GastroenterologyArcher online USMLE Reviews

www.CccsWorkshop.com

These slides are to be used with Archer Gastroenterology Video

lectures

All rights reserved

Esophageal Disorders

Symptoms

• Look for symptoms in the Q and its duration • If Dysphagia – is it progressive or

intermittent? To liquids alone or both solids and liquids? Site ? Oropharyngeal ? esophageal

• If Odynophagia think about ?HIV, ?Immunosuppression ? Reflux esophagitis

• Chest pain ? Quality ? Burning ? Positional changes ? Reflux ? regurgitation

• Warning signs weight loss, iron deficiency anemia, persistent vomiting, symptoms not responding to PPIs, Dysphagia with GERD

Symptoms - Dysphagia• Obstructive lesions (LUMEN PROBLEM) present with

dysphagia predominantly to solids ( liquids slide and may pass esply when there’s no total

obstruction) Cancer ( clue: weightloss) , Stricture ( peptic ( clue:chronic

heartburn) / malignant ) progressive to solids

Schatzki ring ( lower esophagus mucosal ring) intermittent to solids

• Motility disorders present with dysphagia usually both to liquids and solids.

Eg: Progressive Achalasia cardia ( clues : hx of aspiration, regurgitation), Scleroderma ( clues: chronic heartburn)

Intermittent Diffuse esophageal spasm, Nutcrackers esophagus ( clues : severe intermittent chestpain)

Diagnosis - Dysphagia• For the exam – its always barium esophagogram ( what if theres a malignant stricture

– u cant pass scope beyond it may perforate!!)• Barium swallow shows oropharyngeal dysphagia

especially in the old think about neuromuscular diseases CVA, Parkinsons, Myesthenia Gravis, polio, dermatomyositis, hypothyroidism, multiple sclerosis. Videopharyngoesophagoscopy will help in confirming this diagnosis

• Barium Esophagogram shows obstructive lesion irregular (?cancer, stricture), smooth ( achalasia, scleroderma) proceed with upper Endoscopy. EGD shows obstructive lesion biopsy, dilatation if benign stricture is more likely

If Endoscopy is Normal suspect motility disorder ( even if ur clinical scenario points to a motility disorder u still have to do endoscopy) Proceed with Manometry

Diagnosis - Dysphagia

• Manometry – evaluates contractile function of esophagus.

- Used to determine the possibility of motility disorders in pts with dysphagia and NORMAL findings on upper endoscopy.

- Used to rule out esophageal motility disorders prior to surgical fundoplication (GERD)

OdynophagiaPainful swallowing ( Inflammatory) ( Esophagitis)• GERD ( Reflux esophagitis)• Scleroderma ( chronic heartburn) look for skin signs like sclerodactyly,

telangiectasias• Infectious candida ( clue: thrush), HSV, CMV ( Clue: CD4<50) In HIV

pt coming with oralthrush and odynophagia , no need for EGD, First treat with fluconozole. If no improvement EGD and biopsy Single, shallow ulcer ( CMV) ( Rx Ganciclovir)

Multiple, punched out ulcers, raised edges HSV ( Acyclovir. Use foscarnet for resistant cases)

• Also keep in mind Giant aphthus ulcers associated with HIV. If EGD & Biopsy negative for infectious etiology think about this ( rx with corticostroids, antiretroviral therapy)

• Pill Esophagitis Doxycycline, Alendronate ( Bisphosphonates), NSAIDS, Ascorbic acid, Quinidine, KCL account for 90% cases of pill esophagitis Diagnosis is made with air contrast barium studies which usually show circumferentially distributed superficial ulcers and erosion. Typical location is in the midesophagus near the anatomic site of compression by the aortic arch and the left main stem bronchus. Symptoms resolve about 7 to 10 days after the offending agent is discontinued.

