GI Board Review Elizabeth Paine, MD Division of Digestive Diseases

GI Board Review Elizabeth Paine, MD Division of Digestive Diseases
The University of Mississippi Medical Center

Esophagus Proximal 1/3 esophagus- striated muscles under CNS control
Distal 2/3 esophagus- smooth muscle under vagal and myenteric nervous system control UES and LES are normally in a contracted state Initiation of swallow relaxes both of the sphincters

Question 70 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 CT Answer – 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

Dysphagia Oropharyngeal Dysphagia - Structural disorders
- Neurological disorders (Stroke, ALS, myasthenia gravis, Parkinson’s, myotonic dystrophy) Esophageal Dysphagia Oropharyngeal: - 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

Esophageal Dysphagia Solids Only: Solids and Liquids: Characteristic
Etiology Treatment Intermittent Schatzki’s ring Dilation Progressive + heartburn Peptic stricture Dilation + PPI Progressive + weight loss Esophageal cancer Depends on stage Solids+ Liquids usually motility d/o. Adeno CA: Barretts/GERD Squamous cell carcinoma: Older, smoking Characteristic Etiology Treatment Intermittent + chest pain Diffuse esophageal spasm PPI + nitrates/CCB Progressive + heartburn Scleroderma PPI Progressive + no GERD Achalasia Heller myotomy, pneumatic dilation

Schatzki’s Ring 45yo M with longstanding GERD presenting with 6 months of intermittent solid food dysphagia

Odynophagia Ulcerative Esophagitis - Due to infection or pill
- Viral (HSV,CMV) - Candida - most common Pill-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.

Question 55 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 cancer B. Esophageal stricture C. Achalasia D. Esophageal ring Answer C. Achalasia is a primary motility disorder of the esophagus and requires manometric diagnosis.

Achalasia Failure of the LES to relax with swallowing
Progressive dysphagia for solids and liquids and regurgitation Barium esophagram with esophageal dilation with classic “bird’s beak” appearance distally Esophageal manometry shows lack of relaxation of the LES with swallowing and aperistalsis of the esophageal body Achalasia 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

Achalasia treatment Laparoscopic Heller myotomy Pneumatic dilation
Botox injection just proximal to LES Nitrates/CCB offer temporary relief Smooth 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.

Pseudoachalasia If obstruction at LES is caused by a malignant lesion, the disorder is designated “pseudoachalasia” Mimics manometric findings of achalasia EGD is recommended in all suspected cases of achalasia

GERD Most common cause of non-cardiac chest pain Indications for EGD
Inappropriate LES relaxation Empiric PPI - first dx/tx Refractory GERD needs EGD, pH monitoring and/or eso manometry Indications for EGD Failure of treatment Age > 50 Symptoms > 5 years Alarm 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.

GERD 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.

Risks of PPI Enteric infections (C. difficile) Pneumonia
Hip fractures (Osteoporosis) B12 deficiency

Dyspepsia 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/symptoms Dyspepsia 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

Dyspepsia

Question 59 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 monitoring Barium swallow study EGD H2 Blockers C. Long-standing symptoms of gastroesophageal reflux disease should prompt an esophagogastroduodenoscopy to evaluate for Barrett esophagus.

Barrett’s Esophagus Normal squamous epithelium of the distal esophagus is replaced by columnar epithelium Obese/white/male/smoker with GERD Pre-malignant condition Increased risk of esophageal adenocarcinoma Long segment BE > 3 cm Histologically diagnosed by detection of specialized intestinal metaplasia and goblet cells Annual incidence of B

Barrett’s Esophagus

Management of Barrett’s esophagus (AGA guidelines 2011)
Finding Management No dysplasia EGD every 3-5 years Low-grade dysplasia EGD every 6-12 months High-grade dysplasia without eradication tx EGD every 3 months Mucosal irregularity within Barrett’s Endoscopic mucosal resection Invasive cancer Surgery EGD not BE

Esophageal Squamous Cell Cancer
More common in men, especially black men Risk factors: Smoking, alcohol, nitrosamine exposure, corrosive injury to esophagus, achalasia, HPV Clinical presentation: Dysphagia, weight loss, GI bleed, anorexia Dx: Endoscopy. Mass usually involves upper esophagus Rx: Surgery/Chemo/Radiation Adeno CA involves lower esophagus.

