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54 Cards in this Set

  • Front
  • Back
Stomach Gross anatamy
Top to bottom:
folds = Rugae
Stomach Epithelium
-same in all compartments
-tall simple columnar w/ deep pits:
Superficial Part-Foveolar compartment
Deep part-Glandular compartment w/ gastric glands
Stomach Glands
Vary by part:
Cardia - Mucous
Fundus/Body - Parietal(acid), Chief(pepsin)
Antrium/Pylorus - mucous, G cells(gastrin)
Helicobacter Pylori Basics
Gram(-) spiral Rod
Seen on Silver Stain
H Pylori, where it lives
lives in layer of mucus on GASTRIC FOVEOLAR cells only
-concentrates at intracell jxns(more urea)
Adaptation to gastric:
1.bind to foveolar epithelial cells and gastric mucin
2.synthesize urease → degrade urea → ammonia → buffers local pH
H pylori pathogenesis
make these injurious molecules:
1.Proteases->degrades mucous barrier->indirect epithelial cell injury
2.ammonia-> direct epithelial cell injury
3.cytotoxins-> direct epithelial cell injury
H Pylori Natural History
epithelial cell injury →:
1.acute inflammation → acute gastritis
2.chronic inflammation → chronic gastritis
3.necrosis → peptic ulcer disease
4.chronic inflammation → gastric lymphomas, ?(gastric adenoCA)
Gastritis (def/etiology)
Inflammation associated with mucosal injury
-autoimmune processes
Gastropathy (def/etiology)
Epithelial cell damage and regeneration without associated inflammation
-bile reflux
Gastric injury presentation
-Dyspepsia “Stomach ache”
-Nausea and vomiting
-Weight loss
-Hypertrophic gastropathy(diarrhea, severe protein loss)
Gastric injury Tests
endoscopy w/ Biopsy is ultimate
-Serum anti-parietal and anti-intrinsic factor antibodies(autoimmune)
-Vitamin B12 level
-Serum gastrin
-Helicobacter pylori testing(serology, rapid urease test)
Acute Gastritis Definition
Acute inflammation of mucosa (PMNs)
can →:
-necrosis (erosion)
Acute Gastritis Etiology
-Drugs(NSAIDs, CA chemo.)
-Complication of other diseases(uremia, infections)
- Mucosal hypoxia (shock, trauma, burns, surgery) = ‘Stress’
Acute Gastritis Pathogenesis
Causative agents:
1. Directly injure gastric mucosa
2. (and/or) interfere with normal gastric protective mechanisms(e.g. mucus prod., prostaglandin level, epithelial repair, intramural pH)
->Gastric contents injure unprotected gastric mucosa
->Acute inflammatory response
Acute Gastritis Gross/histopathology
-Acute inflammation(neutrophils)
-Patchy mucosal necrosis (erosions)
-Petechial hemorrhage

(Rarely confirmed by biopsy since profuse hemorrhage may occur at the biopsy site.)
Chronic Gastritis Etiology
1.Infectious : Helicobacter pylori
3.Other (gastric surgery)
Chronic Gastritis Pathogenesis
Etiology (X)
->chronic inflammatory cells(lymphocytes, plasma cells, macs)
->cell and humoral mediated immune responses(T-cells)
->epithelial cell necrosis:
can → atrophy(glands and eventually mucosa)
can → intestinal metaplasia(which can progress to dysplasia → cancer)
Chronic Gastritis Gross
thin, atrophic gastric wall
Chronic Gastritis Histopath
chronic inflammation
+/- gastric gland and mucosal atrophy
+/- intestinal metaplasia(Goblet cells & brush border
Autoimmune Chronic Gastritis Inheritance
Autosomal Dominant
Autoimmune Chronic Gastritis basic pathogenesis
autoAb to Parietal Cell proteins(IF, etc) (BODY/FUNDUS)
->cell-mediated destruction of Parietal Cells(lymphocytes, cytotox Tcells)
->loss of Parietal Cells:
can → atrophy of glands/mucosa, ↓ HCl, ↓ IF (intrinsic factor)
Autoimmune Chronic Gastritis pathogenesis-results of less parietal cells:
1: ↓ Acid production(hypochlorhidria or achlorhidria)
->Loss of negative feedback on G cells in antrum
->Hyperplasia of antral G(G cells are neuroendocrine cells which secrete gastrin)
2:Atrophy of gastric glands(body, fundus)
3:↓Intrinsic factor
->↓ B12 absorption
->Anemia(When anemia is present, disease is re-named Pernicious anemia)
Ulcer Definition
A defect in the mucosal surface penetrating through the muscularis mucosa
Ulcer Epidemiology
-mortality goes up over age 65
-Hospitilazations for Gastric Ulcers has gone up with more incedence of bleeding(from more NSAID use)
Ulcer pathophysiology
-Balance b/w aggressive and Defensive factors
-H. pylori
-Hypersecretory states
-Genetic & environmental
Ulcer Aggressive Factors
H. pylori
Gastric acid/Bile
Ulcer Defensive Factors
Mucus barrier
Cellular resistance
Mucosal blood flow
HCO3 secretion
Mucus Barrier
-Secreted by superficial mucus cells
-Stomach and duodenum
-15% Glycoprotein and 85% water
-Relatively impermeable to pepsin
-Hydrogen ions flow relatively freely
-pH=2 out of mucus, =7 at cells in mucus
Mucus Barrier Stim/Inhib
-Cephalic-vagal stage
-Cholinergic agonists
-Bacterial Toxins

