Stomach and duodenum

Omar alnoubani MD,MRCS

• asymmetrical, pearshaped,most proximal abdominal organ of the digestive tract.

• Cardia connected to esophagus.

• Fundus bounded superiorly by diaphragm and laterally by the spleen.

• The angel of His is where the fundus meets the left side of the GE junction.

• The body contain most of parietal cells .

• Antrum the distal 25-30 percent of the stomach .

The organs that commonly abut the stomach are the liver,

colon, spleen, pancreas, and occasionally the kidney

The lesser curvature is tethered to the liver by the hepatogastric ligament

the left (anterior) and right (posterior) vagal trunks mnemonic LARP

The antrior to liver ,hepatoduodenal ligament as ant. N. of laterjet

The post. To celiac plexus .

The Ns of laterjet terminate near the angularis incisura as crow’s foot

criminal nerve of Grassi The branch that post vagus send to post. Fundus arise above the esophageal hiatus

Easley missed durning truncal vagotomy and HSV

The Ach is the most imp. Neurotransmitter in acid secretion .

The sympathatic supply T5-T10

• Parietal: • Location: Body • Function: secrete acid and intrinsic factor • Mucus: • Location: Body, Antrum • Function: mucus production • Chief: • Location: Body • Function: produce Pepsin

• Surface epithelium: • Location: Diffuse • Function: produce mucus, bicarb, prostaglandins • ECL: • Location: Body • Function: Histamine production • G cells: • Location: Antrum • Function: Gastrin production • Other cells ….

Acid Secretion

• Two forms:

• Basal Acid Secretion

• Stimulated Acid Secretion

Stimulated Acid Secretion

• Three Phases:

• Cephalic phase

• Gastric phase

• Intestinal Phase

• These phases occur concurrently NOT consecutively.

Cephalic Phase

• Originates with the sight, smell, thought or taste of food.

• Stimulates the cortex and hypothalamus.

• Signals cause Vagus to release Ach, Ach causes increase in parietal cell acid production.

• Accounts for 20-30% of acid production.

Gastric Phase

• Begins when food enters the gastric lumen (gastric distention).

• Digestion products stimulate the G cells, they release gastrin, parietal cells release acid.

• Distention alone can increase acid production.

• Accounts for 60-70% of acid production.

• Phase lasts until the stomach is empty.

Intestinal Phase

• Poorly understood.

• initiated by chyme entering the small bowel.

• Accounts for ~10% of acid production.

Gastric Hormones

• Gastric Hormones: • Chemical messengers that regulate intestinal and

pancreatic function. • The “gut” is the largest endocrine organ in the

body. • The messengers can act as: • Endocrine: distant target • Paracrine: close target • Autocrine: self target • Neurocrine: neurotransmitter or stimulator

Gastric Hormones

• Gastrin

• Somatostatin

• Gastrin-releasing peptide (GRP)

• Histamine

• Leptin

• Ghrelin

Gastrin

• Synthesis: G-cells in the antrum

• Release: AA, protein, vagal tone, antral distention, GRP, pH > 3.0, ETOH, Histamine.

• Inhibition: pH < 3.0, somatostatin, secretin, CCK, VIP, GIP, glucagon.

• Target cells: Parietal and Chief cells

Gastrin

• Action:

Stimulates acid secretion : Direct action on parietal cells

Potentiating interaction with histamine

Possible: releasing of histamine

• Increases release of lytes & water from stomach, pancreas, liver and Brunner’s glands

• Stimulates motility in stomach, intestine, and gall bladder

• Inhibits contraction of pylorus and sphincter of Oddi.

• Stimulates GI mucosal growth.

Somatostatin

• Synthesis:

CNS, antrum, fundus, sm. bowel, colon, and D cells in pancreas.

• Release:

Antral acidification

Fats, protein, acid in duodenum

Pancreatic: glucose, amino acids, CCK

• Inhibition:

Release of acetyl-choline from vagal nerve fibers

• Action: • The “master off switch” Inhibits the release of most GI hormones • Inhibits pancreatic and GI secretion(s) Inhibits intestinal motility. • Clinical: Octreotide- decrease fistula output Treatment of esophageal variceal bleed Can ameliorate symptoms of endocrine tumors

Gastrin-Releasing Peptide.

