Transcript ABIM_Gastroenterology

GI Board Review
Esophagus
GERD
Middle aged overweight male with retrosternal burning and
regurgitation worse with citrus and smoking.
GERD
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Symptoms
Retrosternal burning – post prandial/recumbant
 Regurgitation
 Dysphagia
 Water Brash
 Chronic Cough
Historical clues: Pregnancy, Scleroderma, Obesity,
hiatal hernia
Gold standard – 24 hour pH probe
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GERD
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Complications
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Barrett’s
Adenocarcinoma
Strictures/Rings
Hoarseness/Asthma
Empiric treatment – Sensitivity of 80%
When refer for endoscopy?
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Evaluate for Barrett’s/anatomy
Don’t respond to therapy
Alarm symptoms – dysphagia, bleeding, weight loss,
anemia, odynophagia
Chronic
GERD - treatment
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On the Boards, remember to be cost effective
Lifestyle modification (Weight loss most important and avoidance of foods
that cause LES relaxation i.e. peppermint, chocolate, alcohol, fatty foods)
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Acid suppression
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Promotility – Reglan/Cisapride (Minimal Data)
Surgery – Nissen Fundoplication
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PPI > H2 blocker(80% control symptoms)
PPI better in endoscopically proven esophagitis
Equivalent to PPI therapy – 0.2% mortality
2/3 will be on acid suppression in 5 years
No evidence that prevents Barrett's or CA
Endoscopic Therapy (Stretta, Endocinch, etc)
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Rarely performed.
Barrett’s Esophagus
55 year old white male with 10 years of
pyrosis, mildly improved over past year, on
PPI daily.
Barrett’s Esophagus
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Middle aged and older, M>F (2:1)
Whites and Hispanics predominantly
About 5-10% of patients with GERD (though in multiple
studies, also present in 0%-25% of asymptomatic patients)
Defining characteristic: Change in squamous esophageal
epithelium to intestinal metaplasia
0.5% per person per year chance of developing adenocarcinoma
Treatment
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Control GERD Symptoms – PPI vs. surgery
No therapy definitively shown to reduce risk of progression to
malignancy
Surveillance endoscopy
Esophageal Cancer
75 year old female with history of tobacco use and alcohol
use with progressive solid food dysphagia and 15 pound
weight loss over past year.
Esophageal Cancer
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Essentially equal prevalence in United States
of esophageal SCC and adenocarcinoma
Squamous Cell – proximal esophagus
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Smoking
Tylosis
Achalasia
Plummer-Vinson
Lye
Ethanol
Sprue/Scleroderma
Adenocarcinoma – Distal esophagus
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GERD/Barrett’s, Obesity, Tobacco
Esophageal Cancer
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Symptoms
Progressive Solid Food Dysphagia
 75% also weight loss/anorexia
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Endoscopy with Biopsy – Diagnostic
Staging
1. CT chest/abd/pelvis vs. PET for Mets
 2. EUS for T and N staging
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Dysphagia
Dysphagia
Solids
Solids/liquids
Intermittent
Progressive
Intermittent
Progressive
Ring or Stricture
Esophageal CA
DES
Achalasia / Scleroderma
Dysphagia
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History and Physical
Solid vs. liquid
 Intermittent vs. progressive
 Oropharyngeal vs. Esophageal
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Barium swallow (13mm pill)
EGD (with possible dilation)
Esophageal manometry
Peptic Stricture
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Progressive solid food dysphagia
History of GERD
No weight loss
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Patients have normal appetite
Majority (60-70%) are peptic in origin
Result of chronic esophageal inflammation
Esophageal Ring
38 year old female with frequent heartburn, controlled on
PPI, with intermittent solid food dysphagia.
Achalasia
35 year old male with progressive solid and liquid food
dysphagia and fatigue, with regurgitation of undigested
food.
