# Clinical Cases: Gastric Disorders

## Case 1: Peptic Ulcer Disease with Upper GI Bleeding

### Patient Presentation
**Demographics:** 58-year-old male

**Chief Complaint:** Black tarry stools and lightheadedness for 2 days

**History of Present Illness:** The patient noticed black, tarry, foul-smelling stools (melena) starting 2 days ago. He has had mild epigastric discomfort for several weeks that he attributed to "indigestion." Today he felt lightheaded upon standing and nearly fainted. He denies hematemesis. He has been taking ibuprofen 600 mg three times daily for knee pain for the past 3 weeks.

**Past Medical History:** Osteoarthritis, hypertension

**Medications:** Ibuprofen, lisinopril, aspirin 81 mg daily

**Social History:** Occasional alcohol use, non-smoker

### Physical Examination
- **Vital Signs:** BP 98/62 mmHg (supine), 78/50 mmHg (standing); HR 108 bpm (supine), 128 bpm (standing)
- **General:** Pale, diaphoretic male
- **Abdomen:** Mild epigastric tenderness, no peritoneal signs
- **Rectal:** Black, tarry stool, guaiac positive

### Workup and Results
- **CBC:** Hemoglobin 7.2 g/dL (baseline 14), MCV 82 fL, platelets 285,000
- **BMP:** BUN 42 mg/dL, Cr 1.1 mg/dL (elevated BUN:Cr ratio suggests upper GI bleeding)
- **Upper Endoscopy:** 1.5 cm posterior duodenal bulb ulcer with visible vessel (Forrest IIa), no active bleeding
- **H. pylori:** Positive on biopsy urease test

![Duodenal Ulcer with Visible Vessel](case_01_image.jpg)
*Endoscopic image of a posterior duodenal ulcer with a non-bleeding visible vessel (Forrest IIa), a high-risk stigmata indicating significant rebleeding risk without endoscopic therapy.*

**Image Source:** Wikimedia Commons, CC BY-SA 3.0

### Diagnosis
**NSAID-induced and H. pylori-associated Posterior Duodenal Ulcer with Upper GI Bleeding**

### Clinical Correlation
Peptic ulcer disease results from an imbalance between aggressive factors (acid, pepsin, NSAIDs, H. pylori) and protective factors (mucus, bicarbonate, prostaglandins, mucosal blood flow). NSAIDs inhibit cyclooxygenase, reducing prostaglandin synthesis and compromising mucosal defenses. H. pylori infection causes chronic inflammation. Posterior duodenal ulcers are particularly dangerous because they can erode into the gastroduodenal artery, causing massive hemorrhage. The Forrest classification guides treatment: a visible vessel (IIa) carries ~40% rebleeding risk without therapy.

### Treatment
- IV PPI bolus (80 mg) followed by continuous infusion (8 mg/hour for 72 hours)
- Endoscopic therapy: combination of epinephrine injection plus clip application to visible vessel
- Blood transfusion targeting hemoglobin 7-8 g/dL (restrictive strategy)
- Discontinue NSAIDs and aspirin (discuss with cardiology regarding aspirin)
- H. pylori eradication: bismuth quadruple therapy for 14 days
- Confirm eradication with urea breath test or stool antigen 4+ weeks after treatment

---

## Case 2: Gastric Adenocarcinoma

### Patient Presentation
**Demographics:** 72-year-old male of Korean descent

**Chief Complaint:** Unintentional weight loss, early satiety, and epigastric discomfort for 4 months

**History of Present Illness:** The patient reports 20-pound unintentional weight loss over 4 months. He feels full after only a few bites and has lost interest in food. He has vague epigastric discomfort but denies severe pain. He recently noticed that his stools appear dark. He has never had an upper endoscopy.

**Past Medical History:** H. pylori infection treated 15 years ago (cure not confirmed), chronic atrophic gastritis

**Social History:** Born in Korea, immigrated 30 years ago; heavy smoker (45 pack-years, quit 5 years ago); no alcohol

**Family History:** Father died of "stomach cancer" at age 65

### Physical Examination
- **Vital Signs:** BP 126/78 mmHg, HR 84 bpm, BMI 19 (previous 24)
- **General:** Thin, cachectic male
- **Abdomen:** Mild epigastric tenderness, no palpable masses, no hepatomegaly
- **Lymph Nodes:** 1.5 cm firm, non-tender left supraclavicular node (Virchow's node)

### Workup and Results
- **CBC:** Hemoglobin 9.8 g/dL (iron deficiency anemia pattern)
- **Upper Endoscopy:** Large ulcerated mass in the gastric antrum; biopsies obtained
- **Histopathology:** Intestinal-type gastric adenocarcinoma; H. pylori organisms identified
- **CT Chest/Abdomen/Pelvis:** 6 cm gastric mass with perigastric lymphadenopathy; no liver metastases
- **EUS:** T3N2 disease with invasion of muscularis propria and multiple perigastric nodes

