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157 Cards in this Set

  • Front
  • Back
define: peptic ulcer disease?
chronic, most often solitary, lesions that occur in any portion of the GIT exposed to the aggressive action of acid-peptic juices
what is the most common location, and next most common location, for PUD to occur?
1) duodenum, first portion; 2) stomach, usually antrum
where will these ulcers occur in setting of GE reflux or Barrett esophagus?
at gastroesophageal junction
where do they occur in patients with Zollinger-Ellison syndrome?
1) duodenum; 2) stomach; 3) jejunum
what procedure can cause them, and where do they occur?
gastrojejunostomy stoma
what is the lifetime likelihood of developing a peptic ulcer for males and females?
10% for males, 4% for females (in USA)
what is the pathogenesis of PUD?
an imbalance between gastroduodenal defence mechanisms, and the damaging forces, particularly gastric acid and pepsin
in what % of duodenal ulcers and stomach ulcers is H. pylori infection present?
virtually all patients with duodenal ulcers, about 70% of those with gastric ulcers
what drugs can increase likelihood of ulcers (2)?
1) aspirin; 2) NSAIDs; 3) corticosteroids
what was said to impair mucosal blood flow and healing?
cigarette smoking
what is Zollinger-Ellison syndrome?
excessive gastrin production by a tumor
what are other risk factors (2)?
1) alcohol; 2) stress
how deep to ulcerations generally extend?
beyond muscularis mucosae, usually into the muscularis propria
what zones are demonstrable in active ulcers (4)?
1) exudate (neutrophils/fibrin); 2) necrosis; 3) granulation tissue; 4) scar
what type of pain do most ulcers cause?
gnawing, burning, or aching pain
when does the pain tend to be worse (2)?
1) at night; 2) 1 to 3 hours after meals during the day
what is the pain classically relieved by?
1) alkalis; 2) food
what is the most frequent complication of PUD?
what complication accounts for 2/3 of ulcer deaths?
what are other complications (2)?
1) penetration into adjacent organ; 2) obstruction from edema or scarring
what are the two forms of IBD (different, but chronic, relapsing inflammatory diseases with common features)?
1) Crohn's disease (CD); 2) ulcerative colitis (UC)
what has higher incidence and prevalence, and what is the trend?
fairly similar, steadily rising
what populations are these diseases most common in (3)?
1) Western developed populations; 2) Jews; 3) whites
what age can it occur in, and what are peak ages of detection (2)?
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
what % of patients have first degree relatives?
what are the etiology and pathogenesis?
what mutation is associated with predisposition?
NOD2 mutation in CD
what is it postulated that IBD results from?
unregulated and exaggerated local immune responses to commensal microbes in the gut, in genetically susceptible individuals
what antibody is only elevated in CD?
ASCA - anti-Saccaromyces servisiae
what other antibody can help distinguish between these diseases, and what % of UC and CD patients have it?
pANCA - 75% in UC, 11% in CD
what is the most important technique in diagnosis of IBD and differential diagnosis between CD and UC?
pathologic examination of tissue
what happens if a distinction cannot be made?
it is called IBD, intermediate type
where can CD occur in the GIT?
any part
where does inflammation occur, and what is seen in the inflamed areas?
transmural inflammation and lymphoid aggregates
what is GIT wall like?
markedly thickened
what may be seen on X-ray, and what does it represent?
string sign - stenosis / obstruction
are areas of involvement continuous or discontinuous?
discontinuous involvement - "skip" lesions
what type of ulcers might be seen (3)?
1) apthous; 2) linear (cobble stone mucosa); 3) fissuring ulcer
how common are granulomas?
<50% on resection specimens
what are two other pathological findings we must know that are common in Crohn's disease?
1) fistula formation; 2) perianal disease
where was metaplasia said to occur?
what happens to muscularis mucosa?
what happens to neurons?
what are clinical manifestations like, and how do they compare to UC?
extremely variable, and generally more subtle than those of UC
besides diarrhea, what are two common symptoms?
fever, abdominal pain
what protein is lost from the blood?
albumin (protein-losing enteropathy)
what types of malabsorption were mentioned to occur (3)?
1) generalized malabsorption; 2) B12 malabsorption; 3) malabsorption of bile salts
what does malabsorption of bile salts lead to?
what are five extraintestinal manifestations?
