Gastroenterology III

Inflammatory Bowel Disease -Crohn's Disease * S/Sxs

*often patients have sxs for months to years before going to doc to get it diagnosed. -hx of fatigue, wt. loss, abd. pain, often steady and localized in RLQ -occult blood loss common (melena), blood in stool if colonic involvement (hematochezia) -stools usu. formed, mb loose if extensive colonic involvement or terminal ileum (because of bile salt malabsorption) *If it's more in the colon, they're more likely to have chronic diarrhea. If it's in the SI, they're less likely to have diarrhea -fat malabsorption increases risk of gallstones, renal oxalate stones

Inflammatory Bowel Disease -Crohn's Disease * S/Sxs continued

-1/3 of pt. have PERI-ANAL Dz.. - fissures, fistulas, perianal abscess (Ppl w/ colitis usually don't have these but need to differentiate these from people w/ chronic constipation -from straining to pass hard stool) -1/2 of pt. have pathognomonic sarcoid-type EPITHELIOD GRANULOMAS in the intestinal wall and occ in the involved mesenteric nodes *often crampy pain/discomfort after meals *may feel a mass from the inflammation *different areas of the GI tract can be inflamed at different times so symptoms can vary. *recurrent apthous ulcers in the mouth -may present as an acute abd. simulating appendicitis, esp. in young pts. * 4 patterns may present- a) inflammation: RLQ pain, tenderness, like appendicitis b) obstruction: severe colic, abd. distention, constipation, vomiting c) diffuse jejunoileitis: both inflam and obstruction leading to chronic debility d) abd. fistulas and abscesses: usu. late, with fever, painful masses, wasting

Appendicitis -Etiology

-FECALITHs form when calcium salts and fecal debris become layered around a nidus of fecal material located within the appendix. -LYMPHOID HYPERPLASIA is associated with a variety of inflammatory and infectious disorders including: * Crohn's disease * gastroenteritis * amebiasis * respiratory infections * measles * mononucleosis. -OBSTRUCTION of the appendiceal lumen has less commonly been associated with: * parasites + (e.g., Schistosomes species, Strongyloides species) * foreign material + (e.g., intrauterine device, tongue stud, activated charcoal) * tuberculosis * tumors

Irritable Bowel Syndrome -Diagnosis Part 4

-IBS can be confidently diagnosed by identifying typical symptoms, performing a complete physical examination and excluding alarm features. -The presence of alarm features should prompt a more detailed diagnostic evaluation directed by the patient's predominant symptoms. -Current evidence does not support the performance of exhaustive testing to exclude organic diseases in patients fulfilling symptom-based IBS criteria without alarm features. -Preliminary evidence suggests that celiac disease may be more prevalent in patients with suspected IBS. -Patients 50 years of age or greater with IBS symptoms should undergo colonoscopy (or other acceptable regimen) for age appropriate colorectal cancer screening. -If alarm features are not present and the patient fulfills symptom-based criteria, a confident diagnosis of IBS should be made and symptom-directed therapy should be initiated. -A crucial aspect of this approach is adequate and timely follow-up. If, after appropriate therapeutic interventions, the patient reports no significant improvement, a more extensive diagnostic evaluation may be indicated.

Malabsorption C. Celiac Disease -description Part 3

-In celiac disease, dietary gluten causes inflammation of the small intestine, which may affect absorption of important nutrients including iron, folic acid, calcium, and fat-soluble vitamins. -Studies show celiac disease to be a common disorder, possibly affecting 1 in 150 of the general population, the majority of patients being diagnosed in adulthood. -Many patients have minimal symptoms, and gastrointestinal symptoms are frequently absent. -Celiac disease should be considered in a wide range of clinical situations including anemia or osteoporosis and in patients with a range of associated disorders such as type 1 diabetes. -The diagnosis and screening for celiac disease has been facilitated by testing for endomysial autoantibodies. -Treatment consists of permanent withdrawal of gluten from the diet, which results in complete remission.

Inflammatory Bowel Disease -Ulcerative Colitis * DDx

-Inflammatory bowel disease (Crohn's, celiac) -Irritable bowel disease -microscopic colitis (inflammation can only be seen on biopsy) -drug induced -infectious -ischemia

Inflammatory Bowel Disease -Crohn's Disease

-Intestinal obstruction is a frequent complication. * In the initial stage, obstruction from edema and inflammation commonly in the ileum are reversible. * As disease progresses, fibrosis develops, leading to more constipation and intractable obstruction from fixed luminal narrowing. -Fistula formation is common and can cause indolent abscess, malabsorption, cutaneous fistula, persistent urinary tract infection, or pneumaturia. -perforation and hemorrhage are rare due to thickened mucosa *Increased incidence of gallstones in Crohn's disease patients because of fat malabsorption *increased susceptibility to kidney stones + (recurrent kidney stones in s/o who is following the recommendations of drinking more water think of this or something else predisposing this) *Hydronephrosis more common too from malabsorption.