• GRP is the mammalian equivalent of bombesin, a hormone discovered more than two decades ago in an extract of skin from a frog.

• Synthesis: Gastric antrum, small bowel mucosa

• Release: vagal stimulation

GRP

• Action:

• The “master on switch”

• Stimulates the release of all GI hormones (Secretin).

• Stimulates GI secretion

• Stimulates GI motility

• most important: stimulates gastric acid secretion and release of antral gastrin

• Stimulates bowel and pancreatic mucosal growth

Histamine

• Stimulates parietal cells

• Found in the acidic granules of ECL cells and resident Mast cells.

• Release is stimulated by:

• Gastrin, acetyl-choline, epinephrine

• Inhibited by Somatostatin.

Leptin and ghrelin

• Leptin is a protein primarily synthesized in adipocytes.

• It is also made by chief cells in the stomach, the main source of leptin in the GI tract.

• Leptin works at least in part via vagally mediated pathways to decrease food intake in animals.

• Not surprisingly, leptin, a satiety signal hormone, and ghrelin, a hunger signal hormone, are both primarily synthesized in the stomach.

PEPTIC ULCER DISEASE

• Peptic ulcers are focal defects in the gastric or duodenal mucosa that extend into the submucosa or deeper.

• They may be acute or chronic and, ultimately, are caused by an imbalance between mucosal defenses and acid/peptic injury.

Epidemiology

• PUD is one of the most common GI disorders in the United States with a prevalence of about 2%, and a lifetime cumulative prevalence of about 10%, peaking around age 70 years .

• Recent studies have shown an increasein the rates of hospitalization and mortality in elderly patients for the peptic ulcer complications of bleeding and perforation.

• This may be due in part to the increasingly common use of NSAIDs and aspirin in this elderly cohort, many of whom also have H. pylori infection.

Pathophysiology and Etiology

• No acid no ulcer

• In general H. pylori predisposes to ulceration, both by acid hypersecretion and by compromise of mucosal defense mechanisms.

• NSAID use causes ulcers predominantly by compromise of mucosal defenses.

Helicobacter pylori Infection

• With specialized flagella and a rich supply of urease, H. pylori is uniquely equipped for survival in the hostile environment of the stomach.

• About50% of the world’s population is infected with H. pylori, a major cause of chronic gastritis

• Have a role in gastric lymphoma

• The organism possesses the enzyme urease, which converts urea into ammonia and bicarbonate, thus creating an environment around the bacteria that buffers the acid secreted by the stomach.

• The ammonia is damaging to the surface epithelial cells.

Gastric ulcers

• The most common, Johnson type I gastric ulcer, is typically located near the angularis incisura on the lesser curvature, close to the border between antral and corpus mucosa.

• Patients with type I gastric ulcer usually have normal or decreased acid secretion .

Nonsteroidal Anti-Inflammatory Drugs in Peptic Ulcer Disease

• Chronic use of NSAIDs (including aspirin) increases the risk of peptic ulcer disease about 5-fold and upper GI bleeding about 4-fold.

• Complications of PUD (specifically hemorrhage and perforation) are much more common in patients taking NSAIDS

Indications of acid suppression in patients taking NSAIDs

Clinical Manifestations

• More than 90% of patients with PUD complain of abdominal pain.

• The pain is typically nonradiating, burning in quality, and located in the epigastrium.

Medical management

Surgical Treatment of Peptic Ulcer Disease

• Indications :

• Bleeding

• Perforation

• Obstruction

• Intractability or nonhealing

• Malignancy .

• Mainly oversewing of the bleeders and patch closure for perforating .

• The use of vagotomy is increasingly uncommon because of PPI.

Before PPI !!!

Bleeding

• The most common complication

• Three-fourths of the patients who come to the hospital with bleeding peptic ulcer will stop bleeding if given acid suppression and nothing by mouth.

• However, one fourth will continue to bleed or will rebleed after an initial quiescent period, and virtually all the mortalities (and all the operations for bleeding) occur in this group .

• Patients with massive bleeding from high-risk lesions (e.g., posterior duodenal ulcer with erosion of gastroduodenalartery, or lesser curvature gastric ulcer with erosion of left gastric artery or branch) should be considered for early operation.

