Lecture 80 -- Disease of the stomach Flashcards
Peptic Ulcer Disease:
Erosion vs Ulcer
Erosion – a break in the mucosal lining
Ulcer -a break with depth into the submucosa
Peptic Ulcer Disease: causes
Causes: “PH, HP, nough SAID”
pH, H. Pylori, NSAID – 90%
Peptic Ulcer Disease:
pathogenesis
Pathogenesis:
1) Injurants to the lining –
Gastric acid or bile acid
NSAIDs
2) Impaired mucosal Defenses: Impaired mucus and bicarbonate secretion Poor Blood Flow
what are Stress Ulcers ?
who get’s them?
what’s a Cushing’s ulcer?
what’s a Curling ulcer?
Stress Ulcers – -occur with severe physiological distress
ICU Patients, Intubated Patients, Post Trauma Patients,
Cushing's Ulcer = patients with increased Intra cranial pressure
Curling Ulcer — in burn patients
4 complications of Ulcers?
which is the most common?
why is incidence decreasing?
Perforations – non sterile contents of the GI lumen break open into the peritoneal cavity
Bleeding - the most common complication
Penetration – ulcer breaks into adjacent organ
Obstruction – such as with an ulcer situated at the pyloric outlet
have largely been resolved with the use of PPIs
H. Pylori –
where will the ulcers be?
course of the infection ?
Gastric + Duodenal Ulcers
90% of Duodenal Ulcers; 80% of Gastric Ulcers are H pylori associated?
Initial Infection —>
Almost everyone will get chronic gastritis
10% Gastric or Duodenal Ulcers
Atrophic Gastritis – precursor for gastric cancer
Lymphoproliferative MALT Lymphoma (MALToma)
H. Pylori –
diagnostic techniques
serum antibody – this can be used for initial detection, but not thereafter as it will always be positive
stool antigen
Breath test – H pylori is urease producing; therefore give patient radiolabelled Urea, and detect if CO2 on exhalation is also radiolabelled; indicates presence of urease
Biopsy – spiral shaped bacteria in the mucosa
Giemsa, Genta or Silver Stains
CloTest – bx of the stomach and put in on an assay
If urease is present it will be positive
H. Pylori –treatment
Treatment – 2 antibotics + PPI
Amoxcillin, tetracyclin, metronidazole, clarithromycin
If you eradicate the organism, risk of recurrent ulcer decreases
NSAIDs and Gastric Ulcers
pathogenesis?
NSAIDS = COX inhibition
therefore there is less: prostaglandins, thromboxane and prostacyclin
These are very important for protection of the gastric Mucosa
NSAID Ulcers: Risk factors:
concurrnet use of what drug is bad?
> 60 yo, past hx of ulcer, high doses of NSAID
Concomitant Steroid Use
NSAID Ulcers:
treatment and prevention
Prevention:
Avoid NSAIDs, Use COX2 selective NSAIDs (Celebrex)
Concomitant use of H2 blockers or PPI –
Misoprostol – PGE1 analog
Treatment: Stop NSAID, start PPI
Zollinger Ellison Syndrome and Ulcers
what is ZE?
Prevalence in the US?
what % have Multiple endocrine neoplasia?
What is it? Gastrin secreting non beta cell tumor of the pancreas (Gastrinoma); which constitutively secretes Gastrin (loss of negative feedback from low pH), leading to gastric acid hypersecretion from parietal cells
25% of ZE patients have MEN
1 in a million Americans have ZE
Manifestations of ZE
Gastric and Small intestinal ulcers,
Diarrhea (due to the volume of the extra acid and malabsorption from inhibition of pancreatic enzymes),
Severe GERD
Diagnosis of ZE
hypergastrinemia in the setting of Low pH
Secretin Provocation Test (normally secretin inhibits gastrin release)
Localizing the Tumor:
Ocreotide
Treatment of ZE
Treatment:
Resection
High Dose PPI
Ocreotide – somatostatin analog