Malabsorption D. Lactase Deficiency -description -demogaphics

-Lactose intolerance is a common disorder -due to the inability to digest lactose into its constituents, glucose and galactose, secondary to low levels of lactase enzyme in the brush border of the duodenum. In the US: -The prevalence of primary lactose intolerance varies according to race. -As many as 25% of the white population -among black, Native American, and Asian American populations, prevalence is estimated at 75-90%. Internationally: -Of the world's population, 75% is estimated to be lactose-deficient. -Lactose intolerance is very common among Asian, South American, and African persons.

Diverticulitis -S/Sxs Part 1

-abdominal pain * mostly in the LLQ * tends to be steady, severe, and deep -fever -previous episodes of dull, colicky, and diffuse abdominal pain accompanied with flatulence, distention, and change in bowel habits (diverticulosis) -altered bowel habits including diarrhea, increased constipation, tenesmus -nausea and vomiting -dysuria, pyuria, and urinary frequency if bladder or ureter are irritated -history of pneumaturia or recurrent urinary tract infections (colovesicular fistulas)

Inflammatory Bowel Disease -Ischemia Colitis * Imaging

-abdominal plain film is usually an initial examination undertaken in most cases involving acute abdominal problems. -CT after the plain radiography can exclude many other causes of abdominal pain and establish the diagnosis of intestinal ischemia.

Appendicitis -S/Sxs Part 2

-anorexia is present in 74-78% of patients -diarrhea or constipation in as many as 18% of patients -duration of symptoms is less than 48 hours in approximately 80% of adults but tends to be longer in elderly persons and in those with perforation. -an inflamed appendix near the urinary bladder or ureter can cause irritative voiding symptoms and hematuria or pyuria. Cystitis in male patients is rare in the absence of instrumentation. Consider the possibility of an inflamed pelvic appendix in male patients with apparent cystitis. -often presents atypically so need to use all the indicators for dx.

Inflammatory Bowel Disease -Ulcerative Colitis * Etiology

-autoimmune: * serum and mucosal autoantibodies against intestinal epithelial cells may be involved. -immune-mediated: * abnormalities of humoral and cell-mediated immunity and/or generalized enhanced reactivity against intestinal bacterial antigens may be causes. * A loss of tolerance against indigenous enteric flora is believed to be the central event in the pathogenesis of inflammatory bowel disease (IBD). -genetic susceptibility (chromosomes 12 and 16) is a factor associated with ulcerative colitis. * A positive family history (observed in 1 in 6 relatives) is associated with a higher risk for developing the disease. -smoking is not associated with ulcerative colitis (reversed in Crohn's disease). -environmental factors may be involved. -dietary factors - dairy

Appendicitis -PE

-male infants and children occasionally present with an inflamed hemiscrotum due to migration of an inflamed appendix or pus through a patent processus vaginalis. This is often initially misdiagnosed as acute testicular torsion. -RLQ tenderness, guarding (typically over McBurney's point) is present in 96% of patients, but this is a nonspecific finding. -most specific physical findings are: * rebound tenderness * pain on percussion * rigidity * guarding. Present in a Minority of Appendicitis Cases: -Rovsing sign * (RLQ pain with palpation of the LLQ) -Obturator sign * (RLQ pain with internal rotation of the flexed right hip) -Psoas sign * (RLQ pain with hyperextension of the right hip)

Inflammatory Bowel Disease -Crohn's Disease * description * demographics * first signs

-characterized by acute & chronic inflammation extending through all layers of the intestinal wall and involving mesentery as well as regional lymph nodes. -early mucosal involvement consists of longitudinal and transverse APHTHOUS ULCERs, which are responsible for COBBLESTONE appearance. As the disease progress, deep FISSURES, SINUSES and FISTULAs develop. -Can occur anywhere in the GI tract, but is DISCONTINUOUS along the GI tract. (normal tissue -> SKIP LESIONs -> normal tissue) -Can often first be seen in the mouth in the form of mouth apthous ulcers. These people get apthous ulcers often and they take longer to heal. (whereas in food sensitivities they may get them occasionally or just when eating large amts. Of that food & they heal quicker). -Age: Bimodeal peak age of onset/diagnosis (15-25 and 55-65)

Malabsorption D. Lactase Deficiency -Etiologies

-congenital lactose intolerance is inherited as an autosomal recessive trait and is very rare. -primary lactose intolerance is due to low levels of lactase, which develop after childhood. -secondary, or acquired, lactase deficiency may develop in a person with a healthy small intestine during episodes of acute illness. This occurs because of mucosal damage or from medications. Some causes of secondary lactase deficiency are as follows: * acute gastroenteritis * ascariasis * carcinoid syndrome * celiac sprue * chemotherapy * Crohn's disease * diabetic gastropathy * gastrinoma * giardiasis * HIV enteropathy * Kwashiorkor * radiation enteritis * tropical sprue * Whipple syndrome

Diverticulitis -DDx

-discomfort and pain upon defecation suggests hemorrhoids or/ anal fissures. -history of weight loss and mucus in the stools indicates inflammatory bowel disease.

