Path Exam III - GI

Esophageal Achalasia presents as
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Terms in this set (49)
**Barrier effectiveness of tonically contracted lower esophageal sphincter can be altered by loss of lower esophageal sphincter tone;
- Increased frequency of transient relaxations of lower sphincter (response to ^gastric distention)
- Loss of secondary peristalsis after a transient
- Increased stomach volume or pressure
- Increased production of acid
Cause of Acid-Peptic DiseaseH pylori,Corrosive agents (acid and pepsin)H. pylori infection in acid peptic disease leads toinflammation, ↓ mucosal defenses and ↑ acid production, toxins producedGastric Ulcers-Penetrate the mucosa -Area of intact but inflammed mucosa surrounds ulcer -Occur on the lesser curvature of stomach -Motility defects -NSAID's, smoking, stress, H. pyloriMotility defects in gastric ulcers are due to1) reflux due to incompetent pyloric sphincter. 2) delayed emptying of gastric contents 3) delayed gastric emptying hence food retentionAcute Erosive Gastritis-inflammation resulting from superficial mucosal injury, mucosal erosion, or shallow ulcers caused by alcohol, drugs, and stress (commonly) -ETOH usually causes gastritis but can cause a gastric ulcerChronic Atrophic Gastritis-inflammatory cell infiltration with gastric mucosal atrophy and loss of glands -capacity to secrete gastric acid is progressively reduced, and the serum levels of gastrin are elevated -Autoantibodies to parietal cells, intrinsic factor, and gastrin are common findings -Associated w/H. pyloriDuodenal Ulcer-consequence of H pylori infection -Excessive acid secretion plays a secondary role -Various other risk factors, including diet, smoking, and excessive alcohol consumption -Genetic factors also play a role -StressClinical Manifestations of ulcers**Acute or chronic GI bleeding (↓ Hct) **Acute massive hemorrhage (> 10% of blood volume over minutes to hours) is manifested by - hypotension - tachycardia - orthostatic blood pressure and heart rate changes on standing (dizziness) **Life-threatening perforation and obstructionGastroparesis presents as-development of bezoars from retained gastric contents -bacterial overgrowth -erratic blood glucose control - nausea/vomit-->weight loss,bloating, either constipation or diarrheaGastoparesis caused by-Poorly controlled Diabetes mellitus -alterations in a number of normal gastric functionsCholelithiasis presents as- mild nausea or abdominal discomfort after fatty or fried foods - RUQ or epigastric pain - jaundice -Loss of muscular wall motility -Excessive sphincteric contractions (impaired emptying)Cholelithiasis risk factors-Female in her 40's -HX of high fat intake -Prior pregnanciesCholelithiasis forms by*if Patients w/chronic hemolytic disease--> bilirubin stones may form *May have large individual stones, many small stones or sludge *stones are composed of cholesterol w/wo calciumCholelithiasis can cause-Cholecystitis (acute or chronic) -Can progress to pancreatitis -Gallbladder can become infected or undergo infarction and necrosis ->systemic sepsisDiarrhea- stools that are excessive in volume, frequency, or liquidity - acute (infections) or chronic - SE of medicationssecretory diarrheasecretagogues maintain elevated rates of fluid transport out of epithelial cells into the GI tract lumenosmotic diarrheamalabsorbed nutrients or poorly absorbed electrolytes that retain water in the lumenmalabsorbtive diarrheathe ability to digest or absorb a particular nutrient is defective and can be due to disordered mixing (altered motility), pancreatic insufficiency (altered digestion), or damage to enterocytes or their surface transporters (altered absorption).Diarrhea can cause-Dehydration -Malnutrition -Weight loss -Vitamin deficiencies (glossitis, cheilosis, stomatitis)Viral gastroenteritis (young children) is associated witha high mortality rate from dehydration from diarrhea when supportive measures are not promptly provided.Some individuals with diarrhea from parasitic infections remainasymoptomatic (mostly)Inflammatory Bowel Disease described