• Radiation Esophagitis Depending on the dose given, radiation can cause immediate esophagitis. Rx is sUpportive – stop medication, if acid refulx + control it with PPIs

GERD• Symptoms• PPI Trial, Lifestyle changes• Sx if no response or if chronic and pt opts for sx rather than

PPIs – fundoplication/ manometry before fundoplication.• Warning signs• When to do EGD Either warning signs or greater than 5

years of chronic GERD• Important problem recognize various presentations

Asthma, Nocturnal cough, Hoarseness, sorethroat, malignancy• Complications reflux esophagitis, stricture, Barretts

esophagus, adenoca, Asthma• When to do 24 hr ambulatory Ph monitoring? this helps to

quantitate esophageal exposure to acid, Should be done in pts with persistent typical or atypical symptoms of GERD without evidence of esophageal mucosal damage (i.e; normal endoscopy) Should be done prior to antirefulx surgery to confirm that refux does exist

Barretts Esophagus

• Do EGD 5 years after Chronic GERD ( to r/o barretts) or persistent symptoms not responding to PPIs ( to r/o other causes) or warning signs ( dysphagia, bleeding, weightloss, choking)

• 10% pts with chronic heartburn and regurgitation progress to Barretts esophagus. Adenoca develops in barretts esophagus at a rate of 0.5% per year.

• Barretts is suspected by findings at upper endoscopy and is confirmed by histopathology of biopsy.

• If Barretts present enroll this pt in endoscopic surveillance program to identify progression to high grade dysplasia. If no dysplasia do EGD and biopsy every 2 years. If low grade dysplasia every 6 months to one year. If high grade dysplasia esophagectomy to prevent progression to adenoca.

Case study• A 75 y/o female presents to you with two day symptoms of burning

pain in the retrosternal area that increases on lying down. She also has hoarseness. Her medications include calcium carbonate and alendronate for osteoporosis that was started 1 week ago, enalapril for hypertension and glipizide for her diabetes. She does not report weightloss of hemetemesis. Physical exam is unremarkable except for mild livedo reticularis on her extremities. An EKG, Cardiac enzymes are negative and CBC does not reveal Anemia. Her pastmedical history is significant for smoking 1ppd x 30 years. Most appropriate statement about this patients condition is:

• A) Avoiding smoking would have prevented this condition• B) Life style changes like reducing the aggravating foods and lying

with head end elevated would have prevented her symptoms• C) She most likely has a cancer in view of her smoking history• D) She could have prevented this by drinking at least 4 ounces of

fluid with alendronate and avoiding supine position post alendronate ingestion

• E) She has scleroderma

GI bleeding

• Occult bleeding

• Obscure bleeding - management

• Upper GI bleeding

• Lower GI bleeding

• Iron deficiency anemia

Occult Bleeding

• Stool Guaic

• False negatives

• Approach to work up

Variceal Bleeding

• Causes – portal hypertension

• Management strategies

• Gastric varices without esophageal varices splenic vein thrombosis Rx is splenectomy

Ishemic disease - GI

• Mesenteric Ischemia acute, chronic

• Ischemic Colitis look for Pneumatosis intestinalis on x-ray management

Q• A 24-year-old woman is hospitalized after a sudden episode of lightheadedness

followed by passage of maroon-colored stools. She denies abdominal pain or weight loss. One year ago, she was hospitalized for similar findings and required transfusion of 4 units of packed erythrocytes. Upper endoscopy, colonoscopy, and small bowel radiograph series were normal at that time. Following volume replacement with isotonic saline, the patient is pale but has no other abnormalities on physical examination. Hemoglobin is initially 8.4 g/dL but increases to 11.2 g/dL after transfusion of 3 units of packed erythrocytes. The hemoglobin level remains stable, and stool color normalizes. Upper endoscopy, colonoscopy with terminal ileoscopy, and enteroscopy of the proximal small bowel are normal. Radionuclide scanning using 99m-Tc pertechnetate (Meckel's scan) is negative.Which of the following is the most appropriate next step in evaluating this patient?