Diverticulitis -S/Sxs Part 2

-feculent vaginal discharge * (fistulas with the uterus or vagina) -severe and generalized abdominal pain (diffuse peritonitis) -back or lower extremity pain (perforation) -lower GI bleeding from diverticulosis occurs in the form of bright red-colored or wine-colored stools. * onset of bleeding typically is sudden, painless, and accompanied by an urge to defecate. * amount of bleeding typically is massive and tends to stop spontaneously.

Irritable Bowel Syndrome -Diagnosis Part 1

-historically, a diagnosis of exclusion rather than a primary diagnosis. AGA position statement: in the absence of 'alarm features' or 'red flags' and/or any positive screening studies, additional diagnostic testing is not typically necessary. Red flags or alarm features include: 1. symptom onset after age 50 2. severe, unrelenting diarrhea 3. nocturnal symptoms 4. unintentional weight loss 5. hematochezia 6. family history of organic gastrointestinal diseases such as IBD, celiac sprue or malignancy *Gastroenterologists want GPs to diagnose & treat this because these cases are so common & just as easily treated by GP. *Do not send to gastroenterologist if the patient does not have any of these alarm symptoms, and make the presumptive diagnosis of IBS *If the patient has any of these symptoms, we do not make a presumptive diagnosis of IBS! *We then treat them as if they have IBS. If better in 1 month we continue treatment *If they come back in a month and they are not better, then we initiate the workup to figure out what it is if not IBS.

Inflammatory Bowel Disease -Ischemia Colitis

-inflammatory disease of the colon due to diminished blood flow leading to bowel wall ischemia and a secondary inflammation. -simulates inflammatory disease (looks like Crohn's in elderly)

Diverticulitis -PE

-localized tenderness -rebound tenderness -guarding -assess vital signs to determine hemodynamic stability -low-grade fever -rectal examination * identifies tenderness * establishes the color of stools * determines the presence and extent of GI bleeding. * A mass may be seen in the cul-de-sac. -diffuse abdominal tenderness, rebound, absent bowel sounds, and/or high-grade fever may indicate possible complications of perforation and/or peritonitis. -abdomen may be distended and tympanic.

Diverticulitis -Etiology

-low-fiber diet is the highest risk factor → low-bulk stool → increased intraluminal pressure and formation of diverticula. -high fat and grain-fed beef diets associated with diverticular disease -genetic causes exist : * Asians have right-sided diverticula preponderance * westerners mostly on the left side. -aging leads to change in collagen structure -colonic motility disorders -corticosteroids but not NSAIDs increase the risk -colonic segmentation - non-propulsive contractions produce isolated segments or little chambers with high pressure within. -defects in colonic wall strength

Diverticulitis -description

-mostly occurs in elderly people -inflammation of 1 or more diverticula -potentially leading to obstruction or perforation and to abscess and fistula formation -may heal spontaneously (microabscess) or may enlarge. -If enlarges, may then adhere to adjacent organs (bladder, vagina), fistula may form. -Repeated inflam may lead to obstruction and potentially dangerous perforation

Malabsorption B. Tropical Sprue -description

-occurs in residents and prolonged visitors of the tropics -may not appear until as long as 10 years after the patient has left there. -No definitive marker exists -unknown etiology -suggested to be caused by infection (bact., viral), parasites, vitamin def. (folic acid) -multiple nutritional deficiencies * folate, vitamin B-12, and iron deficiencies are the most common -impaired absorption (esp. fats) and motor abnormalities (increased peristalsis)

Appendicitis -DDx

-often difficult to tell - 20-30% of normal appendix are removed -increased WBC count helpful, although may be absent (esp. elderly) DDx: -PID * (R/O by hx, pelvic exam) -acute gastroenteritis * N/V, pain more generalized -pancreatitis -Crohn's -cholecystitis -pyelonephritis -IBS -children- volvulus, intussusception

Malabsorption A. Insufficient digestive elements

-pancreatic enzymes -bile salts -hypochlorhydria -also post-surgical syndromes are common in practice