![Gastric Adenocarcinoma](case_02_image.jpg)
*Endoscopic view of gastric adenocarcinoma appearing as an ulcerated, irregular mass in the gastric antrum with raised, nodular borders characteristic of malignancy.*

**Image Source:** Wikimedia Commons, CC BY 2.0

### Diagnosis
**Intestinal-type Gastric Adenocarcinoma (Stage III)**

### Clinical Correlation
Gastric adenocarcinoma is the third leading cause of cancer death worldwide, with highest incidence in East Asia. H. pylori infection is the dominant risk factor, classified as a WHO Class I carcinogen. The progression from chronic gastritis to atrophic gastritis, intestinal metaplasia, dysplasia, and carcinoma explains the importance of H. pylori eradication. Intestinal-type adenocarcinoma (forming glands) is associated with H. pylori and has a relatively better prognosis than diffuse-type. The Virchow node represents metastatic spread via lymphatics.

### Treatment
- Perioperative chemotherapy (FLOT regimen: 5-FU, leucovorin, oxaliplatin, docetaxel)
- Surgical resection: subtotal gastrectomy with D2 lymphadenectomy
- Adjuvant chemotherapy post-operatively
- H. pylori eradication
- HER2 testing (trastuzumab if HER2-positive)
- Nutritional support and B12 supplementation after gastrectomy

---

## Case 3: Autoimmune Gastritis with Pernicious Anemia

### Patient Presentation
**Demographics:** 55-year-old female

**Chief Complaint:** Progressive fatigue, tingling in feet, and glossitis for 8 months

**History of Present Illness:** The patient describes worsening fatigue that limits her daily activities. She has noticed tingling and numbness starting in her toes and progressing up her feet. Her tongue has been sore and appears smooth. She has had intermittent episodes of loose stools. She denies weight loss, abdominal pain, or blood in stool.

**Past Medical History:** Hashimoto's thyroiditis (on levothyroxine), vitiligo

**Family History:** Mother had "thyroid problems" and anemia requiring injections

### Physical Examination
- **Vital Signs:** BP 118/70 mmHg, HR 92 bpm
- **General:** Pale female with visible vitiligo patches
- **HEENT:** Smooth, beefy-red tongue (atrophic glossitis); pale conjunctivae
- **Cardiac:** Mild tachycardia, systolic flow murmur
- **Neurologic:** Decreased vibration sense in feet, diminished position sense in toes
- **Skin:** Depigmented patches on hands and face (vitiligo)

### Workup and Results
- **CBC:** Hemoglobin 8.4 g/dL, MCV 122 fL (macrocytic), WBC 3.4, Platelets 145
- **Peripheral Smear:** Macro-ovalocytes, hypersegmented neutrophils
- **Vitamin B12:** 88 pg/mL (severely low)
- **Methylmalonic Acid:** Markedly elevated
- **Fasting Gastrin:** 1,250 pg/mL (elevated due to achlorhydria)
- **Anti-Parietal Cell Antibodies:** Positive
- **Anti-Intrinsic Factor Antibodies:** Positive
- **Upper Endoscopy:** Atrophic mucosa limited to gastric body and fundus; antrum normal; small polyps in body

![Autoimmune Gastritis Endoscopy](case_03_image.jpg)
*Endoscopic appearance of autoimmune atrophic gastritis showing pale, thin mucosa in the gastric body with loss of normal rugal folds and visible submucosal vessels, contrasting with normal antral mucosa.*

**Image Source:** Case courtesy of Radiopaedia.org

### Diagnosis
**Autoimmune Gastritis (Type A Gastritis) with Pernicious Anemia**

### Clinical Correlation
Autoimmune gastritis is characterized by autoantibodies targeting parietal cells and intrinsic factor, leading to destruction of acid-secreting cells in the gastric body and fundus. This results in: (1) achlorhydria - loss of acid production; (2) intrinsic factor deficiency - causing B12 malabsorption and pernicious anemia; (3) hypergastrinemia - loss of acid-mediated feedback inhibition of G cells; (4) ECL cell hyperplasia - from chronic gastrin stimulation, with potential for carcinoid tumors. The condition associates with other autoimmune diseases (thyroiditis, vitiligo, type 1 diabetes). Neurologic manifestations (subacute combined degeneration) result from B12 deficiency affecting myelin synthesis.

### Treatment
- Intramuscular vitamin B12 (cyanocobalamin) 1000 mcg daily for 7 days, then weekly for 4 weeks, then monthly lifelong
- Monitor for hypokalemia during early treatment
- Surveillance endoscopy for gastric carcinoid tumors and adenocarcinoma
- Monitor chromogranin A levels
- Screen for concurrent autoimmune conditions
- Family screening for autoimmune gastritis