Presentation on theme: "GI Board Review Elizabeth Paine, MD Division of Digestive Diseases"— Presentation transcript:
1GI Board Review Elizabeth Paine, MD Division of Digestive Diseases The University of Mississippi Medical Center
2Esophagus Proximal 1/3 esophagus- striated muscles under CNS control Distal 2/3 esophagus- smooth muscle under vagal and myenteric nervous system controlUES and LES are normally in a contracted stateInitiation of swallow relaxes both of the sphincters
3Question70 year old female with PMH of Parkinson’s disease, HTN, DM presents with dysphagia and occasional choking while eating for past several weeks. She notices dysphagia as soon as she initiates a swallow. CXR is normal. Which modality is the most sensitive in the diagnosis of this patient’s dysphagia? A. Esophageal manometry B. Modified barium swallow C. EGD D. Chest CTAnswer – B.In patients with dysphagia, immediate onset of symptoms with initiation of a swallow, difficulty swallowing liquids, and cough associated with swallowing difficulty are characteristic of oropharyngeal rather than esophageal dysphagia.In this patient, the immediate onset of symptoms with the initiation of a swallow, difficulty swallowing liquids, and the cough associated with the swallowing difficulty make oropharyngeal, or transfer, dysphagia more likely than esophageal dysphagia.Videofluoroscopy, which allows real-time radiographic analysis of swallowing function, is the most sensitive test for oropharyngeal dysphagia
4Dysphagia Oropharyngeal Dysphagia - Structural disorders - Neurological disorders(Stroke, ALS, myasthenia gravis, Parkinson’s,myotonic dystrophy)Esophageal DysphagiaOropharyngeal:- Cervical osteophytes, Zencker’s Diverticulum,Thyromegaly are structural causes- Occurs immediately with swallowing and usually associated with neurological diseases such as stroke, ALS, muscular dystrophy
6Schatzki’s Ring45yo M with longstanding GERD presenting with 6 months of intermittent solid food dysphagia
7Odynophagia Ulcerative Esophagitis - Due to infection or pill - Viral (HSV,CMV)- Candida - most commonPill-Induced Esophagitis- Tetracyclines, FeSO4,Bisphosphonates,NSAIDs, Quinidine,Potassium- Endoscopy is usually required for DX. Avoid the offending agent. Large fluid bolus with pills- Patient presents with oral thrush + odynophagia ….Dx Candida esophagitis (top picture) Empiric Treatment with Diflucan No need of endoscopy.If no improvement endoscopy.- Systemic sclerosis-induced esophageal dysmotility can result in dysphagia, stricture, and increased risk for pill-induced esophagitis.Patients with systemic sclerosis often develop pill-induced esophagitis due to stasis in the distal esophagus.
8Question55 y/o man presents with progressive dysphagia for both solids and liquids, intermittent regurgitation of food, and wt loss of 30 lbs over the course of 1 year. Symptoms not relieved with PPI. Barium esophagram shows a dilated esophagus with an air/fluid level and tapered narrowing of the distal esophagus. What is the most likely diagnosis?A. Esophageal cancerB. Esophageal strictureC. AchalasiaD. Esophageal ringAnswer C.Achalasia is a primary motility disorder of the esophagus and requires manometric diagnosis.
9Achalasia Failure of the LES to relax with swallowing Progressive dysphagia for solids and liquids and regurgitationBarium esophagram with esophageal dilation with classic “bird’s beak” appearance distallyEsophageal manometry shows lack of relaxation of the LES with swallowing and aperistalsis of the esophageal bodyAchalasia is thought to be caused by degeneration of the myenteric plexus with resulting loss of inhibitory neurons in the lower esophageal sphincter, which remains tonically contracted.Barium radiography is the primary screening test, and esophageal dilatation with the classic “bird's beak” appearance distally and the to-and-fro movement of barium (loss of peristalsis) suggest the diagnosis
10Achalasia treatment Laparoscopic Heller myotomy Pneumatic dilation Botox injection just proximal to LESNitrates/CCB offer temporary reliefSmooth muscle relaxants such as nitrates and calcium channel blockers may provide temporary relief for some patients, but do not appear to retard progression of disease.Injection of botulinum toxin into the sphincter provides symptomatic relief in up to three quarters of patients, but the effect is not usually durable; this therapy is now rarely used as first line in patients with acceptable risk for dilatation.Endoscopic pneumatic balloon dilatation provides long-lasting improvement in most patients but is associated with an approximately 5% risk of esophageal perforation.Fundoplication to prevent GERD.