Question 39y/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. Achalasia B. Severe GERD C. Eosinophilic esophagitis D. Schatzki’s ring Answer C Rx Ppi and Oral Steroids.

Eosinophilic Esophagitis
Young adults with dysphagia and food impaction and with h/o other allergic disorders Endoscopic Dx : - Mucosal longitudinal furrowing - Circumferential rings Pathology shows > Eos/HPF TX : PPI and swallowed fluticasone

H.Pylori Diagnosis Stool Antigen Test Urea Breath test
Serum antibody test Endoscopic histology (gold standard) Stool antigen test 94% sensitive. Good positive and negative predictive value irrespective of prevalence; can be used before and after therapy Urea breath test 90%–96%; can be used before and after therapy; sensitivity affected by use of PPI, bismuth, antibiotic should be off PPI for 2-4 weeks before postTx assessment

Treatment of H.pylori Triple Therapy
PPI BID+ Amox 1 Gm + Clarithromycin 500mg BID X days With PCN Allergy PPI BID + Metronidazole 500mg BID + Clarithromycin 500 mg BID X Days Quadruple Therapy PPI 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 TX The 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.

Peptic Ulcer Disease Causes
H.Pylori NSAIDS ZE Syndrome Malignancy Crohn’s disease Viral infections A 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.

Peptic Ulcer Disease Complications
Bleeding (most common) (Risk factors: Age and NSAIDS) Perforation Gastric outlet obstruction Anemia Bleeding 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.

Management of PUD Stop NSAIDS Eradicate HP if present
PPI BID x 8 weeks Follow up EGD in 8 weeks for gastric ulcers Surgery for those refractory to medical therapy

Zollinger-Ellison Syndrome
Involves gastrinoma causing ulcers and diarrhea Gastrinomas are frequently in the duodenum or pancreas Can be associated with MEN 1 Initial tests are 3 fasting serum gastrin levels off PPI on different days Additional testing includes secretin stimulation test, octreotide scan, CT/MRI to localize gastrinoma, EUS

Upper GI Bleeding Causes
Non-Variceal: Gastric and DU Ulcers Esophagitis/Gastritis Mallory-Weiss tear Malignancy GAVE (watermelon stomach) Hemobilia AVMs (Age, CRI, AV, OWR) Dieulafoy lesion Hemosuccus pancreaticus Aortoenteric fistula Variceal Gastric and duodenal ulcers and accounting for 35% to 50% Most peptic ulcers occur secondary to Helicobacter pylori infection or use of NSAIDs Esophagitis and gastritis, which account for up to 25% of UGIB Mallory-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.

Question 57 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? EGD UGI series Angiography Insert large-bore IV’s and T/C match for blood EGD/Colon exam Answer D.

Management of UGI Bleed
Fluid resuscitation Blood transfusion 2 large bore IV’s or Central Line Placement PPI infusion initially Octreotide infusion (Variceal Bleed) EGD Epinephrine inj + Coag and/or clips IR or Surgery if endoscopy fails

Management of UGI Bleed
Evaluate severity of bleed NGT lavage that does not clear = emergent endoscopy Coffee ground or NGT that clears in hemodynamically stable patient can wait Hemodynamically unstable patient should be admitted to the ICU Remember ABCs Elevated BUN (normal creat) = UGI bleed Look for signs of liver disease

Gastric Adenocarcinoma
Risk factors: smoking, blood type A, H.Pylori, family history of gastric cancer, environmental Clinical Presentation: wt. loss, abd pain, early satiety, GOO, anemia Diagnosis: Endoscopy with biopsy EUS for depth of invasion

Gastroparesis Causes - Idiopathic - DM - Postoperative
- Autoimmune disorders Diagnosis - Rule out mechanical obstruction with EGD/UGI - 4 hr Gastric emptying test Retention 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

Gastroparesis Management
Low fat and low fiber diet Small/frequent meals Antiemetics Prokinetics GES Feeding jejunostomy tube TPN

Gastric Bypass Roux-en-Y is the most common in US
PE is the most common cause of death post-procedure IDA B12 deficiency Calcium and Vit D deficiency