• Early operation should also be considered in patients more than 60 years of age, those presenting in shock, those requiring more than four units of blood in 24 hours or eight units of blood in 48 hours, those with rebleeding, and those with ulcers >2 cm in diameter

• The Mortality rate of surgery is around 20%.

Perforation

• 2nd M.C.C.

• Acute abdominal pain

• Initially chemical peritonitis then bacterial

• 80% of x-rays show free air .

• Mx : resuscitation

• Operative vs non operative

• Graham patch

G.O.O

• occurs in no more than 5% of patients with PUD.

• Presented with nonbiliuos vomiting

• It is usually due to duodenal or prepyloric ulcer disease, and may be acute from inflammatory swelling or chronic from scarring .

• Always role out malignant cause .

• The standard operation for obstructing PUD is vagotomy and antrectomy

Intractable or Nonhealing Peptic Ulcer

• Should raise red flags for the surgeon:

• Maybe the patient has a missed cancer

• maybe the patient is noncompliant (not taking prescribed PPI, still taking NSAIDs, still smoking)

• maybe the patient has Helicobacter despite the presence of a negative test or previous treatment.

Zollinger-Ellison Syndrome

• ZES is caused by the uncontrolled secretion of abnormal amounts of gastrin by a duodenal or pancreatic neuroendocrine tumor (i.e.,gastrinoma).

• Most cases (80%) are sporadic, but 20% are inherited.

• Familial with MEN I usually the have multiple gastrinoma tumors, and surgical cure is less common.

• sporadic gastrinomas are more often solitary and are more often amenable to surgical cure

• Currently, about 50% to 60% of gastrinomas are malignant, with lymph node, liver, or other distant metastases at operation.

• Five-year survival in patients presenting with metastatic disease is approximately 40%.

• The larger the primary gastrinoma, the higher the likelihood of metastatic disease.

• More than 90% of patients with sporadically, completely resected gastrinoma will be cured

• The most common symptoms of ZES are epigastric pain, GERD, and diarrhea.

• More than 90% of patients with gastrinoma have peptic ulcer.

• Most ulcers are in the typical location (proximal duodenum), but atypical ulcer location (distal duodenum, jejunum, or multiple ulcers) should prompt an evaluation for gastrinoma.

• About 80% of primary tumors are found in the gastrinoma triangle , and many tumors are small (<1 cm), making preoperative localization difficult.

• Transabdominal ultrasound is quite specific, but not very sensitive.

• CT will detect most lesions >2 cm in size and MRI is comparable.

• EUS is more sensitive than these other noninvasive imaging tests, but it still misses many of the smaller lesions, and may confuse normal lymph nodes for gastrinomas

• Currently, the preoperative imaging study of choice for gastrinoma is somatostatin receptor scintigraphy (the octreotide scan).

• When the pretest probability of gastrinoma is high, the sensitivity and specificity of this modality approach 100%.

• All patients with sporadic (nonfamilial) gastrinoma should be considered for surgical resection and possible cure.

• The lesions should be located in 90% of patients, and the large majority is cured by extirpation of the gastrinoma.

• The management of gastrinoma in patients with MEN I is controversial because the patients are often not cured by operation, and the tumors tend to be small and multiple.

• If the tumor can be imaged preoperatively, operation by an experienced gastrinoma surgeon is reasonable

GASTRITIS AND STRESS ULCER

• Gastritis is mucosal inflammation.

• The most common cause of gastritis is H. pylori.

• Other causes of gastritis include alcohol, NSAIDs, Crohn’s disease, tuberculosis, and bile reflux

• different mechanisms ,immune cell infiltration , disruption the mucosal barrier.

• Stress gastritis and stress ulcer are probably due to inadequate gastric mucosal blood flow during periods of intense physiologic stress.

• The rationale for routine acid suppression in the ICU, supported by excellent data from clinical trials and the laboratory, is that less mucosal injury will be caused in the potentially weakened gastric mucosa if there is less luminal acid

• There are some studies suggesting that routine acid suppression leads to overgrowth of gastric bacteria, which increases the incidence and/or severity of aspiration pneumonia in the ICU.

MALIGNANT NEOPLASMS OF THE STOMACH

Adenocarcinoma

• Epidemiology : Globally, gastric cancer is the fourth most common cancer type and the second leading cause of cancer death.

