| How is blood supply of stomach? | Greater curvature: Right and left gastroepiploic arteries
Lesser curvature: Right and left gastric arteries
Pylorus: Gastroduodenal artery
Fundus: Short gastric arteries |
| How is innervation of stomach? | Anterior gastric wall: Left vagus nerve
Posterior gastric wall: Right vagus nerve
Sympathetic afferents from level T5 (below nipple line) to T10 (umbilicus) are responsible for sensation of gastroduodenal pain |
| How is physiology of the stomach? | Storage, mixing, trituration, and regulated emptying are accomplished by the muscular apparatus of the stomach.
Peristaltic waves originate in the body and pass toward the pylorus. The thickness of the smooth muscle increases in the antrum and corresponds to the stronger contractions that can be measured in the distal stomach. |
| What are stomach cell functions? | Parietal cells: Located in fundus and body.
Secrete Intrinsic factor for absorption of vitamin B12 in the terminal ileum. Pernicious anemia is characterized by atrophy of the parietal cell mucosa, deficiency FI Secrete hydrochloride (HCl), accounting for highly acidic pH of stomach.
Chief cells:Located in fundus and body
Secrete pepsinogen, which digests protein.
G cells:Located in antrum.
Secrete gastrin
Mucous cells and pyloric gland areas : Mucus ,
provides a weak barrier to the diffusion of H+ and
probably protects the mucosa.
Gastric Juice : 500 and 1500 mL/d |
| How is duodenum anatomy? | Duodenum is the first part of small intestine.
It is C – shaped structure.
It is only 25 cm long.
It is retroperitoneal and fixed to posterior abdominal wall.
It Begins at pylorus and ends at the ligament of Treitz.
It becomes jejunum opposite the second lumbar vertebra.
Duodenum is divided into four portions:
First or Superior part .
Second or Descending part .
Third or Horizontal part .
Fourth or Ascending part |
| How is duodenum blood supply? | Because duodenum is developing from foregut and midgut, it is supplied by branches of celiac and superior mesenteric arteries.
Proximal: Superior pancreaticoduodenal artery, branch of gastroduodenal artery (first branch of proper hepatic artery).
Distal: Inferior pancreaticoduodenal artery (branch of superior mesenteric artery [SMA]). |
| How is venous and lymphatic drainage of duodenum? | Venous drainage:
Anterior and posterior pancreaticoduodenal veins drain into the superior mesenteric vein (SMV).
Lymphatic drainage: is to the gastroduodenual, pancreaticoduodenal and hepatic group of lymph nodes. |
| What is PUD? | PUD consists of duodenal ulcers (DUs) and gastric ulcers (GUs).
EPIDEMIOLOGY
Two times more common in men.
Incidence increases with age.
Smoking and alcohol increase risk. |
| What are gastric ulcers? | PATHOPHYSIOLOGY
Decreased protection against acid
Can be caused by reflux of duodenal contents (pyloric sphincter dysfunction) and decreased mucus and bicarbonate production
CAUSES
NSAIDs and steroids inhibit production of PGE.
(PGE stimulates production of the gastric mucosal barrier)
H. pylori produces urease, which breaks down the gastric mucosal barrier. |
| What are classifications of gastric ulcers? | CLASSIFICATION
Type I: Ulcer in lesser curvature at incisura angularis. (Most common location)
Type II: Simultaneous gastric and duodenal ulcer.
Type III: Prepyloric ulcer.
Type IV: Ulcer in gastric cardia.
Type V: Medication-induced (NSAID/acetylsalicylic acid): anywhere in stomach. |
| What are S&S and dx of gastric ulcers? | SIGNS AND SYMPTOMS
Burning, gnawing epigastric pain that occurs with anything in the stomach: Pain is worst 30 minutes after food.
Anorexia/weight loss
Vomiting
Associated with blood type A
DIAGNOSIS
Via endoscopy.
Three percent of GUs are associated with gastric cancer so all GU are biopsied |
| How is tx of gastric ulcers? | Medical
Discontinue NSAIDs, steroids, smoking.
Proton pump inhibitors (Mainstay): 90% cure rate after 4 weeks.