Inflammatory Bowel Disease -Ulcerative Colitis * Imaging

-plain abdominal radiograph: * might show colonic dilatation in severe cases, suggesting toxic megacolon. * Also, evidence of perforation, obstruction, or ileus can be observed. -barium enemas may precipitate toxic megacolon in severe cases. Barium enemas can be performed safely in mild cases. * They may show a narrow, tubular, shortened colon with loss of haustral folds, pseudopolyps, and small ulcers * "lead pipe" appearance * flexible sigmoidoscopy can provide the diagnosis of colitis. -colonoscopy with biopsy confirms a diagnosis. * Also, useful for documenting the extent of the disease, for monitoring disease activity, and for surveillance for dysplasia or cancer * however, be cautious in attempting colonoscopy with biopsy in a patient with severe disease because of the possible risk of perforation or other complications.

Inflammatory Bowel Disease -Crohn's Disease * Imaging

-plain radiography, double-contrast barium enema examination -single-contrast upper GI series with small-bowel follow-though barium x-ray shows: * irregularity, nodularity, stiffness, thickening of terminal ileum, narrowed ileum lumen. * In advanced cases, string sign shows marked stricturing of the ileum -CT and double-contrast evaluation of the small bowel. (b/c other imaging modalities often cannot image the SI well) -Ultrasonography and MRI can be used as adjuncts if radiation exposure is an issue in monitoring disease activity. -colonoscopy - "SKIP areas", "COBBLESTONE appearance", LONGITUDINAL ULCERs, rectal sparing, narrowing, FISTULAs (& exudative inflamed areas) *ppl often get multiple surgeries to remove pieces of the SI/colon (usu. the area w/ the string sign)

Diverticular Disease

-refers to diverticulosis of the colon (although mb throughout GI) -rare in people < 40 years, increases with age - 30% of 60 yo, 80% of 80 yo -90% are asymptomatic

Inflammatory Bowel Disease -description -demographics

-refers to idiopathic bowel disorders, Crohn's dz., ulcerative colitis, celiac -400,000+ people affected -more frequently in Jewish people, whites, pt. in higher socioeconomic group, Type A- can't relax, never satisfied, feel inadequate, compulsive about everything -increased intestinal permeability and an imbalanced microflora may trigger IBD. Healthy gut flora can block translocation of gut pathogens and decrease overactive immune response (J Endotox Res 2000;6(3): 205-212) -www.scdiet.org (specific CHO diet) helps many of these patients - grain restricted/ CHO restricted diet -antibodies are present to colon epithelium -psychological stress exacerbates the conditions- always < under stress

Inflammatory Bowel Disease -Ulcerative Colitis * description

-relatively uncommon, chronic, recurrent inflammatory disease of the colon or rectal mucosa. -Often a lifelong illness, the condition has profound emotional and social impact on the affected individual. -superficial ulceration of the colon almost always involves rectum (95%) and if any portion of remaining colon is involved, it is in a continuous manner extending proximally from the rectum -Ulcerative proctitis (limited to anus & rectum), is a common, limited form of the dz., usu. remains localized to the rectum

Malabsorption B. Tropical Sprue -PE

-reveals vitamin deficiency symptoms: * glossitis * stomatitis * cheilosis * cutaneous hyperpigmentation * dry rough skin * abd. distention, tenderness and edema (late) * weight loss * dehydration

Diverticula

-saccules anywhere in the colon, but most commonly in the sigmoid due to: * factors that chronically increase intraluminal pressure: + low fiber diet + high refined carbohydrates -usually asymptomatic -may have chronic or intermittent LLQ abd. pain -often constipation -often observed on barium studies -may cause rectal bleeding if erosion of mucosa

Diverticulitis -Imaging

-sigmoidoscopy * shows narrowing and inflammation -barium x-ray is hazardous in acute phase, may cause a perforation

Inflammatory Bowel Disease -Ulcerative Colitis * S/Sxs

-sloughing of colon tissue causes bleeding? -low grade fever, colicky abdominal cramps, distension, fluid & electrolyte imbalance, wt. loss, anorexia, weakness cachexia -causes depression, anger, frustration -stress often causes exacerbation (often in type A, anxiety ridden people) -Both Crohn's & UC have exacerbations & remissions *an exacerbation of UC puts the person on bed/house rest. *63% have tenesmus (colon spasming) *47% have hard or formed stools. *could be rectal bleeding or blood coated stool from higher up bleeding in colon. *Patients with colitis seek help! They are in serious distress!

