Dental Management 11 – Gastrointestinal Disease

Peptic Ulcer Disease

 Well defined break in the GI mucosa (.5mm)

o results from
 chronic acid or pepsin secretion
 H. pylori
o Develops in GI tract, proximal to acid and pepsin secretion
 first portion of duodenum in western populations
 gastric in Asian populations
 rarely upper jejunum
 only 10% of patients have more than 1 ulcer
 Epidemiology
o more common in men
o Alcohol and smoking ↑ risk
o Hyperparathyroidism ↑ risk
o Hypersecretion ↑ risk
 Renal disease, ZE syndrome
o Type O blood ↑ risk
o If diagnosed in young children → probably have systemic disease
 usually burn injury or major trauma
 Etiology
o Primary factor is H. pylori
 80% of duodenal and gastric ulcers in the US
 90% in the world
o Use of NSAIDS is the second most common cause of PUD
o H. pylori
 Characteristics
 Microaerophilic
 gram-negative
 spiral-shaped
 4-6 flagella
 Noninvasive bacteria
 Produces urease
 hydrolyzes urea → ammonia and carbon dioxide
 increase local pH
 Humans are only known host
 resides in the oral cavity
o NSAIDs
 Ulcers from NSAIDS are located more often in the stomach than duodenum
 Use of alcohol, steroids, anticoagulants or ASA ↑ risk
 Pathophysiology and Complications
o Body’s defense against ulcers
 mucosa
 mucus and PG production
 blood flow
 bicarbonate secretion
 ion carrier exchange
 antibacterial proteins
o Normal process
 Food → gastrin release → histamine release from enterochromaffin-like cells
→ H+ and HCl release from parietal cells
o Aggressive process
 Vagal hyperstimulation
 Hypersecretion of gastrin, histamine and pepsin
 Stress
 OCD
 parasitic infections
 Drugs
 caffeine, steroids, phenylbutazone
 Alcohol and NSAIDS
 damage stomach mucosa
o H. pylori process
 inflammation of gastric mucosa by producing proteases and ↑ gastrin release
from G cells
 Can cause you to develop MALT lymphoma
 Class I carcinogen
o Complications
 superficial ulcers
 necrotic debris
 fibrin
 inflammatory infiltrate
 granulation tissue
 fibrosis
 Muscularis ulcers
 perforation of peritoneal cavity
 involvement of head of pancreas
 Bleeding ulcers
 from erosion of arteries and veins
 acute hemorrhage
 anemia
 shock
 Untreated ulcers heal by fibrosis
 pyloric stenosis
 gastric outlet obstruction
 dehydration
  alkalosis
 Clinical Presentation
o Signs and Symptoms
 many asymptomatic
 Most have sharp, localized, epigastric pain
 Duodenal Ulcer discomfort on an empty stomach
 frequently awakens at night
 Food, milk and antacids can relieve pain
 Gastric ulcer
 eating may cause pain
 Vomiting a few hours after meal = gastric outlet obstruction
 Laboratory and Diagnostic Findings
o Dx from endoscopic biopsy
 biopsy of marginal mucosa adjacent to the ulcer
 rapid urase test to detect presence of H. pylori in biopsy
 H. pylori staining with
 Giemsa
 acridine orange
 Warthin-Starry
 Methylene blue (in case 4)
 Culture is not routinely performed – unless need AB resistance
o Urea breath test
 measures C13 and C14 ratios in CO2 broken down from urea
 Medical Management
o If not H. pylori → antisecretory drug (such as a PPI)
o If H. pylori is present → triple therapy
 Gastric acid inhibitors
 rapid pain relief and accelerated healing
 At least wo antibiotics
 eradicates H. pylori in 90% of patients
o If an area where there is high Antibiotic resistance → Quadruple therapy
 Metronidazole + amoxicillin + PPI + pepto-bismol
o Once H. pylori is eradicated cigarette smoking does not increase the risk of recurrence
 Dental Management
o Recommendations
 Antibiotics
 ABs used during PUD therapy should keep most dental infections in
check
 may need to alter additional ABs you proscribe
 Bleeding
 GI bleeding → delay treatment
 Drug considerations
 Do not proscribe
 o ASA, or NSAIDS (except celecoxib with a PPI)
 Use APAP instead
 H2 receptor antagonists are not beneficial
 May need to use lower doses of diazepam, lidocaine or TCAs if taking
acid-blocking drugs (cimetidine)
o will lead to ↓ metabolism and ↑ half-life
o Oral complications and manifestations
 H. pylori is found in dental plaque
 If using antibiotics → may get candidiasis or median rhomboid glossitis
 proscribe antibiotics
 Vascular malformations of lip and erosion of the enamel
 Medications
 PPIs → altered taste perception
 Cimetidine and ranitidine → toxic effect on bone marrow
o Also can cause mucosal ulcerations, mucosal pallor, gingival
bleeding or petechiae
 Anticholinergic drugs → xerostomia
 Omeprazole and lansoprazole (+ cimetidine and ranitidine) →
erythema multiforme

