gel that binds to proteins in the ulcer crater , creating a protective barrier against acid and pepsin.

Question 34

What is the major side effect and a key drug interaction of Sucralfate?

Answer 34

Side Effect: Constipation. Interaction: It binds to and delays absorption of drugs like Ciprofloxacin Digoxin, and Phenytoin.

Question 35

Why is H. pylori eradication a cornerstone of PUD treatment?

Answer 35

It prevents ulcer relapse promotes healing, and reduces the risk of gastric cancer.

Question 36

Name the key antibiotics and adjuncts used in H. pylori eradication therapy.

Answer 36

Antibiotics: Metronidazole , Clarithromycin, Amoxicillin, Tinidazole. Adjuncts: PPIs, Bismuth Subcitrate.

Question 37

Describe a standard Triple Therapy regimen for H. pylori.

Answer 37

PPI (e.g., Lansoprazole 30mg BD) + Clarithromycin 500mg BD + Amoxicillin 500mg TDS (or Metronidazole if penicillin allergic). Duration: 7-14 days. Efficacy: ~90%.

Question 38

How do NSAIDs cause ulceration?

Answer 38

By inhibiting the Cyclooxygenase (COX) enzyme , which catalyzes the formation of cytoprotective prostaglandins (PGE2, PGI2) in the stomach.

Question 39

Which NSAID is considered the mildest in terms of ulcer risk and which drug class carries a lower risk?

Answer 39

Mildest: Ibuprofen. Lower Risk: Selective COX-2 inhibitors (e.g., Celecoxib), though cardiac toxicity must be monitored.

Question 40

What is the first step in treating an NSAID-induced ulcer?

Answer 40

Immediate withdrawal of the offending NSAID.

Question 41

What is the first-line drug treatment for an active NSAID-induced ulcer?

Answer 41

Proton Pump Inhibitors (PPIs).

Question 42

List the major clinical uses of PPIs.

Answer 42

Gastric & Duodenal ulcers , GERD, Ulcers refractory to H2 blockers, Zollinger-Ellison Syndrome.

Question 43

List the major clinical uses of H2 Receptor Antagonists.

Answer 43

Gastric & Duodenal ulcers GERD, Prophylaxis of stress ulcers (e.g., Ranitidine in major trauma/burns), Zollinger-Ellison Syndrome, Add-on therapy for chronic urticaria.

Question 44

What is the pathophysiological defect in GERD?

Answer 44

Reflux of acidic gastric contents into the esophagus due to a compromised Lower Esophageal Sphincter (LES) often from hiatus hernia or excessive relaxation.

Question 45

What are the four pillars of GERD management?

Answer 45

1. Lifestyle modifications 2. Antacids/Alginates 3. PPIs (first-line for esophagitis) 4. Prokinetic drugs (e.g. Domperidone).

Question 46

How do prokinetic drugs like Domperidone help in GERD?

Answer 46

They enhance gastric emptying and increase the basal tone of the LES , reducing reflux.

Question 47

Name four types of drugs that can worsen GERD.

Answer 47

Nitrates , Calcium Channel Blockers (CCBs), Theophylline, and drugs with antimuscarinic activity (e.g., TCAs) - they relax the LES.

Question 48

How long is a typical course of PPI therapy for healing endoscopically proven esophagitis?

Answer 48

4 to 8 weeks.

Question 49

Why might bile reflux not respond to PPI therapy?

Answer 49

Because bile is alkaline , and PPIs only suppress acid. Prokinetic therapy may be more effective.

Question 50

What is Zollinger-Ellison Syndrome?

Answer 50

A rare condition caused by a gastrin-secreting tumor (gastrinoma) , leading to extreme gastric acid hypersecretion and multiple, refractory ulcers.

Question 51

What is the mainstay of pharmacological treatment for Zollinger-Ellison Syndrome?

Answer 51

High-dose Proton Pump Inhibitors (PPIs) , e.g., Omeprazole 120mg or more per day.

Question 52

Clinical Scenario: A 75-year-old woman on chronic Naproxen for arthritis presents with melena (black stool). What is the most likely cause and the first-line treatment?

Answer 52

Cause: NSAID-induced ulcer with GI bleeding. Treatment: 1. Immediately stop Naproxen. 2. Start a high-dose PPI (e.g., Omeprazole).

Question 53

Clinical Scenario: A patient on Warfarin for a mechanical heart valve is prescribed Cimetidine for dyspepsia. What is the major concern?

Answer 53

Cimetidine is a potent CYP450 inhibitor. It will reduce the metabolism of Warfarin, leading to dangerously high Warfarin levels and a significantly increased risk of bleeding. The INR must be monitored closely, and a safer alternative like Ranitidine or a PPI should be used.

Question 54

Clinical Scenario: A 45-year-old man is diagnosed with an H. pylori-positive duodenal ulcer. What is the standard first-line treatment?

Answer 54

A triple therapy regimen for 14 days, e.g., PPI (Lansoprazole 30mg BD) + Clarithromycin 500mg BD + Amoxicillin 500mg TDS.

Question 55

Clinical Scenario: A patient requires long-term low-dose Aspirin for cardiovascular protection but has a history of a gastric ulcer. How can you protect them?

Answer 55

Co-prescribe a Proton Pump Inhibitor (PPI) for gastroprotection. Misoprostol is an alternative but is less tolerated due to side effects.