• Decreased in Western industrialized countries

• This decrease has been largely in the so-called intestinal form rather than in the diffuse form of gastric cancer.

• In general, gastric cancer is a disease of the elderly, and it is twice as common in blacks as in whites.

• In younger patients, tumors are more often of the diffuse variety and tend to be large, aggressive, and more poorly differentiated, sometimes infiltrating the entire stomach (linitis plastic).

Etiology

• Gastric cancer is more common in patients with pernicious anemia, blood group A, or a family history of gastric cancer.

• Environmental factors appear to be more related etiologically to the intestinal form of gastric cancer than the more aggressive diffuse form.

Genetics

Gastric polyps

• Benign gastric polyps are classified as neoplastic (adenoma and fundic gland polyps) or nonneoplastic (hyperplastic polyp, inflammatory polyp, hamartomatous polyp).

• In general, inflammatory and hamartomatous polyps have little or no malignant potential.

• Fundic gland polyps, commonly seen in patients on long term ppi therapy, are not premalignant but in patients with FAP, dysplasia in these lesions is not uncommon.

• Hyperplastic polyps usually occur in the setting of chronic inflammation.

• Large hyperplastic polyps (>2cm) may harbor dysplasia or carcinoma in situ.

• Gastric adenomas are premalignant, similar to colon adenomas.

• Patients with FAP have a high prevalence of gastric adenomatous polyps (about 50%), and are 10 times more likely to develop adenocarcinoma of the stomach than the general population.

Early Gastric Cancer

• defined as adenocarcinoma limited to the mucosa and submucosa of the stomach, regardless of lymph node status.

• The entity is common in the Orient, where gastric cancer is a common cause of cancer death, and where aggressive surveillance programs have therefore been established.

• Approximately 10% of patients with early gastric cancer will have lymph node metastases

• Approximately 70% of early gastric cancers are well differentiated, and 30% are poorly differentiated.

• The overall cure rate with adequate gastric resection and lymphadenectomy is 95%.

Gross Morphology and Histologic Subtypes

• polypoid, fungating, ulcerative, and scirrhous • In the first two, the bulk of the tumor mass is

intraluminal. • In the latter two gross subtypes, the bulk of the

tumor mass is in the wall of the stomach • scirrhous tumors infiltrate the entire thickness of

the stomach and cover a very large surface area. • Scirrhous tumors (linitis plastica) have a

particularly poor prognosis, and commonly involve the entire stomach.

Histology

• The most important prognostic indicators in gastric cancer are both histologic: lymph node involvement and depth of tumor invasion.

• Tumor grade (degree of differentiation: well, moderately, or poorly) is also important prognostically.

WHO and Ming classification

• The Ming classification also is useful and easy to remember, with only two types—expanding (67%) and infiltrative (33%).

Lauren classification

• commonly used separates gastric cancers into intestinal type (53%), diffuse type (33%), and unclassified (14%).

• The intestinal type is associated with chronic atrophic gastritis, severe intestinal metaplasia, and dysplasia, and tends to be less aggressive than the diffuse type.

• The diffuse type of gastric cancer is more likely to be poorly differentiated and is associated with younger patients and proximal tumors

Pathologic Staging

• Ultimately, prognosis is related to pathologic stage.

• The most widespread system for staging of gastric cancer is the tumor-node-metastasis (TNM) staging system based on depth of tumor invasion, extent of lymph node metastases, and presence of distant metastases.

• This system was developed by the American Joint Committee on Cancer and the International Union Against Cancer, and has under gone several modifications since it was originally conceived

Clinical Manifestations

• Most patients have advanced stage

• Weight loss , anorexia ,dysphagia,early satiety.

• Abdominal pain ,nausea ,vomiting .

• Acute upper GI bleeding …

• Paraneoplastic syndromes such as Trousseau’s syndrome , acanthosis nigricans .

Physical exam

• Signs of wt loss and malnutrition

• Virchow’s node ,Irish node, Krukenberg’s tumor , Sister Joseph’s nodule ,Blumer’s shelf ascites .

Diagnostic Evaluation

• Upper endoscopy and Bx.

• Virtual endoscopy

• Magnifying endoscopy with narrow-band imaging (NBI) has undergone technological improvements and can observe the microvascular architecture of the mucosa and microsurface pattern of the lesion.