Eradication of H. pylori:
Proton pump inhibitor, clarithromycin, and amoxicillin/metronidazole × 14 days: ∼90% cure rate
Bismuth, metronidazole, tetracycline × 14 days: ∼85% cure rate.
H2 blockers: 85–95% cure rate after 8 weeks. |
| What are surgical options for gastric ulcers? | Surgery is rarely indicated except for complications or lack of healing (to rule out malignancy).
Antrectomy for types I and II.
Highly selective vagotomy for type III.
Subtotal gastrectomy followed by Roux-en-Y esophagogastrojejunostomy for type IV. |
| What are duodenal ulcers? | PATHOPHYSIOLOGY
Increased acid production.
ETIOLOGY
Helicobacter pylori: A bacterium that produces urease, which breaks down the protective mucous lining of the stomach.
10 to 20% of persons with H. pylori develop PUD.
NSAIDs/steroids: Inhibit production of PGE, which stimulates mucosal barrier production |
| What are clinical features of duodenal ulcers? | Burning gnawing epigastric pain that occurs with an empty stomach:
Pain is relieved within 30 minutes by food.
Nighttime awakening (when stomach empties)
Nausea, vomiting
Zollinger–Ellison (ZE) syndrome:
gastrin-secreting tumor in or near the pancreas.
0.1–1% of patients with ulcer.
20% of ZE patients have associated multiple endocrine neoplasia 1 (MEN-1).
Two thirds are malignant.
Diarrhea is common.
Can see jejunal ulcers |
| How is dx of duodenal ulcers? | Endoscopy; however, most symptomatic cases of DU are easily diagnosed clinically.
If patient responds to DU therapy, there is no need to do the biopsy.
Most common location for DU: Posterior duodenal wall within 2 cm of pylorus.
H. pylori:
Endoscopy with biopsy—for H. pylori (organism is notoriously hard to culture—multiple specimens required during biopsy).
Serology: Anti-H. pylori immunoglobulin G (IgG) indicates current or prior infection.
Urease breath test: C13/14 labeled urea is ingested. If gastric urease is present, the carbon isotope can be detected as CO2 isotopes in the breath.
ZE: A fasting serum gastrin level > 1,000 pg/mL is pathognomonic for gastrinoma.
Secretin stimulation test: Secretin, a gastrin inhibitor, is delivered parenterally and its effect on gastrin secretion is measured.
In ZE syndrome, there is a paradoxical astronomic rise in serum gastrin |
| How is tx of duodenal ulcers? | Medical
Discontinue NSAIDs, steroids, smoking.
Proton pump inhibitors (Mainstay): 90% cure rate after 4 weeks.
Eradication of H. pylori:
Proton pump inhibitor, clarithromycin, and amoxicillin/metronidazole × 14 days: ∼90% cure rate
Bismuth, metronidazole, tetracycline × 14 days: ∼85% cure rate.
H2 blockers: 85–95% cure rate after 8 weeks. |
| How is surgical tx of duodenal ulcers? | Since the advent of highly effective medical therapy, elective surgery for PUD is quite rare.
Surgery is indicated when ulcer is
refractory to 12 weeks of medical treatment or
hemorrhage,
obstruction,
perforation.
Surgical options:
Truncal vagotomy with pyloroplasty
Truncal vagotomy with antrectomy + Billroth I gastroduodenostomy or a Billroth II loop gastrojejunostomy.
Highly selective vagotomy
Truncal vagotomy and selective vagotomy : not commonly performed anymore due to associated morbidity (high rate of dumping syndrome) despite good protection against recurrence.
Procedure of choice is highly selective vagotomy (parietal cell vagotomy, proximal gastric vagotomy). |
| What is highly selective vagotomy? | Individual branches of the anterior and posterior nerves are divideded .
The terminal branches to the pylorus and antrum are spared, preserving pyloroantral function and thus obviating the need for gastric drainage.
Preferred due to its lowest rate of dumping; however, it does have the highest rate of recurrence.
Prepyloric ulcers have the highest recurrence rate : 30%.
