Gastrointestinal Problems

Claire Nowlan MD

Jan 16, 2004

Peptic Ulcers

Ulceration of either the gastric or duodenal mucosa

Risk factors for Peptic Ulcers H. Pylori (cause of 70%-90% of ulcers) NSAIDs (Steroids and Bisphosphonates) Alcohol Smoking Ages 30-50 Stress Medical conditions

– Hyperparathyroidism– Zollinger Ellison Syndrome– Renal Dialysis

Etiology

Imbalance of Aggressive/protective factors H. Pylori produces urease

– urea > ammonia and CO2– This invokes immune response and starts

inflammation cascade– infection increases with age and poor

socioeconomic conditions– only 20% of infected develop disease

Etiology

NSAIDs– reduced mucosal prostaglandin

production, resulting in impaired prostaglandin dependent mucosal defense and repair mechanisms

Inflammation cascade

ca ta lyzed b y cox-2

L eu ko trien es

A rach id on ic ac id p ros tag lan d in s

P h osp h o lip id s

d is tu rb an ce o f ce ll m em b ran es

S tim u lu s

Complications

Depends on depth of ulcer More common in the elderly

– Perforation– Hemorrhage - more serious if patient on

anticoagulants– Pyloric stenosis– Carcinomatous transformation

Signs and Symptoms

Variable Red flags - vomiting, bloody or tarry

stools, new ab pains in an elderly person, signs of blood loss (pale, lightheaded, orthostatic hypotension)

Lab findings

Serology or 13C 14C urea breath tests for H. Pylori

Barium swallow Endoscopy

Medical treatment

Eradication of H. Pylori usually cures ulcer Regiments – 7 to 14 days of:

– PPI (Omeprazole/Lansoprazole/Pantoprazole)– PLUS 2 antibiotics

(Clarithromycin/Metronidazole/Amoxicillin/Tetracycline)

– PLUS/MINUS Pepto-Bismol

Stop NSAIDs

Dental Management If active, untreated disease - refer If possible, NSAIDs should be avoided in

patients with high GI risk– Previous GI bleeding– Previous peptic ulcers– Age > 75 years– Steroid use

COX-2 selective inhibitors were created as a NSAID alternative as it does not inhibit Cox-1 present in the GI mucosal barrier, but inhibits Cox-2 present in the inflammation cascade

Treatment algorithm for ill/elderly patient who requires NSAIDs

Y E SU se a tra d it io n a l N S A ID ,

p lu s cytop ro tec tion

If G I ris k > C V riskU se co x -2

If G I ris k < C V riskU se N S A ID p lu s cyto p ro te c tion

N OE va lu a te G I ris k a nd

th e C V risk

T a k in g A S A ?

Cyclo-oxygenase-2 (COX-2) inhibitors Vioxx refecoxib/Celebrex celecoxib(not in patients

with Sulfa allergy)/Bextra valdecoxib Mobicox meloxicam

Similar efficacy to older NSAIDs Early trials suggested decreased endoscopic

ulceration No difference in dyspepsia Recent trials show INCREASED risk (.6%) of

MI ?stimulate endothelial cells and encourage vasoconstriction

Medications to prevent NSAID associated peptic ulcers Misoprostol 200ug TID

– Don’t use in fertile women PPIs

– Omeprazole 20 mg od– Lansoprazole 30 mg od– Pantoprazole 40 mg od

Irritable bowel

Affects up to 30% of the population Symptoms include

• diarrhea• constipation• abdominal pain• bloating

Difficult to control symptoms Treatment includes dietary changes, stress

management, medications

Pseudomembranous colitis

A severe colitis that results from broad spectrum antibiotics killing healthy gut bacteria and allowing C. difficile to flourish (already present in 2% asymptomatic people, up to 50% of the elderly)

C. difficile binds to intestinal mucosa and alters cell permeability

Worst antibiotic – Clindamycin, amoxil and cephalosporins to a lesser extent

Symptoms usually develop 1 week later, can be as long as 8 weeks

Pseudomembranous colitis

Symptoms - Watery profuse diarrhea and low grade fever, if severe - bloody diarrhea, fever, abdominal pain and death

Diagnosis – enterotoxin A/B found in the stool sample

Medical Management• Stopping the antibiotic cures up to 25% of patients• Flagyl or Vancomycin for 7 to 10 days• Hand washing

Pseudomembranous colitis

Dental management– Use broad spectrum antibiotics wisely

especially in elderly patients or those with a previous history

Inflammatory Bowel Disease (IBD) Inflammatory disease of the GI tract Unknown origin Patient experiences diarrhea,

abdominal pain Peak age of onset 20 to 40 years Systemic findings –arthritis, iritis,

uveitis, skin manifestations

Inflammatory Bowel Disease (IBD) Ulcerative Colitis Limited to the large

intestine Limited to mucosa Continuous lesions Remissions/

exacerbations common Rectal bleeding

common

Crohn’s Disease Affects any portion

of the bowel Transmural Segmental Usually slowly

progressive Fever, weight loss

common

Inflammatory Bowel Disease (IBD) Ulcerative Colitis Complications

hemorrhage, toxic megacolon, anemia, volume depletion, electrolyte imbalance, malignancy

Crohn’s Disease Complications

anemia, malabsorption, fistulae, stricture, abscess

Operations more common

Inflammatory Bowel Disease (IBD) - lab findings May see anemia, malabsorptions

causing low B12, folate, iron, albumin, and increased ESR

Really diagnosed with colonoscopy/biopsy

Medical management

Supportive therapy– Nutritional supplementation, bowel rest, replacing

fluid and electrolytes Antiinflammatory drugs

• 5 ASA compounds - Sulfasalazine• Olsalazine, mesalamine• Steroids

Immunosupressives• methotrexate, cyclosporin

Antibiotics Surgery – curative in UC

Dental management - IBD

Precautions if on steroids Immunosupressants cause pancytopenia in

5% of patients, increase risk of lymphoma and oral infections

Methotrexate can cause hypersensitivity pneumonia and hepatic fibrosis

Cyclosporin can cause renal damage Sulfsalazine associated with pulmonary,

nephrotic damage

Dental management - IBD

Analgesics acetaminophen plus

– NSAIDs OK– opioids fine, unless during acute severe

exacerbation - can cause toxic megacolon Only urgent care during exacerbation