Path 3 Pub/ibd/stomach

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PUB/IBD/STOMACH - LEE - WEDNESDAY FEB 14

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PEPTIC ULCER DISEASE

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define: peptic ulcer disease?

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chronic, most often solitary, lesions that occur in any portion of the GIT exposed to the aggressive action of acid-peptic juices

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what is the most common location, and next most common location, for PUD to occur?

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1) duodenum, first portion; 2) stomach, usually antrum

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where will these ulcers occur in setting of GE reflux or Barrett esophagus?

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at gastroesophageal junction

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where do they occur in patients with Zollinger-Ellison syndrome?

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1) duodenum; 2) stomach; 3) jejunum

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what procedure can cause them, and where do they occur?

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gastrojejunostomy stoma

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what is the lifetime likelihood of developing a peptic ulcer for males and females?

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10% for males, 4% for females (in USA)

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what is the pathogenesis of PUD?

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an imbalance between gastroduodenal defence mechanisms, and the damaging forces, particularly gastric acid and pepsin

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in what % of duodenal ulcers and stomach ulcers is H. pylori infection present?

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virtually all patients with duodenal ulcers, about 70% of those with gastric ulcers

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what drugs can increase likelihood of ulcers (2)?

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1) aspirin; 2) NSAIDs; 3) corticosteroids

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what was said to impair mucosal blood flow and healing?

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cigarette smoking

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what is Zollinger-Ellison syndrome?

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excessive gastrin production by a tumor

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what are other risk factors (2)?

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1) alcohol; 2) stress

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how deep to ulcerations generally extend?

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beyond muscularis mucosae, usually into the muscularis propria

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what zones are demonstrable in active ulcers (4)?

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1) exudate (neutrophils/fibrin); 2) necrosis; 3) granulation tissue; 4) scar

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what type of pain do most ulcers cause?

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gnawing, burning, or aching pain

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when does the pain tend to be worse (2)?

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1) at night; 2) 1 to 3 hours after meals during the day

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what is the pain classically relieved by?

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1) alkalis; 2) food

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what is the most frequent complication of PUD?

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bleeding

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what complication accounts for 2/3 of ulcer deaths?

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perforation

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what are other complications (2)?

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1) penetration into adjacent organ; 2) obstruction from edema or scarring

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IDIOPATHIC INFLAMMATORY BOWEL DISEASE (IBD)

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what are the two forms of IBD (different, but chronic, relapsing inflammatory diseases with common features)?

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1) Crohn's disease (CD); 2) ulcerative colitis (UC)

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what has higher incidence and prevalence, and what is the trend?

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fairly similar, steadily rising

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what populations are these diseases most common in (3)?

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1) Western developed populations; 2) Jews; 3) whites

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what age can it occur in, and what are peak ages of detection (2)?

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can occur at any age, but peak ages of detection are second and third decades of life, with a minor peak in the sixth and seventh decades

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what % of patients have first degree relatives?

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15%

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what are the etiology and pathogenesis?

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unknown

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what mutation is associated with predisposition?

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NOD2 mutation in CD

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what is it postulated that IBD results from?

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unregulated and exaggerated local immune responses to commensal microbes in the gut, in genetically susceptible individuals

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what antibody is only elevated in CD?

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ASCA - anti-Saccaromyces servisiae

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what other antibody can help distinguish between these diseases, and what % of UC and CD patients have it?

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pANCA - 75% in UC, 11% in CD

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what is the most important technique in diagnosis of IBD and differential diagnosis between CD and UC?

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pathologic examination of tissue

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what happens if a distinction cannot be made?

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it is called IBD, intermediate type

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CROHN'S DISEASE

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where can CD occur in the GIT?

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any part

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where does inflammation occur, and what is seen in the inflamed areas?

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transmural inflammation and lymphoid aggregates

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what is GIT wall like?

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markedly thickened

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what may be seen on X-ray, and what does it represent?

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string sign - stenosis / obstruction

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are areas of involvement continuous or discontinuous?

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discontinuous involvement - "skip" lesions

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what type of ulcers might be seen (3)?

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1) apthous; 2) linear (cobble stone mucosa); 3) fissuring ulcer

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how common are granulomas?

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<50% on resection specimens

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what are two other pathological findings we must know that are common in Crohn's disease?

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1) fistula formation; 2) perianal disease

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where was metaplasia said to occur?

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pylorus

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what happens to muscularis mucosa?

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thickened

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what happens to neurons?

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hyperplasia

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what are clinical manifestations like, and how do they compare to UC?

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extremely variable, and generally more subtle than those of UC

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besides diarrhea, what are two common symptoms?

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fever, abdominal pain

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what protein is lost from the blood?

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albumin (protein-losing enteropathy)

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what types of malabsorption were mentioned to occur (3)?

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1) generalized malabsorption; 2) B12 malabsorption; 3) malabsorption of bile salts

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what does malabsorption of bile salts lead to?

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steatorrhea

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what are five extraintestinal manifestations?

