Chapter 13: GI Stomach Flashcards

1
Q

Zymogen, or chief, cells secrete:

Parietal, or oxyntic cells secrete:

Endocrine cells secrete:

A

Zymogen/Chief cells: Pepsinogen

Parietal/Oxyntic: HCl and intrinsic factor

Endocrine: Biogenic amines (serotinin, polypeptide hormones - gastrin, somatostatin). VIP.

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2
Q

A white two-week old infant presents with projectile vomiting. Labs show hypochloremic alkalosis.

A

Congenital pyloric stenosis.

Genetic basis - Turner syndrome, trisomy 18, esophageal atresia. Rubella, thalidomide.

Deficiency of nitric oxide synthase.

Pathology shows concentric pyloric enlargement and narrowing of the pyloric canal. Extreme hypertrophy of the circular muscle coat.

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3
Q

It is discovered that some of an infant’s abdominal organs have migrated into the thoracic cavity.

A

Congenital diaphragmatic hernia.

Often occurs with congenital malrotations of the intestine.

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4
Q

What are some congenital abnormalities of the stomach?

A

Duplications, diverticula, cysts: Usually asymptomatic, muscle coats deficient in diverticula and cysts.

Sinus inversus

Ectopic pancreatic tissue: Usually asymptomatic, can cause pain/pyloric obstruction

Partial gastric atresias: Lack of development of body, antrum, and pylorus or stomach ends blindly.

Congenital pyloric and antral membranes: Failure of stomach to canalize. Commonly symptomatic in adults.

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5
Q

A patient presents with epigastric pain. He injured his arm a week ago while doing yardwork and has been self-medicating with several doses of aspirin daily.

Endoscopy of the stomach looks like this.

A

Acute hemorrhagic erosive gastritis (charcterized by mucosal necrosis).

Can extend to deeper tissues to form an ulcer. Associated with corticosteroids, NSAIDs, alcohol, ischemic injury.

Curling ulcer: Stress ulcer/erosion in a severely burned person

CNS trauma -> Cushing ulcer

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6
Q

A patient with recurrent gastric ulcers receives a biopsy. The left microscopic image shows lymphocytic and plasma cell infiltrate.

The picture on the right is a silver stain.

A

Helicobacter pylori-associated gastritis. H. pylori causes atrophic gastritis, peptic ulcer disease, MALT lymphoma, and gastric carcinoma.

Pathogenicity related to cag pathogenicity island

vac A gene associated with duodenal ulcer disease.

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7
Q

A patient presents with chronic inflammation in the lamina propria of the antrum and corpus of the stomach. Biopsy shows reduction in the number of glands and transformation of the epithelium into intestinal-type cells.

A

Multifocal Atrophic Gastritis. Believed to be caused by H. pylori and diet.

Greater risk of carcinoma of the stomach. Typically asymptomatic unless present with pernicious anemia (B12 deficiency, loss of intrinsic factor).

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8
Q

A 55 year-old patient with chronic gastritis presents with weight loss, dyspepsia, and abdominal pain. A biopsy is shown below.

A

MALToma - low grade B-cell tumor.

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9
Q

A patient presents with fatigue and lethargy. A CBC is obtained and reveals macrocytic anemia. Antibodies against parietal cells are discovered.

Endoscopy reveals chronic, diffuse inflammation of the body and fundus of the stomach.

A

Pernicious anemia AND autoimmune atrophic gastritis. PA = malabsorption of B12 due to a lack of intrinsic factor. Related to autoimmune atrophic gastritis. RISK FOR DYSPLASIA AND ADENOCARCINOMA, LIKE MULTIFOCAL ATROPHIC GASTRITIS.

Antibodies to parietal cells + intrinsic factor

Reduction in or absence of gastric secretion, including acid (achlorhydria)

Increased serum gastrin (G-cell hyperplasia of antral mucosa)

Enterochromaffin-like cell hyperplasia in atrophic oxyntic mucosa - gastrin stimulation causes.

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10
Q

Biopsy of a stomach shows villiform projections with fibromuscular proliferation in the lamina propria.

Surface foveolar cells show prominent reactive nuclear atypia out of proportion to the sparce inflammatory infiltrate.

There is a history of NSAID use and gastroduodenostomy/gastrojejunostomy.

A

Reactive (chemical) Gastropathy.

Due to injection of NSAIDs or bile reflux.

