Dr Aqeel Shakir Mahmood Consultant General and Laparoscopic Surgeon Stomach and Duodenum Dr Aqeel Shakir Mahmood Assistant Professor Consultant General and Laparoscopic Surgeon FICMS General Surgery CABS General Surgery FICMS-GIT Gastrointestinal Surgery (subspecialty ) MRCS –( Ireland) General Surgery FRCS –( London) General Surgery

Stomach and Duodenum Anatomy Physiology Pathology Gastritis Peptic ulcer diseases Operative procedures Tumors Carcinoma of the stomach

Anatomy

Has four regions Cardia Fundus Body Pyloric

Surgical importance of blood supply Celiac trunk 1. left gastric artery 2. Splenic artery Left gastroepiploic artery Short gastric artery 3. Hepatic artery Right gastric artery Gastroduodenal artery which give right gastroepiploic artery

PHYSIOLOGY Function: Digestion of food, reduce the size of food Acts as reservoir Absorption of Vit. 12, iron and calcium

Types of Cells Parietal cells most distinctive cells in stomach (HCl & intrinsic factor) Chief cells pepsinogen Mucus neck cells: - HCO3- - Mucus

Types of Cells G Cells: Gastrin (hormone) ---> HCl secretion D Cells: Somatostatin (antrum) Enterochromaffin-like cell: Histamine

Physiology The mucosa lining of proximal stomach contains the parietal (acid and intrinsic factor)and chief cells(pepsinogen) The mucosa lining the more muscular antropyloric segment secretes an alkaline mucus but contains specialized endocrine (G) cells that release gastrin

Pathology Gastritis (inflammation of the gastric mucosa) is a common GI problem. Gastritis may be acute, lasting several hours to a few days, or chronic, resulting from repeated exposure to irritating agents or recurring episodes of acute gastritis. Acute gastritis is often caused by dietary indiscretion—the person eats food that is contaminated with disease-causing microorganisms or that is irritating or too highly seasoned.

Gastritis Other causes of acute gastritis include overuse of aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs), Excessive alcohol intake, bile reflux, and radiation therapy. Severe form of acute gastritis is caused by the ingestion of strong acid or alkali, which may cause the mucosa to become gangrenous or to perforate.

Gastritis Chronic gastritis and prolonged inflammation of the stomach may be caused by either benign or malignant ulcers of the stomach or by the bacteria Helicobacter pylori. Chronic gastritis is sometimes associated with autoimmune diseases such as pernicious anemia; dietary factors such as caffeine; the use of medications, especially NSAIDs; alcohol; smoking; or reflux of intestinal contents into the stomach.

Clinical Manifestations The patient with acute gastritis may have abdominal discomfort, headache, lassitude, nausea, anorexia, vomiting, and hiccupping. Some have no symptoms. The patient with chronic gastritis may complain of anorexia, heartburn after eating, belching, a sour taste in the mouth, or nausea and vomiting. Patients with chronic gastritis from vitamin deficiency usually have evidence of malabsorption of vitamin B12 caused by antibodies against intrinsic factor.

Peptic ulcer diseases Major types ; duodenal ulcer Other types ; gastric ulcer stomal ulcer Other types ; stress ulcer ulcers caused by gastric irritants steroid induced ulcer

Pathogenesis of peptic ulcer Lack of protection of the mucosa Acid production

Peptic Ulcer Disease Pathogenesis : Protective factors vs. hostile factors

Duodenal ulcer ;pathogenetic factors Increased acid secretion Environment ; NSAIDS, Helicobacter Mucosal defense ; decreased bicarbonate production, decreased gastric prostaglandin production

Comparing Duodenal and Gastric Ulcers

Clinical features of peptic ulcers Pain The pain is epigastric, may radiate to the back. Eating may sometimes relieve the discomfort. The pain is normally intermittent rather than intractable. Periodicity Symptoms may disappear for weeks or months to return again. This periodicity may be related to the spontaneous healing of the ulcer. Vomiting Although this occurs, it is not a notable feature unless stenosis has occurred. Alteration in weight Weight loss or, sometimes, weight gain may occur. Patients with gastric ulceration are often underweight but this may precede the occurrence of the ulcer. Bleeding All peptic ulcers may bleed. The bleeding may be chronic and presentation with anaemia is not uncommon. Acute presentation may be haematemesis and melaena.

