Stomach

Question 1

Gastroschisis

Answer 1

exposure of the abdominal contents since there is a malformation of the anterior abdominal wall

Question 2

Omphalocele

Answer 2

herniation of the bowel into umbilical cord (failure to return to the body cavity during development)

*bowel will be covered by peritoneum and amnion

Question 3

Pyloric Stenosis

Answer 3

hypertrophy of the pyloric SM presenting 2 weeks after birth (especially in males) which can be treated with myotomy

1. projectile vomiting (no bile)
2. visible peristalsis
3. olive-like mass in the abdomen

Question 4

Acute Gastritis

Answer 4

acidic damage to the mucosa (too much acid, too little protection) causing inflammation, erosion (superficial layer) or ulcer (mucosal layer)

defenses: mucin layer (foveolar cells), bicarbonate secretion (by epithelial cells), normal blood supply (nutrients and takes away acid)

risk factors:

1. burn (Curling ulcer)–> hypovolemia–> decreased blood supply
2. NSAIDs (decreased PGE2)
3. alcohol
4. chemotherapy (knocks out cells that turn over)
5. intracranial pressure (Cushing ulcer)–> vagus nerve stimulation–> acid
6. shock

Question 5

Chronic Gastritis

Answer 5

chronic inflammation

-<b>autoimmune</b>: destruction of parietal cells in the body and fundus by T-cells (T4HSR) causing atrophy of mucosa, intestinal metaplasia, achlorhydria, increased gastrin levels, antral G-cells hyperplasia, megaloblastic/pernicious anemia from lack of intrinsic factor and increased risk of gastric adenocarcinoma

• <b>H pylori</b>: most common; bacteria increases ureases, proteases, inflammation presenting with epigastric abdominal pain causing increased risk for ulceration, gastric adenocarcinoma, MALT lymphoma
• treatment: triple therapy which resolves gastritis/ulcer and reverses intestinal metaplasia
• confirmation of eradication: negative urea breath test and lack of stool antigen

Question 6

Peptic Ulcer Disease

Answer 6

ulcer involving proximal duodenum or distal stomach

• <b>duodenal ulcer</b>: in anterior duodenum from H. pylori or ZE syndrome presenting with epigastric pain (improves with eating), hypertrophy of Brunner glands
• when present in posterior duodenum, rupture may lead to bleeding from gastroduodenal artery or acute pancreatitis
• not malignant (small, sharply demarcated, punched out)
• <b>gastric ulcer</b>: on lesser curvature of the antrum from H. pylori, NSAIDs or bile reflux causing epigastric pain (worse with eating), and bleeding from left gastric artery if rupture occurs
• from gastric carcinoma (large, irregular, heaped up margins)

Question 7

Gastric Carcinoma

Answer 7

malignant proliferation of surface epithelial cells that presents late with weight loss, abdominal pain, anemia and early satiety (can present with acanthosis nigricans or Leser-Trelat sign)
*spreads to lymph nodes (Virchow node) or distant metastases like liver

• <b>intestinal</b>: large, irregular ulcer with heaped up margins involving lesser curvature of the antrum (like gastric ulcer)
• risk factors: intestinal metaplasia (H. pylori or autoimmune gastritis), nitrosamines in smoked foods and blood type A
• periumbilical region (Sister Mary Joseph nodule) metastasis
• <b>diffuse</b>: signet ring cells that diffusely infiltrate the gastric wall; desmoplasia results in thickening of stomach wall (linitis plastica)
• bilateral ovaries (Krukenberg tumor) metastasis