• ( A ) Wireless capsule endoscopy• ( B ) Technetium-labeled red blood cell scan (bleeding scan)• ( C ) Mesenteric angiography• ( D ) Barium examination of the small bowel after intubation of the duodenum

(enteroclysis)• ( E ) No additional studies at this time

Ans. A

• Wireless capsule endoscopy used to evaluate obscure gastrointestinal bleeding and small intestinal pathology.

• Capsule endoscopy disadvantages : not very useful in detecting esophageal lesions, cannot obtain biopsies. Some times capsule can get impacted and requires surgical removal.

Peptic Ulcer Disease

Peptic ulcer disease

• Site : Gastric vs. Duodenal

• Complicated vs. Uncomplicated

• Causes

• Diagnosis – mainly clinical

• Management

H.Pylori Screening

Testing not indicated1. Screening of healthy asymptomatic individuals

(including close contacts of infected patients) for H. pylori is not indicated.

2. The value of testing and treating for H. pylori is not proven in the following circumstances:

• family history of peptic ulcer disease or gastric malignancy

• gastroesophageal reflux • remote partial gastrectomy for gastric cancer • chronic NSAID use without evidence of an

ulcer

H.Pylori Screening

• Testing Recommended only if you plan to treat. As for :

Persistent dyspepsia/ recurrent dyspepsia

MALT lymphomas

H.Pylori Screening• Remember Endoscopy should be

considered for initial diagnosis of H.Pylori in pts with age>55 yrs because of high risk of gastric cancer and in the presence of Alarm symptoms.

H.pylori• Associations• Diagnosis / Screening Antibody tests ( May be used for screening. –ve test rules out infection.

+ve test does not differentiate b/w present vs. past infection) urea breath tests ( H.pylori has urease – we use this in diagnosis).

Beware of false –ves! no PPIs for atleast 2 weeks before undergoing urea breath test!!!

Stool for H.pylori antigen. most specific are endoscopic tests like urease on biopsy, histology and

culture of biopsy specimen.( but EGD is invasive)• Treatment – triple Therapy ( OCM/ OAM bid x 1 wks) Rx failure/

resistance , use Quadruple therapy• Determining H.pylori eradication after RX: reinfection rates are low at 2% of pts per year. So persistent H.pylori after

eradication therapy is more likely due to failure than due to reinfection If Resistance, treat with QUADRUPLE therapy ( Bismuth+ triple therapy)

no antibody tests endoscopic tests are invasive and expensive Urea breath test is reliable but cannot be done untill 4 weeks after

eradication treatment ( before that false –ves) So, options are STOOL ANTIGEN TESTING 7 days after RX or Urea

breath test 4 wks after Rx!!! - However, endoscopic tests when indicated are the best for diagnosis of

Rx failure

H.Pylori Screening tests

H.Pylori regimens

CASE STUDY

• Urea breath test

DYSPEPSIA

A common complaint seen in Internist’s office

Dyspepsia

• Bloating• Flatulence• Water brash, heartburn• Upper Abdominal discomfort/ pain - epigastric• Early satiety• Nausea/ vomiting

MCC of Dyspepsia is functional or non-ulcer dyspepsia

DyspepsiaDifferential Diagnosis of Dyspepsia• Functional or nonulcer dyspepsia Up to 60 percent • Dyspepsia caused by structural or biochemical disease  • Peptic ulcer disease 15 to 25 percent  • Reflux esophagitis 5 to 15 percent  • Gastric or esophageal cancer < 2 percent  • Biliary tract disease Rare  • Gastroparesis Rare  • Pancreatitis Rare  • Carbohydrate malabsorption (lactose, sorbitol, fructose, mannitol) Rare  • Medication effects Rare  • Infiltrative diseases of the stomach (Crohn's disease, sarcoidosis) Rare  • Metabolic disturbances (hypercalcemia, hyperkalemia) Rare •  Hepatoma Rare •  Ischemic bowel disease Rare  • Systemic disorders (diabetes mellitus, thyroid and parathyroid disorders,

connective tissue disease) Rare  I• ntestinal parasites (Giardia species, Strongyloides species) Rare  • Abdominal cancer, especially pancreatic cancer

Questions to Ask When Determining Common Causes of Dyspepsia

• Peptic ulcers Does the patient have a personal history of ulcers? Does the patient have a strong family history of ulcers? Does the patient report melena? Is the patient a smoker?

