PEPTIC ULCER
TREATMENT
If H.pylori present: eradicate
Re-appearance= 1% per annum
Due to failed eradication rather then re-infection
False -ve of breath test
Clears 85-90%
2 out of 3:
Metronidazole
Clarithromycin
Amoxicillin
No acid= no ulcer: Proton Pump Inhibitor (PPI)
Duodenal ulcer
Never malignant
Nocturnal
Pain when hungry
Gastric ulcer
1% = malignant
Pain releived with food
INVESTIGATIONS
H. pylori
UREA breath test
Shud do 2 c if got rid of HP
Most sensitive
C13/ radioactive C14
Must biopsy if gastric ulcer as 1% are malignant
CLO test
Histology
Serology
Barium meal
Gastroscopy
ERECT CXR: gas/air under diaphragm = perforated ulcer
Blood tests
Amylase= >3 times upper limit of normal = Pancreatitis
Biochemistry: Electrolytes; Renal function (urea & creatinine); LFT's
FBC
Thrombo-cytopaenia = decreased platelet count
Chronic iron deficiency anaemia
CAUSE
NSAID's/ aspirin
H.pylori
HP= class 1/grade A carcinogen (like smoking with lung cancer)
= Risk factor (3-5 fold increase) for gastric carcinoma
Only HP has UREASE= enzyme that breaks down urea & produces CO2 (acid)
Gastric ulcer: found in 70% of cases with no NSAID's/ aspirin
Duodenal ulcer: found in 100% of cases with no NSAIDs/aspirin
Lives in gastric antrum
Acquired in childhood
Prevalence= 50% in 50yr olds; 20% in 20 yr olds
SYMPTOMS
Bleed/haemorhage: 15% mortality
Melena
Haematemesis
Perforation
Epigastric pain
Smoking= secretagon: increases acid production
Lasts for 4 weeks at a time
Eased with antacids
May radiate thru to back
Constant