Pathology of the Stomach PDF

Pathology of the Stomach Stomach Anatomy and Histology Anatomic regions of stomach (5): o Cardia o Fundus o Corpus (body) o Antrum o Pylorus Histology of the Stomach o Mucosa (innermost) o Submucosa o Muscularis externa o Serosa (outermost) Stomach Histology (layers) Mucosa (innermost layer) o Epith...

Pathology of the Stomach Stomach Anatomy and Histology Anatomic regions of stomach (5): o Cardia o Fundus o Corpus (body) o Antrum o Pylorus Histology of the Stomach o Mucosa (innermost) o Submucosa o Muscularis externa o Serosa (outermost) Stomach Histology (layers) Mucosa (innermost layer) o Epithelium (aka gastric foveolae) o Lamina propria (space btwn epithelium) o Muscularis Mucosa (layer of muscles) Submucosa o Fats o Fibrous tissue o Blood vessels o Lymphatics Muscularis Propria/externa o Inner Oblique § Additional layer seen only in stomach § Helps further churn food o Middle circular o Outer longitudinal Serosa (outermost layer) o Epithelium o Connective tissues Gastric Surface Epi Histology Gastric foveolae at surface of epi (Mucosa layer) o Mucous neck cells o Contains cytoplasmic mucus globules o Secrete alkaline mucus to protect stomach lining from acidity/autodigestion Glandular Gastric Epi Histology Histo varies btwn location in stomach Cardia: o Robust muscularis mucosa, submucosa o Coiled gastric glands rich in mucous cells § Forms columnar epi of cardia § Protects stomach lining from acid Corpus/Body: o Slimmer submucosa, muscularis o Many Gastric glands that are less coiled o Contain ECL, Parietal, Chief, mucus cells Pylorus: o Deep gastric pits o Gastric glands rich in G, D cells Stomach Pathology Terminology Gastropathy o Gastric mucosa damaged o No inflammation is present Gastritis o Inflammation of gastric mucosa Acute Gastritis o Short-term sudden inflammation or swelling in the stomach mucosa o Neutrophils are present Chronic Gastritis o Long-term stomach lining inflammation o Lymphocytes and Plasma cells present o Helicobacter pylori gastritis: primary cause and subgroup of chronic gastritis Mechanism of Gastric Injury Normal Conditions o Under normal conditions, damaging factors are: § Gastric acidity § Peptic enzymes o Protective factors (6): § Mucus secretion on surface: alkaline pH § Bicarb secretion into mucus § Mucosal blood flow to take away damaging factors § Epithelial barrier function § Epithelial regenerative capacity § High prostaglandins for increasing defense mechanisms (ex. Mucus, bicarb) In Injured State o Increased Damage: § H Pylori infection § NSAIDs § Tobacco § Alcohol § Gastric hyperacidity § Duodenal-gastric reflux o Impaired Defenses: § Ischemia § Shock § NSAIDs When injury is not treated o Ulcer formation § Mucosal lining fully damaged § Necrotic debris present § Acute inflammation § Granulation tissue § Fibrosis Acute Gastritis o o o o No mucous cells left Very damaged epithelial layer Lots of neutrophils present and spread from epithelium to lamina propria Muscularis mucosa is slimmed down Acute Gastritis caused by: o Infection § Most common o Frequent/Long-term NSAID use § Inhibits COX pathways à Inhibits prostaglandin formation § No defense mechanisms are made/stimulated § Acute and Chronic gastritis o Extreme Physiological Stress (illness, surgery, etc) § Uremia inhibits gastric bicarb transporters o Bile § Bile reflux into stomach § Alkalinity of bile imbalance creates irritation in stomach lining o Elderly § Reduced mucin secretion § Reduced bicarb secretion o Alcohol, Smoking § Direct injury to mucosal cells § Increased ROS presence Stress Related Mucosal Injury “Stress induced Acute Gastritis” Most assc w critically ill pts: o Trauma, shock, sepsis o Extensive burns o Major surgeries, serious medical dz o Severe physiological stress o Intracranial dz Results in ulcer-related minimal to severe GI blood loss Factors for identification: Location & Complication o Curling Ulcers § In proximal duodenum à assc w severe burns, trauma § Leads to Hypovolemia à ischemia o Cushing Ulcers § Gastric, duodenal and esophageal ulcers: assc w intracranial dz § High incidence of perforation Signs/Symptoms of Acute Gastritis Lasts for short