Gastric disease Notes

NOTES NOTES GASTRIC DISEASE GENERALLY, WHAT IS IT? PATHOLOGY & CAUSES ▪ Diseases affecting gastric mucosa, gastric outlet, etc. ▪ Inflammation due to infection; ulceration SIGNS & SYMPTOMS ▪ May be asymptomatic ▪ Epigastric pain, nausea, vomiting ▪ Anemia; fecal, urinary incontinence; ulcers; bleeding DIAGNOSIS DIAGNOSTIC IMAGING ▪ Endoscopy LAB RESULTS ▪ Biopsy 228 OSMOSIS.ORG TREATMENT MEDICATIONS ▪ Proton pump inhibitor (PPI) ▪ Correct fluid, electrolyte deficits ▪ Discontinue nonsteroidal anti-inflammatory drugs (NSAIDs) SURGERY ▪ Endoscopic ligation/coagulation ▪ Surgical repair OTHER INTERVENTIONS ▪ Dietary modification; exercise ▪ Avoid smoking

Chapter 31 Gastric Disease CYCLIC VOMITING SYNDROME osms.it/cyclic-vomiting PATHOLOGY & CAUSES ▪ An uncommon disorder characterized by recurrent episodes of vomiting separated by asymptomatic periods ▪ Median onset age: 5–6 years old CAUSES ▪ Cause unknown; triggers may include psychological stress (e.g. interpersonal conflict, holidays) or physical stress (e.g. infections, exhaustion), certain foods (e.g. cow’s milk, chocolate, cheese, monosodium glutamate) menses RISK FACTORS ▪ Children > adults ▫ In children: mitochondrial DNA deletions and polymorphisms ▪ Females > males ▪ Family history of migraines ▪ Autonomic abnormalities (elevated sympathetic tone) ▪ Hypothalamic-pituitary-adrenal activation (Sato variant) ▪ Chronic cannabis use COMPLICATIONS ▪ ▪ ▪ ▪ ▪ Erosive esophagitis Mallory-Weiss tear Dehydration Electrolyte imbalance Unintended weight loss SIGNS & SYMPTOMS ▪ Symptoms tend to develop at night, in the early morning hours, or upon awakening ▪ Prodromal period is common ▪ Gastrointestinal: vomiting which may include bile or blood; retching, abdominal pain, diarrhea ▪ Autonomic: lethargy, pallor, excessive salivation, low grade fever ▪ Neurologic: headache, photophobia, phonophobia, vertigo ▪ Social withdrawal DIAGNOSIS OTHER DIAGNOSTICS ▪ History and physical examination ▫ No identifiable organic cause ▪ Diagnostic criteria (Rome IV criteria) ▫ ≥ three recurrent, discrete episodes of vomiting in the prior year, with two episodes in the past six months occurring at least one week apart ▫ Variable intervals between vomiting episodes and asymptomatic baseline ▫ Stereotypical characteristics regarding timing of onset, symptoms, and duration TREATMENT OTHER INTERVENTIONS ▪ During cyclic vomiting episodes ▫ IV fluids, antiemetics, sedatives; comfort care in dark, quiet room Prevention ▪ Prophylactic therapy ▫ H1-antagonists (e.g. cyproheptadine) for children ≤ five years old ▫ Tricyclic antidepressants (e.g. amitriptyline) > years of age ▪ Abortive therapy ▫ Triptans; neurokinin-1 receptor antagonists ▪ Avoidance of triggers OSMOSIS.ORG 229

GASTRIC DUMPING SYNDROME osms.it/gastric-dumping DIAGNOSIS PATHOLOGY & CAUSES ▪ Iatrogenic post-gastric surgery syndrome; impaired gastric motility → rapid stomach emptying ▪ Surgical intervention → disruption in gastric anatomy, mucosal function, fundus tone, antropyloric regulatory mechanisms, duodenal feedback on motility → rapid emptying of stomach contents into duodenum ▪ 50% of individuals undergoing gastric surgical procedures ▪ More common in individuals who are biologically female SIGNS & SYMPTOMS ▪ GI: early satiety; abdominal colic; nausea, vomiting; explosive diarrhea; bloating; malabsorption ▪ Vasomotor: diaphoresis; palpitations; vertigo ▪ Early dumping syndrome ▫ 30–60 minutes post-meal ▫ Accelerated stomach emptying → hyperosmolar contents poured into small bowel → osmotic activity → bowel distention, motility stimulated → GI symptoms ▪ Late dumping syndrome ▫ 60–180 minutes post-meal ▫ Accelerated stomach emptying → ↑ carbohydrate concentration in proximal intestine → rapid glucose absorption → rapid, sustained insulin response → hypoglycemia → vasomotor symptoms 230 OSMOSIS.ORG DIAGNOSTIC IMAGING ▪ Endoscopy LAB RESULTS ▪ Oral glucose challenge test elicits symptoms ▪ Hydrogen breath test after glucose ingestion OTHER DIAGNOSTICS ▪ Gastric emptying study ▪ Clinical indices ▫ Sigstad’s diagnostic index: > 7 ▫ Visick classification: heart rate variations after oral glucose challenge TREATMENT MEDICATIONS Acarbose ▪ Interferes with carbohydrate reabsorption Octreotide ▪ Inhibits insulin release OTHER INTERVENTIONS Dietary modification ▪ Avoid simple sugars, fluid intake during meals; low carbohydrate, high protein diet