Achalasia “failure to relax”
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1/100,000
M:F 1:1
Age 25-60 (If older>60, think pseudoachalasia especially
gastric cancer)
Increased risk for squamous cell cancer
Hallmarks:
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Aperistalsis
Failure of LES to relax
Dysphagia to solid and liquid
Postural changes to help swallowing
Regurgitation of undigested food
Autoimmune vs. Viral
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Chagas Disease (Trypanosoma cruzei)
Achalasia - diagnosis
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Barium Swallow – Dilated esophagus with
column of barium and “Birds Beak” taper. Test of
choice if suspected
Endoscopy – rule out pseudoachalasia
Manometry (Used to confirm diagnosis)
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(1)Loss of peristalsis,
(2)failure of LES to relax,
(3)possibly LES high pressure
Chest X-ray – wide mediastinum and air fluid level
Eosinophilic Esophagitis
20 year old male with history of asthma and eczema
with recurrent food impactions.
Eosinophilic Esophagitis
Atopic history and food impactions
 Ringed esophagus / linear furrows
 >15 eosinophils per high power field
 Some (minority) have peripheral eosinophilia
 Oral fluticasone 220 mcg/puff 2 puffs bid for 6-8
weeks. Recurrence frequent.
 Other possible treatments:
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PPI, singulair (large doses up to 100 mg), elimination diets
(children predominantly) and dilation
Scleroderma
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Historical Key: 70 year old woman with sclerodactyly
telangiectasias, Raynaud’s with GERD, resistant to
PPI
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75% have esophageal involvement
Severe GERD, frequently resistant to PPI
Incompetent LES and lack of peristalsis
Control GERD with PPI
Stomach
Upper GI bleed
Presentation
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Hematemesis (Not to be confused with hemoptysis)
Melena (Black, Tar-Like – not solid)
Nausea/vomiting common with PUD
Orthostasis (Bedside orthostatics)
Abdominal pain
Hematochezia (10% of maroon stool from upper source –
On test will be unstable)
Upper GI Bleed
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Peptic Ulcer Disease – 55%
Esophageal Varices – 14%
AVM’s / GAVE – 6%
Mallory-Weiss tear – 5%
Dieulafoy’s – 1%
Cameron’s lesion
Tumors
Esophagitis (Most common cause of UGIB in
hospitalized patients, likely due to NGT and reflux in
supine position)
Peptic Ulcer Disease
65 year old female with arthritis, taking ibuprofen, with
melena and lightheadedness.
Risk Factors for NSAID-induced
Ulcers
Definite:
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Prior PUD
Advanced age
Concomitant use of
glucocorticoids
Concomitant use of anticoagulants
High doses or combinations of
NSAIDs, including low-dose
aspirin
Comorbid illness (RA, CAD, etc)
Ethanol use
Possible:
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H. pylori infection
smoking
Helicobacter pylori
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Most peptic ulcers caused by Helicobacter pylori
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60-80% of GU’s and 90% DU’s
2 clinical presentations of H. pylori
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Antrum predominant
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Body predominant
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Increased acid production, Duodenal Ulcers, no cancer
Decreased acid production, Gastric Ulcers, Gastric Cancer (<1% of
those infected, Cag A strain)
Eradication of Hp dramatically decreases PUD and its
complications
Tests for H. pylori
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Serologic Antibody (90% sens / 90% spec)
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Endoscopy with Histology (95% sens / 98% spec)
Endoscopy w/Rapid Urease Test (CLO) (90% /98%)
Urease Breath Test (C13 / C14) (95% / 95%)
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Remains positive for several years
Do not use for evaluation for eradication
Best test for eradication
Stool Antigen (92% / 90%)
All tests (except serology) less reliable if on PPI in last 2
weeks, or antibiotics or bismuth in past 4 weeks.
Rx of H. pylori
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Standard : Amoxicillin, Clarithromycin, PPI bid
x 14 days
75-80% eradication rate
Major antibiotic resistance to clarithromycin and
metronidazole.