11PseudoachalasiaIf obstruction at LES is caused by a malignant lesion, the disorder is designated “pseudoachalasia”Mimics manometric findings of achalasiaEGD is recommended in all suspected cases of achalasia
12GERD Most common cause of non-cardiac chest pain Indications for EGD Inappropriate LES relaxationEmpiric PPI - first dx/txRefractory GERD needs EGD, pH monitoring and/or eso manometryIndications for EGDFailure of treatmentAge > 50Symptoms > 5 yearsAlarm symptoms- Wt Loss- Dysphagia- Anemia- Inappropriate Relaxation of LES; most common etiology- Decreased esophageal acid clearance Esophageal acid is cleared by peristalsis, gravity, and neutralization from saliva and alkaline esophageal secretions. Failure of these mechanisms (which may be caused by xerostomia, cigarette smoking, medications, and esophageal motility disorders [for example, scleroderma]) can increase esophageal acid.
13GERD Treatments Life style modifications PPI H2 Blockers Fundoplication- Although H2RA therapy relieves symptoms and heals esophagitis in 50% to 60% of patients, PPI therapy provides results in 80% range.- Relief of symptoms with surgery is significant but not always long-lasting; more than half of patients who have surgery for GERD resume regular PPI therapy within 10 to 15 years after surgery. Side effects of surgery, which include dysphagia, gas-bloat syndrome, and diarrhea, occur in approximately 25% of patients.Antireflux surgery is most effective if done by an experienced surgeon in a high-volume center.
14Risks of PPI Enteric infections (C. difficile) Pneumonia Hip fractures (Osteoporosis)B12 deficiency
15Dyspepsia Definition Alarm signs - Age >55 years with new-onset symptoms- Family history of gastric cancer- Unintentional wt. loss- GI bleeding- Dysphagia/Odynophagia- Gastric outlet obstruction signs/symptomsDyspepsia is chronic or recurrent discomfort in the upper mid-abdomen.Can have peptic ulcer disease (5% to 15%), reflux esophagitis (5% to 15%), and malignancy (2%). Up to 60% of patients with dyspepsia have functional dyspepsia, which consists of a 3-month history of dyspepsia in patients who do not have peptic ulcer disease
17Question59 y/o white male with h/o GERD for the last 5-6 years. Symptoms have gotten worse lately. OTC tums don’t help much. Recent cardiac work up was negative. Denies N/V or weight loss. Also has HTN, DM, and Obesity. He is a smoker. Meds include HCTZ , Metformin. Other than BMI of 32 rest of PE is normal. Which of the following is the most appropriate management of this patient?Ambulatory esophageal pH monitoringBarium swallow studyEGDH2 BlockersC. Long-standing symptoms of gastroesophageal reflux disease should prompt an esophagogastroduodenoscopy to evaluate for Barrett esophagus.
18Barrett’s EsophagusNormal squamous epithelium of the distal esophagus is replaced by columnar epitheliumObese/white/male/smoker with GERDPre-malignant conditionIncreased risk of esophageal adenocarcinomaLong segment BE > 3 cmHistologically diagnosed by detection of specialized intestinal metaplasia and goblet cellsAnnual incidence of B
20Management of Barrett’s esophagus (AGA guidelines 2011) FindingManagementNo dysplasiaEGD every 3-5 yearsLow-grade dysplasiaEGD every 6-12 monthsHigh-grade dysplasia without eradication txEGD every 3 monthsMucosal irregularity within Barrett’sEndoscopic mucosal resectionInvasive cancerSurgeryEGD not BE
21Esophageal Squamous Cell Cancer More common in men, especially black menRisk factors:Smoking, alcohol, nitrosamine exposure, corrosive injury to esophagus, achalasia, HPVClinical presentation: Dysphagia, weight loss, GI bleed, anorexiaDx: Endoscopy. Mass usually involves upper esophagusRx: Surgery/Chemo/RadiationAdeno CA involves lower esophagus.
22Question39y/o male with PMH of seasonal allergies for past several years presented with c/o chest discomfort after he ate pork chops for lunch 2-3 hrs ago. He can’t swallow anything and feels food stuck in his chest. He has had 2 such episodes in the past. Physical examination is unremarkable. EGD is as shown. Histologic examination of the mucosa shows intense inflammation of the lamina propria with more than 15 eosinophils per HPF. No strictures are seen. What is the diagnosis?A. AchalasiaB. Severe GERDC. Eosinophilic esophagitisD. Schatzki’s ringAnswer C Rx Ppi and Oral Steroids.