Chapter 31 Gastric Disease GASTRITIS osms.it/gastritis PATHOLOGY & CAUSES ▪ Inflammation of the lining of the stomach ▪ May occur as a short episode or may be of a long duration TYPES Acute gastritis ▪ Inflammation of gastric mucosa; compare to gastropathy (without active inflammation) ▪ Gastritis, gastropathy ▫ Clinically identical, histologically distinct ▪ Infectious ▫ Most common cause (80%) ▫ H. pylori → chronic gastritis → gastric atrophy → metaplasia → dysplasia → cancer (associated with intestinal-type gastric carcinoma) ▫ Cytotoxin-associated gene A (CagA); carcinogenic virulence factor of H. pylori ▫ Normal gastrin levels, no hypochloridia, no anti-parietal cell/anti-intrinsic factor antibodies (compare to autoimmune atrophic gastritis; hypochloridia, antiparietal/anti- intrinsic factor antibodies) ▫ Gastric ulcers Atrophic gastritis ▪ AKA chronic gastritis, metaplastic gastritis, gastric atrophy ▪ Chronic inflammation of gastric mucosa → epithelial metaplasia, mucosal atrophy, gland loss ▫ Metaplasia: reversible change of one epithelium into another, response to stress ▫ Intestinal metaplasia: goblet cells CAUSES Acute gastritis ▪ Certain medications, alcohol, corticosteroids, uremia ▪ NSAIDs block cyclooxygenase → ↓ prostaglandin E2, I2 production → ↓ gastric defense mechanisms (mucus, HCO3 secretion) → mucosal injury ▪ H. pylori infection → gastric mucosa infiltrates antrum, corpus → inflammation involving neutrophil, mononuclear cells ▪ Alcohol, cigarette smoke, caffeine → irritates, erodes stomach mucosa lining ▪ Extreme physiological stress (e.g. shock, sepsis, burns) Atrophic gastritis ▪ Two main causes: infectious and autoimmune Figure 31.1 A high magnification image of Helicobacter organisms within a gastric crypt. Helicobacter are a common cause of gastritis. ▪ Autoimmune ▫ Most common cause in individuals without H. pylori ▫ Inherited autoimmunity against intrinsic factor, H+/K+ ATPase in parietal cells → inhibition of gastric acid secretion (hypochloridia). ↓ intrinsic factor → OSMOSIS.ORG 231

cobalamin (B12) malabsorption → pernicious anemia ▫ Hypochloridia (impaired iron absorption /G-cell hyperplasia, hypergastrinemia → ↑ neuroendocrine tumor formation) ▫ ↑ gastric adenocarcinoma, neuroendocrine tumors ▫ Damage limited to gastric fundus, body RISK FACTORS Atrophic gastritis ▪ Infectious ▫ Household crowding; rural areas; poor sanitation ▪ Autoimmune ▫ Associated with HLA-DR3, B8, other autoimmune diseases; more common in biologically-female individuals SIGNS & SYMPTOMS ▪ ▪ ▪ ▪ May be asymptomatic Epigastric pain, nausea, vomiting Mucosal ulcers Hemorrhage, hematemesis, melena Autoimmune atrophic gastritis ▪ Iron deficiency anemia ▫ Hypochlorhydria → dietary iron in ferric form → ↓ iron absorption → iron deficiency ▪ Pernicious anemia (symmetrical neuropathy predominantly affecting lower limbs) ▫ Anti-intrinsic factor (IF) antibodies, ↓ cobalamin (B12) absorption → depletion of 5-methyl-tetrahydrofolate → homocysteine cannot convert into methionine → impaired myelin regeneration → subacute combined degeneration of spinal cord posterior columns ▫ Weakness, paraplegia, paresthesias, ataxia, loss of position/vibration sense ▫ Spasticity, clonus; atrophic glossitis; fecal/urinary incontinence; diarrhea; dementia 232 OSMOSIS.ORG DIAGNOSIS LAB RESULTS Endoscopic biopsy ▪ Distinguish gastropathy from gastritis, nonspecific; mucosal erosions, erythema, absence of rugae ▪ Infectious atrophic gastritis ▫ Multifocal atrophy; gastric/duodenal ulcers; erythematous, nodular mucosa; thickened rugal folds in early disease, loss of rugal folds in late disease; damage limited to gastric antrum ▪ Autoimmune atrophic gastritis ▫ Diffuse atrophy, absent rugae, mucosal thinning, visible submucosal blood vessels H. pylori detection ▪ Serology, stool antigen test, urease breath test, biopsy ▪ Atrophic gastritis ▫ H. pylori curved bacilli (hematoxylin, eosin; Giemsa; Warthin-Starry stain); intraepithelial neutrophil, plasma cell invasion Other lab results ▪ Autoimmune atrophic gastritis ▫ Anti-IF antibodies, anti-parietal cell antibodies ▫ ↑ serum gastrin: parietal cell loss → achlorhydria → unrestricted gastrin secretion ▫ ↓ serum pepsinogen: gastric oxyntic mucosa damaged → ↓ chief cells → ↓ serum pepsinogen ▫ Lymphocytosis, eosinophilia, plasma cell invasion; oxyntic gland destruction; metaplasia (intestinal, pyloric, pancreatic)

