1.3b Stomach

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BEI SAMONTE ☺ Page 1 of

1 3B STOMACH

SURG RY

STOMACH

• STORES ingested food

• DIGEST and ABSORB ingested food

• REGULATE appetite

• Has digestive, nutritional, and endocrine functions

ANATOMY

• The stomach is a dilated part of the alimentary canal between

the esophagus and the small intestine.

• It is a muscular sac.• It occupies the left upper quadrant, epigastric, and umbilical

regions, and much of it lies under cover of the ribs.

• Stomach located at level of T10 and L3 vertebral.

• Position of the stomach varies with body habitués.

The stomach is divided into four regions:

1. The cardia, which surrounds the opening of the esophagus

into the stomach.

2. The fundus of stomach, which is the area above the level of

the cardial orifice.

3. The body of stomach, which is the largest region of the

stomach.

4. The pyloric part, which is divided into the pyloric antrum an

pyloric canal and is the distal end of the stomach.

• Openings:

– Gastroesophageal: To esophagus

– Pyloric: To duodenum

BLOOD SUPPLY

Arterial blood supply:

• 3 Branches

• Left Gastric Artery

- Supplies the cardia of the stomach and distal

esophagus

• Splenic Artery

- Gives rise to 2 branches which help supply the

greater curvature of the stomach

Left Gastroepiploic

Short Gastric Arteries

• Common Hepatic or Proper Hepatic Artery

- 2 major branches

Right Gastric- supplies a portion of the lesser

curvature

Gastroduodenal artery

→ Gives rise to Right Gastroepiploic artery

→ Helps supply greater curvature in

conjunction with Left Gastroepiploic Artery

LYMPHATIC DRAINAGE

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1 3B STOMACH Surgery

• Lymph from the proximal portion of the stomach drains along

the lesser curvature first drains into superior gastric lymph

nodes surrounding the Left Gastric Artery.

• Distal portion of lesser curvature drains through the

suprapyloric nodes.

• Proximal portion of the greater curvature is supplied by the

lymphatic vessels that traverse the pancreaticosplenic nodes.• Antral portion of the greater curvature drains into the subpyloric

and omental nodal groups.

INNERVATIONS

• The main innervations are Left and Right Vagus Nerves.

• Parasympathetic innervation of Stomach- Vagus Nerve

- 90% of fiber in vagal trunk is afferent (info

transmitting from stomach to CNS)

• Sympathetic innervation of Stomach- Splanchnic Nerve

- Derived from spinal segement T5-T10

HISTOLOGY

PHYSIOLOGY

• To store food and facilitate digestion by

- Secretory functions

Production of acid, pepsin, intrinsic factor

mucus, and a variety of GI hormones

- Motor functions

Food storage (receptive relaxation and

accomodation), grinding and mixing,

controlled emptying of ingested food, and

periodic interprandial "housekeeping."

IDENTIFYING THE DISEASE

SIGNS AND SYMPTOMS

• Abdominal pain, weight loss, early satiety, anorexia, nausea,

vomiting, bloating, and anemia

• Complete and thorough history and PE

DIAGNOSTIC TESTS

• Esophagogastroduodenoscopy

- 45 years old and above

- Or if with the ff:

Recurrent vomiting

Bleeding

Anemia

Weight loss

Dysphagia

• Radiographic tests - SFA, UGIS with contrast

• CT scan, MRI, arteriography

• Endoscopic ultrasound

• Gastric secretory analysus, H.Pylori Test

• Scintigraphy

• Antroduodenal motility testing and EGG

ENDOSCOPIC ULTRASOUND

1. Superficial mucosa2. Deep mucosa

3. Submucosa

4. Muscularis propria

5. Serosa

PEPTIC ULCER DISEASE

• Focal defects in the gastric or duodenal mucosa that extend

into the submucosa or deeper

• Due to an imbalance between mucosal defenses and

acid/peptic injury

• Caused by:

- Gastrinoma, antral G-cell hyperfunction and/or

hyperplasia, systemic mastocytosis, trauma, burns

and major physiologic stress

- Drugs (all NSAIDS, aspirin, and cocaine), smoking

and psychologic stress

• Helicobacter pylori

• Possess the enzyme urease

Converts urea into ammonia and

bicarbonate

• Ammonia is damaging to the surface epithelial cells

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Aggression Defense Repair

Acid

Pepsin

NSAIDS

H.Pylori

Bicarbonate

Blood flow

Mucus

Cell junctions

Apical resistance

Restitution

Mucoid cap

Proliferation

Growth factors

SIGNS & SYMPTOMS

• Burning, non radiating epigastric pain

• Duodenal ulcer - after a meal, at night

• Gastric ulcer - occurs with eating

• Nausea, bloating, weight loss, stool positive for occult blood,

and anemia

DIAGNOSTIC TESTS

• EGD with or without biopsy• H.Pylori test

COMPLICATIONS

• Bleeding

• Perforation

• Obstruction

TREATMENT

• Lifestyle modification

• Medical

• Surgical

JOHNSONS CLASSIFICATION

PATIENTS TAKING NSAIDS OR ASPIRIN NEED CONCOMITANT ACI

SUPPRESSING MEDICATION IF ANY OF THE FF RISK FACTORS IS

PRESENT

• Age over 60

• History of acid/ peptic disease

• Concurrent steroid intake

• Concurrent anticoagulant intake

• High-dose NSAID or acetylsalicylic acid

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VAGOTOMY

HSV TV

DRAINAGE

Gastrojejunostomy Pyloroplasty

ZOLLINGER ELLISON SYNDROME

• Uncontrolled secretion of abnormal amounts of gastrin by a

duodenal or pancreatic neuroendocrine tumor (i.e.,

gastrinoma).

• 80% are sporadic (mid life 40-50's)

• 20% are inherited (young 20-30's)

• Associated with multiple endocrine neoplasia type I

(MEN I), which consists of parathyroid, pituitary, and

pancreatic (or duodenal) tumors.

SIGNS & SYMPTOMS

• Epigastric pain, GERD, diarrhea

DIAGNOSTIC TESTS

• EGD - atypical ulcer location (distal duodenum, jejunum, or

multiple ulcers)

• Secretin stimulation test

• BAO testing

• Serum calcium

• Parathyroid hormone levels

• Somatostatin receptor scintigraphy (octreotide scan)

• Endoscopic ultrasound, CT scan or MRI

TREATMENT

• PPIs

• Exploratory laparotomy with curative intent

• Chemotherapy

GASTRITIS AND STRESS ULCER

GASTRITIS

• Gastritis = mucosal inflammation

• H.Pylori - most common cause

• Others: Alcohol, NSAIDS, Crohn's disease, TB, and bile reflux

• Infectious and inflammatory causes result in immune cell

infiltration and cytokine production which damage mucosal

cells

• Chemical agents (alcohol, aspirin, and bile) disrupt the mucos

barrier, allowing mucosal damage by back diffusion of luminalhydrogen ions

• Diagnosis is made clinically and with EGD with biopsy

STRESS GASTRITIS

• Due to inadequate gastric mucosal blood flow during periods o

intense physiologic stress

• Mucosal breakdown occurs

• Seen in ICU patients

• Medical treatment: Acid suppression

• Bleeding: Angiographic embolization or endoscopic hemostat

treatment, surgery

MALIGNANT NEOPLASM - ADENOCARCINOMA

• 95% of gastric malignancies

• Elderly

• Younger patients

- Tend to be diffuse, large, aggressive, poorly

differentiated, sometimes infiltrating the entire

stomach (linitis plastic)

• Higher incidence in groups of lower socioeconomic status

FACTORS INCREASING OR DECREASING THE RISK OF GASTRIC

CANCER

• Increase risk

- Family history

- Diet (high in nitrates, salt, fat)

- Familial polyposis

- Gastric adenomas

- Hereditary nonpolyposis colorectal cancer

- Helicobacter pylori infection

Atrophic gastritis, intestinal metaplasia,

dysplasia

- Previous gastrectomy or gastrojejunostomy (>10y

ago)- Tobacco use

- Menetrier's disease

• Decrease risk

- Aspirin

- Diet (high fresh fruit & vegetable intake)

- Vitamin C

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SIGNS& SYMPTOMS

• Abdominal pain, weight loss, anorexia, early satiety, nausea,

vomiting, bloating

• Chronic occult bleeding > acute massive bleeding

• Palpation of mass is rare and if present the stage is most likel

advanced

• Virchow's node, Sister Joseph's nodule

• (+) nodules in the rectal shelf - drop metastasis

DIAGNOSTIC EVALUATION

• EGD with biopsy

• Abdominopelvic CT scan with IV and oral contrast, EUS

• PET scanning

• Staging laparoscopy

TREATMENT

• Perioperative chemotherapy and curative gastric resection wit

lymphadenectomy

• Palliative gastrectomy for stage IV

– Endoscopic removal

< 2cm in sixe

Node negative

Confined to the mucosa on EUS

No other gastric lesions

MALIGNANT NEOPLASMS - LYMPHOMA

• 4% of gastric malignancies

• Most are B-cell type, thought to arise in mucosa associated

lymphoid tissue (MALT)

• 50% are high grade, 50% are low grade

• The normal stomach = no lymphoid tissue

• However, chronic gastritis = acquires MALT -> malignant

degeneration

• H.Pylori = culprit

• Low-grade MALT lymphoma can degenerate

• into high-grade lymphoma

• Remarkably, when the H. pylori is eradicated and the gastritis

improves, the low-grade MALT lymphoma often disappears.