If allergic to PCN, substitute metronidazole for
amoxicillin
Peptic Ulcer Disease – Rebleed
Risk (within 72 hours)
Clean Base
Pigmented Spot
Adherent Clot
Visible Vessel
Active Bleeding
Baseline
PPI
3-5%
7-10%
22-30%
43-52%
55-90%
------0%
12%
73%
PPI/EGD Tx
------6.7%
6.7%
6.7%
Zollinger-Ellison
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Gastrin producing neuroendocrine tumor
1% of PUD (Never seen clinically but all over board
exams)
90% will have PUD (frequently solitary duodenal ulcer
but may be multiple and in unusual places i.e. jejunum)
Frequently with abdominal pain and chronic secretory
diarrhea
70% Duodenum/30% Pancreas
1/3 metastatic at diagnosis
Zollinger - Ellison
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Fasting Gastrin >1000 diagnostic if acidic pH in
stomach (separate low acid states (atrophic gastritis and
pernicious anemia) from ZE)
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Secretin Stimulation Test (secretin infusion promotes
gastrin release by gastrinoma cells but not gastric G
cells)
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150-1000 abnormal but can be secondary to meds (PPI) or H
pylori causing atrophic gastritis
Positive test - Increased Gastrin by at least 120-200 pg/ml
within 20 minutes after secretin infusion
Localize with octreoscan/EUS of pancreas
MEN1
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Pancreatic islet cell tumors seen with MEN1
about 80% of time (parathyroid, pituitary,
pancreas)
50-60% with MEN1 have gastrinoma, but…
 About 20% with gastrinoma have MEN1
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Most common pancreatic islet cell tumor
associated with MEN1 is a “nonfunctioning”
islet cell tumor (i.e. releases hormone that does
not cause symptoms like PPP)
Gastric Cancer
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Diffuse (Infiltrating cells, i.e. linitis plastica) vs.
Intestinal Type (glandular)
Most common in Far East (if Japanese or Korean
patient with stomach complaint, think of gastric cancer)
Risk Factors
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1st degree relative (3x)
H. pylori – Chronic Atrophic Gastritis
Dietary – Nitrates
Tobacco
Gastric Cancer Epidemiology
Pancreas
Acute pancreatitis
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Alcohol or gallstone predominant etiologies
Drugs – DDI, diuretics, estrogen, valproic acid, 5-ASA,
azathioprine, TCN, sulfa
Interstitial (85%) vs. necrotizing (15%)
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Organ failure in 10% vs. 54%
Mortality Rate 3% vs. 17%
33% of patients with sterile necrosis develop infected necrosis
47% mortality with MSOF
Interesting fact – Pain radiates to back only about 50%
of time.
Complications
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SIRS: ARDS, Shock, ARF, GI Bleed
Necrosis: Infection
Pseudocyst/Abscess
Pancreatic Ascites, Fistula (pleural effusion)
Chronic Pancreatitis
Splenic Vein Thrombosis, Pseudoaneurysm
Treatment
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Mild – NPO, pain control, fluid resuscitation
Severe pancreatitis – Likely ICU
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Adequate pain relief,
Adequate IV fluid replacement, especially initially (decrease Hct
over first 24 hours to reduce risk of necrosis)
ERCP for gallstone panc (cholangitis/jaundice) (suspect if ALT or
AST>3x ULN)
Nutritional support
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Enteral feeding better than TPN due to decreased episodes of
hyperglycemia and sepsis
Current teaching to place feeding tube beyond Ligament of Treitz
(controversial)
Enteral Nutrition and Severe
Pancreatitis
16
14
12
10
8
Enteral
TPN
# PTS
6
4
2
0
septic complications
*P<0.01
any complication
**P<0.05
Kalfarentos et al Br J Surg 1997; 84:1665
Treatment
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Severe pancreatitis
Contrast CT recommended at some point beyond
the first 3 days in severe pancreatitis to rule out
necrotizing pancreatitis.
 Otherwise, minimal role for early CT
 No role for prophylactic antibiotics with sterile
necrosis (controversial)
 If concern for infected necrosis (usually after 7 days),
CT guided aspiration.
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Chronic pancreatitis
Chronic Pancreatitis
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Chronic epigastric pain/maldigestion related to
fibrotic pancreas
Diagnosis usually made after disease is well
established.