Irritable Bowel Syndrome -Treatment

-standard treatment is fiber (psyllium, Metamucil), & muscle relaxer to prevent spasming. -Biofeedback is also a possible treatment for someone with anxiety issues or problem recognizing when they're getting stressed -remove food sensitivities

Appendix -Purpose

-the appendix is a reserve population of your microflora. -Part of our evolution because when we got food poisoning & had horrible diarrhea & wiped out our own microflora, these microbes would repopulate the colon (since back then we couldn't take probiotics)

Inflammatory Bowel Disease -Ulcerative Colitis * S/Sxs

-usu. a series of attacks of bloody diarrhea with asymptomatic intervals * the diarrhea usu. is from 5-10X per day. Up to 27 times per day! -usu. begins insidiously, with increased urgency, lower abd. cramps, blood and mucus in stool -if confined to rectosigmoid area, stool may be normal, or hard or dry -rectal d/c of mucus with RBC's and WBC's -if process extends proximally, stools become looser * 10-20 a day with * severe cramps * rectal tenesmus. * Watery stools with pus, blood, mucus * systemic sxs of malaise, fever, anemia, wt. loss

Inflammatory Bowel Disease -Crohn's Disease * Location

-usu. primarily the small intestine, esp. the terminal ileum and then the colon and Crohn's colitis (Crohn's disease & ulcerative colitis) is common, but may occur in any part of the GI from mouth to anus -involves the ileum alone in 35% (ileitis) -ileum and colon, esp. R side, in 45% (ileocolitis) -colon alone in 20% (granulomatous colitis) -entire small bowel occ (jejunoileitis); -rarely may also affect stomach, duodenum, esophagus -inflammation involves all layers of intestinal wall, which becomes thickened patchy distribution with areas of normal bowel (skip areas) (normal tissue and inflam. tissue)

Malabsorption D. Lactase Deficiency -S/Sxs

-varies from: * minor abd. discomfort and bloating * to severe diarrhea in response to even small amounts of lactose * loose stools * abdominal bloating and pain * flatulence * nausea * borborygmi * diarrhea

Irritable Bowel Syndrome -Imaging

-x-ray: * may show altered GI motility (spasm) -sigmoidoscopy: * shows increased mucus & spasm (or often nothing)

Malabsorption D. Lactase Deficiency

1. hydrogen breath test - test of choice - subjects are administered lactose after an overnight fast, after which expired air samples are collected before and at 30-minute intervals for 3 hours to assess hydrogen gas concentrations. -A rise in breath hydrogen concentration > 20 ppm over the baseline after lactose ingestion suggests lactase deficiency. 2. dietary elimination: -Resolution of symptoms with elimination of lactose-containing food products and resumption of symptoms with the reintroduction are findings suggestive of lactose intolerance - drink milk- problems?; try cheese-

Irritable Bowel Syndrome -Etiology Part 1

1. postulated etiologies -abnormal transit profiles and an enhanced perception of normal motility may exist. -local histamine sensitization of the afferent neuron causing earlier depolarization may occur. 2. causes related to enteric infection -colonic muscle hyper -reactivity and neural and immunologic alterations of the colon and small bowel may persist after gastroenteritis. -psychological co-morbidity independently predisposes the patient to the development of post-infectious IBS. -psychological illness may create a pro-inflammatory cytokine milieu, leading to IBS through an undefined mechanism after acute infection.

Irritable Bowel Syndrome -Etiology Part 2

3. central neurohormonal mechanism -abnormal glutamate activation of N-methyl-D-aspartate (NMDA) receptors, activation of nitric oxide synthetase, activation of neurokinin receptors, and induction of calcitonin gene-related peptide have been observed. -limbic system mediation of emotion and autonomic response enhances bowel motility and reduces gastric motility to a greater degree in patients who are affected than in controls. -hypothalamic-pituitary axis may be intimately involved in the origin. Motility disturbances correspond to an increase in hypothalamic corticotropin-releasing factor (CRF) production in response to stress. CRF antagonists eliminate these changes.

Irritable Bowel Syndrome -Etiology Part 3

4. small bowel bacterial overgrowth provides a unifying mechanism for the common symptoms of bloating and gaseous distention in patients with IBS. 5. bloating and distention may also occur from intolerance to dietary fats. 6. psychological stress aggravates symptoms 7. low fiber diet and intolerance to lactose (diarrhea) and other sugars, (glucose intolerant, milk intolerant (casein) → congestion, bronchitis, asthma, mucus; also gluten mb a problem 8. food sensitivities: dairy, gluten 9. genetics - food + genetics -> abnormal biochemistry of the body & brain (stress, poor food hygiene) -> CNS, autonomic nervous system -> thought changes, behavior changes, effects on gut, heart problems

Irritable Bowel Syndrome -description

=Functional Dyspepsia, Spastic Colitis, Mucus Colitis -most common of all GI disorders, up to 50% of pt. to gastroenterologist -a disorder of exclusion when others have been ruled out (consider a dysfunctional GB) -often too quickly used as a diagnosis -counseling is helpful because of pt. frustration with problem

