Pathology Exam 2: Lecture 1 GI Tract – Flashcards

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What area of the GI tract? 2 answer. Mouth, esophagus, stomach, duodenum, (jejunum) (Ileum), appendix, colon, rectum, anus
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Upper gastro-intestinal tract = UGI Lower gastro-intestinal tract = LGI
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Enteric , entero-, enteral = intestinal, GI tract -_______ feedings = using the GI tract -________ feedings = IV, not using the GI tract
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Enteral Parenteral
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*Three answers:* Mouth to duodenum Small bowel to colon Colon to anus
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Foregut Midgut Hindgut
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Contraction of _______ muscle -> bowel constricts Contraction of __________ muscle -> bowel shortens Together they produce Peristalsis.
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Circular Longitudinal
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Rhythmic contraction and relaxation of GI tract muscle propels food and liquid through from mouth to anus. When ________ in small bowel or colon STOPS or DECREASES, patient has an ____. When peristalsis INCREASES, patient has _____.
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Peristalsis, ileus, diarrhea
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Without ________, (or without forward motion due to obstruction), juices and air separate.The air can now be seen, In small bowel on radiographs.
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Peristalsis
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What creates an emulsion, and forward movement through GI tract?
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Peristalsis
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Obstructed structure becomes dilated proximally (before the obstruction), and empty (narrow) distally. Typically causes intermittent cramping pain... -rather than continuous pain. -due to continued peristalsis against an obstruction. What will happen to the following? -Esophageal obstruction -> ________ _______ -Small bowel obstruction -> ______ -Colon obstruction -> _________________
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Difficulty Swallowing Vomiting Fewer Bowel Movements
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Ileus means what?
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Lack of peristalsis
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Lack of forward movement through small bowel allows proliferation of whatever bacteria are present. Once the ileus or obstruction has passed, and forward movement resumes, the patient often has _______... -due to accumulation of unabsorbed intestinal juices. -due to proliferation of bacteria. So at first the patient with either ileus or obstruction was not having bowel movements. Now that the ileus or obstruction has passed.
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Diarrhea
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*GI tract sphincters:* -LES too loose -> _____ -LES too "tight" (does not relax) -> ______ -Infant pylorus too large (hypertrophic pyloric stenosis)->_____________________ -Lack of pylorus (after surgery) -> "_______" -Anal sphincter too loose -? _________ of stool
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-GERD -Achalasia -Gastric Outlet -"Dumping" -Incontinence
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What closes *cystic duct* before it joins common hepatic duct? They join to form the common bile duct (CBD).
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Spiral fold (valve of Heister)
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Embryologically, biliary tree and pancreas bud off from _______. ______ starts as dorsal and ventral sections, which later fuse.
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Duodenum Pancrease
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What is an abnormal communication between structures?
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GI tract Fistulas
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Type of GI tract Fistulas (3 answers). Often presents as intestinal contents coming out of incision or drain site Can be due to colon cancer or diverticulitis, and often presents as recurrent urinary tract infection(UTI). Can result from trauma, surgery, or severe pancreatitis.
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Entero-cutaneous fistula (entero = intestine cutaneous = skin) Colo-vesicle fistula (colo = colon vesicle = urinary bladder) Pancreatic Fistula
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What are four GI developmental Abnormalities?
