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4 Inflammatory Diseases of the Stomach

- acute gastritis, acute peptic ulceration, chronic gastritis, and peptic ulcer disease (PUD)


What does acute gastritis result from? What are four main causes?

- the disruption of the stomach's normal protective mechanisms (mucus and bicarbonate); AKA erosive gastritis/gastropathy
- NSAIDs, alcohol, severe stress, portal HTN


Why are elderly patients and patients using NSAIDs at risk of developing acute gastritis?

- elderly patients have decreased mucin production
- NSAIDs inhibit prostaglandins, which are used to enhance bicarbonate secretion
- (both of these result in decreased protection from gastric acid)


Acute peptic ulceration is a complication of what two things?

- NSAID therapy
- severe physiologic stress


What are the 3 lesion types of acute peptic ulceration? What is each associated with?

- stress ulcers: affect critically ill patients
- curling ulcers: occur in proximal duodenum; associated with severe burns
- cushing ulcers: occur in stomach, duodenum, or esophagus of patients with intracranial disease (increased vagus stimulation leads to increased HCl secretion)


Are symptoms of chronic gastritis more or less severe than those of acute gastritis?

- less severe (ie: hematemesis is quite uncommon in chronic gastritis)


What are the two main causes of chronic gastritis?

- infection with Helicobacter pylori (most common, 90%) and autoimmune gastritis (10%)


H. pylori usually results in gastritis in which parts of the stomach? Is acid production increased or decreased? Will the patient be hyper- or hypogastrinemic? What about in autoimmune gastritis?

- H. pylori: gastritis in the antrum; increased acid production despite hypogastrinemia(???) (H. pylori inhibit D cells and stimulate G cells)
- autoimmune: usually spares the antrum; decreased acid production despite hypergastrinemia


What is chronic gastritis via H. pylori associated with?

- intestinal metaplasia of the gastric tissue, resulting in an increased risk of gastric adenocarcinoma
- also PUD


Which 2 findings on a gastric biopsy would indicate intestinal metaplasia?

- the presence of goblet cells and columnar absorptive cells


What's the pathogenesis of autoimmune gastritis? What are the resulting effects?

- antibodies against parietal cells and intrinsic factor
- leads to decreased HCl (achlorhydria) and intrinsic factor secretion
- decreased HCl will result in a pronounced increase in gastrin (hypergastrinemia) to try and stimulate acid release
- lack of intrinsic factor will result in vitamin B12 deficiency, leading to pernicious anemia (AKA "pernicious anemia gastritis")


Peptic Ulcer Disease (PUD) is highly associated with which two things? It usually develops on a background of what? Which two areas are most commonly affected?

- associated with H. pylori infection and NSAIDs (NOT due to alcohol, stress, or diet)
- develops on a background of chronic gastritis
- commonly affects the proximal duodenum (90%) and the stomach (10%)


Zollinger-Ellison Syndrome; what two pathologies is it associated with?

- gastrin-producing tumors of the pancreas or G-cells result in massive acid production
- associated with peptic ulcer disease and carcinoid tumors


What is the most common gastric malignancy?

- gastric adenocarcinoma (more than 90% of gastric cancers)
- it is the 2nd most common cause of cancer death world-wide


Symptoms of Gastric Adenocarcinoma

- progression from dyspepsia (indigestion), dysphagia, and nausea to weight loss, anorexia, anemia, and altered bowel habits
- often presents with acanthosis nigricans (brown-black velvety hyperpigmentation of the skin)


T or F: PUD only slightly increases the risk of developing gastric adenocarcinoma.

- false!
- PUD, itself, actually does NOT increase the risk (infection with H. pylori does, as does a partial gastrectomy to treat the PUD)


What are the two types/patterns of gastric adenocarcinoma? Which is more common?

- diffuse gastric cancer (20-30%) and intestinal-type gastric cancer (70-80%)


Compare diffuse and intestinal-type gastric adenocarcinomas.

- diffuse (less common, 20-30%): not associated with H. pylori, don't develop from precursor lesions, no discrete mass, look for gastric wall thickening (linitis plastica) and signet ring cells, worse prognosis
- intestinal-type (more common, 70-80%): associated with H. pylori and smoked foods and tobacco, do develop from precursor lesions, is usually a discrete bulky mass


Signet-Ring Cells

- cells associated with diffuse gastric adenocarcinoma
- discohesive cells with large mucin vacuoles that expand the cytoplasm, displacing the nucleus to the periphery and making them crescent-shaped


How common are extranodal lymphomas in the GIT?

- quite common!
- while they only make up 5% of gastric malignancies (majority being adenocarcinoma), extranodal lymphomas are most commonly seen in the GIT
- (they are known as MALTomas in the gut)


What do carcinoid tumors arise from? What two pathologies are carcinoid tumors in the gut associated with? What do we use for diagnose? Where do they most commonly arise in the GIT?

- neuroendocrine organs / neuroendocrine-differentiated GI epithelia (G cells!)
- associated with chronic gastritis and Zollinger-Ellison syndrome
- diagnose with plasma chromogranin A (CgA) levels
- small intestine > rectum > colon > stomach > pancreas > appendix


What is carcinoid syndrome?

- a paraneoplastic syndrome of carcinoid tumors; the tumor secretes hormones/vasoactive substances causing flushing, sweating, bronchospasms, colicky abdominal plain, diarrhea, and right-sided valvular fibrosis
- main 3 symptoms: flushing, diarrhea, and bronchospasms


Why is carcinoid syndrome only seen in 10% of cases involving the GIT?

- because when the cancer is in the GIT, the tumor secretions pass through the liver and get deactivated!
- (therefore, when carcinoid syndrome is seen, it is highly associated with metastatic disease)


A congenital anomaly leading to a split in the abdominal wall, exposing the abdominal contents, is known as:

- gastroschisis


What is an Omphalocele? What is it due to? What does it result in?

- it's the persistent herniation of the bowel into the umbilical cord due to the failure of the herniated intestines to return to the body cavity
- (this herniation is normal during development, but then normally returns to the body cavity)
- it results in the exposure of the abdominal contents


Both Gastrochisis and an Omphalocele result in the exposure of the abdominal contents; What is the major difference between the two?

- in gastrochisis, the contents are bare
- in an omphalocele, the contents are in a bubble of peritoneum and amnion


What is the pathophysiology of congenital pyloric stenosis? How soon after birth does the stenosis usually develop? What do patients present with?

- congenital hypertrophy of the pyloric smooth muscle results in the stenosis
- develops about 2 weeks after birth; present with distension and projectile non-bilious vomiting


What can cause a curling ulcer? A stress ulcer? A cushing ulcer? What's the pathophysiology behind each?

- curling ulceration can occur in patients with severe burns: the large loss of fluid due to severe burns results in hypovalemia, leading to less efficient mucosal protection (less blood flow to the stomach)
- stress ulceration can occur in patients in critical condition: same mechanism as above (hypovalemic shock)
- cushing ulceration can occur due to increased intracranial pressure: the increased pressure results in increased vagal stimulation, leading to increased ACh and therefore increased HCl production


What is the most common cause of vitamin B12 deficiency? What does such a deficiency result in?

- autoimmune gastritis is most common cause
- pernicious anemia can result


Proximal duodenal ulcers are nearly ALWAYS due to H. pylori, but what is the 2nd most common cause? Similarly, ulcers in the distal stomach are MOSTLY due to H. pylori - what is the 2nd most common cause? What age group is each more common in?

- duodenal ulcers: Zollinger-Ellison syndrome; younger patients (30-55)
- gastric ulcers: NSAIDs; older patients (55-70)