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1) migratory polyarthritis; 2) sacroiliitis; 3) ankylosing spondylitis; 4) erythema nodosum; 5) uveitis

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what other disease of the GIT does Crohn's disease increase the incidence of, and how does this compare to UC?

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cancer (but considerably less than UC)

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ULCERATIVE COLITIS

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what part of the GIT is UC limited to, and what is almost always involved?

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limited to the colon, rectum almost always involved

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is involvement continuous or discontinuous?

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continuous - no "skip" lesions

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what is inflammation like?

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severe acute and chronic inflammation

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what happens to crypts (2)?

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1) abscesses; 2) distortion

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what other type of lesions occur (2)?

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1) broad-based ulcers; 2) pseudopolyps

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what layers do crypt abscesses involve?

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entire mucosa, and may extend into the submucosa, but not the muscle layer

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what are local complications of UC (3)?

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1) perforation; 2) toxic megacolon; 3) colon cancer (people with long-standing, extensive disease have a higher risk of colon cancer than the general population)

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what is stool like, and is there pain?

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bloody mucoid diarrhea with cramping lower abdominal pain

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what may precipitate flare-ups?

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emotional or physical stress

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what extraintestinal manifestation is there that we must know?

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primary sclerosing cholangitis

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what are other extraintestinal manifestations (4)?

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1) arthritis; 2) uveitis; 3) erythema nodosum; 4) pyoderma gangrenosum

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ACUTE GASTRITIS / GASTRIC EROSIONS

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what are the two most important causes of acute gastritis?

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1) heavy use of NSAIDs, particularly aspirin; 2) severe stress (trauma, burn, surgery)

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what are other causes (list)?

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alcohol, heavy smoking, uremia, systemic infection, food poisoning, cancer chemotherapy, irradiation

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what three things contribute to the pathogenesis of acute gastritis?

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1) mucosal hypoperfusion (shock, sepsis); 2) impairment of local defense; 3) hypersecretion of gastric acid

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what can cause impairment of local defense through decreased mucus production (2)?

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1) aspirin; 2) steroid

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what can cause impaired defense through decreased prostaglandin production?

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NSAIDs

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what can cause hypersecretion of gastric acid?

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direct stimulation of vagal nuclei by increased intracranial pressure

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what are lesions like, and what is adjacent?

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abrupt lesions, with unremarkable adjacent mucosa

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what else is absent in early lesions?

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inflammatory reaction

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what % of patients go to the ICU?

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5-10%

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what does severity range from?

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asymptomatic to bleeding requiring transfusion

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what is the single most important determinant of clinical outcome?

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the ability to correct underlying conditions

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CHRONIC GASTRITIS

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what is chronic gastritis currently viewed as?

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a histologic abnormality shared by a number of different diseases, each producing mucosal inflammation by a different etiology or mechanism (a histologic rather than a clinical entity)

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what are the four major classes of chronic gastritis?

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1) nonatrophic; 2) atrophic; 3) chemical; 4) miscellaneous

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what causes nonatrophic chronic gastritis?

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H. pylori

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what is H. pylori shaped like, and how does its cell wall stain?

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curved, spiral, or S-shaped gram negative organism

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what substance does it produce, and what cells does it colonize?

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produces urease, and colonizes the mucus-secreting epithelial cells of the stomach (not in the intestinal mucosa)

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in what patients is there a 90% infection rate (what area is affected)?

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those with chronic gastritis affecting the antrum

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what factor do colonization rates increase with?

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age (50% infection rate in asymptomatic Americans over 50)

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what is the mode of transmission of H. pylori?

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not well defined

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what disease does H. pylori have a definitive etiologic role for?

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MALT lymphoma

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what other diseases does H. pylori have a strong causal association with (2)?

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1) PUD; 2) gastric carcinoma

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what are three noninvasive techniques for diagnosing nonatrophic Helicobacter gastritis?

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1) serologic tests for antibodies; 2) urea breath test; 3) stool antigen test (fecal bacterial detection)

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what are four invasive diagnostic techniques?

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1) rapid urease assay; 2) histology (H&E); 3) culture; 4) bacterial DNA detection by polymerase chain reaction

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what is the underlying pathology with Helicobacter gastritis (2)?

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1) "active" inflammation; 2) lymphoid follicle formation

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what are the types of atrophic chronic gastritis (2)?

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1) autoimmune (type A); 2) multifocal (type B)

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where does type A (autoimmune) atrophic gastritis occur, and what things occur there (3)?

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1) intestinal metaplasia; 2) glandular atrophy; 3) inflammation - these are all confined to the gastric body

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what types of antibodies are elevated in the serum?

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1) antibodies to parietal cells; 2) antibodies to intrinsic factor

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what is type A (autoimmune) atrophic gastritis often associated with?

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other autoimmune disorders

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what two things does loss of parietal cells result in?

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1) hypo or achlorydia; 2) loss of intrinsic factor

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what does hypo or achlorydia lead to?

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secondary hyperplasia of gastrin-producing G cells and hypergastrinemia

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what does loss of intrinsic factor lead to?

