1. Gastric and duodenal ulcerGastric and duodenal ulcer
diseasedisease

2. AnatomyAnatomy
 Arterial blood supply
 Lymphatic drainage
 Nerve supply

3. PHYSIOLOGYPHYSIOLOGY
Function:
1. Digestion of food, reduce the size of food
2. Acts as reservoir
3. Absorption of Vit. 12, iron and calcium
Stimulant of Gastric secretion:
1. Gastrin -----> (+) parietal cell
2. Acetylcholine (vagus) ---> (+) gastric cells
3. Histamine (mast cells) ---> parietal & chief
cells

4. PHYSIOLOGYPHYSIOLOGY
BAO: 2 – 5 meq of acid/hr. (vagal tone and basal
histamine secretion)
MAO:
1. Cephalic (vagus) ---> (+) parietal & G cell
 10 meq acid/hr.
1. Gastric: ---> (+) vagus & G cell
 15 – 25 meq of acid/hr pH = < 2.0
1. Intestinal:
 Chyme enters the duodenum
 (-) gastric release
 Secretin, gastric inhibitory peptide, peptide YY
– ACID condition sterilized the area, except for
HELICOBACTER PYLORI

5. Protective factorsProtective factors vs.vs. hostile factorshostile factors
Peptic Ulcer DiseasePeptic Ulcer Disease
PathogenesisPathogenesis ::

6. Peptic ulcerPeptic ulcer
Pathogenesis:
1. For both Duodenal & Gastric Ulcers:
a. Infection w/ H. pylori:
 Decreases resistance of mucus layer from acid
permeation (hydrophobicity)
 Increase acid secretion
 Slow duodenal emptying
 Reduced both duodenal and gastric bicarbonate
secretion

7. Clinical ManifestationClinical Manifestation
1. Abdominal pain:
– Due to irritation of afferent nerves w/in the ulcer by the
acid or due to peristaltic waves passing through the ulcer
 Duodenal: colicky or burning pain relieved w/ food
intake
 Gastric: gnawing or burning usually during or after
eating.
1. N/V
2. Weight loss
3. Epigastric tenderness

8. Peptic ulcerPeptic ulcer
Pathogenesis:
b. Effects of NSAIDs
 Decreases Prostagladin
Prostaglandin – inhibits acid secretion, stimulates mucus
and HCO3 secretion and mucosal blood flow
b. Zollinger-Ellison Syndrome (1%):
 Massive secretion of HCL due to ectopic gastrin
production from non-beta islet cell tumor (gastrinoma)
 Associated w/ type I (MEN) PPP
 20% multiple, 2/3 malignant, w/ slow growing
 Parietal cell mass is increased
 > gastrin 3-6 x the normal

9. Symptoms of gastric ulcer disease:
 epigastric pain after meal or during meal
 upper dyspeptic syndrome – loss of appetite, nauzea,
vomiting, flatulence
 vomiting brings relief
 reduced nutrition
 loss of weight

10. Comparing DuodenalComparing Duodenal
and Gastric Ulcersand Gastric Ulcers

11. Symptoms of duodenal ulcer disease:
epigastric pain 2 hours after meal or on a empty
stomach or during night
pyrosis
good nutrition
obstipation
seasonal dependence (spring, autumn)

12. Diagnosis:Diagnosis:
1. UGIS (double contrast)
2. Endoscopy

13. Therapy:
Conservative
• regular lifestyle
• prohibition of the smoking and alcohol
• diet (proteins, milk and milky products)
• pharmacology (antagonists of H2 receptors,
antacids, anticholinergics
Surgical
• BI, BII resection
• proximal selective vagotomy
• vagotomy with pyloroplastic
• suture of perforated or haemorrhagic ulcer

14.  StomachStomach resections:resections:
 BillrothBillroth I (BI)I (BI) –– gastro-duodenoanastomosis end-to-endgastro-duodenoanastomosis end-to-end
 Billroth II (BII)Billroth II (BII) – gastro-jejunoanastomosis end-to-side– gastro-jejunoanastomosis end-to-side
with blind closure of duodenumwith blind closure of duodenum
 ProximalProximal selective vagotomyselective vagotomy – denervation– denervation of parietalof parietal
gastric cellsgastric cells