• Gastroesophageal reflux disease Does the patient complain of heartburn or sour belches? Are symptoms worse when the patient is lying down? Does the patient have a chronic cough or hoarseness?

• Biliary tract disease Does the patient report any history of jaundice? Does the patient report dark urine? Does pain occur after meals? Is the pain associated with meals or belching?

• Pancreatitis Is the pain stabbing, and does it radiate to the patient's back? Is the pain abrupt, is it unbearable in severity and does it last for many hours without relief? Does the patient have a history of heavy alcohol use?

• Cancer Is the patient over 50 years of age? Has the patient had a recent significant weight loss? Does the patient have trouble swallowing? Has the patient had recent protracted vomiting? Does the patient have a history of melena? Is the patient a smoker?

• Irritable bowel syndrome Is dyspepsia associated with an increase in stool frequency? Is pain relieved by defecation?

• Metabolic disorders Does the patient have a medical history of diabetes mellitus, hypothyroidism or hyperthyroidism, or hyperparathyroidism?

• Medications Is the patient currently taking medications commonly associated with dyspepsia?

Drugs Commonly Associated with Dyspepsia

• Acarbose (Precose) • Alcohol • Alendronate (Fosamax) • Antibiotics, oral (e.g., erythromycin) • Codeine • Corticosteroids (e.g., prednisone) • Herbs (e.g., garlic, ginkgo, saw palmetto, feverfew, chaste tree berry,

white willow)• Iron • Metformin (Glucophage) • Miglitol (Glyset) • Nonsteroidal anti-inflammatory drugs, including cyclooxygenase-2 enzyme

inhibitors • Orlistat (Xenical) • Potassium chloride • Risedronate (Actonel) • Theophylline

Non Ulcer/ Functional Dyspepsia

Rome II Diagnostic Criteria for Functional Dyspepsia

• Patient meets the following criteria for at least 12 weeks (which need not be consecutive) within the preceding 12 months: – Persistent or recurrent symptoms (pain or discomfort

centered in the upper abdomen) – No evidence of organic disease (including on upper

endoscopy) that is likely to explain the symptoms – No evidence that dyspepsia is relieved exclusively

by defecation or associated with the onset of a change in stool frequency or stool form (i.e., not irritable bowel syndrome)

Approaches - Dyspepsia

There are 5 initial approaches to management of dyspepsia:

• empirical acid suppression

• noninvasive H. pylori testing

• H. pylori test and treat

• empirical H. pylori eradication ( No longer recommended)

• early endoscopy.( recommended if age>55yrs or in presence of alarm features)

Dyspepsia – KEY POINTS• Patients 55 years or younger without alarm features should receive H. pylori test

followed by acid suppression. • H. pylori testing should no longer be performed with serologic testing and

instead a 13C-urea breath test or stool antigen test should be used. • In populations with a low prevalence of H. pylori (less than 10%), an empirical

course of PPI therapy is the most cost-effective approach. • PPI is more effective than placebo or H2-receptor blockers in patients with

uninvestigated dyspepsia. • Those who are H. pylori positive should undergo eradication therapy. • Those who are H. pylori negative may be offered a short course of PPI therapy

and longer-term therapy offered if symptoms are not resolved. Long-term therapy should be assessed every 6 to 12 months.

• Endoscopy adds little in young patients. • In patients older than 55 years or for younger patients with alarm features

presenting with new dyspepsia, upper GI malignancy is of concern, and upper endoscopy is indicated.