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-Tracheo-esophageal (TE) fistula -Intestinal atresia/stenosis -Meckel's diverticulum -Malrotation
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What GI developmental abnormalities? Two answers: -Communication between trachea and esophagus -Neonate does not feed well Abnormal blood supply Complete blockage due to malformation -Small bowel - newborn vomits bile -Imperforate anus
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*Tracheo-esophageal fistula* *Intestinal Atresia / stenosis*
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What GI developmental abnormalities? Two answers: -Out-pouching of small bowel -Can contain gastric mucosa or pancreatic tissue -Appendix does not reside in RLQ -Can result in duodenal obstruction or small bowel volvulus
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*Meckel's Diverticulum* *Malrotation*
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2% of the population Within 2 feet of the ileocecal valve 2 types of ectopic mucosa in 73%* -Pancreatic tissue -Gastric tissue --Can bleed or perforate Common complication in adults -bleeding; in kids - obstruction. Risk for complications: age 2cm, abnormal histology
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Meckel's Diverticulum: "Rule of 2s"
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What type of *Hiatal Hernia* (Herniation of stomach up through diaphragmatic hiatus)? -Stomach "slides" up through an enlarged hiatus (opening in the diaphragm). EG junction is now in the chest. -Most common type; can be associated with reflux
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*Axial ("Sliding")* hiatal hernia
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What type of *Hiatal Hernia* (Herniation of stomach up through diaphragmatic hiatus)? Stomach "rolls" up next to esophagus. EG junction still in abdomen. -Might get trapped and become a surgical emergency due to squeezing of blood supply
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*Non-axial ("para-esophageal")* hiatal hernia
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*Incidence:* -Mostly Western adults; 0.5% of US *Pathogenesis:* -*Low esophageal sphincter pressure* allows stomach contents to reflux up into esophagus. -Mucosa becomes inflamed from irritating acid, bile, and pepsin, thickens -; *esophagitis* *Clinical Characteristics:* -Recurrent heartburn is dominant symptom. -Sometimes accompanied by regurgitation of sour brash into mouth
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*Gastroesophageal reflux disease (GERD)*
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*Pathogenesis:* -Normal squamous epithelium of lower esophagus converts to columnar glandular epithelium. --This is *metaplasia.* Metaplasia may be patchy or cover entire surface. -Biopsy reveals mainly columnar epithelial cells, not normal squamous mucosa. -This can progress to become adenocarcinoma.
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*Barrett's Esophagitis*
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*Clinical Characteristics:* -Patients typically also smoke and drink EtOH -Can resolve if reflux is resolved -Can progress to malignancy if left untreated
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*Barrett's Esophagitis*
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"Failure to relax" Incomplete relaxation of lower esophageal sphincter (LES) in response to swallowing Becomes a functional obstruction -Esophagus does not completely empty. -Esophagus becomes dilated over time.
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*Achalasia*
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*Pathogenesis:* 3 abnormalities -Aperistalsis - lack of orderly peristalsis -Partial or incomplete relaxation of LES -*Increased LES pressure* Uncertain etiology In Latin America, commonly caused by Trypanosoma cruzi - known as Chagas Disease
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*Achalasia*
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Incidence - 1 / 100,000 -Male : female equal; 25 - 60 y/o * -Symptoms ~ 4 yrs before diagnosis -Cause unknown - inflammatory? --Decrease in inhibitory neurons -> LES (lower esophageal sphincter) fails to relax --Decreased (or abnormal) peristalsis -Dysphagia for solids AND liquids -Atypical chest pain (not like MI) -Regurgitation of undigested food --It doesn't reach the stomach. -Recurrent aspiration, lung infection -Weight loss
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Achalasia
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What disease in southern South America, achalasia can be associated with Trypanosoma cruzi, a protozoan from feces of bug. Can affect esophagus or colon. Heart is involved more often than GI tract.
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Chagas disease*
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-More common in Asia, where they screen for it by doing EGD. In Western society, we screen for what GI tract cancer? -Two primary types: ________ ____ and adenocarcinoma -________ __________ is precursor for adenocarcinoma.
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*Esophageal Carcinoma,* Colon Cancer, Squamous cell, Adenocarcinoma is a precursor for adenocarcinoma,
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*Clinical Characteristics:* in Western society, usually older patient -Dysphagia (but by then the tumor might be unresectable) -; weight loss -Metastasis to the liver is very common. -Prognosis is poor.
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*Esophageal Carcinoma*
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++-Pouch or sac created by herniation of the lining mucous membrane through a defect in muscular coat (pseudo-diverticuum) *Three primary types:* 1. ______- upper esophagus in ; 60 y/o; most common 2. ______ - midportion of esophagus; older patients; pulled out by inflamed or enlarged mediastinal nodes 3. _______ - immediately above the diaphragm, in those with esophageal motility disorder
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*Esophageal Diverticulum* -*Zenker -Traction -Epiphrenic*
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-Shallow longitudinal tear in esophageal mucosa near EG junction -Seen in alcoholics (or others) after severe retching or vomiting -Most bleeding is self-limited (stops by itself). -Account for 5% - 10% of upper GI bleeding cases
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*Mallory-Weiss tear*
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*Incidence:* -Most commonly caused by aspirin, other NSAIDS -Hyper-secretion of acid and *physiologic stress increase risk* *Pathogenesis:* -Focal patchy necrosis of gastric mucosa -Any serious injury or other physiologic stress makes gastric mucosa more vulnerable to erosion. *Clinical Characteristics:* -Vague epigastric pain, might vomit blood-tinged matter or might have obvious upper GI bleeding.