15. Zeman, M. et al., Speciální chirurgie, ISBN 80-7262-260-9, 2004
Billroth I

16. Billroth II
Zeman, M. et al., Speciální chirurgie, ISBN 80-7262-260-9, 2004

17. Zeman, M. et al., Speciální chirurgie, ISBN 80-7262-260-9, 2004
Gastro-enteroanastomosis on
Roux Y crankle

18. Zeman, M. et al., Speciální chirurgie, ISBN 80-7262-260-9, 2004
Vagotomy

19. TreatmentTreatment
 Primarily medical
– PPI or H2 blocker
– Triple combination (double antibiotic and
PPI=amoxicillin, clarithromycin, pantoprazole for 7-14
days)
 Surgical indications
– Intractibility (after medical therapy)
– Hemorrhage
– Obstruction
– Perforation
– Relative: continuous requirement of steroid
therapy/NSAIDs

20. Treatment:Treatment:
Mechanism of Pharmacologic Therapy:
4. For eradication of H. pylori:
a. Bismuth based triple therapy
 Bismuth + Tetracycline + Metronidazole
a. Proton pump inhibitor
 Omeprazole + Amoxicillin/Clarithromycin
+ metronidazole

21. Treatment:Treatment:
Surgical Treatment:
Indication:
1. Intractability:
– Highly selective vagotomy
 Low septic complication, (-) dumping and diarrhea
– For gastric ulcer:
 Total or subtotal gastrectomy w/ or w/o vagotomy

22. Zeman, M. et al., Speciální chirurgie, ISBN 80-7262-260-9, 2004
A – penetration B – perforation
C – bleeding D - stenosis

23. GI BleedingGI Bleeding

24. Ulcer with recent bleedUlcer with recent bleed

25. Treatment:Treatment:
Surgical Treatment:
Indication:
2. Hemorrhage: s/sx
– Critically ill
– Endoscopy
– Surgery: a. continue bleeding for more
than 6 units
b. recurrent bleeding after
endoscopically controlled
- pyloroduodenostomy + HSV
- pyloroduodenostomy + vagotomy + pyloroplasty

26. Ulcer Perforation

27. Treatment:Treatment:
Surgical Treatment:
Indication:
3. Perforation: S/Sx
 Graham omental patch only for shock, perforation > 48
hrs or other medical problem
 Vagotomy + pyloroplasty; HSV
 Vagotomy + Gastrojejunostomy
4. Obstruction: S/Sx; Saline loading test
 Vagotomy + Antrectomy
 Vagotomy + Gastroenterostomy

28. Gastric outlet obstructionGastric outlet obstruction

29. Elective Surgical TherapyElective Surgical Therapy
Rare; most uncomplicated ulcers heal
within 12 weeks
If don’t, change medication, observe
addition 12 weeks
Check serum gastrin (antral G-cell
hyperplasia or gastrinoma)
EGD: biopsy all 4 quadrants of ulcer (rule
out malignant ulcer) if refractory

30. Modified JohnsonModified Johnson
ClassificationClassification
Type Location Acid
Hypersecretion
I Lesser curvature, incisura No
II Body of stomach, incisura, and
duodenal ulcer (active or healed)
Yes
III Prepyloric Yes
IV High on lesser curve, near
gastroesophageal junction
No
V Anywhere (medication induced) No

31. Elective Surgical TherapyElective Surgical Therapy
Type I

32. Type IType I
Lesser curvature;
incisura
MOST COMMON
Decreased mucosal
protection (no
vagotomy)
Distal gastrectomy
(INCLUDING
UCLER) with BI

34. Billroth IBillroth I

35. Elective Surgical TherapyElective Surgical Therapy
Type II/III

36. Type 2/3 UlcersType 2/3 Ulcers
 Acid hypersecretion
 Antrectomy with ulcer and
bilateral truncal vagotomy
 Billroth II or Billroth I
depending on technical
difficulty
 Parietal cell vagotomy
option but higher
recurrence