Malabsorption B. Tropical Sprue -Labs

CBC - megaloblastic anemia (60% of patients) Stool analysis - increased fecal fat * > 6 g in 24 hours is abnormal (positive for fat malabsorption). * Fatty stools are usually observed when the stool fat content is 15 g or more. Chem. screen - decreased serum protein, calcium, phosphorus, cholesterol and prothrombin - hypochlorhydria - normal pancreatic function D-Xylose absorption test - 25 g D-xylose is administered orally. -In well-hydrated patients with normal renal function, abnormal results (i.e., positive for mucosal malabsorption) -include a 5-hour urine collection of less than 4 g and a 1-hour serum collection of less than 20 mg/dL.

Inflammatory Bowel Disease -Ulcerative Colitis * Labs

CBC: -anemia -platelet count >350,000/mL -elevated ESR and elevated C-reactive protein Chem screen: -hypoalbuminemia -hypokalemia -hypomagnesemia -elevated alkaline phosphatase

Inflammatory Bowel Disease -Ulcerative Colitis * Complications * Prognosis

Complications -hemorrhage most common -toxic megacolon * markedly distended colon (ballooning, over 6 cm) with attenuated walls and IMMEDIATE DANGER OF PERFORATION may occur in severe colitis (> 40% mortality) -cells may become dysplastic with increased risk of colon cancer, increases by 0.5-1% per year Prognosis -most cases are controlled with treatment, with the patient experiencing lifelong exacerbations and remissions. -In more severe cases, surgery is the end result

Inflammatory Bowel Disease -Crohn's Disease * Etiology * Risk Factors

Etiology -largely unknown -genetic, infectious, immunologic and psychological factors have all been implicated in influencing the development of the disease. Risk factors -family history * associated with HLA-DR1 and DQw5 genes -smoking -use of oral contraceptives * 2:1 for women who use them -diet -ethnicity * 2-4X in Jewish population, followed by Caucasians, followed by those in African Americans and Asians -Age: bimodal distribution. * One early peak ages 15-25 years, another smaller peak ages 55-65 years. * in patients <20 years, 88% involve SI, as compared with 58% in those > 40 years.

Peritonitis -PE

Indicative of Peritonitis: -positive cough sign (sharp pain in the RLQ elicited by a voluntary cough) -RLQ pain in response to percussion of a remote quadrant of the abdomen, or to firm percussion of the patient's heel -The Markle sign (pain elicited in a certain area of the abdomen when the standing patient drops from standing on toes to the heels with a jarring landing) -rectal/ vaginal tenderness without marked abd. tenderness

Irritable Bowel Syndrome -Labs

Lab -(only to confirm other possible diagnosis) -CBC screen: * for anemia, inflammation, and infection -Chem screen: * evaluate for metabolic disorders * and to rule out dehydration/ electrolyte abnormalities in patients with diarrhea -Hemoccult test may be useful. -stool examinations - complete GI health panel * lysozyme test normal (= spasm, not IBD) -Hydrogen breath tests * for lactose intolerance. -Celiac testing

Appendicitis -Labs -Imaging

Lab -CBC * 80-85% of adults have a WBC count > 10,000. * Neutrophilia greater than 75% occurs in 78% of patients. * results inconsistent with regard to WBC counts in children and elderly patients Imaging -abdominal CT * has become the most important imaging study in the evaluation of patients with atypical presentations of appendicitis. -ultrasound * sensitivity of 85-90% and a specificity of 92-96%.

Malabsorption C. Celiac Disease -Diagnosis/Testing Part 3

Newest test: • Deamidated gliadin peptide (DGP) IgA - high sensitivity and specificity, esp in elderly that had normal standard tests • When the prevalence is low, as in the general U.S. population, the risk of a false-positive result is high even with an accurate test . IgA Antibody/ Sensitivity/ Specificity Anti-gliadin ELISA/ 57-100%/ 42-98% Anti-endomysial Indirect IF/ 75-98%/ 96-100% Anti-tissue transglutaminase ELISA /98-100%/ 97-98% Celiac Disease Comprehensive Antibody Profile - - endomysial antibodies IgA - tissue transglutaminase IgG - tissue transglutaminase IgA - deamidated gliadin IgA - deamidated gliadin IgG - serum IgA quantitation • small bowel biopsy required to confirm the diagnosis of celiac disease for most patients.