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Acute Erosive Gastritis
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*Pathogenesis:* -Patient develops antibodies to gastric parietal cells, with decreased production of intrinsic factor (IF). -Decreased IF inhibits absorption of B12 --Therefore might result in *pernicious anemia* ----Megaloblastic RBC ----*Neuro symptoms - numbness in legs, etc* -Can result in achlorhydria (absence of hydrochloric acid in stomach)
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Auto-immune Gastritis
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Pathogenesis: -Chronic infection of gastric mucosa by a microorganism. -By age 60, half the population shows a positive antibody titer to Helicobacter pylori. -The *most common* cause of non-erosive gastritis -Also a common cause of peptic ulcer disease (PUD) *Clinical Characteristics:* -Many are asymptomatic. -Should be ruled out when patient is unresponsive to therapy for presumed GERD or peptic ulcers
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*H. Pylori gastritis*
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Urea breath test - *enzyme produced by H. pylori (urease) converts urea to ammonia and CO2.* Exhaled CO2 is measured before and after patient swallows a compound containing urea made from an isotope of carbon. If the isotope is detected in CO2 on exhalation, then the patient has H. pylori.
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*H. Pylori gastritis*
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*Incidence:* -Smokers have predisposition -Increased risk if parents have it -Often associated with H. pylori infection -High stress lifestyle does not appear to contribute.
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*Peptic Ulcer Disease (PUD)* (Gastric or duodenal ulcer)
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*Pathogenesis:* Disruption of mucosa of stomach and / or proximal duodenum caused by gastric secretions -Results in focal loss of mucosa -Might result in shallow to deep erosive ulcers -*______* ulcer can erode through the wall -; perforation gastric secretions in peritoneum -; chemical peritonitis -*_______ duodenal ulcers* can penetrate an artery -; results in hemorrhage into lumen -; UGI or LGI bleeding
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*Peptic Ulcer Disease (PUD)* (Gastric or duodenal ulcer), *Anterior, Posterior*
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What are three presentations of Peptic Ulcer Disease?
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-*Pain -Bleeding -Perforation*
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What presentation of Peptic Ulcer Disease? Three answers. Erodes into blood vessel, discovered before it is deep enough to perforate -slight bleeding -; occult blood in stool -heavy bleeding -; vomiting blood, or blood in stool (melena or hematochezia) Minimal bleeding; no perforation Erodes deeper; no blood vessel between ulcer and outer wall, therefore no major bleeding
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*Bleeding* *Pain* *Perforation*
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*Clinical Characteristics:* _____________ Burning epigastric or RUQ pain ----1-3 h after eating, or patient wakes at night with pain. ----Typically relieved by meals or antacids -Might note dark stools (digested blood), or have occult blood in stool -Many are positive for H. pylori, but many with H. pylori don't have PUD. -50% of patients will get relief from antacids / antibiotics.
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*Non-Emergency*
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*Clinical Characteristics:* ________ -UGI or LGI bleeding - often from posterior ulcer -Perforation - often from *anterior* ulcer -; peritonitis --Causes peritonitis, not bleeding.
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*Emergency*
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10 times more likely in patients with pernicious anemia *________:* -Tumor of smooth muscle of muscularis layer *_______ ____:* -Arise from gastric epithelium --Generally hyperplastic or adenomatous ----Adenomatous polyps are pre-cancerous. ----Gastric polyps warrant further search for cancer. *Endoscopy plus biopsy of the polyp*
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*Benign* Neoplasms of the stomach *Leiomyoma* *Epithelial polyps*
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*Incidence:* -Peaks at older age - many have H. pylori -Most common in Asian population (younger age than Westerners) -Diet - smoked meats, pickled foods increase risk ----Smoking and EtOH also contribute *Pathogenesis:* -95% are _____________ and are most common in distal stomach. ----When gastric ulcer is seen, it is biopsied to r/o cancer. ----No so with duodenal ulcer -Nitrosamines (common in many foods) contribute to development of stomach cancer (Vitamin C inhibits this?)
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*Malignant* Neoplasms of the stomach, Adenocarcinoma
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*Clinical Characteristics:* -Might be discovered as gastric ulcer -Early satiety = feeling of fullness after eating only a little -Might have occult blood in stool due to mild bleeding -Tends to metastasize to liver, lung, and brain
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Malignant Neoplasms of the stomach
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What are three main causes of diarrhea?