Chapter 31 Gastric Disease TREATMENT MEDICATIONS Remove offending agents ▪ NSAIDs, acids/alkalis Eradicate H. pylori ▪ Triple therapy ▫ PPI + clarithromycin + amoxicillin (2 weeks) ▪ Quadruple therapy ▫ PPI + bismuth + metronidazole + tetracycline (1 week) Figure 31.2 Histological appearance of chronic gastritis. The lamina propria contains numerous plasma cells. Correct vitamin deficiencies ▪ For Autoimmune atrophic gastritis Figure 31.3 The histological appearance of intestinal metaplasia, characterized by the presence of goblet cells in the gastric mucosa. OSMOSIS.ORG 233

GASTROPARESIS osms.it/gastroparesis PATHOLOGY & CAUSES ▪ Delayed gastric emptying, no mechanical obstruction CAUSES ▪ Most common cause ▫ Idiopathic/diabetes ▪ Iatrogenic (post-surgical/medication side effect), post-viral ▪ More common among individuals with T1DM than T2DM secondary to neuropathy SIGNS & SYMPTOMS ▪ Chronic nausea, vomiting ▪ Early satiety, bloating ▪ Abdominal pain DIAGNOSIS DIAGNOSTIC IMAGING Endoscopy, CT scan, MRI ▪ Exclude mechanical obstruction Gastric emptying scintigraphy 234 OSMOSIS.ORG

Chapter 31 Gastric Disease TREATMENT MEDICATIONS OTHER INTERVENTIONS ▪ Exercise; low fat diet ▪ Metoclopramide (gastrointestinal prokinetic) ▪ Remove medications that may delay gastric emptying PEPTIC ULCER osms.it/peptic-ulcer PATHOLOGY & CAUSES ▪ Chronic mucosal ulceration of stomach/ duodenum extends into muscularis mucosa. ▪ Most common cause of upper gastrointestinal bleeding; proximal duodenum/gastric antrum ▪ Associated with chronic gastritis ▪ ↑ acid secretion, ↓ protective mechanisms → mucosal damage → ulceration RISK FACTORS ▪ H. pylori infection (most common) ▫ ↑ gastric acid secretion, ↓ duodenal HCO3 secretion ▪ NSAID ▫ Particularly low dose aspirin corticosteroids ▪ Physiologic stress ▫ Cushing’s ulcer (intracranial hypertension), Curling ulcer (severe burns) ▪ Psychological stress ▪ Hyperchlorydia ▪ Smoking ▪ Chronic obstructive pulmonary disease (COPD) ▪ Hypergastrinemia (Zollinger-Ellison syndrome) Figure 31.4 An endoscopic view of the gastric antrum which displays two discrete ulcers. SIGNS & SYMPTOMS ▪ Up to 70% asymptomatic ▪ Epigastric burning pain; may mimic myocardial infarction ▫ Usually occurs few hours after meal, worsens at night ▫ Pain characteristically relieved by food/ antacids ▪ Pain may radiate to back, chest, left/right upper abdominal quadrants ▪ Nausea, vomiting, coffee-ground emesis, bloating, weight loss OSMOSIS.ORG 235

▪ Surgical emergency ▫ Hematemesis, melena, positive guaiac test if slow bleed ▫ Acute abdomen; abdominal guarding, peritonitis ▫ GI obstruction ▪ Gastric outlet obstruction, fistula formation DIAGNOSIS DIAGNOSTIC IMAGING Abdominal CT scan Barium abdominal radiography Endoscopy ▪ Diagnostic, therapeutic TREATMENT MEDICATIONS ▪ Discontinue NSAIDs, avoid smoking ▪ PPI SURGERY ▪ Endoscopic ligation/coagulation of bleeding ulcers 236 OSMOSIS.ORG Figure 31.5 A barium study demonstrating the bullseye sign in a case of a gastric ulcer.