---

BIRAT MEDICAL COLLEGE — Mid-Semester Examination

---

Q1. Distinguish between Ulcerative Colitis and Crohn's Disease. [4 marks]

• Crohn's: right lower quadrant pain, diarrhoea without blood (early), perianal disease, weight loss
• UC: bloody diarrhoea, tenesmus, urgency, mucus in stool

---

Q2. What is the most common cause of Upper GI Bleed? Write the prescription for triple therapy in H. pylori. [1+3=4 marks]

Most Common Cause of UGIB:

• Erosive gastritis/haemorrhagic gastritis
• Oesophago-gastric varices (in portal hypertension)
• Mallory-Weiss tear
• Oesophagitis
• Gastric malignancy

Prescription for H. pylori Triple Therapy (PAC Regimen):

---

• Duration: 14 days preferred over 7–10 days (improves eradication by ~5%)
• Target eradication rate: ≥85–90%
• In penicillin allergy: substitute Amoxicillin with Metronidazole 400 mg BD (PCM regimen)
• Confirm eradication 4 weeks post-therapy with urea breath test or stool antigen test
• Clarithromycin-based triple therapy should be avoided where local resistance >15%

---

Q3. What is the most common cause of Upper GI Bleed? Mention different mechanisms of ascites formation. [4 marks]

---

Q3. H. pylori Related Gastritis [4 marks]

Definition:

Pathogenesis:

1. Flagella — allow motility through viscous mucus
2. Urease — converts urea → ammonia, raising local pH and neutralising gastric acid
3. Adhesins — promote adherence to surface foveolar cells
4. Toxins (CagA, CagE) — stimulate IL-8 release → neutrophil recruitment → mucosal damage and sustained inflammatory response

Pathology (Morphology):

• Initially affects the antrum → stimulates G cells → ↑ gastrin → hyperacidity → peptic ulcer disease
• Later spreads to the body → parietal cell loss → gastric atrophy → intestinal metaplasia → risk of gastric adenocarcinoma
• Histology shows: neutrophilic infiltration, pit abscesses, plasma cells and lymphocytes in lamina propria, submucosal lymphoid aggregates (MALT — may transform to MALT lymphoma)
• Chronic infection → intestinal metaplasia (goblet cells + columnar absorptive cells) — precursor to gastric adenocarcinoma

Clinical Features:

• Often subclinical; presents as dyspepsia, epigastric pain, nausea
• Associated with: chronic gastritis, peptic ulcer disease, gastric adenocarcinoma, MALT lymphoma

Diagnosis:

• Non-invasive: Urea breath test (gold standard non-invasive), stool antigen test, serology (not useful post-treatment)
• Invasive (endoscopy + biopsy): Rapid urease test (CLO test), histology (H&E/Giemsa stain), culture

Treatment:

---

Q4. How do you manage Acute Pancreatitis? Mention different mechanisms of ascites formation. [4 marks]

A. Management of Acute Pancreatitis:

1. Initial Assessment & Severity Scoring

• BISAP score (≥3 = severe): BUN >25 mg/dL, Impaired mental status, SIRS ≥2 criteria, Age >60 yrs, Pleural effusion
• SIRS criteria: Temperature <36° or >38°C, HR >90/min, RR >20/min, WBC >12,000 or <4,000/μL
• APACHE II score ≥8 at 24h indicates severity
• Triage: mild → ward; SIRS persistent at 24h → step-down unit; organ failure → ICU

2. Fluid Resuscitation (most critical intervention)

• Lactated Ringer's solution is preferred (reduces systemic inflammation vs. normal saline)
• Bolus: 10–15 mL/kg IV, followed by 1.5–2 mL/kg/hour
• Target: urine output >0.5 mL/kg/hour; monitor hematocrit and BUN every 8–12h
• Monitor vitals and O₂ saturation every 6–8h; adjust fluids accordingly

3. Analgesia

• IV narcotic analgesics (e.g., morphine, pethidine) for pain control

4. Keep NPO (Nil Per Oral)

• Minimises pancreatic stimulation
• Enteral nutrition (NG/NJ feeding) is preferred over TPN in severe pancreatitis once feasible

5. Supplemental Oxygen

6. Etiology-Specific Management

• Gallstone pancreatitis: ERCP within 24–48h if ascending cholangitis; cholecystectomy in same admission for mild cases
• Hypertriglyceridaemia (TG >1000 mg/dL): IV insulin + fasting 24–36h
• Alcohol-induced: Cessation counselling

7. Complications management

• Necrotising pancreatitis: antibiotics (imipenem/meropenem) only if infected necrosis confirmed; consider necrosectomy
• Pancreatic pseudocyst: drainage if symptomatic

---

B. Mechanisms of Ascites Formation:

---

Q5. How do you approach a case of Dysphagia? [4 marks]

Definition:

---

Step 1: Classify the Type of Dysphagia

---

Step 2: Further Characterise

• Solids only → mechanical obstruction (e.g., carcinoma, stricture, Schatzki ring)
• Liquids and solids → motility disorder (e.g., achalasia, diffuse oesophageal spasm)
• Progressive → malignancy (carcinoma of oesophagus) or worsening stricture
• Intermittent → oesophageal ring, diffuse spasm, eosinophilic oesophagitis (EoE)
• With weight loss, >50 yrs, progressive → red flag for malignancy
• Associated regurgitation → achalasia or Zenker's diverticulum
• Heartburn history → GERD → peptic stricture

---

Step 3: Causes of Esophageal Dysphagia

• Eosinophilic oesophagitis (most common cause in young adults today)
• Peptic stricture (GERD-related)
• Oesophageal carcinoma (adeno- or squamous cell)
• Schatzki ring
• External compression (mediastinal mass, thoracic aortic aneurysm, aberrant subclavian artery — dysphagia lusoria)

• Achalasia (failure of LES relaxation)
• Diffuse oesophageal spasm
• Jackhammer oesophagus
• Scleroderma
• Chagas disease

---

Step 4: Investigations

1. Upper GI endoscopy (OGD) — first-line; visualises mucosa, biopsies, dilatation
2. Barium swallow — shows narrowing, strictures, motility; "bird-beak" in achalasia
3. Oesophageal manometry — gold standard for motility disorders
4. CT chest/abdomen — extrinsic compression, staging of malignancy
5. Video fluoroscopy / modified barium swallow — for oropharyngeal dysphagia
6. ENT referral — if high/cervical dysphagia

---

Step 5: Management Principles

• Structural (peptic stricture): PPI + endoscopic dilation
• Malignancy: Staging → oncology referral; stenting for palliation
• Achalasia: Pneumatic dilation, Heller myotomy, or per-oral endoscopic myotomy (POEM)
• Eosinophilic oesophagitis: Swallowed fluticasone, elimination diet, dilation
• Oropharyngeal: Neurological management + speech therapy, feeding tube if needed

---

Sources: Goldman-Cecil Medicine (International Ed.) | Harrison's Principles of Internal Medicine 22E | Robbins & Kumar Basic Pathology | Yamada's Textbook of Gastroenterology (7th Ed.) | Schwartz's Principles of Surgery (11th Ed.)