period (wks) Inflammation is gone once symptoms dissipate Symptoms: o Loss of appetite o Upper abd Discomfort o Nausea o Vomiting Gastropathy (NOT gastritis) Dmg to stomach mucosa WITHOUT inflammation Etiology: o NSAIDs o Alcohol o Smoking o Physiological Stress Histology: o Surface is intact but damaged o Loss of mucin vacuoles o Corkscrew hyperplasia of gastric epithelium § Runs Deep § causes edema Chronic Gastritis Infiltration of lymphocytes, plasma cells btwn epithelium, lamina propria Upper layer mucosa replaced w metaplastic cells Etiology: o Helicobacter Pylori § Most common cause of Chronic § Long-term can cause atrophic gastritis and metaplasia o WITHOUT H. Pylori: Autoimmune Gastritis o Less Common Causes § Chronic Bile reflux § Mechanical injury (nasogastric tube) § Radiation injury § Toxins (alcohol, tobacco) o Increase risk w age >60 Symptoms o Less severe than acute gastritis o Longer lasting § Nausea § Pain § Vomiting Helicobacter Pylori Gastritis Transmission route in lower socioeconomic: o Fecal-oral o Oral-oral Predominantly occurs at Antrum with normal or increased acid production Can cause mucosa-associated lymphoid tissue that can transform into lymphoma Can induce metaplasia and lead to adenocarcinoma Infection shows Brown staining Invasion (4 steps): o 1. Gram-negative rod bacilli bacteria Flagella allows bacterial motility o 2. Urease produced § Which generates ammonia from urea à Increases gastric pH for survival o 3. Adhesins § Bacteria attaches to epithelial cells § DO NOT penetrate surface mucus cells o 4. Toxins: Cytotoxin-associated gene A (CagA) involved in dz progression causes colonization and proliferation of immune cells Stomach pH is normally 1.5-2 Urease from H. pylori increases pH to 4.5 - 7 for survival Metaplasia: Transformation of normal cells Dysplasia: Presence of abnormal cells Hyperplasia: Increase in # of cells Autoimmune Gastritis Autoimmune metaplastic atrophic gastritis/ Type A gastritis Affects fundus/corpus of the stomach Parietal cells are damaged by: o 90% have Parietal cell antibodies (to the protein pump K/hydrogen ATPase) o 60% have Intrinsic factor antibodies o As a result: Hypochlorhydria (âHCL), low pepsinogen, high gastrin serum concentration. Associated with: o Other autoimmune diseases (Hashimoto’s thyroiditis, Addison’s disease) o NOT assc. with H. pylori o Leads to vit B12 deficiency o Increase risk for dysplasia/carcinoma o Increase risk of gastric neuroendocrine tumors (due to loss of parietal cells that effects ECL cells) Pathogenesis of Autoimmune Gastritis Parietal cells damaged Hyperplasia of G cells in antrum o Increase gastrin secretion o Stimulate ECL cells in corpus (hyperplasia) o Histamine secreted to stimulate parietal cells (missing) § Causes neuroendocrine tumors Antibodies against parietal cells detected via immunofluorescence Shows as Yellow hyperplastic ECL Location Inflammatory Response Acid Production Gastrin Antibody Sequela Association H. pylori vs. Autoimmune gastritis H. pylori gastritis Autoimmune gastritis Antrum Corpus/fundus Neutrophils, plasma cells Lymphocytes, macrophages Increased, slight dmg Decreased Normal, slight increase Increased Antibody to H pylori Antibody to parietal cells, intrinsic factor Peptic ulcer Atrophy Adenocarcinoma Pernicious anemia MALToma Adenocarcinoma Neuroendocrine tumor Low socioeconomic location Autoimmune dz (fecal-oral, oral-oral transmission) Chronic Gastritis: Complications Peptic Ulcer Dz (PUD) o Imbalance btwn mucosal defense and damaging factors (specifically Gastric acid and pepsin) o Duodenal & gastric ulcers o Antral gastric PU caused by: § H. pylori § Smoking § NSAIDs § Bile pancreatic juice reflux § Zollinger-Ellison dz: Pancreatic tumor, inc stomach acidity, dec bicarb Tumors o Gastric Adenocarcinoma o Gastric Lymphoma o Neuroendocrine tumor Gastritis: Diagnosis, Tx Diagnosis: o Test for H pylori § Stool test § Breath test o Upper GI endoscopy w biopsy o Barium swallow test Treatment: o Antibiotic to kill H pylori: take for 7days-2wks with PPI o PPI (decrease acidity) o Antacid (neutralize acidity) Breath Test for H. pylori - Exhale into balloon-like bag - Checks Co2 levels