Most frequently associated with alcohol abuse
Maldigestion with steatorrhea/weight loss
Fat soluble vitamin and B12 deficiency
DM common in advanced disease
Chronic Pancreatitis
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Lipase and amylase normal or only slightly
elevated
May mimic pancreatic cancer or autoimmune
pancreatitis (IgG4, ANA) with duodenal or
biliary obstruction
Complications: pseudocyst, splenic vein
thrombosis, pancreatic cancer (4% lifetime risk)
Diagnosis (difficult)
Clinically useful tests for CP
Function
Secretin stim test
Bentiromide test
Serum trypsinogen
Fecal chymotrypsin
Fecal fat
Structure
ERCP/EUS
CT scan
US
KUB
Treatment
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Pain relief
Non-enteric coated pancreatic enzymes (Viokase)
with PPI
 Narcotics
 Celiac plexus block (CT vs. EUS)
 ERCP with stent or stone removal
 Surgical resection or Peustow procedure
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Maldigestion (steatorrhea)
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Coated Pancreas enzyme (Creon)
Pancreatic Cancer
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2nd most common GI cancer and 4th most common
cancer death in US
Rare before age 45, M>F, African Americans>Whites
28,000 cases per year (27,000 deaths)
85-90% originate from pancreatic ductal cells
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Rarer cancers of acinar cells or neuroendocrine cells
Painful or painless jaundice, acholic stool, dark urine,
weight loss
Elevated CA 19-9
Diabetes frequently diagnosed within past 2 years
Treatment
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Biggest risk factors – Hereditary pancreatitis, smoking,
BRCA-2, chronic pancreatitis
Only 20% resectable at diagnosis
Surgery
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Head – Whipple procedure
Tail – Distal pancreatectomy/Splenectomy
Palliation – Intestinal/Biliary bypass
ERCP – Biliary/Duodenal Metal Stent
Chemo - 5FU and Gemcitabine
Role of XRT controversial
Pancreatic Neuroendocrine Tumors
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Insulinoma
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Glucagonoma
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Necrolytic migratory erythema, weight loss, diarrhea
75% malignancy rate
VIPoma (aka Verner-Morrison Syndrome or WDHA (Watery
diarrhea, hypokalemic and achlorhydria)
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Usually solitary, 5-10% malignancy
Hypoglycemia - 48 hour fast
Secretory diarrhea, flushing, achlorhydria, hypokalemia
Elevated fasting VIP Level
Increased risk of neuorendocrine tumors in MEN1, Von HippelLindau, neurofibromatosis 1, tuberous sclerosis
Choledocholithiasis
EUS
us
MRCP
IOC
ERCP
Common Bile Duct
stones/Cholangitis
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Obstructive jaundice WITH pain
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Rising LFTS after Lap Chole – either retained stone in CBD
vs. Bile leak
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Answer is ERCP
Cholangitis
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Charcot Triad: RUQ Pain, Fever, Jaundice
Reynolds Pentad : Shock, MS changes
ERCP stone extraction/biliary stent placement
IR placed percutaneous GB drain
Antibiotics : Floroquinolone or Unasyn/Zosyn
Gallstones
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Presentation: Usually asymptomatic
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If no symptoms from stones, then no treatment
Type: 75-80% cholesterol stones
Risk factors: 4F’s - fat, fertile, female, forty
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Ethnicity, rapid weight loss
20% pigmented stones
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Biliary colic, acute cholecystitis, CBD obstruction (acute elevation of
ALT, AST, Alk phos and TB with direct predominance), pancreatitis
Black – hemolysis and cirrhosis (calcium bilirubinate)
Brown – Anaerobic bile duct infections (Rare in US)
Diagnosis: Ultrasound best, CT, MRCP
Treatment – If symptomatic, cholecystectomy. If not surgical
candidate, ursodiol.
Biliary Tree Tumors
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Carcinoma of GB is the
leading cause of biliary tree
tumors.
Risks include:
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Gallstones
Choledochal cysts
GB polyps (primarily single
and >1 cm)
Porcelain GB
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Cholangiocarcinoma-rare but
increasing incidence.