The nerve of Latarjet ,nerve of the lesser curvature is a branch of the vagal trunk which supplies the pylorus. It is cut in selective vagotomy and preserved in highly selective vagotomy |
| What are complications of PUD surgery? | Dumping syndrome 1 – 2%
Duodenal stump leak
Marginal ulcer: 10% after Vagotomy , 2-3% with antrectomy
Alkaline reflux gastritis : Billroth I
Anemia : failure to absorb ingested iron, Vitamin B12 deficiency
Postvagotomy diarrhea: 5%–10% after TV
Postgastrectomy stump cancer.
Chronic gastroparesis |
| What are complications of PUD? | Bleeding: 20%
Perforation: 7%
Gastric outlet obstruction, due to scarring and edema.
Cancer in GU |
| What is peptic ulcer hemorrhage? | Most common cause of massive upper GI hemorrhage; chronic gastric and duodenal ulcers have about the same tendency to bleed.
Bleeding duodenal ulcers usually located on posterior surface of duodenal bulb with erosion into gastroduodenal artery.
Gastric ulcers rebleed 3 times more commonly than duodenal ulcers.
Upper GI endoscopy shows bleeding ulcer, visible vessel, ulcer with adherent clot.
Treatment
Replace blood loss with crystalloid and blood products; nasogastric lavage.
Endoscopy for localization and possible treatment |
| What is indication for surgery in peptic ulcer hemorrhage? | Surgery is indicated for
Massive hemorrhage with shock.
Ongoing transfusion requirements (>6 U packed red blood cells).
Recurrent hemorrhage.
Surgery: excise ulcer (gastric) or oversew vessel (Gastro-duodenal art)or antrectomy/Billroth II
Prognosis: 75% managed by endoscopy alone; surgery required in <20% of cases; 15% mortality from massive hemorrhage |
| What is peptic ulcer perforation? | Most perforated ulcers are located anteriorly.
Symptoms and signs:
Usually sudden, severe upper abdominal pain.
Patient is severely distressed, lying quietly.
Rebound tenderness and abdominal rigidity.
Abdominal x-ray reveals free intraperitoneal air in 85% of patients .
Localized or generalized peritonitis |
| How is tx of peptic ulcer perforation? | Treatment (consider medical treatment Taylor)
Surgery is indicated in nearly all cases; rare patient with sealed perforation may be managed without operation.
Surgery: all free perforations should be repaired by
lavage , secure closure with omentum (Graham patch closure) and drainage.
Prognosis: 15% mortality, mostly from delay in treatment, advanced age, and comorbid diseases |
| What is gastric outlet obstruction? what are sx? | COMMON CAUSES
Malignant tumors of stomach and head of pancreas.
Obstructing gastric or duodenal ulcers.
Chronic ulcer causes secondary edema or scarring, which occludes lumen
Early
Early satiety
Gastric reflux
Weight loss
Abdominal distention
Late
Vomiting
Dehydration
Metabolic alkalosis |
| What are dx and tx of gastric oulet obstruction? | DIAGNOSIS
Endsocopy or barium swallow x-ray.
TREATMENT
Endoscopic balloon dilatation if not tumor
Surgical resection + Truncal vagotomy and pyloroplasty after 7 days of nasogastric decompression and antisecretory treatment.
Partial gastrectomy |
| What is gastric bezoars? | Concretions of nondigestible matter that accumulate in stomach.
May consist of hair, vegetable matter (especially in patients who may have eaten persimmon), or charcoal (used in management of toxic ingestions)
May develop after gastric surgery |
| What are S&S, dx and tx of gastric bezoars? | SYMPTOMS
Similar to gastric outlet obstruction
Occasionally causes ulceration and bleeding
DIAGNOSIS
Upper GI endoscopy. CT Scanner
TREATMENT
Proteolytic enzymes—papain
Mechanical fragmentation with endoscope
Surgical removal |
| What is dieulafoy's lesion? | DEFINITION
large tortuous arteriole most commonly in the stomach wall (submucosal) that erodes and bleeds.
SYMPTOMS
Massive, recurrent painless hematemesis.
DIAGNOSIS
Upper GI endoscopy.
TREATMENT
Endoscopic sclerosing therapy or electrocoagulation
Wedge resection |
| What is gastric volvulus? | DEFINITION
Torsion/twisting of stomach typically along long axis. Often associated with paraesophageal hernia. May be acute, but most often chronic.
