Stomach Flashcards
Motility disorders of the stomach
- Gastroparesis
Partial paralysis of the stomach, results in delayed gastric emptying
- gastric motility normally governed by the vagus nerve –> any nerve injury can cause gastroparesis
- Diabetic neuropathy is most common cause
- injury to stomach itself –> connective tissue disorders
Motility disorders of the stomach
- Pyloric stenosis
Hypertrophy of muscle of the pylorus
- may be palpable through the abdominal wall
- prevents movement of food into the duodenum
- idiopathic condition
- presents with projectile vomiting ~2 weeks after birth
Classification of gastritis
By presentation –> acute vs. chronic
- based on the clinical picture
- histologic features won’t always match
- classically acute features = “active” gastritis (PMNs)
- features of active and chronic = “active chronic” gastritis
By cause
- H. pylori
- chemical –> bile, iron, etc.
- autoimmune
- radiation
- stress ulcer
- curling ulcer –> severe burns
- cushing ulcer –> intracranial disease
H. pylori gastritis
- pathogenesis
- histology
- location of h. pylori
Spiral shaped bacterium found in the gastric mucus layer or adherent to the epithelial lining of the stomach
Acute h. pylori is usually asymptomatic –> takes time to develop injury
Pathogenesis –> increased acid production + reduced protection against acid in the stomach and duodenum
Histology –> produces “active” gastritis (PMNs), usually chronic component too = “active chronic”
Organism is present in surface and glandular mucosa –> prefers antrum, but may be pangastritis
Complications of H. pylori infection
- peptic ulcer disease
- intestinal metaplasia –> gastric carcinoma
- short term is good –> h. pylori can’t live in intestinal type epithelium
- long term is bad –> the metaplasia is not wide spread enough to eradicate infection, predisposes to adenocarcinoma - lymphoma –> MALToma
- stimulated by ongoing exposure to h. pylori antigen
- classic appearance = lymphoepithelial lesion –> destruction of glands
- may be treated along with h. pylori antibiotics
Autoimmune gastritis
- morphology
Pernicious anemia –> autoimmune destruction of intrinsic factor and of parietal cells
- characterized by circulating autoantibodies, but mediated by T cells
- associated with other autoimmune diseases
Morphology
- predominates in gastric body and fundus with relative sparing of the antrum –> disruption of the parietal cells, differs from h. pylori
- active chronic gastritis –> resembles h. pylori
- replacement of fundic by antral type mucosa
- “atrophic gastritis” = gradual destruction of mucosa –> incomplete atrophy with foci of epithelial sparing may mimic polyps
Complications of autoimmune gastritis/pernicious anemia
- Anemia
- Peptic ulcer disease
- Intestinal metaplasia
- Neuroendocrine tumors
- loss of acid secretion –> hypergastrinemia –> overgrowth of endocrine cells (ECLs)
- linear hyperplasia –> nodular hyperplasia (timy tumors) –> neuroendocrine tumors
- may be monitored with sequential endoscopy
H. pylori vs. autoimmune gastritis
Location
- H pylori –> mostly antrum
- A.G. –> mostly in fundus/body
Acid production
- h. pylori = normal/increased
- A.G. = decreased
Gastrin
- h. pylori = normal/decreased (due to increased acid)
- A.G. = increased (due to decreased acid)
Antibodies
- h. pylori = anti-HP antibodies
- A.G. = anti-parietal cell antibodies
Associated malignancy
- h. pylori = adenocarcinoma, lymphoma
- A.G. = adenocarcinoma, NET
Chemical gastritis
- histology
Foveolar hyperplasia –> may resemble vili
- complex glandular architecture –> “corkscrew”
- vascular congestion
- typically mild inflammation
- erosions may be associated with more inflammation
Gastropathy
Mild changes with limited inflammation –> uncertain clinical significance, some asymptomatic
Many causes –> most look exactly the same
- NSAIDS
- bile reflux into stomach from duodenum
- alcohol
- coffee
- cocaine
Iron pill gastritis
Severe, chronic gastritis associated with oral iron pills –> causes ulceration of the mucosa