Risks include:
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UC
PSC
Thorotrast
Choledochal cysts
Clonorchis and Opisthorchis
Treatment - Surgery in minority vs. Palliative stent
Colon
Acute Diarrhea
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Virus
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Protozoa
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Norovirus
Rotavirus
Adenovirus
Giardia
Entamoeba histolytica
Cryptosporidium (HIV)
Cyclospora
Toxin mediated
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Bacteria
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Salmonella
Campylobacter
Shigella
E.Coli (0157:H7)
C. Difficile
Yersinia
Vibrio
Listeria
Norovirus
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Nursing homes, hospitals, cruise ships, restaurants
Incubation 24-48 hours (also highest shedding)
Abd cramps followed by vomiting and diarrhea
 Nonbloody watery diarrhea
Myalgias and malaise, low grade fever
Lasts 48-72 hours
Symptomatic treatment
Campylobacter
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Food borne disease – 3 day incubation
Typically with fever, severe abdominal pain (may mimic
appendicitis) and bloody diarrhea
Lasts on average 7 days
Associated with Reactive Arthritis, Guillain-Barre
Syndrome, and pericarditis
Treatment – Mainly supportive as disease usually self
limited
If severe, use Erythromycin (other possibilities include
Flouroquinolones, Macrolides, and Aminoglycosides)
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Most resistant to septra
Salmonella Non-typhoid
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Salmonella typhimurium and Salmonella enteritidis
Largest number of food borne outbreaks in US
Eggs, poultry, undercooked beef, and pet reptiles and
rodents
Nausea, vomiting, diarrhea, fever, abd pain
 4-10 days of diarrhea
Antibiotics have not been shown to be of benefit in
routine cases
 Flouroquinolones or bactrim in severe cases or
comorbidity (HIV)
May become chronic carriers
EHEC (0157:H7)
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Enterohemorrhagic Escherichia coli
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Incubation 3-4 days
>90% will have bloody diarrhea
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Undercooked ground beef, petting zoos, daycare
Differ from other E. coli in the production of Shiga Toxins
 Enter circulation and target endothelial cells causing vascular damage
and prothrombotic state
Abdominal Pain
Often lack a fever
HUS: 6-9% --- 50% dialysis, 3-5% mortality
Treatment – Supportive
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Avoid antimotility agents and antibiotics (risk of causing HUS)
Shigella
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Not susceptible to acid, so few organisms cause
infection
Fever, abdominal cramps, mucoid or bloody diarrhea
3 day incubation, 7 day duration
Rare cause of HUS and reactive arthritis
Associated with seizures and encephalopathy in
children
Treatment – antibiotic recommended (FQ)
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Reduce shedding and person to person transmission
Decrease fever and diarrhea by 2 days
Clostridium dificile
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Associated with antibiotic usage, older age, and possibly
PPI
NAP1/BI/027 strain with larger quantities of toxins A
and B, worse outcomes, and associated with leukemoid
reaction.
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Think C diff in inpatient on antibiotics with WBC 20K.
Treatment - Fluids, Avoid/Hold antibiotics
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Metronidazole 500mg TID or 250mg QID
Oral Vancomycin 125 – 250 mg po QID
20% Relapse rate – retreat with Flagyl or Vancomycin
Other Infectious Causes
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Amebiasis (Entamoeba histolytica)
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Invade and penetrate colonic mucosa
Subacute moderate diarrhea with abdominal pain and bloody
stools and weight loss
Treatment – Metronidazole 500-750 mg tid for 7-10 d
Giardia lamblia (Chronic, large volume)
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Contaminated water source (stream, well), or person
to person (daycare, MSM)
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Watery diarrhea, malaise, steatorrhea, abd cramps and
bloating
Treatment: Metronidazole 250 mg tid for 5 days
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Chronic Diarrhea
Chronic Diarrhea (>4wks)
Diarrhea
Watery
Osmotic
Inflammatory
Fatty
Secretory
Initial Testing: Large Volume (Small Bowel) vs. Small Volume (colon)
1. Stool Osmolar Gap = 290 – 2(Na +K)
<50 is secretory >100 osmotic
2. Fecal Occult Blood Testing and Fecal Leukocytes
3. Fecal Fat - >7g over 24 hours with 100 g fat diet (tends to be
higher (i.e. 30g/day) with maldigestion than malabsorption)
Chronic Diarrhea
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Osmotic