• Biopsy specimens for H. pylori are recommended at the time of endoscopy. • The American College of Physicians recommends endoscopy for those without

response after 7 to 10 days or 6 to 8 weeks of therapy. • The most common diagnosis reached at endoscopy is functional dyspepsia.

Antidepressants and psychological approaches may be considered for functional dyspepsia.

• (AGA RECOMMENDATIONS, 2005)

Note

• Remember Functional dyspepsia can also mimic GERD symptoms.

• If the diagnosis of GERD is uncertain, intraesophageal pH monitoring may help in separating the disease from other causes of dyspepsia.

• A suspected GERD with negative Ph monitoring and no response to PPI therapy is considered as functional heartburn.

Rx Functional Dyspepsia - Summary

• In pts with risk factors, do EGD to exclude GERD, Peptic ulcer disease, malignancy etc

• In patients without risk factors, consideration should be given to empiric therapy with a prokinetic agent (e.g., metoclopramide), an acid suppressant (histamine-H2 receptor antagonist), or an antimicrobial agent with activity against Helicobacter pylori.

• Treatment of patients with H. pylori infection and non ulcer dyspepsia (rather than peptic ulcer) is controversial and should be undertaken only when the pathogen has been identified. ( no emperic therapy)

• Psychotropic agents should be used in patients with comorbid anxiety or depression. Treatment of nonulcer dyspepsia can be challenging because of the need to balance medical management strategies with treatments for psychologic or functional disease

Gall Stones

Clinical scenarios• Acute Cholecystitis - Complications

• Choledocholithiasis

• Acute Cholangitis

• Acute Pancreatitis• ERCP Vs. MRCP

Gallstones• Asymptomatic Do not do anything except

in pts in certain geographical areas with high incidence of ca.gallbladder

• Porcelain gallbladder cholecystectomy• Symptomatic gallstones colic, dyspepsia,

cbd obstruction, cholecystitis, Cholangitis, pancreatitis lap chole

• Complications of lap chole CBD injury get a HIDA scan

This complication can lead to biliary peritonitis

Pancreatitis

Acute and Chronic

Pancreatitis - Etiology• Find out subtle clues regarding the cause a) Alcoholic Pancreatitis History, Liver panel

with AST>ALT, Normal common bile duct on ultrasound

b) Gallstone Pancreatitis Obstructive jaundice, Painful jaundice, ALT increases first, ALP follows, direct bili high

c) Other causes increased triglycerides, drugs ( HCTZ, Didanosine), pancreatic divisum, pancreatic cancer

. Finding the cause of pancreatitis dictates your treatment. Eg: ERCP for gallstone pancreatitis and cholecystectomy ASAP

Topics

• Clinical Features• Investigations• ? Antibiotics – justify the use• Where to admit the patient? ? ICU/FLOOR• Necrotizing pancreatitis• Complications – Pseudocyst, Abscess, Chronic

Pancreatitis• Emergency Chole in Gallstone pancreatitis• ERCP in gallstone pancreatitis• Role of MRCP in gallstone pancreatitis

Pancreatic Pseudocyst

• Asymptomatic

• Complications

• Imaging

• Treatment modalities ? Indications for treatment

Ransons criteria• RANSON'S CRITERIA: For Determining Prognosis of Acute

Pancreatitis• UPON ADMISSION:

– Age > 55 – Blood Glucose > 200 mg/dl – WBC count >16,000 / cu mm – Serum LDH > 700 IU% – SGOT > 250 SF units % (56 units/dl)

• AFTER 48 HOURS: – HCT decrease >10% – Serum Ca2+ < 8mg % (mg/dl) – Base Deficit > 4 meq/l – BUN increase > 5mg % (mg/dl) – Estimated. fluid retention > 6L – Arterial 02 tension < 60 mm hg

• < 3 signs - better prognosis, & < 1% mortality.• > 3 signs - serious acute pancreatitis - may be 25% mortality.