- may have acute features
- iron apparent in lamina propria and crusted along surface
Lymphocytic gastritis
Pain and diarrhea, may present with protein losing enteropathy
- relatively rare
- marked lymphocytosis (>25 lymphocytes/100 epithelial cells) –> lymphocytes in the lamina propria
Causes –> descriptive term associated with multiple possible etiologies
- H. pylori
- HIV
- Crohn’s
- lymphoma
- Celiac disease –> ~1/.3 of celiac patients, may also have lymphocytic colitis, relatively resistant to gluten free diet
- idiopathic
Crohn’s gastritis
1/3 of crohn’s patients have upper tract disease
- pain, nausea, vomiting
- may produce strictures, perforations, etc
- may produce elucers, but histologic changes may be present even in grossly normal tissue
Histology
- granulomas –> relatively rare, more common in kids
- focally enhanced gastritis –> relatively common
- –> typically focal with normal backgroun
- –> periglandular inflammation with lymphocytes, histiocytes and often neutrophils
- –> differential diagnosis includes h. pylori
Zollinger Ellison syndrome
Triad of hypergastremia (due to gastrinoma), increased acid, and duodenal ulcers
- hyperplasia of fundic mucosa in response to stimulation
Heterotopia
Normal tissue in an abnormal place –> not usually significant
- antral heteropia –> histologically unremarkable antral type mucosa located in body or fundus
- pancreatic heterotopia –> umbilicated nodule in stomach; most are submucosal
Fundic gland polyps
Most common gastric polyps –> benign
Two major associations
- long term PPI use
- familial adenomatous polyposis –> polyp itself usually benign, but condition is dangerous
- often multple
- small, same color background as stomach
- histology –> fundic mucosa with cystic dilation
Hyperplastic polyp
Overgrowth of foveolar epithelium
- may be multiple
- smooth surface
- large, cystically dilated glands
- surface inflammation/erosion
- may hardbor intestinal metaplasia –> dysplasia –> carcinoma –> bigger polyps = increased risk
Polyposis
Characterized by multiple gastric polyps
- associated with APC mutations = familial adenomatous polyposis
- increased cancer risk –> screen with colonoscopy
Dysplasia
“gastric dysplasia” refers to a flat lesion –> often grossly inapparent
- may arise in background of intestinal metaplasia
- may regress or progress –> particularly if high grade
- features like those of esophageal dysplasia
Adenoma
Denotes glandular polyp with at least low grade dysplasia
- high grade/malignant potential –> especially >2 cm, most are < 2 cm
Polypnoid
Visible growth of dysplastic epithelium
- often arise in context of inflammation and intestinal metaplasia
- may be
- –> intestinal type (goblet cells ) OR
- –> gastric type (foveolar cells)
Risk factors for adenocarcinoma
- environmental –> diet, h. pylori, smoking
- genetics –> inherited abnormalities in APC + e-cadherin
- genetic abnormalities –> e-cadherin, KRAS, p53, APC
Intestinal type gastric adenocarcinoma
- cohesive glands
- typically discrete fungating masses or ulcers
- associated with intestinal metaplasia
Diffuse type gastric adenocarcinoma
Particularly bad prognosis
- individual cells with “signet ring” morphology –> very poorly cohesive, infiltrate extensively
- generalized thickening of the stomach = “linitis plastic”
- can be subtle endoscopically and microscopically
- often younger patients
- usually sporadic –> rarely associated with e-cadherin mutations
- poor outcomes
Staging of gastric carcinoma
Mostly looking at indirect measures of how aggressive the tumor is
- direct tumor spread –> through muscularis propria, or through serosa
- lymph node metastases
- distant metastases
Predictive markers –> markers that predict response to chemo
- overexpression of her2/neu = response to trastuzimab (~20% of intestinal type cancers)
Neuroendocrine tumors
Classified by associated conditions
- Type I = autoimmune gastritis –> best prognosis
- Type 2 = ZES
