Peptic Ulcer

( 17 pages )

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Peptic Ulcer

Blood supply & venous drainage of stomach:

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Nerve supply of stomach:1/ Sympathetic 2/ Parasympathetic:

- ant.vagal trunk → hepatic branch → descend along lesser curvature & supply ant. wall of stomach - post.vagal trunk → coelic branch → supply back wall of stomach

Vagus ⅔ ⅓

Ant & Post vagus hepatic branch celiac b. Stomach liver & gall bladder -pancreas -S.Intestine -transverse colonHistology:1/ Columnar epith : Lines the whole stomach

2/ Cardiac gland: Secrete mucous and electrolytes Occupy a small ring around the oesophagogastric junction

3/ Oxyntic glands: Occupy the fundus and body of stomacha- parietal cells:produce H+ & intrinsic factorit is double its # in duodenal ulcer & 4х in Zollinger Ellison syndromeits # is ↓ in gastric ulcerb- peptic (chief) cells:in the fundus & produce pepsinogen

4/ Pyloric glands:In the antrumSecrete mucous & electrolytes

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5/ G-cells:In the antrumSecrete gastrinIts # increase only in duodenal ulcer

Surgical Physiology:

1/ Gastric motility:Body & fundus act as a reservoir for food.Antrum acts as a mill, mix & grind the food & expel it to the duodenum.Gastric motility is controlled by intrinsic neural plexus which are regulated by the extrinsic nerve supply (vagus)Truncal vagotomy affects & reduces gastric motility.Also, sympathetic n. inhibit gastric motility.

2/ Gastric secretion: Mucus is secreted in all regions of stomach & protects surface

epith. against acid and pepsin. Acid & pepsin secretion is regulated by a neurocrine, endocrine

& paracrine factors. Neurocrine: Ach from vagus Endocrine: Gastrin from antrum Paracrine: Histamine from cells near to parietal or peptic cells Parietal (w secrete H+) & pepsin (w secrete pepsin) cells has

specific receptor for each of the 3 stimulants. The action of each stimulant is potentiated by the other two. Eg;

Gastrin & Ach release histamine from mucosal stares.Ach stimulate secretion by inhibit the release of somatostatin.In truncal vagotomy not only Ach stimulation is affected, but also gastrin & histamine efficacy is reduced.

Phases of gastric secretion:1/ Cephalic (neural) phase:

Sight, smell, taste or though stimulate vagal center Vagus → stimulate peptic & parietal cells (direct)

→ stimulate gastrin release from antrum (indirect)

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2/ Gastric Phase: Distention of gastric antrum & products of protein digestion

stimulate gastrin release from antral mucosa.

3/ Intestinal Phase: Food in small bowel release enteroxyntin (duodenal gastrin)

that increases acid release.

Pathology:Due to imbalance between gastric acid – pepsin secretion and the ability of the GI mucosa to define against them.This imbalance occurs due to:

a. Hyper secretion of acid and pepsin. (D.U)b. Defect in mucosal defense. (G.U)c. H.pylori infection.

Special Forms of Peptic Ulceration:1/ Stress ulcer:

Occur after major surgery, trauma or sever illness. Multiple small superficial ulcers in the stomach or duodenum.

2/ Curling’s ulcer: In patient with sever burns. In the duodenum.

3/ Cushing’s ulcer: In patient with neuro-surgical illness or head injury. In both stomach or duodenum.

Sites:1) Duodenum:

o The 1st part of the duodenum is the commonest.o If it is in the Ant. surface → perforation.o If it is in the Post. surface → He by erosion of arteries.

2) Stomach:o Type 1 (1ry GU): often in the lesser curvature.o Type 2: same as type 1 plus a D.U. o Type 3: in pyloric channel or prepyloric area.

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3) Esophagus:o At the lower end.o Due to reflux of acid and pepsin from the stomach.

4) Jejunum:o Zollinger-Ellison syndrome.o After gastro-jejunostomy.

5) Meikle’s diverticulum:o Due to the presence of ectopic gastric mucosa.

N.BG.U in Post. wall → erode to pancreasG.U in Ant. wall → erode to liver

Etiology:

1/ Acute peptic ulcer: May be without apparent cause. Or associated with ingestion of alcohol, NSAID or steroidal

therapy. Also it can be associated with stress ulcer, curling’s ulcer or

cushing’s ulcer.