Diarrheas

Osmotic Vs. Secretory

• Important to know which physiological type because etiology varies

• Calculate stool Osmolar gap• Stool osmolar gap = 290 – {2(Na+)+(K+)}• If stool osmolar gap > 50 osmotic diarrhea ( Osmotic

solute draws a lot of water causing dilution and drop in Na+, K+ in stool)

<50 secretory diarrhea• Large volume diarrhea small bowel• Small volume diarrhea large bowel• Daily stool weight more than 200gms is another

definition of chronic diarrhea.

Causes

• Infectious – viral, bacterial, parasitic

• Inflammatory

• Irritable Bowel syndrome

• Malabsorption Sydromes

Diarrheas• Viral some clues cruise ships, large number ppl

affected simultaneouslyNo blood/ wbcs in the stool• Bacterial time of onset is a clue to etiology, wbcs and

presence of occult blood points more towards bacterial when diarrhea is acute

• Inflammatory bowel disease r/o bacterial etiology before you come to this diagnosis

a diarrhea not responding to antibiotics is a clue presence of wbcs/blood colonoscopy with biopsy is diagnostic if biopsy shows CHRONIC colitis ( monolymphocytic infiltrates). Where as bacterial related inflammation should be an acute one! Treatment!!

• Irritable bowel synd ROME criteria diagnosis of exclusion chronicity > 3 mos constipation alternating with diarrhea management

Malabsorption Syndromes – Chronic Diarrheas

• Celiac disease recognize subtle clues like iron deficiency anemia, chronic diarrhea management Associations ( Dermatitis herpetiformis rxed with Gluten free diet + dapsone)

• Whipple disease extraintestinal manifestations ( Lymphadenopathy, mogratory arthritis)

• Chronic Pancreatitis Pancrealipase, avoid high fat foods.

• Tropical Sprue responds to antibiotics - tetracyclines• Crohns disease

Liver Disorders• Viral Hepatitis• Acetaminophen toxicity N-Acetyl Cysteine• Alcoholic liver disease• Non Alcoholic Steato Hepatitis• Ischemic Hepatitis• Autoiimune Hepatitis• Hepatorenal syndrome• Hemochromatosis• Wilsons disease• Alpha antitrypsin deficiency

Fulminant Hepatic Failure

• Defined as development of hepatic encephalopathy within 8 weeks of onset of acute severe hepatitis.

• Causes most common cause is Tylenol toxicity, other causes

• Management

• A 48-year-old woman with Sjögren's (sicca) syndrome develops pruritus that she attributes to dry skin. Physical examination reveals numerous excoriations, xerostomia, and multiple dental fillings. The liver is slightly enlarged. The spleen is not palpable, and there is no ascites. Rectal examination discloses brown stool. Neurologic examination is normal.

• Laboratory Studies• Hemoglobin 11.9 g/dL• Leukocyte count 6800/μL• Platelet count 150,000/μL• INR 1.1• Serum creatinine 0.8 mg/dL• Serum aspartate aminotransferase 45 U/L• Serum alanine aminotransferase 58 U/L• Serum alkaline phosphatase 648 U/L• Serum ?-glutamyltransferase 400 U/L• Serum total bilirubin 0.9 mg/dL• Serum total protein 7.2 g/dL• Serum albumin 3.8 g/dL• Which of the following diagnostic studies is most appropriate at this time?• ( A ) Magnetic resonance cholangiopancreatography• ( B ) Endoscopic retrograde cholangiopancreatography• ( C ) CT scan of the abdomen• ( D ) Serum antimitochondrial antibody titer• ( E ) Serum antiendomysial antibody titer

Primary Biliary Cirrhosis• C/F – Classic scenario “middle aged

woman with pruritis”• Diagnosis Increased ALP, AMA, ERCP• Rx• Ursodeoxycholic acid reduces disease

progression• Corticosteroids for symptomatic pts• Complicationssteatorrhea, vitamin deficiencyOsteoporosis (1/3 pts)

Hepatitis C

• Contraindications for treatment

• Evaluating the need for Rx

• Drugs used

• Complications

• Hepatocellular carcinoma

• When to refer for liver transplant?