23Eosinophilic Esophagitis Young adults with dysphagia and food impaction and with h/o other allergic disordersEndoscopic Dx :- Mucosal longitudinal furrowing- Circumferential ringsPathology shows > Eos/HPFTX : PPI and swallowed fluticasone
24H.Pylori Diagnosis Stool Antigen Test Urea Breath test Serum antibody testEndoscopic histology (gold standard)Stool antigen test 94% sensitive. Good positive and negative predictive value irrespective of prevalence; can be used before and after therapyUrea breath test 90%–96%; can be used before and after therapy; sensitivity affected by use of PPI, bismuth, antibioticshould be off PPI for 2-4 weeks before postTx assessment
25Treatment of H.pylori Triple Therapy PPI BID+ Amox 1 Gm + Clarithromycin 500mg BIDX daysWith PCN AllergyPPI BID + Metronidazole 500mg BID +Clarithromycin 500 mg BID X DaysQuadruple TherapyPPI BID+ Bismuth 525 mg QID + Metronidazole 500 mg BID + Tetracycline 500 mg QID X days- Treatment failure is usually the result of noncompliance with medical therapy or of antimicrobial resistance, given the low reinfection rate (<2% of patients/year)Do not use clarithromycin if Triple therapy failure. Use quadruple TXThe urea breath test and fecal antigen test detect active Helicobacter pylori infection and can be used before therapy to confirm infection and at least 4 weeks after therapy to confirm eradication.Triple therapy consisting of a proton pump inhibitor, amoxicillin, and clarithromycin is the most commonly used initial treatment for Helicobacter pylori infection.
26Peptic Ulcer Disease Causes H.PyloriNSAIDSZE SyndromeMalignancyCrohn’s diseaseViral infectionsA peptic ulcer is an ulcer of the mucous membrane of the alimentary tract caused by gastric acid.HP and NSAIDS account for 90% of ulcers.
27Peptic Ulcer Disease Complications Bleeding (most common)(Risk factors: Age and NSAIDS)PerforationGastric outlet obstructionAnemiaBleeding occurs in 15% of Ulcers. hematemesis, melena, or hematochezia; occult bleeding.Perforation: sudden, severe abdominal pain and hemodynamic compromise. Upper endoscopy is contraindicated in patients with perforation, and emergent surgical consultation is indicated.GOO ulceration in the prepyloric region or pyloric channel. Patients with obstruction present with progressive nausea, vomiting, early satiety, and weight loss.
28Management of PUD Stop NSAIDS Eradicate HP if present PPI BID x 8 weeksFollow up EGD in 8 weeks for gastric ulcersSurgery for those refractory to medical therapy
29Zollinger-Ellison Syndrome Involves gastrinoma causing ulcers and diarrheaGastrinomas are frequently in the duodenum or pancreasCan be associated with MEN 1Initial tests are 3 fasting serum gastrin levels off PPI on different daysAdditional testing includes secretin stimulation test, octreotide scan, CT/MRI to localize gastrinoma, EUS
30Upper GI Bleeding Causes Non-Variceal:Gastric and DU Ulcers Esophagitis/GastritisMallory-Weiss tear MalignancyGAVE (watermelon stomach) HemobiliaAVMs (Age, CRI, AV, OWR) Dieulafoy lesionHemosuccus pancreaticus Aortoenteric fistulaVaricealGastric and duodenal ulcers and accounting for 35% to 50% Most peptic ulcers occur secondary to Helicobacter pylori infection or use of NSAIDsEsophagitis and gastritis, which account for up to 25% of UGIBMallory-Weiss tear of the gastroesophageal junction secondary to retching, which accounts for up to 15%,rare cause but one with high morbidity in a patient with recent vascular surgery is an aortoenteric fistula.
31Question57 year old male presents with c/o weakness and melena for 3 days. No significant abdominal pain. He is orthostatic on exam. Stool is heme positive. NG suction with coffee-grounds material. HCT 30. What is the next step in management?EGDUGI seriesAngiographyInsert large-bore IV’s and T/C match for bloodEGD/Colon examAnswer D.