2/ Chronic peptic ulcer:

I. Genetic & blood groupBlood group O 3x likely to get D.Uα¹- antitrypsine deficiency

II. Neurogenic therapyVagal stimulation → hyper secretion & hyper motility ←Stress & anxiety +→ vagus

III. Accessory causes (factors)AlcoholExcessive smokingVitamine deficiency

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IV. EndocrineZ-E syndrome →↑gastrin →↑acid secretionMultiple adenoma syndromeHyper parathyroidism →↑Ca² →↑gastrin

V. InfectionHelicobacter pylori

H-pylori:A Gm -ve spirochetal bacteriamFound in the antral and duodenal mucosa

Mechanism: It is urease +ve → split urea & lead to formation of ammonia →

alkaline media around the pacteria → 2ry ↑ in acid → ulcer Also it affects the cells through cytotoxin

Diagnosis:1) HistologySpiral bacterial rod adjacent to gastric epith.2) Direct cultureOnly done when an Atb resistant organism is suspected.3) CLO (urease) test4) SerologyHigh anti – H.pylori IgA & IgG titer

Treatment:Triple therapy

Bisthmus Metronidazole Tetracycline or Ampicillin

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History: H.P.I:

D.U G.UAge 30’s – 40’s 50’s – 60’sSex ♂:♀ 4:1 ♂>♀

Occupation Highly professional & managersPain epigastrium Epigastrium & can

radiate to the backOnset 2-3 hrs after eating or

at midnight (empty stomach)

Soon after eating (15-30min)

Aggravated by Hunger (missing meal), anxiety, stress

Eating (pt afraid to eat)

Relieved by Eating (milk, biscuits), anti-acid

Vomiting or by lying down flat, anti-acid

Periodicity More prominent features 4-6 mth

(spring & fall)

Comes & goes in a 2-3 months cycle

Duration of attack

1-2 months Few weeks

Vomiting Uncommon Common to relieve the pain

Appetite Good Pt is afraid to eatDiet Eat every thing Avoid fried food &

curries but like milk, fishWeight No wt loss Loss wt

Hematemesis &

Melena

Hematemesis:Melena40:60

Hematemesis:melena60:40

Ratio of all Hge is more in D.U than G.U

Drug Hx:NSAID, steroid

Social Hx:Smoking, alcohol intake

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Examination:General examination is likely to be normal.Usually there is only mild to moderate epigastric tenderness.If complications develop:

Bleeding → anemia Pyloric stenosis → epigastric fullness & visible peristalsis Malignant changes → wasting

Differential Diagnosis:1. uncomplicated hiatal hernia2. atrophic gastritis3. chronic cholecystitis4. irritable bowel syndrome5. pancreatitis6. functional indigestion7. reflux esophagitis

Investigation:1) Barium meal: (not used anymore)a- gastric ulcer:

A niche (مشكاة) will be seen projecting from the stomach outline.

J-shaped stomach & hangs low in the pelvis.b- duodenal ulcer:

Ulcer crater ( , حفرة بركان filled with Barium (فوهةwich indicate active ulcer.Folds of scar tissue coverage on the ulcer site (rugal convergence).

2) CBC:↓ Hb in chronic blood loss.

3) Stool:Occult blood.

4) Gastroduodenoscopy: (the best one)a- especially in G.U to roll out malignancy

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b- take biopsy.c- View the esophagus, stomach, 1st & 2nd part of

duodenum.5) Serum gastrin level:Specially done in pt with recurrent ulcer or multible ulcers or suspected to have Z-E syndrome.Level > 200 pg/ml is high.In Z-E syndrome > 500 pg/ml

6) Gastrin function studies:a- Measurement of acid production without stimulating

the stomach (Normal basal acid input = 1.5 – 2.5 mEq/hr)b- Measurement of acid production in stimulated

stomach, done by histamine or pentagastrin(Maximal acid output = 20 – 30 mEq/hr)

Complications:1. Hemorrhage.2. Perforation.3. Obstruction (pyloric stenosis/ D.obst)4. Malignant transformation (only in G.U)5. Pancreatitis.6. Biliary obstruction.

Surgical Pathology:

G.U D.USite Single, in lesser

curvatureSingle, in the 1st part,

sometimes doubleEdges Punched out Punched out

Associations Atrophic gastritis DuodinitisMalignancy May become malignant Never become malignantPenetration To near structure like

pancreas or liverLiver, pancreas or post.

abdominal wallHge Minor → from mucosa

Sever → from large art.Gastroduodenal art.

erosionPerforation To lesser sac →

abscessAnteriorly → peritonitis

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To peritoneum→peritonitis

Obstruction If there is ulcer in pylorus or large ulcer

Pyloric stenosis by edema & fibrosis

Duodenal Ulcer Treatment:

Indications for surgery:1/ Failure of medical ttt:

Break through of symptoms during medical ttt. Endoscopy fails to confirm ulcer healing.