Clinical features of peptic ulcers Clinical examination Examination of the patient may reveal epigastric tenderness but, except in extreme case (for instance gastric outlet obstruction), there is unlikely to be much else to find.

Complications of Peptic Ulcer Penetration Stenosis Perforation Bleeding Malignant transformation

Complications: Bleeding - chronic (minor, cause anaemia) - acute (major, form affected vessel) Perforation - mostly bulbus duodeni, anterior gastric wall - acute violent pain - bleeding can be present Penetration - of the ulcer deeply through whole wall into neighbor organ (pancreas, liver) Stenosis - narrow of the lumen caused by scar, oedema or inflammatory infiltration after healing of the ulcer - rise only at pyloric localization - vomiting of huge volume of gastric content

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

DIAGNOSIS PROGRAM 1. History and physical examination. 2. Endoscopy. 3. X-Ray examination of stomach. 4. Examination of gastric secretion by the method of aspiration of gastric contents. 5. Gastric pH metry. 6. Multiposition biopsy of edges of ulcer of stomach. 7. Gastric Dopplerography. 8. Sonography of abdominal cavity organs. 9. General and biochemical blood analysis.

Investigation of the patient with suspected peptic ulcer Gastroduodenoscopy This is the investigation of choice in the management of suspected peptic ulceration and, is highly accurate. In the stomach, any abnormal lesion , numerous biopsies must be taken to exclude the presence of a malignancy. Commonly, biopsies of the antrum will be taken to see whether there is histological evidence of gastritis and a CLO test performe to determine the presence of H. pylori.

Therapy: Conservative Surgical regular lifestyle prohibition of the smoking and alcohol diet (proteins, milk and milky products) pharmacology (antagonists of H2 receptors, antacids, antich-olinergics Surgical BI, BII resection proximal selective vagotomy vagotomy with pyloroplasty suture of perforated or haemorrhagic ulcer

Gastric Ulcer

Location and Type of Ulcer: Type 1: Primary gastric ulcer. Associated with diffuse antral gastritis. Type 2: Gastric ulcers with duodenal ulcers, most likely secondary to duodenal ulcers. Type 3: Prepyloric or channel ulcer. Type 4: Proximal stomach or gastric cardia. Acid hyper secretion common among type 2 and 3 ulcers. Type 1 an 4 pathophysiologycally the same.

Location of gastric ulcers

Type I gastric ulcer 60% of GU Large volume of secretion with low or normal acid secretion

Type II gastric ulcer 25% of GU Usually acid hypersecretor DU usually precedes GU

Type III gastric ulcer 23% of GU Prepyloric ulcer Typically acid hypersecretor

Type IV gastric ulcer Less than 10% of GU High-lying ulcer

Predisposing factors ; gastric conditions Acid and pepsin Gastric stasis Coexisting duodenal ulcer Duodenogastric reflux Gastritis Helicobacter pylori

Predisposing factors ; clinical conditions Chronic alcohol use NSAIDS Smoking Long-term steroid therapy Infection Intraarterial chemotherapy

Comparing Duodenal and Gastric Ulcers DUODENAL ULCER Age 30–60 Male: female 2–3:1 80% of peptic ulcers are duodenal GASTRIC ULCER Usually 50 and over Male: female 1:1 15% of peptic ulcers are gastric

Signs, Symptoms, and Clinical Findings DUODENAL ULCER Hypersecretion of stomach acid (HCl) May have weight gain Pain occurs 2–3 hours after a meal; often awakened between 1–2 AM; ingestion of food relieves pain Vomiting uncommon GASTRIC ULCER Normal—hyposecretion of stomach acid (HCl) Weight loss may occur Pain occurs 1⁄2 to 1 hour after a meal; rarely occurs at night; may be relieved by vomiting; ingestion of food does not help, sometimes increases pain Vomiting common

Comparing Duodenal and Gastric Ulcers DUODENAL ULCER Hemorrhage less likely than with gastric ulcer, but if Present, melena more common than Hematemesis More likely to perforate than gastric ulcers GASTRIC ULCER Hemorrhage more likely to occur than with duodenal ulcer; hematemesis more common than melena

Comparing Duodenal and Gastric Ulcers DUODENAL ULCER Malignancy Possibility Rare Risk Factors H. pylori, alcohol, smoking, cirrhosis, stress GASTRIC ULCER Occasionally H. pylori, gastritis, alcohol, smoking, use of NSAIDs, stress

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