as- recurrent episodes of mucopurulent, bloody diarrhea characterized by lack of positive cultures for infectious organisms - characterized by exacerbations and remissions2 chronic IB diseases areChrohns& ulcerative colitisChrohnsis transmural and granulomatous, -OCCURS distal ileum or the colon, although any region of the GI tract from mouth to anus can be involved, generally in a discontinuous fashion - characterized by ulceration and inflammation involving the entire thickness of the bowel wall -Chronic Inflammatory Bowel DiseaseUlcerative colitissuperficial and limited to the colonic mucosa. -Chronic Inflammatory Bowel DiseaseChrohns causes- microorganisms (bacteria and viruses), dietary factors, genetic factors, defective immune responses, and psychosocial factorsUlcerative colitis causes- infections, allergies to dietary components, immune responses to bacteria and self-antigens, and psychosocial factorsCommon feature to all forms of inflammatory bowel disease ismucosal ulceration and inflammation of the GI tractDiff in ulcerative colitis vs crohnsUC: Higher rectal bleeding, less diarrhea, ALL will have rectal involvement, Extent ismucosal, continuous, colon & rectum CRNS: Most have rectal bleeding, More have diarrhea, <50% have rectal involvement, Extent: transmural, non continuous, mouth to anus **TAKEAWAY:UC IS CONTINUOUS AND CHNS IS NOT!!!Chrohns disease will present as- "cobblestone" appearance - Perforation, fistula formation, abscess formation, and small intestinal obstruction are frequent complications -Can involve adjacent mesentery and lymph nodes -Migratory arthritis -Inflammatory disorders of the skin, eye, and mucous membranes, particularly aphthous ulcers of the buccal mucosa -Nephrolithiasis (1/3rd) -Amyloidosis -Thromboembolic disease -Patient's are often malnourished and show evidence of deficiency statesUlcerative colitis- inflammation in ulcerative colitis is restricted to the mucosa of the colon and rectum - bloody diarrhea and malabsorption - because ulcerative colitis generally is limited to the mucosa, obstruction, perforation, and fistula formation are not typical complications. - Toxic megacolonDiverticular Disease presents as- 80% of Pt's are asymptomatic except for chronic constipation - intermittent and unpredictable griping lower abdominal painCauses of diverticular disease-mucosa and submucosa herniate through the underlying muscularis -Increases with age, starting from about 40 years. -Epidemiologic studies suggest that the consumption of highly refined foods and less fiberA. Diverticulosis pathology- sigmoid colon affected 95% of time - abnormalities in colonic wall connective tissue - connective tissue diseases (Ehlers-Danlos & Marfan's Syndrome)Functional abnormality of divertiulosis- chronic constipation and the development of a transmural pressure gradient from colonic lumen to peritoneal space as a result of vigorous muscle contraction of the colonic wallDiverticulosis decreased dietary fiber makes...Change in dietary habits; decreased dietary fiber makes forward propulsion of feces at normal transmural pressures more difficult -Pain may last hours to days, with sudden relief on passing flatus or feces -Pain meds (opioids) is contraindicatedDiverticular Bleeding is the most common cause ofmost common cause of massive lower GI bleeding in the elderly - bleeding is typically painless -colonic intramural arteries occasionally rupture and bleeding.Diverticulitis is most common complication isa focal area of inflammation response to irritation by fecal material - Symptoms of abdominal pain and fever with a risk of progression to abscess with or without perforation - Perforations usually are self-contained, but the potential for subsequent fistula formation and intestinal obstruction is highIrritable Bowel Syndrome-Altered bowel habits with abdominal pain in the absence of any detectable organic pathological process or specific motility or structural abnormalities -Alternating between diarrhea and constipation -Abdominal pain -Bloating or perceived abdominal distension -Occur during or after a stressful event