32Management of UGI Bleed Fluid resuscitationBlood transfusion2 large bore IV’s or Central Line PlacementPPI infusion initiallyOctreotide infusion (Variceal Bleed)EGDEpinephrine inj + Coag and/or clipsIR or Surgery if endoscopy fails
33Management of UGI Bleed Evaluate severity of bleedNGT lavage that does not clear = emergent endoscopyCoffee ground or NGT that clears in hemodynamically stable patient can waitHemodynamically unstable patient should be admitted to the ICURemember ABCsElevated BUN (normal creat) = UGI bleedLook for signs of liver disease
34Gastric Adenocarcinoma Risk factors:smoking, blood type A, H.Pylori, family history of gastric cancer, environmentalClinical Presentation:wt. loss, abd pain, early satiety, GOO, anemiaDiagnosis: Endoscopy with biopsyEUS for depth of invasion
35Gastroparesis Causes - Idiopathic - DM - Postoperative - Autoimmune disordersDiagnosis- Rule out mechanical obstruction with EGD/UGI- 4 hr Gastric emptying testRetention of more than 10% of the ingested meal at 4 hours is abnormal.The predominant causes of gastroparesis include idiopathic (33%), diabetes mellitus (25%), and postoperative states (20%). Other causes include eating disorders, renal failure, neurologic disorders (such as Parkinson disease), paraneoplastic syndromes, rheumatologic conditions (such as scleroderma), previous lung or heart-lung transplantation, and viral infections. A viral cause is suggested by rapid onset of gastroparesis after a presumed viral infection
37Gastric Bypass Roux-en-Y is the most common in US PE is the most common cause of death post-procedureIDAB12 deficiencyCalcium and Vit D deficiency
38Dumping Syndrome Early: - within 30 minutes of eating - nausea, bloating, and diarrheaLate:- 1-3 hrs after eating- hypoglycemia, tachycardia, sweatingTreatment:- low carb diet- small meals- more protein and fat in diet- Occurs after gastric surgery when ingested foods bypass the stomach too quickly and enter the small bowel largely undigested
39Gastric volvulus Abnormal rotation of the stomach around its axis Acute volvulus: pain in the upper abdomen or lower chest, inability to pass NG tube, vomitingRadiographic findingsAcute gastric volvulus is a surgical emergency. However, if the patient is a poor surgical candidate, endoscopic methods can be tried.Chronic volvulus usually has vague upper abdominal symptomsAcute volvulus can present with peritonitis, signs of complete gastric outlet obstructionThe plain radiograph of the chest shows a large central gas bubble in the thoracic cavity reminiscent of a large hiatal hernia (between white arrows). The classic finding of acute gastric volvulus on plain abdominal radiograph is a single large spherical gas bubble located in the upper abdomen or chest with an air-fluid levelComputed tomography of the lower chest of an elderly female with organoaxial volvulus shows accumulated food and fluid in a distended stomach with evidence of pneumatosis of the stomach wall (yellow arrow). A small gas bubble in the liver represents portal venous air (blue arrow).- Computed tomography (CT) of the abdomen or chest typically demonstrates a dilated stomach, often abnormally positioned in the chest. A swirl sign, in which the esophagus and stomach rotate around each other on transverse plane images, may also be evidentImages from Uptodate.com
40Lower GI Bleeding Etiologies Diverticuli HemorrhoidsIschemic colitis NSAIDs/ulcersAVMs IBDPost-polypectomy bleed Dieulafoy lesionMeckel’s Diverticulum Radiation colitisUGI cause in 10-15%LGIB is distal to the ligament of Treitz.
41Acute Diverticular Bleeding Painless bleeding with hypotension/syncopeUsually elderly patients85% of cases have spontaneous remissionDiagnosis/treatment:- Volume resuscitationwith fluids/blood- Colonoscopy & endo tx- AngiographyUp to 15% of patients with diverticulosis develop bleeding, more frequently in the elderly.Diverticular bleeding accounts for 24% to 50% of cases of lower gastrointestinal bleedingAngiography is 100% specific in identifying the affected artery, but bleeding must be active at the time of the test;
42Ischemic colitisDue to decreased mesenteric blood flow and hypoperfusion in “watershed” areasDue to non-occlusive ischemiaSudden LLQ pain with tenesmus, then passage of red-to-maroon stoolVirtually never embolicDx with colonoscopy or CTRx: Supportive care with IVF, pain control, risk factor modification, +/- antibioticsSegmental in the IMA territory - usually S.Flexure and Recto SigmoidDM,HTM,DLD,CAD, Stroke,Coagulation d/o
43Management of LGIBIdentify contributing factors by history (NSAIDS, antiplatelets, anticoagulants, radiation)Volume resuscitation with blood and IVFColonoscopic treatment with epi/coag/clipsTagged RBC scanAngiography with possible embolizationSmall bowel eval with push enteroscopy or PillcamRed blood cell scanning is positive in 45% of patients with an active bleed and has an overall accuracy for localizing the bleeding of 78%. It can detect ongoing bleeding occurring at a rate of 0.1 to 0.5 mL/min. This scan is more sensitive than angiography and is often the first radiologic test performed.Angiography cannot detect the bleeding site if the bleeding rate is less than 1 mL/min; however, the advantage of angiography as a primary modality is its ability to provide selective embolization. Initial control of hemorrhage with angiotherapy ranges from 60% to 100%.