Dumping Syndrome Early: - within 30 minutes of eating
- nausea, bloating, and diarrhea Late: - 1-3 hrs after eating - hypoglycemia, tachycardia, sweating Treatment: - 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

Gastric volvulus Abnormal rotation of the stomach around its axis
Acute volvulus: pain in the upper abdomen or lower chest, inability to pass NG tube, vomiting Radiographic findings Acute 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 symptoms Acute volvulus can present with peritonitis, signs of complete gastric outlet obstruction The 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 level Computed 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 evident Images from Uptodate.com

Lower GI Bleeding Etiologies
Diverticuli Hemorrhoids Ischemic colitis NSAIDs/ulcers AVMs IBD Post-polypectomy bleed Dieulafoy lesion Meckel’s Diverticulum Radiation colitis UGI cause in 10-15% LGIB is distal to the ligament of Treitz.

Acute Diverticular Bleeding
Painless bleeding with hypotension/syncope Usually elderly patients 85% of cases have spontaneous remission Diagnosis/treatment: - Volume resuscitation with fluids/blood - Colonoscopy & endo tx - Angiography Up 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 bleeding Angiography is 100% specific in identifying the affected artery, but bleeding must be active at the time of the test;

Ischemic colitis Due to decreased mesenteric blood flow and hypoperfusion in “watershed” areas Due to non-occlusive ischemia Sudden LLQ pain with tenesmus, then passage of red-to-maroon stool Virtually never embolic Dx with colonoscopy or CT Rx: Supportive care with IVF, pain control, risk factor modification, +/- antibiotics Segmental in the IMA territory - usually S.Flexure and Recto Sigmoid DM,HTM,DLD,CAD, Stroke,Coagulation d/o

Management of LGIB Identify contributing factors by history (NSAIDS, antiplatelets, anticoagulants, radiation) Volume resuscitation with blood and IVF Colonoscopic treatment with epi/coag/clips Tagged RBC scan Angiography with possible embolization Small bowel eval with push enteroscopy or Pillcam Red 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%.

Obscure GI bleeding Dieulafoy lesion Hemobilia Missed lesions Meckel’s
Picture shows a Dieulafoy lesion

Meckel’s diverticulum
Outpouching of the ileum Can have ectopic gastric mucosa Maroon painless bleeding per rectum Can present with intestinal obstruction or appendicitis-like symptoms Can be diagnosed by Meckel’s scan (99mmtechnetium-pertechnetate study) Picture shows a positive Meckel’s scan

Diverticulitis Acute LLQ pain with fever and leukocytosis Diagnosis:
- CT scan with contrast - Avoid colonoscopy Treatment: - Needs to cover Gram negatives and anaerobes - Cipro/Flagyl - Ampicillin-sulbactum

Pericolonic diverticular abscess
IF < 3-4 cm: - antibiotics supportive care IF > 3-4 cm: - CT guided drainage - antibiotics Diverticular abscess is delineated with *

Acute Mesenteric Ischemia
Do not confuse with ischemic colitis Pain out of proportion to examination, acutely ill Due to loss of blood flow to SB and/or ascending colon Commonly embolic Older patients with h/o CHF, recent MI, cardiac arrhythmias Do angiography unless there are signs of perforation

Chronic mesenteric ischemia
“Intestinal angina” Postprandial abdominal pain, abdominal bruit, weight loss Caused by atherosclerosis of intestinal arteries Often have signs of other PVD and smoking hx Diagnosis often based on sx although MRA or spiral CT have been used Tx: angioplasty with stent placement in patients who can tolerate this In patients who cannot tolerate endovascular repair – could consider long-term warfarin

Question 54 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 disease Mesenteric venous thrombosis Biliary colic Functional abdominal pain Answer 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 states Pain is out of proportion of abdominal exam May cause varices if portal or splenic veins involved CT is the procedure of choice

Colon Cancer Risk factors: Age > 50 H/o adenomatous polyps
H/o breast, ovarian, or endometrial CA Family History (1st degree) Ulcerative colitis/Crohn’s colitis Lifestyle (fat, fiber, obesity) 3rd most common cancer in males (behind prostate and lung) and female (behind breast and lung)

