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57 Cards in this Set

  • Front
  • Back
What are the main regions of the Stomach?
Cardia
Fundus
Body
Antrum
Pylorus
Heterotopic Pancreas
1 cm nodules of pancreatic tissue in Gastic or Intestinal wall

usually in the antrum or pylorus regions

Can become inflammed and may cause obstruction

nipple-like projection, which has normal acini and ducts
Congenital Pyloric Stenosis
Common Congenital abnormality
75% male - monozygotic twins have high concordance rates
Associated with Turner's syndrome, Trisomy 18, and esophageal atresia

projectile vomiting in second week of life, regurgitation and visible peristalsis

thickened pyloric muscle - fusiform mass - 3-5 cm
occludes pyloric channel

treat with pyloromyotomy (split incision)
Acquired Pyloric Stenosis
80% in men
due to hypertrophy of circular muscle fibers

associated with antral gastritis or pyloric ulcer

DDx - keep in mind neoplastic obstruction
Diaphragmatic hernia
Defective closure of the diaphragm - weakness or absence of a region

abdominal contents present in thorax - stomach and small intestine

may be assymptomatic or may have lethal respiratory problems

very rarely acquired
Muscosal Secretion
thin layer covering the lining of the stomach
much lower diffusion coefficient than water

pepsin and acid are secreted through the mucus into the lumen - never contacts epithelial cells
Bicarbonate secretion
epithelial cells in the stomach and duodenum secrete bicarb underneath the mucus layer, directly in contact with the epithelial cells
Mucosal Defenses
Epithelial Barrier - intercellular tight junctions - prevent acid from back flowing

Mucosal Blood flow - supplies oxygen bicarb, and nutrients and removes back diffused acid

Prostaglandin synthesis - favor the production of mucus and bicarb
inhibit parietal cell secretions
vasodilation effects increase mucosal blood flow

drugs than block prostaglandin synthesis (NSAIDS) cause mucosal damage and ulceration by removing this protectionew

when the mucosa is breached the muscularis mucosa limits the injury

healing occurs in hours to weeks
Gastritis
inflamation of the gastic mucosa

gastropathy is mucosal damage without inflammation
Erosion vs. ulcers
erosion - epithelial damage producing a defect in the mucosa
DOES NOT cross the muscularis

ulcer - full thickness defect in the mucosa extending into the muscularis mucosa
Acute Gastritis
transient inflammation

accompanied by hemorrhage into the mucosa
mucosa can be sloughed off

severe disease can cause significant GI bleeding
Pathogenesis of Acute Gastritis
heavy use of NSAIDS
excessive alcohol consumption
heavy smoking
cancer Chemo
Uremia
Salmonellosis or CMV infection
severe stress
Ischemic Shock
Suicide attempts
NG intubation
Mechanisms of Acute Gastritis
increased acid secretion with back diffusion
decreased bicarb buffer
reduced blood flow
disruption of the mucus layer

bile acid regurg
inadequate synthesis of prostaglandins
Morphology of Acute Gastritis
mild - lamina propria exibits moderate edem
intact epithelium, scattered neutrophils
Neutrophils above the basement membrane is ABNORMAL and indicated active inflammation

Severe - muscosal damage, eroision and hemorrhage
robust amounts of inflammatory infiltrate and fibrin -exudate in the fumen
Clinical features of Acute Gastritis
hemorrhages - dark spots on an otherwise hyperemic mucosa or is association with an erosion

when there is erosion and hemorrhage it is termed acute erosive hemorrhagic gastritis

seen in alcoholics as massive hematemesis

can be assymptomatic or cause epigestric pain, nausea and vomiting with melena and fatal blood loss
Chronic Gastritis
chronic inflammatory changes
epithelial metaplasia and mucosal atrophy
erosions are usually ABSENT

epithelial dysplasia and CIS/carcinoma may ensue
Pathogenesis of Chronic Gastritis
Chronic infection of Helicobacter pylori (90% of patients)
Autoimmune - asoociated with pernicous anemia
Alcohol and cigarette smoking
Postsurgical - antrectomy with gastroenterstomy
Obstructions, bezoars, gastric atony
Radiation
Crohn's disease
Helocobacter Pylori
nonsporing, curvlinear gram negatic rod
its niche is the gastic mucus
- has motility
- produces urease (produces CO2 and NH3 which buffers the the acid)
- has adhesins which bind to the Lewis B blood group antigens
-has toxins CagA and VacA
Patterns of H. Pylori gastritis
antral type gastritis with high acid production - elevated risk for duodenal ulcer