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-Infectious (bacterial, viral) -Inflammatory bowel disease (Crohn's disease, Ulcerative colitis) -Malabsorption (Latose intolerance, Different types of sprue)
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*Pathogenesis:* -Chronic granulomatous *inflammation of entire bowel wall (transmural)* -Mostly involves ileum and cecum, but can involve any part of GI tract from mouth to anus *-Inflammation is PATCHY, with normal mucosa between patches (called "skip lesions".)* -Edema and fibrosis can later result in bowel obstruction.
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Inflammatory Bowel Disease - *Crohn's Disease*
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*Clinical Characteristics:* -Abdominal pain, bloody diarrhea, anemia, fever -No cure, but suppression is possible with anti-inflammatory drugs. -Often requires surgery to remove involved areas
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Inflammatory Bowel Disease - *Crohn's Disease*
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*Pathogenesis:* -Most often affects rectum and colon -Inflammation involves *colonic mucosa (NOT transmural).* *Clinical Characteristics:* Symptoms are intermittent, with bouts of diarrhea, rectal bleeding, and abdominal pain. -~ 70% have recurrent episodes. -10% have single episode that heals spontaneously. -20% have fulminant course resistant to medical treatment. --Can lead to life threatening hemorrhage (not common) --Colectomy is the only treatment for these severe cases. -Extra-colonic (outside the colon) manifestations
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Inflammatory Bowel Disease - *Ulcerative Colitis*
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What illness? -Develop where vessels perforate the bowel wall. -Intra-colonic pressure pushes mucosa out through the places where vessels perforate. -These dont include all layers of bowel wall, so they are actually *pseudo-diverticula.* -Possibly related to lack of dietary fiber. -Eat your vegetables.
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Diverticulosis
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*Incidence:* common in industrialized nations. -Unusual in nations with high fiber diets -Mostly in ______ _____; in Asians often in ____ ____ *Pathogenesis:* -Smooth muscle must work harder to propel low-fiber fecal material forward. --This increased pressure contributes to herniation of mucosa through the muscle. --Low fiber diet is most significant contributor. *Clinical Characteristics:* -Often asymptomatic, found incidentally on colonoscopy or barium enema
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Colonic Diverticulosis, Sigmoid colon, Right colon
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Complications of what? -Bleeding -Infection (diverticulitis) ----might lead to perforation and abscess Either bleeding or infection, usually not both at the same time (except for occult bleeding).
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Diverticulosis
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*Pathogenesis:* -Diverticular mucosa becomes inflamed and bleeds -Usually self-limiting, but can be life-threatening. *Clinical Characteristics:* -Rectal bleeding -Not necessarily associated with pain or fever -Supportive care (IV fluids, blood) to prevent / treat hypotension -Might require surgery to remove involved segment
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Complication of diverticulosis - bleeding
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*Pathogenesis:* -Diverticular inflammation due to retained fecal matter -Diverticular mucosa becomes inflamed and swells --Necrosis of tissue can lead to rupture and spillage of contents into pelvis or peritoneal cavity *Clinical Characteristics:* *-Pt c/o pain in ___; eventually has ____, ________. -Look for tender mass in ___.* Antibiotics and supportive treatment usually work unless rupture has occurred. ----With rupture comes either peritonitis or localized abscess.
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Complication of diverticulosis-Diverticulitis, *LLQ, Fever, Leukocytosis*
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Infection that can result in: -perforation abscess -fistula = communication between colon and other structure, such as bladder -bowel obstruction -due to inflammation
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DiverticuLITIS complications
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*Incidence:* Peak incidence in older age group -More common in Western countries than in Asia and Africa -Therefore we screen for it. (screen = test those without symptoms) How? *Pathogenesis:* -*Adenomatous* and *_____* polyps are *pre-cancerous.* ----*Hyperplastic* and juvenile polyps are NOT pre-cancerous -More common in left colon and rectum -Adenocarcinoma - 95% of malignant GI tumors --Remaining 5% are carcinoids, sarcomas, lymphomas *Clinical Characteristics:* -Occult bleeding is common -> anemia -Do rectal exam, obtaining stool for occult blood.