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Fatty
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Mg, PO4, Carb Maldigest
Short gut/Resection
Bacterial overgrowth
Mucosal Disease/Celiac
Pancreatic insufficiency
Inflammatory
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Inflammatory Bowel
Ischemia
Diverticulitis
Chronic infection
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Secretory
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Non-osmotic laxative
Post-cholecystectomy
Bile acid malabsorption
IBS
Gastrinoma
VIPoma
Mastocytosis
Carcinoid syndrome
Hyperthyroid
Vasculitis
Microscopic colitis
Lymphoma, colon ca
History for Chronic Diarrhea
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Osmotic gets better with fasting – others don’t
Bloody BM’s – Inflammatory (UC)
Weight loss – Fatty, Inflammatory
RLQ pain – think Crohn’s
Iron Deficiency – think Celiac sprue
Wakes up at night with symptoms – not IBS
Ask about medications or surgeries
(cholecystectomy or IC valve resection, etc)
Irritable Bowel Syndrome
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Rome III Criteria
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Recurrent abdominal pain or discomfort at least 3
days per month in the last 3 months associated with
2 or more of the following
Improvement with defecation
 Onset associated with a change in frequency of stool
 Onset associated with change in form of stool
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Criteria fulfilled for the last 3 months with symptom
onset at least 6 months prior to diagnosis
Irritable Bowel Syndrome
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Pain poorly localized and inconsistent and often in
BLQ
Need to have bowel movement soon after meals
(gastro-colic reflex)
Symptoms do NOT wake the person from sleep
Symptoms worsened with stress
Less than age 40 at start of symptoms
Depression or Anxiety
Often overlap with other functional syndromes
(Dyspepsia, FMS, etc)
Evaluation for IBS
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If meet Rome III Criteria then testing has not been
shown to be helpful (except for sprue in diarrhea
predominant)
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Celiac Sprue serology has been positive in 5%
Sigmoidoscopy/Colonoscopy no benefit
ESR, FOBT, Stool Culture, O&P etc. no benefit
If they don’t meet the criteria or fit the usual
description then testing is indicated
For testing purposes, avoid performing diagnostic tests
(CT) on patients who meet Rome III criteria
Treatment
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Treat symptoms
Most medications have unproven benefit
Fiber : Metamucil, Citrucel, Benefiber
 Antispasmodics: Bentyl, Levsin, Donnatol
 Tricyclic Antidepressants, SSRI’s
 Imodium (diarrhea), Miralax (constipation)
 Stress Reduction
 Avoid fatty foods, Avoid Dairy
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Celiac Sprue
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40 year old Irish immigrant with history of DM 1 and
hypothyroidism with steatorrhea, microcytic anemia and mild
elevation of ALT (80).
Chronic malabsorption of small intestine secondary to exposure
to dietary gluten (gliadin portion)
1:250 in US
Symptoms include:
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Diarrhea or steatorrhea
Weight loss
Transaminase elevations
Anemia (iron deficiency)
Vitamin deficiency
Asymptomatic
Celiac Disease
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Associated with HLA DQ2 and DQ8
Associated diseases:
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IBS
Osteoporosis
IgA nephropathy
Dermatitis Herpetiformis - Elbows, knees, buttocks
Increased risk of lymphoma (NHL) and GI malignancies
DM 1
IgA deficiency
Thyroid disease
Celiac Sprue
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Diagnose with endomysial Ab or tissue
transglutaminase Ab (both IgA). Confirm diagnosis
with small bowel biopsy.
Activated T-cells damage villous architecture with
inflammatory response (blunted villi, epithelial
lymphocytic infiltrate, crypt hyperplasia).
All testing improves with treatment
Gluten-free diet
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No wheat, rye or barley
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Not in oats, though they are often contaminated with gluten
Nonresponsive or relapse likely due to dietary indiscretion
Lower GI Bleed
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Diverticular (Painless)
Ischemic Colitis (painful)
Angiodysplasia
Cancer / Polyps
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Ulcerative Colitis / Crohn’s
Hemorrhoids
10% LGIB is from upper
source
Diagnose etiology with colonoscopy
If unable to find source of bleeding or if unable to tolerate a colonoscopy
then:
Tagged RBC Scan (Technetium 99m) - Requires .1-.4ml/min of active bleeding
Angiography - Requires .5-1ml/min of active bleeding
Allows directed therapy with gelfoam etc.