pangastritis followed by multifocal atrophy - low acid and high risk for adenocarcinoma
Noninvasive tests for H. Pylori
serological tests for antibodies
fecal bacterial detection
urea breath test
Invasive tests for H. Pylori
gastric biopsy of tissue
detection by visualization of the bacteria in histologic sections, cultures, or PCR
Morphology of H. Pylori Gastritis
antrum is best site for diagnostic biopsy
mucosa is red and coarse
inflammatory cells thicken rugae

mucosa become thin and flat with lymohocytes and plasma cells in the lamina propria

active inflammation has neutrophils within the glandular and surface epithelium
frequent germinal centers
Location of H. Pylori
found in the superficial mucus layer
can be very pathcy and irregular

silver stain is the best, but Giemsa nad HandE is fine

absent from areas with intestinal metaplasia

organisms may be present in foci of pyloric metaplasia and in Barett;s esophagus.
Clinical Features
Chronic Gastritis causes few symptoms
Nausea, vomiting, upper abdominal discomfort
advanced gastritis - causes hypochlordydric - atrophy of mucosa and parietal cell damage

do not develop achlorhydria or pernicous anemia

gastrin is in the usual range or moderately elevated

-- development of peptic ulcer, gastric carcinoma, or gastric lymphoma
Autoimmune Gastritis
less than 10% of chronic gastritis
antibodies against parietal cell ATPases, and gastrin, and IF recepter

can cause hypochlorhydria or achlorhydria and hypergastrinemia

some patients will get pernicous anemia

there is some association to other autoimmune diseases such as Hashimoto, Addison's, and diabetes

significantly increased risk for gastric carcinoma and endocrine

absent antral damage
Reactive gastropathy
common
related to COX inhibition and NSAIDS, bile reflux, mucosal trauma

foveolar hyperplasia with loss of mucin and glandular regeneration

mucosal edema and dilation of capillaries

smooth muscle in the lamina propria

ABSENCE of neutrophils in the epithelium
Peptic Ulcer
breach in mucosa of the alimentary tract - through the muscularis mucosa

occur in the diodenum and stomach

Acute gastric ulcers - severe stress or ingestion of NSAIDS

occur in the duodenum, antrum, GE junction, margins if gastrojejunostomy

Zollinger Ellison Syndrome - gastrin secreting neoplasm
Meckel's diverticulum
Clinical course of Peptic Ulcers
most often diagnosed in middle aged to older adults
relapsing and remitting course

may heal spontaneously

there is an increase in acid secretion but no increase in acidity
Duodneal Ulcers
Rapid gastric emptying enhances acid delivery

H. pylori - enhances acid secretion, and inhibits bicarb in the duodenum

favors gastric metaplasia in the duodenum
have CagA positive strains with VacA toxin
Risk Factors for PUD
chronic NSAIDS - suppress prostaglandins
cigarette smoking
alcohol
corticosteroids
rapid gastric emptying

ulcers more common in alcoholic cirrhosis
COPD
chronic renal failure and hypeerparathyroidism
stress
Pathology of Peptic Ulcer
sharp clean borders with punched out appearance
ulcerating malignant carcinoma

usually occur within a few centimeters of pyloric ring
Gross Morphology
small lesions are more likely to be erosions
over .6 cm is likely to be an ulcer

size and location do not differentiate a benign from malignant ulcer
Classic Peptic Ulcer
round to oveal shaped
sharply punched out defect

heaping up of the margins is indicative of malignant lesions

may perforate into the peritoneal cavity
Histology of Peptic Ulcers
can be necrotic, chronically inflammed, and scaring, to healed tissue

active ulcers have 4 zones
1. fibrous exudate
2. inflammatory cells (PMN's)
3. granulation tissue
4. fibrotic tissue

margins re-epithelialization at margin - it may be atypical, test for adenocarcinoma
Chronic Gastritis and PUD
chronic gastritis
almost always associated with ulcers (duodenal most common)
usually have H. pylori infections
after ulcer heals, gastritis usually remains (ulcer is not connected to the progression of the gastritis)
Clinical features of Peptic Ulcer
Epigastic gnawing/aching pain
-sometimes might present as a patient with iron deficiency anemia

patient is worse at night and occurs a couple hours after meals in the day

food and antacids make the pain better

nausea, vomiting, bloating, belching, weight loss,

penetrating ulcers can have penetrating pain to the back -
Course of Peptic Ulcers
notoriously chronic - recurring lesions
takes 15 years to heal untreated

todays therapies (H2 antagonists, pump inhibitors, antibiotics) heal in weeks
Complications of Peptic Ulcer Disease
bleeding - can be life threatening