Colon Cancer Screening
Average risk: begin at 50 FS q5y, FIT qy - if adenoma found – proceed with colonoscopy Colonoscopy q10y - if incomplete: do BE CT colonography q5y Above-average risk 1 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 than earliest diagnosis Personal history of polyp: q5y - Advanced polyp (>1cm, villous features, high-grade dysplasia): 3y - 3 or more polyps: 3y ACG guidelines – single first degree relative with CRC or advanced adenoma > 60 years, screen as average risk

Familial Adenomatous Polyposis (FAP)
Classic version has >100 adenomatous polyps Classic has 100% CA risk Proctocolectomy by age 20 Periampullary duodenal cancer # 1 cause of cancer death after colectomy FAP Variants Gardner syndrome - FAP + osteomas, desmoid tumors - supernumerary teeth Turcot’s variant - FAP + brain tumors (GBM or medulloblastoma) Attenuated APC adenomatous polyps

What’s wrong with this patient?
Peutz Jegher’s syndrome

Familial Hamartomatous Polyposis Syndromes
Peutz-Jeghers Syndrome Multiple hamartomatous polyps & lip/buccal hyperpigmentation High cancer risk (>90%) - small bowel, colon, breast, ovarian, pancreaticobiliary Common presentation= abd pain due to intussusception or obstruction by large polyp Juvenile Polyposis Hamartomas mostly in distal colon Congenital malformation of GI,GU tract and heart Increased cancer risk - surveillance q1-3y

Hereditary Nonpolyposis Colon Cancer (HNPCC) or Lynch Syndrome
Colon CA in 3 relatives (one first degree) over 2 generations & with one diagnosed < 50 yo microsatellite instability (MSI) MMR gene mutations Lynch I: limited to colon and rectum Lynch II: increased risk of CA in female genital tract, breast, other sites Surveillance: q1-2 yrs beginning age or 10 yrs before the age of youngest family member q1 year after the age of 40

Staging of Colon Cancer
Stage Involvement year survival TNM 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 II Radiation therapy prior to surgery is helpful for rectal lesions only If a cancerous polyp is removed pt must have bowel resection if cancer extends to a blood vessel or to the cautery line

Colon Cancer If a distal lesion is found, the entire colon needs to be “cleared” prior to treatment due to a high risk of concomitant lesions XRT is not used for colonic lesions Remember this because the colon “moves around” and the XRT beam can’t localize the tumor XRT is indicated for rectal cancer

Stage 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 nodes Treatment is with 5-Fluorouracil and leukovorin

Classification of Diarrhea

Acute 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

Infectious Diarrheas Bacteria Key points Treatment Staph aureus
Foodborne in dairy, mayo-based salad, poultry. n/v, short incubation Supportive ETEC (E.coli) Traveler’s diarrhea Supportive, can use FQ Bacillus cereus Reheated fried rice Vibrio cholera Profuse watery diarrhea Copious rehydration. Can use doxycycline Giardia Malabsorption and steatorrhea, daycare, creek water. FQ or nitazoxanide Campylobacter Bloody diarrhea. Uncooked poultry, unpasteurized milk Supportive, erythromycin if septic E.Coli 0157:H7 Can cause HUS. Poorly cooked beef Supportive, avoid abx Vibrio vulnificus Raw seafood, injury in seawater. Skin infection. Can be deadly in cirrhotics. Doxycycline Shigella Acute bloody diarrhea with tenesmus, daycare 3rd generation cephalosporin Salmonella Eggs, chicken, turtles, iguanas, other reptiles. Bloody diarrhea Supportive, avoid antibiotics unless septic, febrile Salmonella: Do not Rx uncomplicated salmonella. Treat if fever, aneurysm, vascular prosthesis and if bacteremic. Salmonella seeds anuerysms. Asstd with sickle cell disease(salmonella osteomyelitis)

Diarrhea Pearls Guilian-Barre Campylobacter Raw eggs  Salmonella
HUS  E.coli O157:H7 Antibiotics  C. diff Bloody diarrhea followed by RUQ pain, fever +/- Jaundice  Amebiasis (tx flagyl + paromomycin) Abd pain, bloating, frothy stool Giardia Rice water stools Vibrio