44Obscure GI bleeding Dieulafoy lesion Hemobilia Missed lesions Meckel’s Picture shows a Dieulafoy lesion
45Meckel’s diverticulum Outpouching of the ileumCan have ectopic gastric mucosaMaroon painless bleeding per rectumCan present with intestinal obstruction or appendicitis-like symptomsCan be diagnosed by Meckel’s scan (99mmtechnetium-pertechnetate study)Picture shows a positive Meckel’s scan
46Diverticulitis Acute LLQ pain with fever and leukocytosis Diagnosis: - CT scan with contrast- Avoid colonoscopyTreatment:- Needs to cover Gram negatives and anaerobes- Cipro/Flagyl- Ampicillin-sulbactum
47Pericolonic diverticular abscess IF < 3-4 cm:- antibiotics supportivecareIF > 3-4 cm:- CT guideddrainage- antibioticsDiverticular abscess is delineated with *
48Acute Mesenteric Ischemia Do not confuse with ischemic colitisPain out of proportion to examination, acutely illDue to loss of blood flow to SB and/or ascending colonCommonly embolicOlder patients with h/o CHF, recent MI, cardiac arrhythmiasDo angiography unless there are signs of perforation
49Chronic mesenteric ischemia “Intestinal angina”Postprandial abdominal pain, abdominal bruit, weight lossCaused by atherosclerosis of intestinal arteriesOften have signs of other PVD and smoking hxDiagnosis often based on sx although MRA or spiral CT have been usedTx: angioplasty with stent placement in patients who can tolerate thisIn patients who cannot tolerate endovascular repair – could consider long-term warfarin
50Question54 y/o WF with protein S deficiency presents with a 2 day history of severe epigastric abdominal pain with nausea/vomiting. She had this CT in the ER. What is the cause of her pain?Peptic ulcer diseaseMesenteric venous thrombosisBiliary colicFunctional abdominal painAnswer B.CT image shows lack of enhancement of the SMV (solid arrow) with stranding in the fat around the vessel, findings consistent with acute thrombosis. Additional subtle infiltration of the peripancreatic and mesenteric fat (open arrows) suggests accompanying pancreatitis.Mesenteric venous thrombosis is associated with hypercoagulable statesPain is out of proportion of abdominal examMay cause varices if portal or splenic veins involvedCT is the procedure of choice
51Colon Cancer Risk factors: Age > 50 H/o adenomatous polyps H/o breast, ovarian, or endometrial CAFamily History (1st degree)Ulcerative colitis/Crohn’s colitisLifestyle (fat, fiber, obesity)3rd most common cancer in males (behind prostate and lung) and female (behind breast and lung)
52Colon Cancer Screening Average risk: begin at 50FS q5y, FIT qy- if adenoma found –proceed with colonoscopyColonoscopy q10y- if incomplete: do BECT colonography q5yAbove-average risk1 first degree relative with CRC or adenoma <60 y/o or 2 first degree relatives with CRC or adenoma: q5y- begin age 40 or 10y younger thanearliest diagnosisPersonal history of polyp: q5y- Advanced polyp (>1cm, villousfeatures, high-grade dysplasia): 3y- 3 or more polyps: 3yACG guidelines – single first degree relative with CRC or advanced adenoma > 60 years, screen as average risk
53Familial Adenomatous Polyposis (FAP) Classic version has >100 adenomatous polypsClassic has 100% CA riskProctocolectomy by age 20Periampullary duodenal cancer # 1 cause of cancer death after colectomyFAP VariantsGardner syndrome- FAP + osteomas,desmoid tumors- supernumerary teethTurcot’s variant- FAP + brain tumors(GBM or medulloblastoma)Attenuated APCadenomatous polyps
54What’s wrong with this patient? Peutz Jegher’s syndrome
55Familial Hamartomatous Polyposis Syndromes Peutz-Jeghers SyndromeMultiple hamartomatous polyps & lip/buccal hyperpigmentationHigh cancer risk (>90%)- small bowel, colon, breast,ovarian, pancreaticobiliaryCommon presentation= abd pain due to intussusception or obstruction by large polypJuvenile PolyposisHamartomas mostly in distal colonCongenital malformation of GI,GU tract and heartIncreased cancer risk- surveillance q1-3y