1) migratory polyarthritis; 2) sacroiliitis; 3) ankylosing spondylitis; 4) erythema nodosum; 5) uveitis
what other disease of the GIT does Crohn's disease increase the incidence of, and how does this compare to UC?
cancer (but considerably less than UC)
what part of the GIT is UC limited to, and what is almost always involved?
limited to the colon, rectum almost always involved
is involvement continuous or discontinuous?
continuous - no "skip" lesions
what is inflammation like?
severe acute and chronic inflammation
what happens to crypts (2)?
1) abscesses; 2) distortion
what other type of lesions occur (2)?
1) broad-based ulcers; 2) pseudopolyps
what layers do crypt abscesses involve?
entire mucosa, and may extend into the submucosa, but not the muscle layer
what are local complications of UC (3)?
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)
what is stool like, and is there pain?
bloody mucoid diarrhea with cramping lower abdominal pain
what may precipitate flare-ups?
emotional or physical stress
what extraintestinal manifestation is there that we must know?
primary sclerosing cholangitis
what are other extraintestinal manifestations (4)?
1) arthritis; 2) uveitis; 3) erythema nodosum; 4) pyoderma gangrenosum
what are the two most important causes of acute gastritis?
1) heavy use of NSAIDs, particularly aspirin; 2) severe stress (trauma, burn, surgery)
what are other causes (list)?
alcohol, heavy smoking, uremia, systemic infection, food poisoning, cancer chemotherapy, irradiation
what three things contribute to the pathogenesis of acute gastritis?
1) mucosal hypoperfusion (shock, sepsis); 2) impairment of local defense; 3) hypersecretion of gastric acid
what can cause impairment of local defense through decreased mucus production (2)?
1) aspirin; 2) steroid
what can cause impaired defense through decreased prostaglandin production?
what can cause hypersecretion of gastric acid?
direct stimulation of vagal nuclei by increased intracranial pressure
what are lesions like, and what is adjacent?
abrupt lesions, with unremarkable adjacent mucosa
what else is absent in early lesions?
inflammatory reaction
what % of patients go to the ICU?
what does severity range from?
asymptomatic to bleeding requiring transfusion
what is the single most important determinant of clinical outcome?
the ability to correct underlying conditions
what is chronic gastritis currently viewed as?
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)
what are the four major classes of chronic gastritis?
1) nonatrophic; 2) atrophic; 3) chemical; 4) miscellaneous
what causes nonatrophic chronic gastritis?
H. pylori
what is H. pylori shaped like, and how does its cell wall stain?
curved, spiral, or S-shaped gram negative organism
what substance does it produce, and what cells does it colonize?
produces urease, and colonizes the mucus-secreting epithelial cells of the stomach (not in the intestinal mucosa)
in what patients is there a 90% infection rate (what area is affected)?
those with chronic gastritis affecting the antrum
what factor do colonization rates increase with?
age (50% infection rate in asymptomatic Americans over 50)
what is the mode of transmission of H. pylori?
not well defined
what disease does H. pylori have a definitive etiologic role for?
MALT lymphoma
what other diseases does H. pylori have a strong causal association with (2)?
1) PUD; 2) gastric carcinoma
what are three noninvasive techniques for diagnosing nonatrophic Helicobacter gastritis?
1) serologic tests for antibodies; 2) urea breath test; 3) stool antigen test (fecal bacterial detection)
what are four invasive diagnostic techniques?
1) rapid urease assay; 2) histology (H&E); 3) culture; 4) bacterial DNA detection by polymerase chain reaction
what is the underlying pathology with Helicobacter gastritis (2)?
1) "active" inflammation; 2) lymphoid follicle formation
what are the types of atrophic chronic gastritis (2)?
1) autoimmune (type A); 2) multifocal (type B)
where does type A (autoimmune) atrophic gastritis occur, and what things occur there (3)?
1) intestinal metaplasia; 2) glandular atrophy; 3) inflammation - these are all confined to the gastric body
what types of antibodies are elevated in the serum?
1) antibodies to parietal cells; 2) antibodies to intrinsic factor
what is type A (autoimmune) atrophic gastritis often associated with?
other autoimmune disorders
what two things does loss of parietal cells result in?
1) hypo or achlorydia; 2) loss of intrinsic factor
what does hypo or achlorydia lead to?
secondary hyperplasia of gastrin-producing G cells and hypergastrinemia
what does loss of intrinsic factor lead to?
failure of absorption of B-12 and pernicious anemia
what does type A (autoimmune) atrophic gastritis carry an increased risk for?
gastric cancer
what things occur in type B (multifocal, environmental) atrophic gastritis (2) and where do they occur?