SYMPTOMS
Intermittent severe epigastric pain and distention .
Inability to vomit.
Difficult passage of nasogastric (NG) tube.
DIAGNOSIS
Upper GI contrast study.
TREATMENT
Surgical repair of accompanying hernia
Gastropexy—fixes stomach to anterior abdominal wall
Gastric resection if there is necrosis |
| What is gastric diverticula? | DEFINITION
Saccular outpouching through all three stomach layers.
SYMPTOMS
Majority are asymptomatic.
DIAGNOSIS
Upper GI contrast study.
TREATMENT
Diverticulectomy only if there are complications (hemorrhage, diverticulitis). |
| What are gastric polyps? | Hyperplastic polyps (>80%): represent overgrowth of normal epithelium, with no relationship to gastric cancer .
Adenomatous polyps: 30% contain a focus of adenocarcinoma; about 10% of benign adenomatous polyps undergo malignant change during prolonged follow-up.
Symptoms and signs: most are asymptomatic or cause vague epigastric discomfort, dyspepsia, occult GI bleeding,
gastric outlet obstruction with nausea and vomiting if polyp is located in distal stomach
Upper GI endoscopy reveals gastric polyp.
Treatment
Endoscopic removal is successful in most cases; laparotomy or laparoscopy if endoscopy is unsuccessful.
Resection if cancer is found in polyp.
Gastrectomy may be required for multiple polyps. |
| What is gastric adenocarcinoma epidemio? | EPIDEMIOLOGY
Highest incidence in age > 60 years.
Adenocarcinoma comprises 95% of malignant gastric cancer.
Male predominance.
Leading cause of cancer-related death in Japan |
| What are risk factors for gastric adenocarcinoma? | Familial adenomatous polyposis
H pylori is known to be a cause of chronic atrophic gastritis,
(6× increased risk)
Post-partial gastrectomy (15+ years)
Pernicious anemia
Diet (foods high in nitrites—preserved, smoked, cured)
Cigarette smoking |
| How is pathology of gastric adenocarcinoma? | Polyploid: 25–50%, no substantial necrosis or ulceration
Ulcerative: 25–50%, sharp margins
Superficial spreading: 3–10%, involves mucosa and submucosa only, best prognosis
Linitis plastica: 7–10%, involves all layers, extremely poor prognosis |
| What are S&S of gastric adenocarcinoma? | Early: Mostly asymptomatic.
Late: Anorexia/weight loss, nausea, vomiting, dysphagia, melena, hematemesis; pain is constant, nonradiating, exacerbated by food. Anemia—from blood loss, pernicious.
Krukenberg’s tumor—metastasis to ovaries
Blumer’s shelf—metastasis to pelvic cul-de-sac, felt on digital rectal exam
Virchow’s node—metastasis to lymph node palpable in left supraclavicular fossa
Sister Mary Joseph’s nodule—metastasis to the umbilical lymph nodes |
| How is dx of gastric adenocarcinoma? | Upper GI endoscopy: Best method, allows for biopsy, definitive >95% sensitivity and specificity
Upper GI series: With double contrast; 80–96% sensitivity, 90% specificity (operator dependent); excellent method in skilled hands.
Abdominal CT: Good for detecting distant metastases; also used forpreop staging, but suboptimal.
Endoscopic ultrasound: Good for detecting depth of invasion |
| How is tx of gastric adenocarcinoma? | Surgical resection is the only curative treatment for gastric cancer.
Aggressive surgical resection (in the absence of distant metastases).
Need negative margins: at least 5 cm from tumor margins.
Extended lymphadenectomy .
Procedure: by location of tumor
Proximal tumors :Total gastrectomy
Distal tumors:
Subtotal gastrectomy
Total gastrectomy: no difference from subtotal (cure)
WITH LYMPHADENECTOMY
Chemotherapy:
Sometimes used palliatively for nonsurgical candidates;
PROGNOSIS
Prognosis depends on stage of disease. Overall 5-year survival is still only 5–15%. |
| What is gastric lymphoma? | Second most common malignant gastric cancer
Comprise only 5% of all gastric tumors
5× risk with human immunodeficiency virus (HIV)
Male predominance 1.7:1
SIGNS AND SYMPTOMS
Nonspecific; include abdominal discomfort, nausea, vomiting, anorexia, weight loss, and hemorrhage.