Constipation

• Causes•Constipation in elderly

•Constipation with Opiates•Different Laxatives and their choice

Types of Laxatives• Bulk forming

• Osmotic

• Stool softeners

• Stimulant laxatives

Ascites

•Etiology – exudate, Transudate•Importance of SAAG in diagnosis

•Management – diuretics, combination diuretics, Paracentesis – Diagnostic

and Therapeutic

Portal Hypertension

• SAAG

• Indications and complications of TIPS

• Subacute bacterial peritonitis prophylaxis and treatment in cases of Ascites.

• Prophylaxis Variceal bleeding

• Treating Variceal bleeding

• A 45-year-old Hispanic male migrant worker has a 2-month history of increasing abdominal girth, intermittent fever, and weakness. Medical history is unremarkable. The patient does not believe that he has ever had hepatitis. He drinks one or two glasses of wine weekly, takes no medications, and denies use of illicit drugs. His

• weight has increased by about 7 kg (15 lb) over the past 2 months. On physical examination, he appears chronically ill. Temperature is 38.5 °C (101.3 °F), pulse rate is 104/min, respiration rate is 26/min, and blood pressure is 110/65 mm Hg. There are no stigmata of chronic liver disease. Abdominal examination reveals distention and shifting dullness without organomegaly.

• Laboratory Studies• Hematocrit 38%• Leukocyte count 12,400/μL (with 46% lymphocytes, 16%monocytes, and 35% neutrophils)• Platelet count 225,000/μL• INR 1.0• Activated partialthromboplastin timeNormal• Blood urea nitrogen 26 mg/dL• Serum creatinine 1.5 mg/dL• Serum electrolytes Normal• Serum aspartate aminotransferase35 U/L• Serum alanineaminotransferase37 U/L• Serum total protein 6.5 g/dLm Serum albumin 3.6 g/Dl . Paracentesis reveals clear fluid that

contains 350 cells/μL (90% mononuclear cells), total protein of 3.2 g/dL, and albumin of 2.8 g/dL. Cultures of ascitic fluid are negative at 48 hours. Which of the following is the most appropriate management at this time?

• ( A ) Administration of furosemide and spironolactone• ( B ) Administration of metronidazole• ( C ) Skin tests for tuberculosis and fungal diseases• ( D ) Diagnostic laparoscopy with biopsy and culture of peritoneal tissue• ( E ) Liver biopsy for tissue culture and histologic studies

Ischemic ColitisUnderlying atherosclerosis with a precipitating event

Bloody DiarrheaUsually pain out of proportion to physical exam

Can lead to peritonitis and shockAXR – Thumb printing

CT scan – HelpfulColonoscopy – Daignostic

Rx – Supportive, if severe partial colectomy

Inflammatory Bowel DiseaseUlcerative ColitisCrohn’s disease

“ Any acute inflammatory ( +Blood, +WBCs in stool) diarrhea that progresses to become chronic and does not

respond to antibiotics should raise suspicion of inflammatory bowel disease – colonoscopy and biopsy is

your next step” Biopsy revealing chronic colitis, cryptitis with

mononuclear infiltrate is indicative of inflammatory bowel disease

• A 19-year-old female college student with a 10-year history of Crohn's ileitis without colitis is hospitalized because of acute right lower quadrant abdominal pain. Her disease was relatively quiescent until last year, when she was hospitalized three times and was forced to withdraw from college temporarily. Flares consist of fever, right lower quadrant abdominal pain, malaise, watery diarrhea, weight loss, and occasional erythema nodosum. The current flare occurred despite therapy with 6-mercaptopurine, 50 mg daily, and mesalamine, 4 g daily, for the past 3½ months and prednisone, 40 mg daily, for the past 3½ weeks. On physical examination, temperature is 37.8 °C (100.0 °F), pulse rate is 110/min, respiration rate is 14/min, and blood pressure is 98/80 mm Hg. BMI is 17. The right lower abdominal quadrant is tender with fullness. Rectal examination discloses loose brown stool. Tender pretibial nodules are present.