perforation in 5% of patients

obstruction from edema or scarring

malignant transformation does not occur with duodenal ulcers and is rare with gastric ulcers
Acute Gastric Ulceration
and
Acute Erosive Gastritis
from NSAIDS
Risk Factors: increasing age, hx of ulcers
anticoagulation

physiological stress -
usually multiple, in the duodenum
can be superficial to deep - are not precursors to gastric ulcers

seen in patients with shock, burns, sepsis, or severe trauma

curling ulcer - proximal duodenum after trauma/burns
cushing ulcer - in stomach, duodenum or esophagus seen after cranial surgery

caused by ischemia, vagal stimulation, hypoxia, and acidosis

can be assyptomatic or have hypoxia and acidosis
Pathology of Acute Gastric Ulceration and Acute Erosive Gastritis
hyperemia, neutrophils within epithelium

erosion - loss of epithelium without disruption the muscularis mucosa

acute erosive gastritis - erosions and hemorrhages

acute ulcers - small circular
Hypretrophic Gastropathy
Giant cerebriform rugal folds

caused by hyperplasia of epithelial cells - mimics infiltrating carcinoma or lymphoma
Menetrier Disease
type 1 - menetrier disease - profound hyperplasia of surface mucous with accompanying glandular atrophy

type 2 -hypertrophic gastropathy - hyperplasia of parietal and cheif cells

type 3 - gastric gland hyperplasia - secondary to excessive gastrin secretion (Zollinger Elision syndrom)
Bezoars
foreign bodies (commonly hair or vegetable matter)
Caliber persistent artery varicies
develop in the setting of portal hypertension

usually within a few cms of gastroesophageal junction - from longitudunal submucosal veins

looks like nodular, tortuous elevations of the mucosa in the cardia or fundus
Stomach Polyps
benign tumors
uncommon and found inceidentally

must investigate histologically due to impossible visual diagnosis

hyperplastic, fundic gland, peutz-Jeghers, juvenille, inflammatory, and adenoma
Hyperplastic Polyps
non-neoplastic
mixture of epithelium, glands, with a lamina propria containing inflammatory cells and smooth muscle

small and sessile located in atrium
frequently seen in the setting of chronic gastritis

no malignant potential
Inflammatory Polyp
submucosal growth
fibromuscular tissue with prominent eosinophilia
Adenocarcinoma
second most common tumor in the world
not so common in the US
most countries see a decline in incidence and death
leading cause of cancer death worldwide

intestinal type - bulky tumors/glandular
diffuse type - poorly differentiated
predisposing factors to Adenocarcinoma of the Stomach
intestinal type - through pattern of dyplasia
diffuse - de novo origin

nitrates, smoked and salted foods, pickled vegetables, lack of fresh fruit and vegetables
low SES
cigarette smoking

chronic gastritis
hypochlorhydria (predisposes to H. pylori)
intestinal metaplasia

type A blood
Family history
Hereditary Non-polyposis cancer syndrom
Pathology of Adenocarcinoma of the Stomach
pylorus and antrum - over half of cases
cardia - 25%

more common on the lesser curvature
Classification of gastric adenocardinoma
depth of invasion - most important factor. advanced extends below the submucosa

macroscopic growth pattern
- exophytic - protrusiion into lumen
- flat - no obvious tumor.
- excavated - shallow or deeply erosive crater. mimics ulcer with heaped up margins
- diffuse pattern - broad region , see in metastatic cancer
Histological difference between intestinal and diffuse adenocarcinoma
intestinal - neoplastic growth of glands permeate the walls. contain mucin vacuoles

diffuse - composed of mucous cells which normally do not form glands, and permeate the tissue. arise from the middle layer of the mucosa. forms a singlet ring conformation
Metastases from Gastric Adenocarcinoma
left supraclavicular node

can spread to the liver and lungs

krukenberg tumor - ovaries

periumbilical subcutaneous nodules - Sister Mary Joseph nodule
Gastric Lymphoma
Most common site for extranodal lymphoma

almost always B cell lymphomas of the MALT

rarely Burkitt lymphomas, AIDS lymphoma, and Hodgkin lymphoma

associated of H. pylori infection

commonly exibit trisomy 3 and t(11, 18) genetic abnormalities
Morphology of Gastric Lymphoma
monomorphic lymphocytic infiltrate in the lamina propria
Gastrointestinal stromal tumors
originate from the interstitial cells of Cajal (control peristalsis)

stain with cKIT and CD34 antibodies

spindle type and apithelioid types
Morphology of GIST
single or multiple
tumor can protrude into the lumen

can have necrotic or cystic components

can exibit spnidle cells, epithelioid cells or both