- Type 3 = sporadic –> worst prognosis
Hard to predict behavior –> called “tumors” rather than carcinomas unless metastatic
- grade 1 = carcinoid
- grade 2 = atypical carcinoid
- ** grade 1 and 2 are well differentiated –> use mitotic rate to tell them apart
- grade 3 = high grade, overtly malignant
GAVE (gastric antral vascular ectasia)
“Watermelone stomach”
- dilated capillaries with fibrin thrombi
- mostly antral
- elderly women
- bleeding –> acute or chronic
- autoimmune association –> also cirrhosis and end stage renal disease
Caliber persistent artery (CAP)
Aka dieulafoy
- large caliber artery going up to the surface
- near GEJ, along lesser curvature
- recurrent bleeding without other symptoms –> may be massive
- typically managed endoscopically –> if resected, try to find to justify the procedure
Causes of peptic ulcer disease
- too much acid –> ZE
- h. pylori
- NSAIDS
- rare causes = CMS, syphillis, lymphocytic gastritis, crohns, granulomatous autoimmune gastritis, cancer
Pathogenesis of peptic ulcer disease
- injurants to the lining –> gastric or bile acids, NSAIDS
- impaired mucosal defense mechanism –> impaired mucous bicarb secretion, poor blood flow
Stress ulcers
Occur with severe physiological stress –> decreased mucsal blood flow = impaired mucus layer
- ICU patients, intubated patients, post trauma patients
- increased intracranial pressure = cushings ulcer
- severe burns = curling ulcer
Complications of ulcers
- perforation –> contents of stomach are not sterile –> when they enter peritoneal cavity = surgical emergency
- bleeding
- penetration –> penetration posteriorly into the head of the pancreas, can cause pancreatitis
- obstruction –> when located at the pyloric outlet
major cause of GI morbidity and mortality
Epidemiology of h. pylori infection
- ~50-60% of worlds population is infected
- major cause of duodenal and gastric ulcers + gastric cancer
- age at acquisition = childhood
- transmission is likely fecal oral
Natural history of infection
Initial infection –> chronic gastritis –>
- gastric or duodenal cancer (10%)
- lymphoproliferative disease = MALToma
- gastric atrophy –> gastric cancer
Evidence that h pylori causes ulcers and gastric cancer
Association with h. pylori infection –> >90% of duodenal ulcers and 80% of gastric ulcers + increased risk of gastric cancer
Eradication of organism results in marked reduction in ulcer relapse + regression of maltoma
Diagnosis of H. pylori
- serum antibody test –> will remain positive even after treatment so not very specific for current active infection, other tests are more specific
- stool antigen test
- urea breath test
- upper endoscopy with gastric biopsy
- Urease test
- microscopic identification of organism
Treatment of h. pylori
2 antibiotics + PPI
- amoxicillin, tetracycline, metronidazole, clarithromycin
- higher eradication rates with longer treatment –> eradication rate = 90%
- antibiotic resistance and patient non-adherence to treatment are major reasons for failure
NSAID induced ulcers
PGs are important for maintaining a healthy mucous lining in the stomach
NSAID gastrophathy
- superficial erosions
- ulcers
- absence of chronic gastritis
- frequently asymptomatic in elderly
- usually occur in the antrum
- very common
Risk factors for NSAID complications
- age >60 years
- past history of ulcers
- high dose
- concomitant corticosteroid therapy –> prevents healing of ulcers but does not cause them
- highly selective COX 2 inhibitors appear to be safer for the stomach but increase risk of CV disease
Prevention and tx of NSAID induced ulcers
Prevention –> avoid NSAIDS, use less NSAIDS, concomitant H2 blocker of PPI
- misoprostol = PGE1 analog
treatment –> stop NSAID, start PPI
Zollinger ellison syndrome
Gastrin secreting non-beta islet cell tumor with gastric acid hypersecretion
- causes gastric and small intestinal ulcers
- 1/3 have severe esophageal reflux
- diarrhea is common –> due to high acid load and acid inhibition of pancreatic enyzmes