Inflammatory Bowel Disease

 Encompasses Ulcerative colitis and Crohn disease

o UC: mucosal disease limited to large intestine and rectum
o CD: transmural (full thickness of bowel wall) → patchy ulcerations from mouth to anus
 most commonly distal ileum and proximal colon
 Epidemiology
o Higher in Jews and whites than in African Americans and very common in the US
 median age is 20-40
o Smoking
 ↑chance of getting Crohn disease
 ↓chance of getting ulcerative colitis
 Etiology
o Genetics is a factor
 Usually a mutation in leukocyte migration → ↓ microbe clearance
 Pathophysiology and Complications
o Both trigger TH17 response
o Ulcerative Colitis
 Targets large intestine
 cycles of remission and exacerbations
 starts in colon and rectum can spread → entire large intestine
 Histology
 Epithelial necrosis
 edema
  vascular congestion
 monocellular infiltration
 Life long disease → can progress
 Toxic megacolon
o disease extends through muscular layer → dilated colon →
perforation
 Carcinoma of the colon
o Crohn Disease
 Chronic, relapsing disease
 Segmental distribution of ulcers called “skip lesions”
 usually effects distal ileum and proximal colon
 but can affect any portion of the bowel
 Relapses are more common in smokers
 Patients will require at least 1 operation
o Both
 Characterized by inflammatory infiltrative lesions of the bowel wall with
noncaseating granulomas
 Clinical Presentation
o Signs and Symptoms
 Ulcerative Colitis
 3 main symptoms
o Diarrhea
o Rectal bleeding
o Abdominal cramps
 Sudden on slow onset, usually chronic either way
 Extraintestinal manifestations
o arthritis
o erythema nodosum
o pyoderma gangrenosum
o eye disorders
o growth failure
 Crohn Disease
 Symptoms
o Recurrent diarrhea (without blood)
o RLQ abdominal pain
o anorexia and weight loss
o Fever
o arthritis
o uveitis
 3 major patterns
o disease of ileum and cecum
o disease confined to small intestine
o disease confined to the colon
  Most patients require surgery
 Laboratory and Diagnostic Findings
o Based on endoscopy/biopsy
 Ulcerative colitis
 friable, granular, erythematous and eroded colon mucosa
 Crohn disease
 patchy erosions and ulcerations and noncaseating granulomas in any
part of GI tract
 Malabsorption leads to anemia in CBC
 ↓ serum total protein and albumin
 Medical Management
o Symptoms can be managed but not cured
o First line
 Antidiarrheal and antiinflammatory
 Especially 5-ASA for Crohn disease
o Second line
 immunosuppressants and antibiotics
o Third line
 biologic agents (monoclonal antibodies against inflammatory markers)
 infliximab
o 5-ASA drugs for Crohn disease
 Sulfasalazine, mesalamine, pentasa, olsalazine, balsalazide
 MOA
 bound to ASA – when metabolized by bacteria delivers local
antiinflammatory
 Deliver
 extended release oral or suppository
 Side effect
 nephrotoxic
o Steroids for acute flare-ups
 need to taper
o Immunosuppressants
 for disease unresponsive to steroids
o Biologics are reserved for sever disease
o Antibiotics for treatment of Crohn disease
 Dental Management
o Identification and Risk Assessment
 < 4 BMs a day and ESR <20mm/hr = mild disease → can have treatment
 5 BMs a day 20-30mm/hr = moderate → refer to PCP
 > 6 BMs a day >30mm/hr = severe → refer to PCP
o Recommendations
 Antibiotics
 those taking immunosuppressives ↑ risk of infection
  Clindamycin and penicillins have ↑ risk of PMC
 Appointments
 only urgent care during acute attacks
 Bleeding
 not an issue unless thrombocytopenia
 get CBC if taking 5-ASA drugs (sulfasalazine)
 Capacity to Tolerate Care
 Steroids → decrease stress tolerance
 Drug Considerations
 antiinflammatory drugs
o avoid NSAIDs
 Can use celecoxib + PPI
o Can use APAP
 Immunosuppressors
o can lead to pancytopenia
o increased risk of lymphoma and infection
o Oral complications
 Ulcerative colitis
 Aphthous-like lesions
 Pyostomatitis vegetans in ulcerative colitis
o raised papillary, vegetative projections on erythematous base of
labial mucosa, gingiva and palate
o tongue is rarely involved
 Crohn disease
 may show up before GI symptoms by several years
 mucosa ulcerations
o linear ulcers with hyper plastic margins
o look like cobblestones
o often in the buccal vestibule and soft palate
 swelling of lips and cheeks
 Sulfasalazine
 can lead to toxic effect on bone marrow
o anemia
 “bald tongue”, mucosal pallor
o agranulocytosis
 oral infection and ulcerations
o thrombocytopenia
 bleeding

Pseudomembranous Colitis

 Fatal form of Colitis from overgrowth of C. difficile in large colon

o results from
 loss of bacterial competition
  heavy metal intoxication
 sepsis
 organ failure
o C. dif produces enterotoxins → colitis and diarrhea
 Epidemiology
o Most common nosocomial GI infection
 Etiology
o C. dif is causative in 90-99% of PMC
 gram-positive
 spore forming
 anaerobic
 rod shaped
o Antibiotic use
 Clindamycin (2-20%)
 Ampicillin or Amoxicillin (5-9%)
 3rd generation Cephalosporins <2%)
 Oral antibiotics more causative than parenteral
 Pathophysiology and Complications
o C. dif produces 3 toxins
 A
 cytoskeletal degeneration
 B
 altered vascular permeability
 Binary toxin
 both effects
o Mild disease
 patchy distribution
o Severe disease
 large plaques
 Clinical Presentation
o Signs and Symptoms
 Diarrhea is most common symptom
 watery and loose
 if severe → bloody diarrhea with pain and cramping and fever
 Laboratory and Diagnostic Findings
o Leukocytosis → leukocytes in stools
o C. dif in stools
o Pseudomembranes in colon biopsy
 Medical Management
o Discontinue use of antibiotic
o Start antibiotic that will eradicate C. dif
 Metronidazole for moderate disease
 Vancomycin for severe disease
 Dental management
o Antibiotics
 Caution with clindamycin, ampicillin and cephalosporins
o Appointment
 Delay until after PMC is resolved
o Drug considerations
 Antibiotics for C. dif can cause oral candidiasis
 Metronidazole can cause peripheral neuropathy, nausea and metallic taste