Transcript Diagnosis and management of PUD

Diagnosis and management of
PUD
Ermias (MD)
History
• Abdominal pain (epigatric burn)
– Common for DU, GU, NUD
– 10% present with complications with out antecedent
pain, eg after NSAID
– DU – 90min-3hr after meal, past midnight,
- relieve with food, antacids
– GU – worse with meal, nausea and weight
loss are common
• Mechanism of pain
– Acid induced chemoreceptor activation in duodenum
– Enhanced duodenal sensitivity to bile acids and
pepsin
– Altered gastro-duodenal motility
History conti…
• Alterations in pain may show complications
– Persistent dyspepsia radiating to the back penetrating ulcer to pancreas
– Sudden onset severe generalized pain –
peritonitis due to perforation (6-7%)
– Worsening vomiting with meals – GOO (1-2%)
– Tarry stool, coffee ground vomits - bleeding
(15%)
Physical examination
• Epigastric tenderness
• 20 % slightly to the right of the mid line
• In complications
– Tachycardia, hypotension
– Signs of peritonitis
– Succussion splash
DDx
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NUD (functional, essential)
Proximal GI tumors
GERD
Pancreaticobiliary diseases
Crohn’s disease (gastro-duodenal)
diagnosis
• Empiric tx as NUD (<45 yrs age)
• Ba studies
– Single contrast -80%, double contrast 90% sensitivity
– See as well defined crater
– Negative in <0.5cm ulcer, post op or scars
• Endoscopy
– Photography, tissue biopsy, source of blood loss,
detection of small ulcers
• H. pylori
• Serum gastrin, gastric acid analysis - ZES
H. Pylori detections
– INVASIVE (ENDOSCOPY/BIOPSY REQUIRED)
• Rapid urease – (80–95/95–100) - Simple, false negative
with recent use of PPIs, antibiotics, or bismuth
compounds
• Histology – (80–90/>95) - Requires pathology
processing and staining;
• Culture - Time-consuming, expensive, allows
determination of antibiotic susceptibility
– NON-INVASIVE
• Serology – (>80/>90) - Inexpensive, convenient; not
useful for early follow-up
• Urea breath test – (>90/>90) - Simple, rapid; useful for
early follow-up; false negatives with recent therapy
– Stool antigen – (>90/>90) - Inexpensive,
convenient; promising for eradication
treatment
• Schwartz – “no acid no ulcer” (old dictum)
• New concept
– Eradication of H. pylori,
– prevention of NSAID induced ds.
Acid neutralizing
• Antacids – symptomatic relief
– Al(OH)3 Mg(OH)2
– CaCO3, NaHCO3
• H2 receptor blockers – for active ulcer tx with H
pylori eradication (4-6wk)
– Antiandrogenic, cyt P450 inhibitor,
– Elevation of transaminases, cr, prolactin;
pancytopenia
• Proton pump inhibitors
– Irreversibly inhibit H+K+ATPase
– Rapid onset and prolonged half life
– Hypergastrinemia, carcinoid tumors (in animals),
hypochlorhydria (interfere with drug absorption)
Cytoprotective agents
• Sucralfate
– Complex sucrose salt of Al(OH)3 and sulfate
– Forms viscous paste in the stomach
– Gives physicochemical barrier from further tissue
injury
– Induce trophic effect on growth factors
– Stimulate mucous and bicarbonate secretion
– Enhance prostaglandin secretion
– SE – constipation, neurotoxicity (Al) in renal
failure
• Bismuth preparations (colloidal bismuth subcitrate,
subsalicylate)
– Anti H pylori effect
– Mech. for ulcer not clear
– Prostaglandin analogues – misoprostal
– Enhance mucous bicarbonate secretion, stimulate
mucosal blood flow, decrease mucosal cell turn
over
– Se – diarrhea, uterine bleeding and contraction
– 200ug QID
Therapy of H pylori
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Dramatic decrease in ulcer recurrence
GU 59% - 4%
DU 67% - 6%
Aim of initial eradication – 85-90%
Efficacy, pt tolerance, resistance pattern,
cost
• dual tx not recommended < 80% eradication
• Unnecessary tx – drug resistance
• Infection recurrence in 6 mnth is likely from
recrudescence than reinfection
• TRIPLE THERAPY
• 1. Bismuth subsalicylate plus
Metronidazole plus
Tetracycline
• 2 tablets qid
250 mg qid
500 mg qid
• 2. Ranitidine bismuth citrate plus
Tetracycline plus
Clarithromycin or metronidazole
• 400 mg bid
500 mg bid
500 mg bid
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• 20 mg bid (30 mg bid)
250 or 500 mg bid
500 mg bid
1 gr bid
3. Omeprazole (lansoprazole) plus
Clarithromycin plus
Metronidazole or
Amoxicillin
• QUADRUPLE THERAPY
• Omeprazole (lansoprazole)
Bismuth subsalicylate
Metronidazole
Tetracycline
• 20 mg (30 mg) daily
2 tablets qid
250 mg qid
500 mg qid
Tx of NSAID related gastric injury
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Stop the injurious agent
Use acid inhibitory agent (PPI, H2 blocker)
Prevention – misoprostol, PPI
Use of COX -2 inhibitors
• Clinical Setting
• Active ulcer
• Recommendation
• Prophylactic
therapy
• Misoprostol
PPI
Selective COX-2 inhibitor
– NSAID discontinued • H2 blocker or PPI
PPI
– NSAID continued
• H. pylori infection
• Eradication if active ulcer
or a past history of peptic
ulcer disease
UGIE
4wk
GU vs DU
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GU (body, fundal) – likely to be malignant
Repeat endoscopy and biopsy at 8-12 wk
Non healing DU (8wk), GU (12wk) – refractory
Causes:
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Poor compliance
NSAID use
Cigarette smoking
Malignancy
Gastric hyper secretary state (ZES)
Ischemia, Crohn’s ds, Amyloidosis, Sarcoidosis,
Lymphoma, Eosinophilic gastroenteritis, CMV infection,
Tuberculosis, syphilis
surgery
• Elective and emergency
• Medically refractory ulcer and complicated
ulcers (bleeding, perforation and GOO)
• Surgical mx decreased with increased
endoscopic interventions
• Procedures:
– 1. vagotomy with drainage
– 2. highly selective vagotomy
– 3. vagotomy with antrectomy
complications
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Depend on the extent of anatomic modification
Complications of intra abdominal procedure
Recurrent ulcerations
Afferent loop syndrome
Dumping syndrome
Post vagotomy diarrhea
Bile reflux gastropathy
Maldigestions and malabsorption
Gastric adenocarcinoma