ARCHER NOTES

1. Gastroenterology
Archer’s online USMLE Reviews
www.CccsWorkshop.com
All rights reserved

2. Esophageal
Disorders

3. 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

4. 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)

5. 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

6. 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)

7. Odynophagia
Painful 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

8. 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

9. 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.

10. Case study
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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

11. GI bleeding
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Occult bleeding
Obscure bleeding - management
Upper GI bleeding
Lower GI bleeding
Iron deficiency anemia

12. Occult Bleeding
• Stool Guaic
• False negatives
• Approach to work up

13. Variceal Bleeding
• Causes – portal hypertension
• Management strategies
• Gastric varices without esophageal
varices  splenic vein thrombosis  Rx
is splenectomy

14. Ishemic disease - GI
• Mesenteric Ischemia  acute, chronic
• Ischemic Colitis  look for Pneumatosis
intestinalis on x-ray  management

15. Q
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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

16. 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.

17. Peptic Ulcer
Disease

18. Peptic ulcer disease
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Site : Gastric vs. Duodenal
Complicated vs. Uncomplicated
Causes
Diagnosis – mainly clinical
Management

19. H.Pylori Screening
Testing not indicated
1. 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

20. H.Pylori Screening
• Testing Recommended only if you plan to
treat. As for :
Persistent dyspepsia/ recurrent
dyspepsia
MALT lymphomas

21. 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.

22. •
•
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

23. H.Pylori Screening tests

24. H.Pylori regimens

25. CASE STUDY
• Urea breath test

26. DYSPEPSIA
A common complaint seen in
Internist’s office

27. Dyspepsia
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Bloating
Flatulence
Water brash, heartburn
Upper Abdominal discomfort/ pain - epigastric
Early satiety
Nausea/ vomiting
MCC of Dyspepsia is functional or non-ulcer
dyspepsia

28. Dyspepsia
Differential 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

29. Questions to Ask When Determining Common Causes of
Dyspepsia
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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?

30. Drugs Commonly
Associated with Dyspepsia
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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

31. 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)

33. 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)

34. Dyspepsia – KEY POINTS
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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)

35. 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.

36. Rx Functional Dyspepsia Summary
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In pts with risk factors, do EGD to exclude GERD, Peptic ulcer
disease, malignancy etc
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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

37. Gall Stones

38. Clinical scenarios
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Acute Cholecystitis - Complications
Choledocholithiasis
Acute Cholangitis
Acute Pancreatitis
ERCP Vs. MRCP

39. 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

40. Pancreatitis
Acute and Chronic

41. 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

42. Topics
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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

43. Pancreatic Pseudocyst
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Asymptomatic
Complications
Imaging
Treatment modalities  ? Indications for
treatment

44. Ransons criteria
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RANSON'S CRITERIA: For Determining Prognosis of Acute
Pancreatitis
• UPON ADMISSION:
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AFTER 48 HOURS:
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Age > 55
Blood Glucose > 200 mg/dl
WBC count >16,000 / cu mm
Serum LDH > 700 IU%
SGOT > 250 SF units % (56 units/dl)
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.

45. Diarrheas

46. 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.

47. Causes
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Infectious – viral, bacterial, parasitic
Inflammatory
Irritable Bowel syndrome
Malabsorption Sydromes

48. Diarrheas
• Viral  some clues  cruise ships, large number ppl
affected simultaneously
No 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

49. 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

50. Liver Disorders
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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

51. 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

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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

53. 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
• Complications
steatorrhea, vitamin deficiency
Osteoporosis (1/3 pts)

54. Hepatitis C
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Contraindications for treatment
Evaluating the need for Rx
Drugs used
Complications
Hepatocellular carcinoma
When to refer for liver transplant?

55. Constipation
• Causes
•Constipation in elderly
•Constipation with Opiates
•Different Laxatives and their choice

56. Types of Laxatives
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Bulk forming
Osmotic
Stool softeners
Stimulant laxatives

57. Ascites
•Etiology – exudate, Transudate
•Importance of SAAG in diagnosis
•Management – diuretics, combination
diuretics, Paracentesis – Diagnostic
and Therapeutic

58. Portal Hypertension

59. • SAAG
• Indications and complications of TIPS
• Subacute bacterial peritonitis prophylaxis
and treatment in cases of Ascites.
• Prophylaxis Variceal bleeding
• Treating Variceal bleeding

60. •
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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

61. Ischemic Colitis
Underlying atherosclerosis with a precipitating event
Bloody Diarrhea
Usually pain out of proportion to physical exam
Can lead to peritonitis and shock
AXR – Thumb printing
CT scan – Helpful
Colonoscopy – Daignostic
Rx – Supportive, if severe partial colectomy

62. Inflammatory Bowel
Disease
Ulcerative Colitis
Crohn’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

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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

64. 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 steroidrelated side effects.

65. Smoking & IBD
- Smoking protects against Ulcerative
colitis. Sometimes, UC is diagnosed
immediately after pts quit smoking.
- Smoking aggravates the course of
Crohn’s disease

66. 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

67. Treatment
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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.
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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).
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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

68. Primary Sclerosing
Cholangitis
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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.