Multiple endocrine neoplasia type 1 –> 25% of ZE patients
- autosomal dominant
- hyperplasia/adenoma of…
1. parathyroids
2. pancreatic islets
3. pituitary glands
Epidemiology of ZE
1/1 million –> rare
- male > female
- mean age at dx ~50 –> range = 7-90
- ~25% associated with MEN1 –> 60% of MEN1 patients have gastrinomas
Diagnosis and tx of ZE
Dx
- gastric hypersecretion
- hypergastrinemia > 150 pg/mL in face of increased acid secretion –> normally when there is high acid levels there should be neg feedback to inhibit g cells, but this does not occur in ZE
- –> other causes of hypergastrinemia = H2 blockers, PPIs, gastric atrophy, antral resection
- secretin provocation test –> gastrin should fall when you give IV secretin, but it rises in ZE
- CT scan, endoscopic ultrasound to localize tumor –> >50% have multiple tumors
- octreotide scan
Tx –> high dose PPIs, surgery, chemo
Acute gastritis
erosive and hemorrhagic –> as opposed to ulcers and erosions where there are breaks in the lining, gastritis is inflammation without breaks
causes
- toxins and drugs –> ethanol, KCl, aspirin, nsaids, chemo
- radiation
- vascular –> ischemia, vasculitis
- gastroduodenal reflux
- stress gastritis
Chronic gastritis
- infection –> h. pylori (common), TB, syphilis, viral, funal (rare)
- autoimmune –> pernicious anemia
- vit B1`2 deficiency caused by gastric atrophy and loss of IF production
- associated with other autoimmune diseases
- familial tendency
- corticosteroids may help
- diagnosis –> low serum B12, IF and parietal cell antibodies, achlohydria, schilling test - generalized GI diseases –> crohn’s, eosinophilic gastroenteritis
- systemic –> sarcoidosis, chronic granulomatous and GVHD
Benign gastric tumors
- hyperplastic polyp
- adenomatous poly
- leiomyoma
- lipoma
Malignant gastric tumors
- adenocarcinoma –> most common, declining incidence in developed countries
- distal stomach = associated with h. pylori infection
- proximal stomach = not associated with h. pylori infection - lymphoma –> second most common
- GIST = GI stromal tumor
- Carcinoid tumors
- Kaposi sarcoma
Findings in gastric cancer
Symptoms
- early = none –> presents late = poor prognosis
- late = anorexia, early satiety, nausea, vomiting, weight loss, anemia, GI bleeding, dysphagia (cardia tumor)
Physical findings
- early = none
- late = mass
- metastasis –> hepatomegaly, supraclavicular, rectal shelf, umbilical
Diagnosis of gastric cancer
- indirect –> UGI x ray + CT scan
- UGI endoscopy with biopsy –> optimal
Gastric vascular lesions
- angiodysplasias –> cause of occult GI bleeding
- GAVE = gastric antral vascular ectasia –> dilated venules in gastric antrum
- associated with chronic liver disease –> poral hypertensive gastropathy and gastric varices
Vomiting
- GI causes
Obstruction
- Gastric –> tumor, ulcer, volvulus
- small intestine –> obstruction, ileus
- large intestine –> obstruction, crohn’s, etc
Inflammation –> infection, crohn’s
Motility disorder = gastroparesis –> delayed gastric emptying when no mechanical obstruction
- disordered peristalsis
- diabetes is most common cause –> also autoimmune (scleroderma), post-viral, idiopathic, meds (anti-cholinergics + narcotics)
- diagnosis –> rule out obstruction + gastric emptying test
- treatment –> metoclopramide, erythromycin, gastric pacing
Upper GI bleeding
- symptoms
- causes
Symptoms
- hematemesis
- –> bright red = vomiting blood
- –> coffee grounds = acid/pepsin break down blood
- melena = dark, tarry, foul smelling stool
- hematochezia = red blood per rectum
- occult blood loss = heme + stool, can cause iron deficiency anemia
Causes
- ulcer
- gastritis
- esophagitis
- mallory weiss tear
- GI varices
- vascular malformation
- tumors
- aortoenteric fistula
Evaluation
- Stabilize the patient
- two large bore IVs
- isotonic fluids –> replace lost fluids
- blood products - check labs
- start PPIs
- nasogastric lavage
- urgent endoscopy
- endoscopic therapy –> cautery, hemoclips, epinephrine injection, banding