Staging

• Abdominal/pelvic CT scanning with IV and oral contrast.

• EUS .. Depth of tumor

• Whole-body PET scan in evaluation of distant mets .

• Staging Laparoscopy and Peritoneal Cytology

Treatment

• Surgical resection is the only curative treatment for gastric cancer .

• The goal of curative surgical treatment is resection of all tumor (i.e., R0 resection).

• Grossly 5 cm margins , more in diffuse type

• Frozen section

• At least 15 lymph node should be resected .

• Extent of Lymphadenectomy D1 vs D2

• D1 lymphadenectomy in total gastrectomy requires dissection of stations 1 through 7 and in D2, from 8a to 12a too.

Chemotherapy and Radiation for Gastric Cancer

• Role of neoadjuvant chemotherapy .

• Different agents , 5-fluorouracil (5-FU), cisplatin, doxorubicin, methotrexate, taxanes, and camptothecin.

• 5-year survival for resected gastric adenocarcinoma stages I, II, and III is about 75%, 50%, and 25%, respectively .

Endoscopic Resection

• differentiated tumors , less than 2 cm , not ulcerated , when there is a low risk for L.N mets .

Gastric Lymphoma

• 4 % of cases

• B-cell ,non-Hodgkin’s lymphoma.

• Stomach is the commonest site .

• MALT lymphoma .

• systemic symptoms in 50 % of pts.

• May cause obstruction or bleeding

• Tx mainly chemo-radiotherapy .

Gastrointestinal Stromal Tumor

• Arise from (ICC) .

• Prognosis depends mostly on size , mitotic count, and metastasis.

• hematogenous spread

• Express c-KIT (CD117) or the related PDGF receptor A, as well as CD34.

• 2/3 of all GISTs occur in the stomach.

• Epithelial cell stromal GIST is the most common cell and cellular spindle type is the next most common.

• The glomus tumor type is seen only in the stomach

GIST

• almost always solitary.

• Wedge resection with clear margins is adequate surgical treatment.

• Imatinib (Gleevec), a chemotherapeutic agent that blocks the activity of the tyrosine kinase product of c-kit, yields excellent results in many patients with metastatic or unresectable GIST

Gastric Carcinoid Tumor

• 1% of all carcinoid tumors and less than 2% of gastric neoplasms.

• Arise from (ECL) .

• Type I is the commonest ,75% associated chronic hypergastrinemia secondary to pernicious anemia or chronic atrophic gastritis.

• Type II gastric carcinoids are associated with MEN1 and ZES.

• Type III gastric carcinoids are sporadic tumors the most aggressive .

BENIGN GASTRIC NEOPLASMS

• Leiomyoma : umbilicated appearance , Asymptomatic

• Lipoma : small , asymptomatic .

Other stomach conditions

• Ménétrier’s Disease : epithelial hyperplasia +PLE +hypochlorhydria .

• Watermelon Stomach (GAVE) :dilated mucosal blood vessels that often contain thrombi, in the lamina propria.

• Dieulafoy’s Lesion a congenital arteriovenous malformation characterized by an unusually large tortuous submucosal artery , my erode and bleed .

• Mallory-Weiss Syndrome : longitudinal tear in the mucosa of the GE junction, caused by forceful vomiting , common in alcoholic.

• Bezoars: concretions of indigestible matter , Trichobezoars Phytobezoars

• Isolated Gastric Varices .

Volvulus

Associated with hiatus hernia

Borchardt's triad

Organo-axial from a line connected the cardia to pylorus

Mesntro-axial from a line connected the greater and lesser curvature .

POSTGASTRECTOMY PROBLEMS

• Dumping Syndrome : phenomenon caused by the destruction or bypass of the pyloric sphincter.

• symptoms caused by abrupt delivery of a hyperosmolar load into the S.B .

• Early occurs after 15-30 minutes ,crampy abdominal pain ,diaphoresis ,diarrhea .

• Late 2-3 hours “reactive hypoglycemia” .

• Diarrhea .

• Gastric Stasis.

• Bile Reflux Gastritis and Esophagitis .

• Roux Syndrome .

• Weight Loss .

• Anemia .

• Bone Disease

• Gallstones .

• Thank you