37. Billroth IIBillroth II

38. R-Y limb (subtotalR-Y limb (subtotal
gastrectomy)gastrectomy)

39. Elective Surgical TherapyElective Surgical Therapy
Type IV

40. Type 4 UlcersType 4 Ulcers
 Least common (5% of all
gastric ulcers)
 Ulcers 2-5cm from cardia
can be treated with distal
gastrectomy, extending
resection along the lesser
curvature and BI
(Pauchet/Shoemaker
procedure)
 Ulcers closer to GEJ,
tongue-shaped resection
high onto lesser curve
(Csendes’ procedure with
Roux-en-Y
reconstruction)
Cardia

41. CSENDES RESECTION
(Line of transection; Roux-en-Y anastomosis)

42. Elective Surgical TherapyElective Surgical Therapy
Giant Gastric
Ulcer

43. Giant Gastric UlcerGiant Gastric Ulcer
Giant gastric ulcer: >3cm; 30% malignancy
risk
Subtotal gastrectomy with Roux-en-Y (high
morbidity and mortality)
Kelling-Madlener procedure: less
aggressive, antrectomy, BI reconstruction,
bilateral truncal vagotomy, leave ulcer,
multiple biopsies, cautery of ulcer

44. Complications after stomach resection:
 Early – dehiscence, stenosis of anastomosis, bleeding,
pancreatitis, obstructive icterus, affection of neighbour
tissues
 Late - days, weeks
- early dumping syndrome
- late dumping syndrome
- incoming crankle syndrome
- outcoming crankle syndrome
- ulcer in anastomosis or in outcoming crankle

45. Early Complications (1)Early Complications (1)
1. Failure of the stomach or stomach remnant to empty occurs after
any procedure. It was formerly common after vagotomy and
drainage. Causes are:
A. Prolonged paralysis of stomach (doubtful)
B. Edema at a stoma
C. Fluid and electrolyte disorder, especially hypokalaemia.
Management is conservative with NG suction, fluid, electrolyte
and nutritional replacement.

46. Early Complications (2)Early Complications (2)
2. Intestinal obstruction.
Causes are:
A. Adhesive.
B. As a consequences:
(a) Twisting of the loop of a gastrojejunostomy after polya
gastrectomy.
(b) Herniation of loops through a mesenteric defect.
(c) Retrograde intussusception of the efferent loop of a
gastrojejunostomy (rare).
Prophylaxis: avoid causes – such as mesenteric cul de sacs or holes
Treatment: operative

47. Early Complications (3)Early Complications (3)
3. Fistulae. Can occur after any operation,
which involves a suture line. Most usual
sites are:
1. After polya gastrectomy
i. Duodenal stump
ii. Pancreases from trying to dissect
out a
difficult ulcer
2. Occasionally at a Pyloroplasty

48. Early Complications (4)Early Complications (4)
4. Acute pancreatitis. May follow any
procedure. Its etiology is unknown, but
some cases are traumatic

49. Late Complications (1)Late Complications (1)
1. Anastomotic and recurrent ulceration
Causes:
a. Inadequate resection of parietal cell mass.
b. Isolated antrum left after polya gastrectomy.
c. Zollinger – Ellison syndrome.
d. Incomplete vagotmy.
e. Persistent suture in the anastomosis. More usually this is merely a suture
exposed as a consequence of ulceration from another cause.
Prophylaxis: adequate primary treatment.
Management is related to cause and requires investigation to ascertain the level
of acid secretion or the completeness of vagotomy. Recurrence after
vagotomy is best managed by polya gastrectomy.

50. Late Complications (1)Late Complications (1)
2. Gastrojejunocolic fistulae.
Occurs when a recurrent ulcer after gastrojejual anastomosis penetrates into the colon. It should
arouse the suspicion of Zollinger-Ellison syndrome.
Clinical features: Severe diarrhea occurs due to enteritis caused by cronic contents passing directly
into the small bowel and acidosis, dehydration, potassium loss, anaemia and cachexia will result
in death if the fastula is not interrupted surgically.
Treatment:
1. Good risk patient. Excision of the gastric, jejunal and colonic components and the construction of a
higher gastrectomy.
2. Poor risk patient. A staged procedure:
(a) Stage 1: Proximal colostomy which, diverts the faecal stream from the fistula and thus stops the
enteritis.
(b) Stage 2: Excision of fistula and its visceral components and the construction of a higher
gastrectomy and colonic anastomosis.
(c) Stage 3: Closure of colostomy.