56Hereditary Nonpolyposis Colon Cancer (HNPCC) or Lynch Syndrome Colon CA in 3 relatives (one first degree) over 2 generations & with one diagnosed < 50 yomicrosatellite instability (MSI)MMR gene mutationsLynch I: limited to colon and rectumLynch II: increased risk of CA in female genital tract, breast, other sitesSurveillance: q1-2 yrs beginning age or 10 yrs before the age of youngest family memberq1 year after the age of 40
57Staging of Colon Cancer Stage Involvement year survivalTNM I/Duke’s A mucosa/ submucosa 95%TNM II/Duke’s B muscularis or serosa %/85%TNM III/Duke’s C regional LN’s 35%-65%TNM IV/Duke’s D metastasis 5%Note: CEA levels are only helpful for recurrence of colon & only if elevated pre-colectomy & normal afer surgery- Surgical resection is the first treatment option.Adjuvant chemo is effective only for stage III or locally advanced stage IIRadiation therapy prior to surgery is helpful for rectal lesions onlyIf a cancerous polyp is removed pt must have bowel resection if cancer extends to a blood vessel or to the cautery line
58Colon CancerIf a distal lesion is found, the entire colon needs to be “cleared” prior to treatment due to a high risk of concomitant lesionsXRT is not used for colonic lesionsRemember this because the colon “moves around” and the XRT beam can’t localize the tumorXRT is indicated for rectal cancer
59Stage C Colon Cancer Common Board Question Stage C = tumor penetrated into and/or through muscularis propria of bowel wall + pathologic evidence of colon cancer in lymph nodesTreatment is with 5-Fluorouracil and leukovorin
61Acute Diarrhea Duration Acute (< 3 weeks)Infectious, drugs, ingestion of osmotic substances.Usually self-limited (given a competent immune system)Treatment usually only with severe dehydration/toxic
62Infectious Diarrheas Bacteria Key points Treatment Staph aureus Foodborne in dairy, mayo-based salad, poultry. n/v, short incubationSupportiveETEC (E.coli)Traveler’s diarrheaSupportive, can use FQBacillus cereusReheated fried riceVibrio choleraProfuse watery diarrheaCopious rehydration. Can use doxycyclineGiardiaMalabsorption and steatorrhea, daycare, creek water.FQ or nitazoxanideCampylobacterBloody diarrhea. Uncooked poultry, unpasteurized milkSupportive, erythromycin if septicE.Coli 0157:H7Can cause HUS. Poorly cooked beefSupportive, avoid abxVibrio vulnificusRaw seafood, injury in seawater. Skin infection. Can be deadly in cirrhotics.DoxycyclineShigellaAcute bloody diarrhea with tenesmus, daycare3rd generation cephalosporinSalmonellaEggs, chicken, turtles, iguanas, other reptiles. Bloody diarrheaSupportive, avoid antibiotics unless septic, febrileSalmonella: Do not Rx uncomplicated salmonella. Treat if fever, aneurysm, vascular prosthesis and if bacteremic.Salmonella seeds anuerysms. Asstd with sickle cell disease(salmonella osteomyelitis)
63Diarrhea Pearls Guilian-Barre Campylobacter Raw eggs Salmonella HUS E.coli O157:H7Antibiotics C. diffBloody diarrhea followed by RUQ pain, fever +/- Jaundice Amebiasis (tx flagyl + paromomycin)Abd pain, bloating, frothy stool GiardiaRice water stools Vibrio
64Clostridium difficile Often will have a leukocytosisManagement depends on severity and recurrenceInitial episode:- Mild: metronidazole 500mg TID x days- Severe: vancomycin 125mg po QID x daysFirst relapse: repeat same treatment as initial episodeSecond relapse: tapering vancomycin or fidaxomicin 200mg po BID x 10 daysSubsequent relapse: fidaxomicin if not used previously vs. fecal transplantID Society of America Guidelines (also on Up to Date)
65Chronic Diarrhea Duration More complex work-up and treatment Chronic (> 3 weeks)More complex work-up and treatment
66Osmotic vs. Secretory Diarrhea Osmotic gap = (Na + K)
67Osmotic Diarrhea Etiologies Bacterial overgrowthLactase deficiency/malabsorptionDrugs (colchicine, neomycin, magnesium-containing laxatives, lactulose)Celiac diseaseTropical spruePancreatic insufficiencyWhipple’s diseaseTropical sprue – unknown etiology. Asia, Central/South America, Central/South Africa. Exposure in as little as 1 month. Tx with tetracycline and folic acid