DIAGNOSIS
Made by endoscopic biopsy, not readily distinguishable from adenocarcinoma by simple inspection.
Bone marrow aspiration and gallium bone scans can diagnose metastases. |
| How is staging and tx of gastric lymphoma? | STAGING (ANN ARBOR CLASSIFICATION)
Stage I: Disease limited to stomach
Stage II: Spread to abdominal lymph nodes
Stage III: Spread to lymph nodes above and below the diaphragm
Stage IV: Disseminated lymphoma
TREATMENT
MALT (low grade)—Treat H. pylori.
MALT (high grade) or non-MALT—Radiation/chemo
Resection reserved for patients with bleeding or perforation
PROGNOSIS
Poor prognostic factors include:
Involvement of the lesser curvature of the stomach
Large tumor size
Advanced stage |
| What is gastrica sarcoma? | EPIDEMIOLOGY
Equal incidence in men and women
Usual age at diagnosis is 65 to 70 years
HISTOLOGY
Most are leiomyosarcomas.
Spread is hematogenous ( No lymphatic metastasis).
TREATMENT: Surgical resection with free margins.
PROGNOSIS
Low-grade tumors: Five-year survival rate is ∼80%
High-grade tumors: Five-year survival rate is ∼30%. |
| What is duodenal diverticula? | Duodenal pulsion diverticula are acquired outpouchings of the mucosa and submucosa;
Found in 20% of autopsies and 5–10% of upper GI series;
90% are on medial aspect of duodenum.
Most are solitary and within 2.5 cm of the ampulla of Vater
Symptoms are uncommon; patients may have chronic postprandial abdominal pain or dyspepsia
Complications : hemorrhage, perforation, pancreatitis, biliary obstruction
Diverticulum is visualized on upper GI contrast radiographic studies or upper GI endoscopy |
| How is tx of duodenal diverticula? | Only 1% of cases found by x-ray warrant surgery
Operation includes excision and 2-layer closure.
Endoscopic sphincterotomy or stent placement may be preferable to treat biliary obstruction.
Surgery is indicated for all complications; severe persistent postprandial abdominal pain or dyspepsia.
Prognosis: good with excellent surgical treatment of complications. |
| What are benign duodenal tumors? | Adenomas are sessile or pedunculated; may be associated with familial adenomatous polyposis;
Types are tubular, villous, Brunner gland.
Tubular: low malignant potential
Villous: high malignant risk; 30% of those >3 cm have malignant focus; often periampullary
Brunner gland: hyperplasia of exocrine glands
Hamartomas: associated with Peutz-Jeghers syndrome
Lipomas: no malignant potential
Symptoms and signs
gastric outlet obstruction, biliary obstruction and jaundice, upper GI bleeding.
Diagnosis
Duodenal tumor evident on upper GI endoscopy or contrast radiography. |
| How is tx of benign duodenal tumors? | Endoscopic removal if feasible
Surgery is indicated for failure of endoscopic removal If malignancy, pancreaticoduodenectomy usually indicated
Prognosis:
If benign, most tumors cured by complete removal; may recur after incomplete resection. |
| What are malignant duodenal tumors? | Adenocarcinoma: 67% periampullary
Risk factors are Crohn disease, ulcerative colitis, polyposis syndromes, villous adenomas, hereditary nonpolyposis colon cancer
Also include lymphoma; GIST (10–30% malignant).
Symptoms and signs
Abdominal pain, GI or biliary obstruction, GI bleeding (hematochezia or melena), weight loss; lymphoma: fever, night sweats, palpable abdominal mass.
Endoscopy and biopsy are usually diagnostic |
| How is tx of malignant duodenal tumors? | Pancreaticoduodenectomy is necessary for complete resection of most proximal duodenal malignancies.
Surgery is indicated for localized disease; resect all adenocarcinomas and GIST.
Medications: imatinib mesylate for GIST.
Prognosis: after curative resection, overall 5-year survival rate is 30%; for adenocarcinoma, 5-year survival for stage I is 80%; stage III, 10–15% |