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failure of absorption of B-12 and pernicious anemia

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what does type A (autoimmune) atrophic gastritis carry an increased risk for?

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gastric cancer

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what things occur in type B (multifocal, environmental) atrophic gastritis (2) and where do they occur?

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1) intestinal metaplasia; 2) atrophy - these occur in any part of the stomach, but most commonly in the antrum

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what is type B atrophic gatritis caused by, initially?

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H. pylori (in conjunction with other unknown factors)

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what is gastric acid secretion like in type B (multifocal, environmental) atrophic gastritis?

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low or normal

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what are gastrin levels like?

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normal

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how common is pernicious anemia in type B (multifocal, environmental) atrophic gastritis?

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does not occur in type B

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what is type B atrophic gatritis the most common precursor of?

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intestinal type gastric carcinoma

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what are two causes of chemical chronic gastirits?

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1) NSAIDs; 2) bile reflux

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what are causes of miscellaneous chronic gastritis (list)?

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eosinophilic, infectious, CD, sarcoidosis, granulomatous

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CARCINOMA OF THE STOMACH

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how does stomach cancer rank in the list of most common cancers in the world, and where is it most common?

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second most common cancer in the world - 60% of them occur in developing countries - very common in Eastern Asia, South and Central America, and Eastern Europe

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what is the trend in incidence?

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steady decline in last six decades

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what are common dietary risk factors, mainly for intestinal type carcinoma of the stomach (4)?

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1) lack of refrigeration; 2) consumption of preserved, smoked, and salted foods; 3) water contamination with nitrates; 4) lack of fresh fruit and vegetables

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what increases the risk for developing gastric carcinoma by five or six fold?

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H. pylori

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how does this infection initiate events that lead to carcinoma?

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causes chronic gastritis

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what chain of events leads from chronic gastritis to carcinoma?

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chronic gastritis --> atrophy --> intestinal metaplasia --> dysplasia --> carcinoma

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do all H. pylori infections increase cancer risk?

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no - not all do, and the vast majority of infected patients do not develop cancer

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what genetic factors are associated with gastric carcinoma (2)?

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1) p53 mutation; 2) E-cadherin germ-linke mutation - also mentioned were allelic losses in various loci, and microsatellite instability

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what are other risk factors/precursors to gastric carcinoma (4)?

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1) autoimmune atrophic gasritis; 2) previous partial gastrectomy (bile reflux); 2) adenomas; 4) Menetrier disease

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what is the most common location of gastric carcinoma, and what % of cases occur in these locations (2)?

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1) antrum; 2) pylorus

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in what location is cancer occuring with increasing frequency, and what is the frequency in this location?

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cardia (proximal gastric cancer): 25% (increasing frequency)

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what are the three possible gross appearances of these cancers, and what is the frequency of each?

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1) polypoid/fungating (one third); 2) ulcerating (one third); 3) diffusely infiltrative (one tenth)

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what else is the diffusely infiltrative type known as?

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"linitis plastica" - leather bottle stomach

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what do almost all of these look like microscopically?

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almost all are adenocarcinomas

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what are the two main classifications of gastric carcinoma?

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1) intestinal; 2) diffuse

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what do the intestinal type, and the diffuse type look like grossly?

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intestinal: polypoid/fungating; diffuse: ulcerative, infiltrative

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which type is well differentiated, and what does it look like?

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intestinal - gland formation

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what cells are seen in the diffuse form?

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signet ring cells

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what type of metaplasia is seen in the intestinal type?

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intestinal metaplasia - less frequent in diffuse type

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what is the mean age for the intestinal and the diffuse type?

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intestinal type: 55; diffuse type: 38

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which has a higher prevalence in a certain sex, and which sex is that?

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intestinal: predominates in males, 2 to 1

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which has a known etiology, and what can be causes (3)?

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intestinal: 1) diet; 2) environment; 3) H. pylori - the etiology of the diffuse type is unknown

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what is carcinoma of the stomach like clinically early in the course?

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generally asymptomatic until late in course

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what are some symptoms (list)?

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weight loss, abdominal pain, anorexia, nausea, vomiting, GI bleeding (melena, hematemesis), anemia

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where does stomach carcinoma generally metastasize?

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to local or distant lymph nodes, and to distant organs

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what distant organs are sites for metastasis (3)?

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1) liver; 2) lungs; 3) ovaries

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where does it invade locally (3)?

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1) duodenum; 2) pancreas; 3) retroperitoneum

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what is it called when stomach carcinoma metastasizes to the ovaries?

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Krukenberg tumor

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what does prognosis depend primarily on?

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staging - depth of invasion and extent of nodal and distant metastasis

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what is the five year survival rate for advanced gastric carcinoma?

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<15%

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what is early cancer limited to, regardless of nodal status?

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mucosa and submucosa

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what % of newly diagnosed cancers does early stomach cancer account for in the United States?

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10-15% (35% in Japan)

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what is the 5 year survival rate if diagnosed early?

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90-95%