68Laxative abuse High volume, frequent, watery diarrhea Often associated with crampy abdominal painOsmolar gap >50Usually female and may be in medical fieldStool magnesium often >108 mg/dL (45 mmol/L or 90 mEq/L) with magnesium-based laxativesTesting for laxativesWith chronic laxative use – will have hypokalemia and metabolic alkalosisTesting for laxatives – urine testing has 10x > yield than plasma. Broad screening methods for both diphenolic laxatives and anthraquinones can be done in most hospital laboratories with mass spectrometry or gas chromatography, although the accuracy of these methods is incompletely understood. Polyethylene glycol containing laxatives should specifically be measured in the stool or urine because of the widespread use of these agents
69Secretory Diarrhea Etiologies: Most common cause is infectionEnterotoxins from infections interacting with receptors causing increased anion secretionCongenital defect in transport moleculesExogenous agentsDrugs and poisonsEtiologies:Enterotoxins from E.coli, V. cholera, S. aureusVillous adenomasGastrinomasVIPomas with secretion of VIPLymphocytic colitisCollagenous colitisBile acids
70Secretory “Structural” Diarrhea There must be an adequate mucosal surface area for transport to occurCompromise water absorptionIleal resection length>100cm: Malabsorption due to decreased bile acids<100cm: Bile acid diarrheaBile acid diarrhea – managed with bile acid binding resins (such as cholestyramine)
71Carcinoid syndromeClinical symptoms: flushing, diarrhea, hypotension, hyperthermia, tachycardiaScreen with urine 5-HIAAMost tumors located in terminal ileum but can be located rarely in the bronchusTreat symptoms with octreotide
73Celiac DiseaseAbd discomfort, bloating, diarrhea, weight loss, flatulenceIDA, Vit A,D,E,K, Folic acid deficiencySteatorrhea & enteropathyAphthous stomatitisAssociated with dermatitis herpetiformis or other autoimmune disorders
74Celiac Disease Gluten-sensitive enteropathy Allergy to wheat, rye, barley, oatsDiagnosisAnti-tissue transglutaminase (tTG) most usefulIgG/IgA antigliadin antibodiesAnti-endomysial antibody less sensitiveHLA –DQ2 or HLA-DQ8Treat with gluten free dietSteroids for refractory disease
75Celiac DiseaseThe gold standard for diagnosis is biopsy from the duodenum, with the biopsy specimen showing intraepithelial lymphocytes, crypt hyperplasia, and partial to total villous atrophy.The recommended serologic test is measurement of IgA antibodies to antitissue transglutaminase
76Whipple’s Disease Tropheryma whipplei (G + Bacilli) PAS positive material in macrophagesDx by PCR on Biopsy or CSF
77Whipple’s Disease Clinical Features - Intermittent episodes of polyarthritis- Diarrhea with wt. loss- CNS: Dementia, myoclonus, ophthalmoplegia- Psych: Depression and personality changes- Card: pericarditis, myocarditisTreatment:IV Ceftriaxone x 2 weeks followed by oral Bactrim x months
78Toxic megacolon Acute toxic colitis with colonic dilation Complication of ischemic colitis, infectious colitis, C.diff, IBD, etcSigns of sepsisCan result in perforationManagement: IVF, replete electrolytes, IV antibiotics, colonic decompression, consult surgeonSurgery indicationsUsually transverse colon >6cm in diameter- Surgery indications: perforation, massive hemorrhage, increasing toxicity, no improvement in dilation on max medical therapy after h
79Colonic inertia Severe form of slow-transit constipation Disordered colonic motor functionSitz marker testConservative measures tried firstIf symptoms persist, may need surgerySitz marker test – ingestion of Sitz markers with follow up x-ray 5 days after ingestion. Retention of markers throughout (as shown in picture at right) is indicative of colonic inertiaConservative measures – increase fiber, exercise, osmotic laxative, stimulant laxative