1) intestinal metaplasia; 2) atrophy - these occur in any part of the stomach, but most commonly in the antrum
what is type B atrophic gatritis caused by, initially?
H. pylori (in conjunction with other unknown factors)
what is gastric acid secretion like in type B (multifocal, environmental) atrophic gastritis?
low or normal
what are gastrin levels like?
how common is pernicious anemia in type B (multifocal, environmental) atrophic gastritis?
does not occur in type B
what is type B atrophic gatritis the most common precursor of?
intestinal type gastric carcinoma
what are two causes of chemical chronic gastirits?
1) NSAIDs; 2) bile reflux
what are causes of miscellaneous chronic gastritis (list)?
eosinophilic, infectious, CD, sarcoidosis, granulomatous
how does stomach cancer rank in the list of most common cancers in the world, and where is it most common?
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
what is the trend in incidence?
steady decline in last six decades
what are common dietary risk factors, mainly for intestinal type carcinoma of the stomach (4)?
1) lack of refrigeration; 2) consumption of preserved, smoked, and salted foods; 3) water contamination with nitrates; 4) lack of fresh fruit and vegetables
what increases the risk for developing gastric carcinoma by five or six fold?
H. pylori
how does this infection initiate events that lead to carcinoma?
causes chronic gastritis
what chain of events leads from chronic gastritis to carcinoma?
chronic gastritis --> atrophy --> intestinal metaplasia --> dysplasia --> carcinoma
do all H. pylori infections increase cancer risk?
no - not all do, and the vast majority of infected patients do not develop cancer
what genetic factors are associated with gastric carcinoma (2)?
1) p53 mutation; 2) E-cadherin germ-linke mutation - also mentioned were allelic losses in various loci, and microsatellite instability
what are other risk factors/precursors to gastric carcinoma (4)?
1) autoimmune atrophic gasritis; 2) previous partial gastrectomy (bile reflux); 2) adenomas; 4) Menetrier disease
what is the most common location of gastric carcinoma, and what % of cases occur in these locations (2)?
1) antrum; 2) pylorus
in what location is cancer occuring with increasing frequency, and what is the frequency in this location?
cardia (proximal gastric cancer): 25% (increasing frequency)
what are the three possible gross appearances of these cancers, and what is the frequency of each?
1) polypoid/fungating (one third); 2) ulcerating (one third); 3) diffusely infiltrative (one tenth)
what else is the diffusely infiltrative type known as?
"linitis plastica" - leather bottle stomach
what do almost all of these look like microscopically?
almost all are adenocarcinomas
what are the two main classifications of gastric carcinoma?
1) intestinal; 2) diffuse
what do the intestinal type, and the diffuse type look like grossly?
intestinal: polypoid/fungating; diffuse: ulcerative, infiltrative
which type is well differentiated, and what does it look like?
intestinal - gland formation
what cells are seen in the diffuse form?
signet ring cells
what type of metaplasia is seen in the intestinal type?
intestinal metaplasia - less frequent in diffuse type
what is the mean age for the intestinal and the diffuse type?
intestinal type: 55; diffuse type: 38
which has a higher prevalence in a certain sex, and which sex is that?
intestinal: predominates in males, 2 to 1
which has a known etiology, and what can be causes (3)?
intestinal: 1) diet; 2) environment; 3) H. pylori - the etiology of the diffuse type is unknown
what is carcinoma of the stomach like clinically early in the course?
generally asymptomatic until late in course
what are some symptoms (list)?
weight loss, abdominal pain, anorexia, nausea, vomiting, GI bleeding (melena, hematemesis), anemia
where does stomach carcinoma generally metastasize?
to local or distant lymph nodes, and to distant organs
what distant organs are sites for metastasis (3)?
1) liver; 2) lungs; 3) ovaries
where does it invade locally (3)?
1) duodenum; 2) pancreas; 3) retroperitoneum
what is it called when stomach carcinoma metastasizes to the ovaries?
Krukenberg tumor
what does prognosis depend primarily on?
staging - depth of invasion and extent of nodal and distant metastasis
what is the five year survival rate for advanced gastric carcinoma?
what is early cancer limited to, regardless of nodal status?
mucosa and submucosa
what % of newly diagnosed cancers does early stomach cancer account for in the United States?
10-15% (35% in Japan)
what is the 5 year survival rate if diagnosed early?