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11
Q

Granulomas are found in the stomach.

A

Granulomatous gastritis.

Infection (myobacterium tuberculosis, fungus)

Systemic illness (sarcoid, Crohn)

Idiopathic

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12
Q

A patient with history of food allergies presents with obstructive GI symptoms. Biopsy shows eosinophilic involvement in all layerts of the stomach wall.

A

Eosinophilic gastritis.

Give corticosteroids.

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13
Q

A patient with celiac disease presents with prominent intraepithelial lymphocytes in the stomach.

A

Lymphocytic gastritis.

Associated with celiac disease, unknown etiology, or H. pylori infection.

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14
Q

A patient with chronic gastritis undergoes endoscopy. The findings are described as “watermelon stomach”.

A

Gastric antral vascular ectasia (vascular gastropathy), GAVE.

Another vascular cause of chronic gastritis is portal hypertensive gastropathy.

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15
Q

A child presents with post-prandial pain that is relieved by antacids. 2+ pitting edmea is found bilaterally on physical exam.

The folds of the greater curvature of the fundus and body of the stomach are taller and thicker.

A

Menetrier Disease - enlarged gastric rugae. In children associated with CMV, in adults associated with overexpression of TGF-alpha. **CONSIDERED PRECANCEROUS CONDITION, REGULAR ENDOSCOPY RECOMMENDED.

Loss of protein from altered gastric mucosa.

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16
Q

What is the association of H. Pylori and duodenal/gastric ulcers?

A

Associated with nearly all duodenal ulcers

Associated with 75% of gastric ulcers, other 25% associated with other cases of chronic gastritis.

17
Q

Risk factors for peptic ulcers include…

A

Aspirin, NSAIDs, cigarettes, genetics (type O blood), high pepsinogen I.

High parietal cell mass. Chief cell mass can also be increased, causing increased pepsinogen. G-cell hyperfunction. Accelerated gastric emptying. Acidic pH in the duodenal bulb.

18
Q

Most patients with gastric ulcers demonstrate what secretory pattern with respect to HCl?

A

They tend to secrete less acid than those with duodenal ulcers and even less than normal people.

  1. Back diffusion of acid into the mucosa
  2. Decreased parietal cell mass
  3. Abnormalities of parietal cells.
19
Q

Patient presents with abdominal pain that worsens after eating. A biopsy of the stomach is taken and reveals the following.

A

Gastric ulcer.

Characteristic sharp demarcation from surrounding mucosa with radiating gastric folds. Base of the ulcer is gray owing to fibrin deposition.

20
Q

What are some diseases associated with peptic ulcers?

A

Cirrhosis: Duodenal ulcers 10x more frequent

Chronic renal failure: Peptic ulceration, bleeding, perforation

Hereditary endocrine syndromes: MEN1, Zollinger-Ellison syndrome (gastric hypersecretion cause dby a gastrin-producing islet cell adenoma of the pancreas)

Alpha1-antitrypsin deficiency: 1/3 patients have peptic ulcers.

Chronic lung disease: 1/4th with peptic ulcers.

21
Q

A patient presents with epigastric pain that follows meals and awakens him at night. Antacids and food relieve thses symptoms.

A biopsy shows the following.

A

Duodenal ulcers - sharply demarcated ulcers surrounded by inflamed duodenal mucosa.

22
Q

Patient presents with epigastric pain. Endoscopy reveals unusual lesions in the stomach, so a biopsy is taken.

A superficial zone of fibropurulent exudate is found covering necrotic tissue, granulation tissue, and fibrotic tissue with variable degrees of chronic ifnalmmation.

Muscle layers are interrupted and replaced with scar tissue after healing.

A

Gastric ulcer.

Full thickness replacement of gastric muscularis with connective tissue.

Photomicrograph of peptic ulcer with superficial exudate over necrosis, granulation tissue, and fibrosis.

23
Q

Complications of peptic ulcers include:

A

Hemorrhage - often occult, no symptoms. Iron deficiency anemia. Massive life-threatening bleeding possible.

Perforation: Rare. Can lead to accumulation of air in abdominal cavity - pneumoperitoneum. If penetrate pancreas, liver, or greater omentum bad. Biliary tract fill with air. High mortality**. Shock, abdominal distention, pain.

Pyloric obstruction: Muscular spasm, edema, hypertrophy, contraction of scar tissue.

Malignant transformation of benign gastric ulcers.