Irritable Bowel Syndrome -PE

Physical Exam -abd. tenderness over course of colon- some areas worse, some areas fullness

Inflammatory Bowel Disease -Crohn's Disease * PE * Labs

Physical Exam -may reveal RLQ tenderness with an associated fullness or mass. Lab -mild anemia -leukocytosis, and an increased ESR (inflammation) + fecal lysozyme and + AACT suggestive of IBD Rule out food intolerances/enzyme deficiencies -celiac dz./gluten sensitivity -lactase deficiency -carbohydrate sensitivity (sorbitol) -stool chymotrypsin/stool fat (pancreatic insufficiency)

Malabsorption C. Celiac Disease -Diagnosis/Testing Part 1

Routine tests that can suggest celiac disease • Anemia -(microcytic, hypochromic or normocytic, normochromic with ↑RDW) • ↑AST • ↓Albumin/plasma protein • Low or "too good" cholesterol (total, LDL, HDL) • ↑ alkaline phosphatase • histological identification of gluten sensitive enteropathy is the accepted basis - in classic cases, a characteristic villous atrophy is found.

Malabsorption C. Celiac Disease -Diagnosis/Testing Part 2

Standard Testing has been: • Serum immunoglobulin A (IgA) endomysial antibodies (IgA) and IgA tissue transglutaminase (tTG) antibodies. Sensitivity and specificity > 95%. • The tTG antibody test is less costly because it uses an enzyme-linked immunosorbent assay; it is the recommended single serologic test for celiac disease screening in the primary care setting. • Testing for gliadin antibodies is no longer recommended because of the low sensitivity and specificity for celiac disease. • Confirmatory testing, including small bowel biopsy, is advised. - requires 4 or more samples from 2nd and 3rd portion of SI - must include gluten in diet a minimum of 2 weeks, preferably 4+ weeks

Irritable Bowel Syndrome -Diagnosis Part 3 / Supporting Sxs

Supporting symptoms include the following: -altered stool frequency -altered stool form -altered stool passage (straining and/or urgency) -mucorrhea -abdominal bloating or subjective distention clinical picture is some combination of: i) crampy abdominal pain ii) constipation, diarrhea, both, or alternating iii) increased colonic mucus production iv) flatulence, nausea, anorexia v) anxiety or depression vi) sxs related to stress vii) appearance of health viii) chronic sxs

Irritable Bowel Syndrome -Diagnosis Part 2

The Rome III criteria (2006) for the diagnosis of IBS require that patients must have recurrent abdominal pain or discomfort at least: - 3 days per month -during the previous 3 months -that is associated with 2 or more of the following: 1. relieved by defecation 2. onset associated with a change in stool frequency 3. onset associated with a change in stool form or appearance

Inflammatory Bowel Disease -Ischemia Colitis * Etiology

Two mechanisms may cause bowel ischemia 1. most common is diminished bowel perfusion due to low cardiac output often seen with in patients with cardiac disease (CHF) or in prolonged shock of any etiology. 2. occlusive disease of the vascular supply of bowel due to atheroma, thrombosis, or embolism in which the collateral circulation is not adequate to maintain bowel integrity. -disease of the elderly. It is rarely seen in those younger than 60 years

Appendicitis -S/Sxs Part 1

classic history: (occurs in only 50% of cases) -anorexia -periumbilical pain -followed by: * nausea * RLQ pain * vomiting * mild fever -migration of pain (persistent, steady, well localized, < movement, deep resp., coughing, sneezing) from the periumbilical area to the RLQ is the most discriminating feature of the patient's history. * This finding has a sensitivity and specificity of approximately 80%. -when vomiting occurs, it nearly always follows the onset of pain. Vomiting that precedes pain is suggestive of intestinal obstruction * nausea is present in 61-92% of patients

Inflammatory Bowel Disease -Ischemia Colitis * S/Sxs + acute

i) acute -sudden onset of localized left side abd. pain, tenderness -rectal bleeding (FRANK BLOOD) -may be associated with: * fever * hypotension * tachycardia -peritoneal signs (muscle guarding, rebound tenderness) -severe ischemia may lead to bowel necrosis and perforation resulting in an acute abdomen and shock -most cases resolve over several weeks with supportive tx

Malabsorption B. Tropical Sprue -S/Sxs

i) begins with bulky, pale, foul smelling, greasy, floating stools -worse after fat meals (typical of fat malabsorption) ii) second stage is marked weight loss, flatulence, abdominal cramps -pallor, weakness and irritability -parasthesias and mm. cramps -improves after leaving the tropics -symptoms may reappear years later (all due to vit/min deficiencies)

Inflammatory Bowel Disease -Ischemia Colitis * S/Sxs + chronic

ii) chronic - longer periods of vague abd. pain, tenderness -rectal bleeding varies -diarrhea -can lead to narrowing, obstruction and need for surgery -rectum spared (like Crohn's, unlike UC) -A reliable diagnosis of ischemic colitis can be made only when the radiologic findings are correlated with the clinical results.