80Question55 y/o F presented with a 2-month history of profuse watery diarrhea up to 5 times per day without bleeding, abdominal pain or vomiting. She had lost 5lbs but there was no history of iritis, arthritis, rashes or aphthous ulcers. Exam was normal. Labs revealed a normal CBC, CMP, and CRP. There was no growth on stool culture. Colonoscopy was normal without ulceration. Her biopsies are shown. What is causing her symptoms?Crohn’s diseaseUlcerative colitisMicroscopic colitisIrritable bowel syndrome – diarrhea predominantC. Microscopic colitis consists of collagenous colitis and lymphocytic colitis.Often occur in middle-aged females. There is a higher incidence of autoimmune conditions such as celiac diseaseColonoscopy is often normal or near normal. Changes are often patchy so multiple biopsies must be taken to catch thisIn lymphocytic colitis – colonic biopsies reveal increased lymphocytes in the surface epithelium and in the lamina propriaIn collagenous colitis, the features of lymphocytic colitis are present, along with a thickened subepithelial collagenous layer
81Irritable bowel syndrome Chronic crampy abdominal pain, alternating bowel habits, improves with defecationRome criteriaTreatment:- Reassurance- Dietary modifications including low FODMAPdiet- adjunctive medical therapyRome criteria: Recurrent abdominal pain or discomfort at least 3 days per month in the last 3 months associated with 2 or more of the following: (1) improvement with defecation (2) onset associated with a change in frequency of stool (3) onset associated with a change in form of stoolDietary modifications: exclusion of gas producing foods, lactose avoidance, low FODMAP dietLow FODMAP: low fermentable oligo-, di-, and monosaccharides and polyols – these short chain carbs are poorly absorbed and are osmotically active in the intestinal lumen where they are rapidly fermented, resulting in symptoms of abdominal bloating and painMed tx: For constipation predominant – osmotic laxatives, lubiprostone. For diarrhea-predominant, antidiarrheals, bile acid binders (cholestyramine). For abdominal pain – antispasmodics (dicyclomine, hyoscyamine), TCAs (elavil).
83IBD Clinical Pearls GI CA UC >>> Crohn’s Toxic megacolon BothBE contraindicated in acute exacerbationSmoking & CD risk exacerbationSmoking & UC UC symptoms can start w/tobacco cessation
84Crohn’s Disease: Pearls Bimodal age distributionPeak 20-30sSmaller one in 70-80sASCA+ in 50-60%Granulomas are pathognomonic……but seldom seen“String sign” in TI on SBFT30% colon, 40% SB, 30% both“mouth to anus”
85Ulcerative Colitis: Pearls Area of involvementproctitisleft-sided colitispancolitis (“universal colitis”)70-80% P-ANCA +
86IBD Treatments 5 ASA Several designer drugs “col” = colon (Asacol, Colazal…)Steroids—avoid if possibleBudesonide (Entocort)Azathioprine/6-MPImmunomodulatorSteroid-sparing agentMonitor for SEsMethotrexateAntibioticsAnti-TNF therapiesFistulizing diseaseUnresponsive to conventional therapy
87IBD Extraintestinal Manifestations Usually seen in colitis therefore more common in UCSeronegative arthropathyUveitis, Ankylosing Spondylitis (HLA-B27)Erythema nodosumPyoderma gangrenosumPrimary sclerosing cholangitis (HLA-B8)PSC, check ALP annually 2X ULN ERCP/MRCPOsteoporosisHLA associated manifestations do not correlate with course of colitis
88UC and Cancer Duration & extent of disease, age at dx increases risk Ulcerative Proctitis has no risk CA10 years 2%20 years 15%Pancolitis- begin at 8 years (AGA guidelines)Left sided colitis- begin at 15 years (AGA guidelines)Colonoscopies are generally performed q1-2 years after surveillance is started, depending on findingsHigh-grade dysplasia or cancer colectomyLow grade dysplasia management is controversial
89Physical Exam Pearls Emaciation, cheilosis, glossitis Severe malabsorptionAssociated dermatitis herpetiformisCeliac sprueAssociated pyoderma gangrenosum-- IBDArthritisIBD or Whipple’sPulmonic stenosis and tricuspid regurgitationCarcinoid syndrome
90Physical Exam Pearls Associated neuropsychiatric findings Whipple’s diseaseAbdominal massMalignancy, Crohn’s, diverticulitisLocalized abdominal tendernessInflammatory conditionPerianal ulcers/fistulas, reduced sphincter tone/incontinence/right sided abdominal pain Crohn’sPeripheral or autonomic neuropathyMay correlate with visceral neuropathy in DM and intestinal pseudo-obstruction