51. Early dumping syndrome:
 group of symptoms approved shortly after meal
 appears after BII resection
 vasomotoric sy. - face redness, fall of blood pressure,
dizziness
 GI sy. - vomiting, diarrhoea
 Th.: diet, no sugar, low quantities of food, change BII to
BI resection

52.  LateLate dumping syndrome:dumping syndrome:
 hhypoglycaemiaypoglycaemia (sugar is not enough digested)(sugar is not enough digested)
 appears after BII resectionappears after BII resection
 weakness, perspiration, dizzinessweakness, perspiration, dizziness,, tremor ccatremor cca 3h3h afterafter
mealmeal
 Th.:Th.: no sugar, change BII to BI resectionno sugar, change BII to BI resection

53. AnemiaAnemia
Partial gastrectomy and polya reconstruction
interferes with duodenal absorption of iron and
a macrocytic anemia may result
More rarely, sufficient stomach has been
removed to cause failure of release of intrinsic
factor and thus a macrocytic anemia
Malnutrition may contribute to both.

54. Weight loss and its complicationsWeight loss and its complications
Particulary after partial gastrectomy when
patients are unwilling to eat sufficiently,
weight loss is common
Severe malnutrition is rare, but there is an
increased risk of nutrition-associated
diseases such as tuberculosis.

55. Bilious vomitingBilious vomiting
Any operation which, destroys or bypasses the
pylorus allows bile to reach the stomach.
Not only does this produce atrophic gastritis but
also it may be associated with bilious vomiting.
This is more likely after a polya gastrectomy
where characteristically a patient eats a meal
and some to 10 to 20 minutes later vomits bile
only.
In severe cases, either normal anatomy should
be restored or the bile diverted more distally
into the intestine.

56. DiarrheaDiarrhea
Apart from the dumping syndrome, all
vagotomies except highly selective ones
seem to cause diarrhea
Matters are made worse if cholecystectomy
has been done or is subsequently done

57. Acute Gastritis (erosive)Acute Gastritis (erosive)
 Stress erosions are usually multiple, small punctuate
lesion in the proximal acid secreting portion of the
stomach
Clinical Settings:
1. Severe illness, trauma, burns (Cushing ulcer) or
sepsis
– Due to (-) mucosal defense (ischemia)
1. Drug and Chemical ingestion
– Aspirin / NSAIDs
1. CNS trauma:
– Increase gastrin ---> elevated acid secretion
– Curling ulcer

58. Acute GastritisAcute Gastritis
Pathogenesis:
1. Aspirin, bile salts (backflow), alcohol
2. Mucosal ischemia
Clinical manifestations:
1. Gastrointestinal bleeding
2. Abdominal pain
Diagnosis:
– Endoscopy / radionuclide scanning / visceral
angiography

59. Acute GastritisAcute Gastritis
Treatment:
– NPO
– NGT / Saline lavage
– Antacids / omeprazole / sucralfate
– Intra-arterial infusion of vasopressin
– Surgery --> if 6-8 units over 24 hrs
 Mortality ---> 40%
1. Near total gastrectomy
2. Vagotomy + pyloroplasty + over sewing of bleeder
3. Partial gastrectomy + vagotomy

60. Zollinger-Ellison SyndromeZollinger-Ellison Syndrome (Gastrinoma)(Gastrinoma)
 Symptoms tends to be more severe, unrelenting and less
responsive to therapy.
Clinical Manifestation:
1. Pain
2. Diarrhea
3. Steatorrhea
Diagnosis:
1. Acid secreting studies (50meq/hr)
2. UGIS
3. Radio-immuno assay for serum Gastrin level
 Diff: a) Pernicious anemia
b) Renal insufficiency
c) Antral gastrin hyperplasia or hyperfunction
1. CT scan and angiography to localize gastrinoma
2. Venous sampling