Appendicitis -Age

incidence of appendicitis gradually rises from birth, peaks in the late teen years, and gradually declines in the geriatric years.

Malabsorption C. Celiac Disease -DDx

• Anorexia nervosa • Autoimmune enteropathy • Bacterial overgrowth • Collagenous sprue • Crohn's disease • Giardiasis • Human immunodeficiency virus enteropathy • Hypogammaglobulinemia • Infective gastroenteritis • Intestinal lymphoma • Irritable bowel syndrome • Ischemic enteritis • Lactose intolerance • Pancreatic insufficiency • Soy protein intolerance • Tropical sprue • Tuberculosis • Whipple's disease • Zollinger-Ellison syndrome

Malabsorption C. Celiac Disease -description Part 2

• Celiac Disease is a very specific type of damage done to the digestive tract resulting from a gluten intolerance. • Body attacks normal tissue resulting in damage to lining of small intestinal villi -Villi contain blood vessels which absorb nutrients -Villi increase area for absorption of nutrients -Digested nutrients are carried away by circulating blood • If villi are damaged, vitamins, minerals, calcium, carbohydrates, protein, and fats are not absorbed well • This damage is the result of an autoimmune reaction that results in villous atrophy. Without villous atrophy, you don't have celiac disease.

Malabsorption C. Celiac Disease -description Part 1

• Celiac disease is an autoimmune condition • Occurs in genetically susceptible individuals - Most all patients with celiac disease express human leukocyte antigen (HLA)-DQ2 or HLA-DQ8, which facilitate the immune response against gluten proteins • can occur at any age, but in adults the peak incidence is in the fifth decade. • Females are more commonly affected than males, ratio of almost 3 to 1 • in childhood has become increasingly uncommon. • A unique autoimmune disorder because: both the environmental trigger (gluten) and the autoantigen (tissue Transglutaminase) are known • elimination of the environmental trigger leads to a complete resolution of the disease

Malabsorption C. Celiac Disease -Evidence for Negative Celiac, Positive Gluten Intolerance

• Tissue Transglutaminase antibody negative • Biopsy negative • Gliadin antibody positive (IgA or IgG) • Total IgA normal Gliadin Antibodies • Not predictive of celiac disease. • A great assessment of an immune reaction to gluten. • Therefore a great assessment of gluten intolerance

Malabsorption C. Celiac Disease -S/Sxs

• Infancy (< 2 years) - more fulminent presentation likely but not common now -diarrhea - chronic (miserable, pale) -abdominal distension (enlarged abdomen) -failure to thrive (low weight, lack of fat, hair thinning) -anorexia, vomiting -psychomotor impairment (muscle wasting) • Childhood (median age of presentation is 4 yo) -diarrhea or constipation -anemia -loss of appetite (short stature, osteoporosis) • Adulthood -Intestinal symptoms may be absent -diarrhea or constipation -anemia -aphthous ulcers, sore tongue and mouth (mouth ulcers, glossitis, stomatitis) -dyspepsia -abdominal pain -bloating (weight loss) -fatigue -infertility -neuropsychiatric symptoms (anxiety, depression) -bone pain (osteoporosis) -weakness (myopathy, neuropathy) -dermatitis herpetiformis - typical pruritic vesicular rash.

Malabsorption C. Celiac Disease -What if there is no villous Atrophy?

• Most of these are also signs and symptoms that can be associated with gluten intolerance even when villous atrophy is not present. • Celiac disease (villous atrophy) is a gluten intolerance • Gluten intolerance is not always celiac disease (villous atrophy).

Malabsorption C. Celiac Disease -pathogenesis

• inappropriate immune response to the dietary protein gluten, which is found in rye, wheat, and barley. • after absorption in the small intestine these proteins interact with the antigen-presenting cells in the lamina propria causing an inflammatory reaction that targets the mucosa of the small intestine. -what makes a particular individual susceptible to gluten? * hereditary factors play a significant role, but the disease is concordant in only 60% to 70% of identical twins. * additional factors such as infectious agents and hormonal status are likely to be involved. -the associated HLA alleles present gluten-derived gliadin peptides to stimulate T-cells • Delaying exposure to gluten may alter disease • Viral exposures may trigger an immunologic response • Adenovirus type 12 implicated • T cells may react with tissue transglutaminase (the principal component of the endomysium autoantigen), and set in motion a series of inflammatory events that result in the characteristic celiac mucosal lesion.

Malabsorption C. Celiac Disease -Associated Diseases

• increased prevalence of celiac disease in certain conditions such as: - type 1 diabetes -autoimmune thyroid disease. -This may also be true of other autoimmune disorders - for example, primary biliary cirrhosis and Sjögren's syndrome.