Cellular Resistance
Mucosal restitution(rapid migration of mucus cells to cover:
-No cell division required
-Maintain intracellular pH

Regeneration(new epith cells:
-Requires cell division
Mucosal blood flow
-Delivers oxygen, nutrients, & bicarbonate
-Removes back diffused acid
-If reduced by more than 50%, mucosa is vulnerable
Bicarbonate Secretion
-Secreted by surface mucus cells
-Maintains pH gradient
(1-2 in lumen, 6-7 at epithelial surface)
-Pepsin is inactive at pH 5
-Stimulate mucous and bicarb secretion
-Increase mucosal blood flow
-Inhibit acid secretion

-Rate limiting catalytic step in arachadonic acid to prostaglandins conversion
-COX 1--constitutively expressed
-COX 2-- inducible
Peptic Ulcer Disease Definition
Chronic ulcers (necrosis extending below mucosa) in GI tract regions exposed to pepsin-acid lumenal contents (stomach, duodenum > other areas)
PUD Etiology
-H. pylori
-↑ gastric acid (including Zollinger-Ellison)
PUD Pathogenesis
H. pylori or ↑ gastric acid or NSAIDs
->epithelial cell necrosis
PUD Gross Pathology
-Single (usually)
-‘Punched out', 'cookie cutter' i.e. clean/smooth base and perpendicular/overhanging sides, flat margins
-Stomach : lesser curvature of antrum, prepylorus
-Duodenum : proximal
PUD Histopathology
Four characteristic zones outter to inner:
-Fibrinopurulent exudate
-Necrotic tissue
-Granulation tissue
-Fibrotic tissue
NSAID mechanism of injury
can still cause ulcers even if given by IV
PUD clinical features
-Abdominal pain-60% sensitive finding
•Postprandial and nocturnal
•Relieved or exacerbated with food or medication
PUD diagnosis
-radiography (Ba swallowa)
PUD treatment
-Medical therapy
-Endoscopy for acute bleeding
-Surgery for refractory bleeding and complications
PUD medical therapy
-Acid Reduction(Proton Pump Inhibitor for 8 weeks)
-Antibiotic Therapy for HPylori positive patients(prevents ulcer recurrence in > 90%)
-Reduce/discontinue NSAIDs
-Smoking cessation
Zollinger-Ellison syndrome (ZE) definition
-severe ulcer disease
-gastric acid hypersecretion
-non-β islet cell tumors of the pancreas
Zollinger-Ellison syndrome (ZE) underlying cause
-Gastrinoma (often in pancreas) causing ↑ gastric HCl secretion, which leads to severe peptic ulceration.
-uncommon cause of peptic ulcers.
PUD complications
-Ranges from occult to severe

-Uncommon in stomach (more common in duodenum)
-Causes peritonitis

-Especially in pylorus → gastric outlet... obstruction
-Arises from edema, scar contraction, muscle hypertrophy, of nearby ulcer
Gastrinomas Epidemiology
-True incidence not known
-Responsible for 0.1-1.0% of all DU
-Responsible for 1 in 50 recurrence after surgery
-Sporadic (75%)
-MEN I(mult endocrine neoplasia) (25%)
1.pituitary, parathyroid, pancreas (3P’s)
2.autosomal dominant
3.chromosome 11q
Gastrinomas Symptoms
-Peptic Ulcer Disease
(multiple, refractory, recurrent)
-Gastroesophageal Reflux
Gastrinomas Diagnosis
-Basal Acid Output (BAO) > 15 meq/h
-BAO/MAO > 6
-Fasting gastrin >1000 pg/ml
.gastric pH < 3
.No further work up necessary
-Fasting gastrin 100-999 pg/ml
.Secretin Stimulation Test
.Gastrin level increase > 200 pg/ml
Gastrinoma Provacotive test
Secretin Test:
-Secretin directly activates the secretin receptor expressed on gastrinoma cells
-This receptor is not found on antral G cells
-Secretin is infused IV
-Serum collected for gastrin measurement 10 minutes and 1 minute prior to infusion and at 2, 5, 10, 15, 20 and 30 minutes post infusion
-With gastrinoma see rise within 15 minutes of infusion
-Rise of 200 pg/ml or more positive test
Gastrinomas causes of chronic hypergastrinemia
Low Gastric Acid:
-pernicious anemia
-chronic atrophic gastritis

High Gastric Acid:
-antral hyperplasia
-chronic renal failure
-short bowel syndrome
-gastric outlet obstruction
Gastrinoma location
-85% occur in gastrinoma triangle
.medially head and body of pancreas
.inferiorly 2nd and 3rd portion of duodenum
.superiorly junction of cystic duct and common bile duct
-Multiple in more than half
-Size can range from 0.1-20 cm
-Malignant in 50-90%
.mets to lymph nodes and liver
.40% will have metastatic disease at time of dx
Gastrinoma Localization
-CT scan
-Endoscopic Ultrasound
-Nuclear Scan (SRS)
-Exploratory laparotomy
Gastrinoma Treatment
-Proton Pump Inhibitors