CASE 1 – THE HEAVY DRINKER

1. COMPLICATIONS OF PUD

Hemorrhage Hematemesis (vomit fresh blood/coffe ground)

Bloody stools/ black tary stools (melena)
Weakness, syncope, thirst, sweaty cause blood loss
Penetration May into duodenum or adjacent space (peritoneal cavity) or adjacent
organs (liver, pancreas)
Pain maybe persistent, intensed and referred
CT/MRI to confirm diagnosis
Free perforation Into peritoneal cavity
CXR/CT show air under diaphragm
Ttt : nasogastric suction, antibiotics, medical and surgical
Gastric outlet obstruction Scarring, spasm/ inflammation
Recurrent vomit, loss appetite, bloating, dehydration, alkalosis
Stomach cancer Patient with H.pylori infection 3-6x > malignancy

2. CAUSES OF EARLY DUMPING’S SYNDROME

i. Autonomic reflex
ii. Intravascular volume contraction
iii. Release of vasoactive peptides from small intestine
iv. Reactive hypoglycemia/ late dumping
v. Mechanical problems
vi. Ulcer recurrence

3. PATHOPHYSIOLOGY OF PUD

DU GU
(increase acid load to duodenum due to) (breakdown of gastric mucosa)
 increase acid secretion because increase parietal cell  gastritis attack body and antrum
mass and increase gastric secretion  local epithelial damage because cytokinine released by
 decrease inhibition of acid secretion (H.pylori damaging H.pylori
somatostatin cells)  parietal cell damage
 smoking : gastric mucosal bleeding
 blood group O
 bicarbonate secretion decrease in duodenum by
H.pylori

4. HELICOBACTER PYLORI

i. Gram –ve, spiral, has multiple flagella at one end

ii. Transmit : oro-oral/ feco-oral
iii. No reservoir in animal/ water supply
iv. Any acidity buffered by organism produces enzymes increase catalyes urea > ammonia, increase pH
v. Stimulates chronic gastritis by provoking local inflammatory response

5. EFFECTS OF H.PYLORI ON GASTRIC HORMONE

i. Increase acid secretion

ii. Increase gastrin released from G-cells
iii. Depletion of antral-D-somatostatin
iv. Increase acid load to duodenum (gastric metaplasia)
v. Inflammation and ulceration

jubahblack@gmail.com
Faculty of Medicine Mansoura University
6. NSAIDs

Inhibit production of prostaglandin precussor from fatty

acid results in
 Decrease mucous and bicarbonate production
 Decrease mucosal blood flow
 Decrease cell renewal
 Generate O2-free-radical > ulceration
Induces mucosal injury by
 Convert superficial to deep mucosal necrosis
 Interfere homeostasis / platelet aggregation
 Impaired ulcer healing

7. DIAGNOSIS

Ulcer (DU/GU) Endoscopy

H.pylori Non-invasive (C13, C14, urea breath test, stool antigen test, IgG titter (serology)
Invasive (gastric mucosal biopsy, rapid urea test)

8. GASTRIC FUNCTION TEST

i. Histamine test : parietal cell mass, total acid secretory potential, true/false hyperacidity
ii. Pentagastrin test
iii. Insulin test (Hollander) : integrity of vagotomy
iv. Clear spit test
v. Gastrin level

jubahblack@gmail.com
Faculty of Medicine Mansoura University