Clostridium difficile
Often will have a leukocytosis Management depends on severity and recurrence Initial episode: - Mild: metronidazole 500mg TID x days - Severe: vancomycin 125mg po QID x days First relapse: repeat same treatment as initial episode Second relapse: tapering vancomycin or fidaxomicin 200mg po BID x 10 days Subsequent relapse: fidaxomicin if not used previously vs. fecal transplant ID Society of America Guidelines (also on Up to Date)

Chronic Diarrhea Duration More complex work-up and treatment
Chronic (> 3 weeks) More complex work-up and treatment

Osmotic vs. Secretory Diarrhea
Osmotic gap = (Na + K)

Osmotic Diarrhea Etiologies
Bacterial overgrowth Lactase deficiency/malabsorption Drugs (colchicine, neomycin, magnesium-containing laxatives, lactulose) Celiac disease Tropical sprue Pancreatic insufficiency Whipple’s disease Tropical sprue – unknown etiology. Asia, Central/South America, Central/South Africa. Exposure in as little as 1 month. Tx with tetracycline and folic acid

Laxative abuse High volume, frequent, watery diarrhea
Often associated with crampy abdominal pain Osmolar gap >50 Usually female and may be in medical field Stool magnesium often >108 mg/dL (45 mmol/L or 90 mEq/L) with magnesium-based laxatives Testing for laxatives With chronic laxative use – will have hypokalemia and metabolic alkalosis Testing 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

Secretory Diarrhea Etiologies:
Most common cause is infection Enterotoxins from infections interacting with receptors causing increased anion secretion Congenital defect in transport molecules Exogenous agents Drugs and poisons Etiologies: Enterotoxins from E.coli, V. cholera, S. aureus Villous adenomas Gastrinomas VIPomas with secretion of VIP Lymphocytic colitis Collagenous colitis Bile acids

Secretory “Structural” Diarrhea
There must be an adequate mucosal surface area for transport to occur Compromise water absorption Ileal resection length >100cm: Malabsorption due to decreased bile acids <100cm: Bile acid diarrhea Bile acid diarrhea – managed with bile acid binding resins (such as cholestyramine)

Carcinoid syndrome Clinical symptoms: flushing, diarrhea, hypotension, hyperthermia, tachycardia Screen with urine 5-HIAA Most tumors located in terminal ileum but can be located rarely in the bronchus Treat symptoms with octreotide

Fat Malabsorption Celiac Disease Small-Intestinal Bacterial Overgrowth
Short-bowel syndrome Pancreatic Insufficiency

Celiac Disease Abd discomfort, bloating, diarrhea, weight loss, flatulence IDA, Vit A,D,E,K, Folic acid deficiency Steatorrhea & enteropathy Aphthous stomatitis Associated with dermatitis herpetiformis or other autoimmune disorders

Celiac Disease Gluten-sensitive enteropathy
Allergy to wheat, rye, barley, oats Diagnosis Anti-tissue transglutaminase (tTG) most useful IgG/IgA antigliadin antibodies Anti-endomysial antibody less sensitive HLA –DQ2 or HLA-DQ8 Treat with gluten free diet Steroids for refractory disease

Celiac Disease The 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

Whipple’s Disease Tropheryma whipplei (G + Bacilli)
PAS positive material in macrophages Dx by PCR on Biopsy or CSF

Whipple’s Disease Clinical Features
- Intermittent episodes of polyarthritis - Diarrhea with wt. loss - CNS: Dementia, myoclonus, ophthalmoplegia - Psych: Depression and personality changes - Card: pericarditis, myocarditis Treatment: IV Ceftriaxone x 2 weeks followed by oral Bactrim x months

Toxic megacolon Acute toxic colitis with colonic dilation
Complication of ischemic colitis, infectious colitis, C.diff, IBD, etc Signs of sepsis Can result in perforation Management: IVF, replete electrolytes, IV antibiotics, colonic decompression, consult surgeon Surgery indications Usually transverse colon >6cm in diameter - Surgery indications: perforation, massive hemorrhage, increasing toxicity, no improvement in dilation on max medical therapy after h