• Laboratory Studies• Hemoglobin 9.4 g/dL• Mean corpuscular volume 100 fL• Leukocyte count 5200/μL (normal differential)• Platelet count 190,000/μL• Erythrocyte sedimentation rate 100 mm/h• C-reactive protein 8.2 mg/dL• Liver chemistry studies Normal• A CT scan of the abdomen shows marked ileal wall thickening without evidence of a mass or bowel

obstruction.• The colon appears normal.• Which of the following is the most appropriate therapy for this patient?• ( A ) Stop 6-mercaptopurine; begin azathioprine• ( B ) Stop mesalamine; begin sulfasalazine• ( C ) Increase prednisone to 60 mg daily• ( D ) Administer infliximab by infusion• ( E ) Refer for surgical resection of the diseased ileum

Ans. D

• This patient has moderately active Crohn's disease with systemic complications that has not responded to immunosuppressive therapy, an aminosalicylate, and a recent course of corticosteroids. Drugs such asinfliximab that antagonize cytokines (specifically tumor necrosis factor-a) are effective for inducing and maintaining remission in patients with this disorder and should be tried before surgery is considered.

• There is no evidence that azathioprine is more effective than 6-mercaptopurine in treating Crohn's disease or that sulfasalazine is more effective than mesalamine in managing this disorder. The patient is already taking prednisone, 1 mg/kg daily. Higher doses are unlikely to induce remission and are more likely to cause steroid-related side effects.

Smoking & IBD

- Smoking protects against Ulcerative colitis. Sometimes, UC is diagnosed immediately after pts quit smoking.

- Smoking aggravates the course of Crohn’s disease

Antibodies & IBD

• Antibodies to Sacharomyces.cerviceae (ASCA) are +ve in Crohn’s disease• p-ANCA are positive in Ulcerative colitis• Sometimes (in about 5% patients with

indeterminate colitis) it’s very difficult to differentiate between crohn’s and UC on colonoscopy and biopsy Presence of ASCA and absence of p-ANCA is pretty diagnostic of Crohn’s in such cases

Treatment• Medical Therapy : Sulfasalazine is mainly useful in colonic disease

because the active compound, 5-aminosalicylic acid (5-ASA), is released in the large bowel by bacterial degradation of the parent compound. Sulfasalazine does not alleviate small-bowel disease. Products such as mesalamine (Asacol) that release 5-ASA in the distal small bowel secondary to pH changes are more useful in patients with small intestinal Crohn disease. Long-term maintenance with mesalamine (800 mg tid) may delay clinical relapse. Sulfasalazine does not have an additive effect or a steroid-sparing effect when used in conjunction with corticosteroids. In contrast to its action in UC, it does not seem to maintain remission in Crohn disease.

• A short course of steroid therapy is indicated in patients with severe systemic symptoms (eg, fever, nausea, weight loss) and in those who do not respond to anti-inflammatory agents. Prednisone (40-60 mg/d) is generally helpful in acute inflammation. Once remission is achieved, slowly taper steroids (5-10 mg q1-2wk).

• Fistulae: Metronidazole If refractory Infliximab, an anti-TNF antibody used for fistulizing

crohns disease. Make sure to do a PPD test and hepatitis b, c testing – as it can reactivate latent TB and Chronic hepatitis

Primary Sclerosing Cholangitis

• Associated with Ulcerative colitis• Extra intestinal manifestation of UC• Leads biliary cirrhosis• Presents with obstructive jaundice/ pruritis• Increased D.Bili, ALP• Diagnosis : ERCP criterion standard for establishing

the diagnosis of PSC. Liver biopsy if ERCP non suggestive• Rx: Address complications like cirrhosis and portal

hypertension Liver transplant useful in children Ursodeoxycholic acid can help improve

symptoms (pruritis) and biochemical abnormalities.