Inflammatory Bowel Disease
String sign – seen with Crohn’s
Ulcerative Colitis
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Recurring episodes of inflammation limited to
the mucosal layer of the colon. Invariably
involving the rectum and extends proximally in a
continuous fashion.
Bloody diarrhea
Rectal urgency
Abdominal cramps
Fever, weight loss, anorexia, N/V
UC - Complications
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Massive hemorrhage
Toxic megacolon
Colonic perforation (5%)
Extraintestinal Manifestations
Lead pipe – chronic UC
UC - treatment
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Inducing remission
Mild = 5-ASA (mesalamine, sulfasalazine)
 Moderate = Steroid taper
 Severe = IV steroids, Cyclosporine, colectomy, TNF
alpha antagonists (i.e. Remicade or Humira)
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Maintenance
5-ASA
 Azathioprine/6-MP
 TNF alpha antagonists
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Crohn’s Disease
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Chronic recurring transmural inflammation associated
with fibrosis and sinus tracts that penetrate serosa
giving rise to microperforations and fistulae presenting
as skip lesions in any area of the GI tract
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Mucosal
Stricturing
Penetrating
Based upon location
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50% ileocolitis, 30% ileitis, 5% Gastroduodenal
Crohn’s complications
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74% require surgery
Right lower quadrant pain
Diarrhea
Weight loss/Anorexia
Small Bowel Obstruction
Fistulas
Perirectal Abscess/Intraabdominal abscesses
Osteoporosis
Extraintestinal Manifestations
Enterocolonic
fistula and
string sign
Crohn’s - Treatment
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Induction of Remission
?5-ASA = target to area of disease
 Ciprofloxacin / Flagyl
 Steroids (Prednisone or Budesonide)
 TNF alpha antagonists
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Maintenance
5-ASA
 6-MP/Azathioprine/MTX
 TNF alpha antagonists
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Extraintestinal Manifestations
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Arthropathy (20%)
Large joint – follows disease activity
 Small joint – independent of disease
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Ankylosing Spondylitis (10%)
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Erythema Nodosum (10%)
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Not associated with disease activity
Associated with disease
Pyoderma Gangrenosum (10%)
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Not associated with disease activity
Extraintestinal Manifestations
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Episcleritis / Uveitis – 5%
Nephrolithiasis
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Primary Sclerosing Cholangitis
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Calcium oxalate stones with ileal Crohn's
5% of UC, 75% of PSC have UC
25% cancer at 10 years after PSC diagnosis
Colon Cancer
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1% per year after 15 years
Start surveillance at 8-10 year after diagnosis in pancolitis and
after 15 years in left sided colitis
IBD = Indication for surgery
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UC
Toxic megacolon/Perforation
 Failure to control symptoms
 Dysplasia on surveillance
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Crohn’s
Strictures with obstruction
 Complicated fistula
 Unresponsive inflammatory mass
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Dermatologic and GI Associations
Dermatitis Herpetiformis
Chronic, symmetric, intensely pruritic eruption including
vesicles, papules and urticarial wheals
Celiac Disease
Acanthosis Nigricans
Diffuse, velvety thickening and hyperpigmentation of skin in
axilla and other body folds
Gastric Cancer
Tricholemmomas
Cowden’s Syndrome
Cowden’s syndrome more associated with thyroid and
breast cancer as well as GI hamartomas
Necrolytic Migratory Erythema
Superficial migratory necrolytic erythema with central blisters or
erosions that crust and heal with hyperpigmentation, a beefy red
tongue, and angular cheilitis
Glucagonoma
Peutz Jeghers Syndrome
Intussusceptions and Malignancies
Pancreatic Neuroendocrine tumors
Neurofibromatosis-1
Tuberous Sclerosis
MEN1, And…
Von Hippel-Lindau
Hemagioblastomas and retinal angiomas
Clear cell RCC
Pheochromocytoma
Endolymphatic sac tumors of middle ear
Pancreatic serous cystadenoma or neuroendocrine tumors
Papillary cystadenomas of epididymis and broad ligament
Questions?
Good luck on Boards