Colonic inertia Severe form of slow-transit constipation
Disordered colonic motor function Sitz marker test Conservative measures tried first If symptoms persist, may need surgery Sitz 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 inertia Conservative measures – increase fiber, exercise, osmotic laxative, stimulant laxative

Question 55 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 disease Ulcerative colitis Microscopic colitis Irritable bowel syndrome – diarrhea predominant C. 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 disease Colonoscopy is often normal or near normal. Changes are often patchy so multiple biopsies must be taken to catch this In lymphocytic colitis – colonic biopsies reveal increased lymphocytes in the surface epithelium and in the lamina propria In collagenous colitis, the features of lymphocytic colitis are present, along with a thickened subepithelial collagenous layer

Irritable bowel syndrome
Chronic crampy abdominal pain, alternating bowel habits, improves with defecation Rome criteria Treatment: - Reassurance - Dietary modifications including low FODMAP diet - adjunctive medical therapy Rome 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 stool Dietary modifications: exclusion of gas producing foods, lactose avoidance, low FODMAP diet Low 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 pain Med tx: For constipation predominant – osmotic laxatives, lubiprostone. For diarrhea-predominant, antidiarrheals, bile acid binders (cholestyramine). For abdominal pain – antispasmodics (dicyclomine, hyoscyamine), TCAs (elavil).

Inflammatory Bowel Disease
Crohn’s disease Ulcerative colitis Lesions Focal, skip, deep Shallow, continuous Clinical Course Indolent More acute Steroids Less responsive Very responsive Granuloma Pathognomonic None Rectal Involvement Rectal sparing Rectum involved Perianal disease Abscesses, fistulas

IBD Clinical Pearls  GI CA  UC >>> Crohn’s
Toxic megacolon  Both BE contraindicated in acute exacerbation Smoking & CD   risk exacerbation Smoking & UC  UC symptoms can start w/tobacco cessation

Crohn’s Disease: Pearls
Bimodal age distribution Peak 20-30s Smaller one in 70-80s ASCA+ in 50-60% Granulomas are pathognomonic… …but seldom seen “String sign” in TI on SBFT 30% colon, 40% SB, 30% both “mouth to anus”

Ulcerative Colitis: Pearls
Area of involvement proctitis left-sided colitis pancolitis (“universal colitis”) 70-80% P-ANCA +

IBD Treatments 5 ASA Several designer drugs
“col” = colon (Asacol, Colazal…) Steroids—avoid if possible Budesonide (Entocort) Azathioprine/6-MP Immunomodulator Steroid-sparing agent Monitor for SEs Methotrexate Antibiotics Anti-TNF therapies Fistulizing disease Unresponsive to conventional therapy

IBD Extraintestinal Manifestations
Usually seen in colitis therefore more common in UC Seronegative arthropathy Uveitis, Ankylosing Spondylitis (HLA-B27) Erythema nodosum Pyoderma gangrenosum Primary sclerosing cholangitis (HLA-B8) PSC, check ALP annually  2X ULN  ERCP/MRCP Osteoporosis HLA associated manifestations do not correlate with course of colitis

UC and Cancer Duration & extent of disease, age at dx increases risk
Ulcerative Proctitis has no  risk CA 10 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 findings High-grade dysplasia or cancer  colectomy Low grade dysplasia management is controversial

Physical Exam Pearls Emaciation, cheilosis, glossitis
Severe malabsorption Associated dermatitis herpetiformis Celiac sprue Associated pyoderma gangrenosum -- IBD Arthritis IBD or Whipple’s Pulmonic stenosis and tricuspid regurgitation Carcinoid syndrome

Physical Exam Pearls Associated neuropsychiatric findings
Whipple’s disease Abdominal mass Malignancy, Crohn’s, diverticulitis Localized abdominal tenderness Inflammatory condition Perianal ulcers/fistulas, reduced sphincter tone/incontinence/right sided abdominal pain Crohn’s Peripheral or autonomic neuropathy May correlate with visceral neuropathy in DM and intestinal pseudo-obstruction

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GI Board Review Elizabeth Paine, MD Division of Digestive Diseases

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GI Board Review Elizabeth Paine, MD Division of Digestive Diseases

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