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*Colon Cancer, Villous*
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*Incidence:* -Most common in middle-aged to elderly *Pathogenesis:* -Most common cause is *colon cancer* -Some other causes of _____ ________ --Volvulus --Diverticulitis *Clinical Characteristics:* -May be fatal (due to perforation) if not diagnosed and treated promptly
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*Colon Obstruction*
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*Incidence:* Mostly in middle-aged to elderly *Pathogenesis:* -Section of bowel twists and closes the lumen, causing complete obstruction. -Usually because of congenital abnormality of bowel or mesentery -Occluding circulation leads to ischemia of bowel -Can involve sigmoid colon, cecum, or small bowel *Clinical Characteristics:* -May be fatal if not diagnosed and treated promptly - due to bowel ischemia and perforation
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*Colon Obstruction-Volvulus*
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-Lack of relaxation of internal anal sphincter (due to lack of ganglia in wall of distal colon)(similar to what condition of esophagus?) -Colon does not empty well. -Stool collects in colon, sometimes escaping uncontrollably as pressure increases. Usually discovered in childhood. -Treatment - remove portion of colon that has no ganglia.
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Hirschsprung's
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*Pathogenesis:* most common causes are: -Incarcerated hernia (world-wide) -Adhesions from previous abdominal surgery (Western countries - where people have abdominal surgery!)
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Small Bowel Obstruction (SBO)
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*Incidence:* any age -Weeks, months years after abdominal surgery -Common cause of SBO in Western countries *Pathogenesis:* -Scarring, fibrosis, and contraction can kink the small bowel, causing obstruction *Clinical Characteristics:* -Cramping abdominal pain and vomiting -Can be fatal due to impairing bowel circulation
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Small Bowel Obstruction due to adhesions
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*Incidence:* any age -Most common cause of SBO world-wide *Pathogenesis:* -Knuckle of bowel becomes trapped in opening in abdominal wall. -Trapped bowel can swell and become ischemic and necrotic, resulting in *strangulation.* *Clinical Characteristics:* -With acute incarceration, patient will have tender mass in groin, and cramping abdominal pain. -Rapid diagnosis and emergency surgery is necessary to prevent strangulation. *Don't say "strangulated " when you mean "incarcerated."*
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Small Bowel Obstruction due to incarcerated hernia
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*Incidence:* usually young children (around age 2) *Pathogenesis:* -One section of bowel telescopes into adjacent section (usually small bowel into colon) -Polyp, diverticulum, tumor, stricture, etc, can be the cause, but often no cause is found. *Clinical Characteristics:* -Intermittent ("colicky") abdominal pain -Young child will be writhing in pain for few minutes, then fine for a few minutes, then inconsolable again. -Diagnosis and treatment is what?
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Small Bowel Obstruction due to intussusception, Barium enema (or just air)
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What are four other causes of small bowel obstructions?
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-Internal hernia (can cause SBO without the usual clues, No abdominal wall or groin hernia, no previous abdominal surgery) -Volvulus -Tumor of small bowel -Crohn's Disease
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*Incidence* - usually older people with PVD *Pathophysiology:* --Occlusion of mesenteric vessels (esp SMA) -Chronic bowel ischemia --"Food fear" - post-prandial (after eating) abd pain --Weight loss - constant finding *Acute bowel ischemia* -Severe diffuse abdominal pain due to ischemic bowel -*"Pain out of proportion to physical findings"* --No signs of peritonitis initially --But later after bowel is dead -? bloody stools (colonic ischemia, sloughing of mucosa)
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Mesenteric ischemia
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*Pathogenesis:* obstruction, distention, infection Fecal material (or inflammation of lymphatic tissue in appendix) -;-; distention of lumen -; ischemia of appendiceal wall -; bacterial invasion (*infection*)
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Appendicitis
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*Incidence:* -Can occur at any age, mostly big kids and young adults -In addition to gallbladder disease, a *common surgical emergency in pregnancy* -Delayed diagnosis in very young and old results in increased incidence of perforation. *Clinical Characteristics:* -Starts as mid abdominal pain, then localizes over hours to RLQ after inflammation of wall has started. -Usually with vomiting, eventually fever and leukocytosis
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Appendicitis
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*Pathology:* -*Obstruction* of lumen -*Distention* of appendix -Appendix wall starts to lose blood supply bacteria invade wall -; *infection* (suppurative appendicitis) -Appendix wall perforates -Feces and bacteria spill out (perforated appendicitis)
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Appendicitis
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*Symptoms/Signs:* -Periumbilical pain -Nausea, later vomiting -Not tender yet -Pain and tenderness RLQ -Low grade fever -Mildly increased WBC -More pain and tenderness -More fever -Higher WBC
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Appendicitis
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