2/ Development of complication: Perforation Bleeding Pyloric stenosis

3/ Other: Combined duodenal & gastric ulcer. Highly level of gastric secretion.

Principle of surgery:It is to reduce acid & pepsin secretion to certain levels no longer associated with ulceration.

Operations for D.U:1/ Truncal vagotomy & drainage:

The aim of vagotomy is to reduce gastric acidity. We cut the major trunk of vagus to the stomach to; a- reduce acid & pepsin secretion.b- Impair antral motility & draiage. So we have to drain by either:a- pyloroplastyb- gastrojejunostomy

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2/ Highly selective vagotomy: (parietal cells vagotomy) With or without drainage. We cut the branch of vagus to the body & fundus ( where more

parietal cells are located) → ↓ HCl secretion. Here the antrum & the pylorus branches are intact, so we may

not need drainage. Many surgeons consider it the procedure of choice, although its

recurrence rate is higher than truncal vagotomy.

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3/ Truncal vagotomy + Anterectomy: Combination of vagal denervation & emoval of the major area

of gastric production. Gastrointestinal continuity is restored by gastroduodenal

(Billroth 1) anastomosis OR gastrojejunal (Billroth 2) anastomosis.

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4/ Partial gastrectomy: We remove the antrum & proportion of the body of the stomach. GI continuity was usually restored by closing the duodenal

stump & anastomosing the gastric remnant to the jejunum.

Complication of vagotomy:Esophagus → Post. vagotomy strictureGall bladder → Gall stonesSmall bowel → Post. vagotomy diarrheaVagus nerve → failed vagotomy1) Post vagotomy stricture:

o The lower part of esophagus gets narrowed.o The cause is not known but may be due to:

i. Peri-esophagus hematoma.ii. Excessive denervation of lower esophageal end.iii. Prolong nasogastric intubation → hiatal herniaiv. Mucosal edema.

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o Pt comes with sever dysphagia.o Diagnosis: by Barium meal & endoscopy.o ttt: Bougie nage (dilater).

2) Gall stones:o Due to denervated gall bladder which will loose its contraction

→ biliary stasis → gall stone

3) Post-vagotomy diarrhea:o It is passage of watery stool up to 20x a day with the fallowing

character: a- expulsive b- urgent c- watery o Occur in 2% of truncal vagotomy.o Can be controlled by cholesteramine.

4) Failed vagotomy:

o It will lead to recurrent ulceration either stomal ulcer or anastomatic ulcer.

Gastric Ulcer Treatment:

Indication for surgery:1/ Failure of medical ttt:A benign G.U which fails to heal clinically or endoscopically after 1 mth of adequate ttt.

2/ Development of complication:Perforation, bleeding or stenosis (hourglass stomach).

3/ Suspicion of malignancy.

Operations for chronic gastric ulcer:Type 1 & 2:Partial gastrictomy OR truncal vagotomy & drainage.Partial gastrectomy:Fallowed by gastroduodenal anastomosis or gastrojejunal anastomosis (Billroth 1, 2)

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Complication of gastrectomy:

(1) Immediate (1st day):a- Bleeding:

Usually from the gastric side of anastomosis. Can be sever & require re-exploration.

(2) Early (1st week):a- Anastomotic leak with its complication:

Sub-phernic abscess. Pelvic abscess. Abdominal collection. Jaundice.

b- Obstruction: Afferent loop → bilious vomiting Efferent loop → food vomiting

c- Internal herniation: Usually fallows gastrojejunal anastomosis.

(3) Late (1st month):a- Dumping syndrome:

Feeling of epigastric fullness after food, associated flushing, sweating.

Pt feels faint after the meal.

b- Intestinal hurry (diarrhea): 2 – 4% of pt.

c- Iron def. anemia: Due to post operative anemia, inefficient absorption of dietry

Iron post operative or chronic blood loss from gastritis.

d- Stomal (anastomotic) ulcer: Recurrence may occur in duodenum or jejunum.

e- Reactive hypoglycemia:

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Due to rapid glucose absorption from the upper small bowel → hyperglycemia → ↑↑ insulin secretion → reactive hypoglycemia.

Usually 90 – 120 min after meal.

f- Small stomach syndrome: Vomiting → loss wt.

Written by: ??????Typed & modified by : Hanan Bousbait

Good luck

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