Thus, low- grade MALT lymphoma is not a surgical lesion.

SIGNS & SYMPTOMS

• Obstruction, bleeding, fever, weight loss, night sweats,

lymphadenopathy

DIAGNOSTIC TESTS

• EGD with biopsy, CT scan of abdomen, pelvis and chest,

bone marrow biopsy, endoscopic ultrasound

TREATMENT

• H. pylori regimen

• radiotherapy (early stage) or chemotherapy with or without

radiation (advanced)

• Surgery: tube jejunostomy, gastrectomy (definitive, palliative

MALIGNANT NEOPLASMS - GIST

• GIST – gastrointestinal stromal tumor

• Arise from interstitial cells of Cajal (ICC)

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• Prognosis depends mostly on tumor size and mitotic count

• Metastasis is by the hematogenous route

• Any lesion >1 cm can behave in a malignant fashion and may

recur

• Almost all express c-KIT (CD117) or the related PDGF receptor

A, as well as CD34

• Low grade – 80% survival in 5 years• High grade – 30% survival in 5 years

• Submucosal tumors that are slow growing

SIGNS & SYMPTOMS

• Small lesions: asymptomatic or impressive bleeding

• Larger lesions: weight loss, abdominal pain, fullness, early

satiety, bleeding, palpable abdominal mass

DIAGNOSTIC TESTS

• EGD with biopsy and IHC staining, CT scan (abdomen, chest

and pelvis)

TREATMENT

• Wedge resection with clear margins is adequate surgicaltreatment.

• If there is invasion of adjacent structure, en bloc removal is

done.

• Chemotherapy: Imatinib (gleevec) 400mg once a day for 3

years for high risk of recurrence

MALIGNANT NEOPLASMS - CARCINOID

• Rare

• Arise from gastric enterochromaffin-like (ECL) cells and some

have malignant potential

• 3 types:

– Type I

Most common, 75%

Occur in patients with chronic hypergastrinemia

secondary to pernicious anemia or chronic

atrophic gastritis

More frequent in women

Often multiple and small

Low malignant potential (2 cm)

More commonly in men

Not associated with hypergastrinemia

Most patients have nodal or distant metastases

at the time of diagnosis, and some present with

symptoms of carcinoid syndrome.

30% survival in 5 years

DIAGNOSTIC TESTS

• EGD and biopsy

• If small, EUS and biopsy

• CT scan and octreotide scan for staging

TREATMENT

• If small (type I and II) and

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MASSIVE UPPER GI BLEEDING

• Acute bleeding proximal to the ligament of Treitz which

requires blood transfusion

• Most common source - stomach and proximal duodenum

• Causes:

• Peptic ulcer, gastritis, Mallory-Weiss tear, and

esophagogastric varices, neoplasm, angiodysplasia,

Dieulafoy’s lesion, portal gastropathy,ie’s disease, and

watermelon stomach, arterioenteric fistula

• IMPORTANT: resuscitation and risk stratification

A. What is the magnitude and acuity of the hemorrhage? Does

the patient have signs and symptoms that suggest that large

blood loss has occurred over a short period of time?

B. Does the patient have significant chronic disease which

compromises physiologic reserve?

C. Is the patient anticoagulated, or immunosuppressed?

D. On endoscopy, is the patient bleeding from varices, or is

there active bleeding, or is there a visible vessel, or is there

a deep ulcer overlying a large vessel? Could the patient be

bleeding from an Arterio enteric fistula?

• NO: low risk

• Most patients will stop bleeding

• supportive treatment

• IV PPI

• Selected patients may be discharged from the emergency

room and managed on an outpatient basis.

UPPER GI BLEEDING

• YES: high risk

• Type and cross-match for blood transfusion

• Admit to ICU

• Consult surgeon and gastroenterologist.

• Resuscitate and correct coagulopathy

• Medical vs. Surgical therapy

DIEULAFOY'S LESION

• Congenital AVM of a submucosal artery

• Usually 6cm from GEJ at lesser curvature

• Middle-aged or elderly men

• More common in patients with liver disease

SIGNS & SYMPTOMS

• Recurrent/intermittent melena, hematemesis, hematochezia

• EGD: Pulsatile bleeding

DIAGNOSTIC TESTS

• Angiography/RBC tagging – if no active bleeding on

TREATMENT

• Endoscopic hemostatic therapy

• Angiographic embolization

• Oversewing/resection

BEZOAR

• Concretions of indigestible matter

– Trichobezoars (hair)

– Phytobezoars (vegetable)

SIGNS & SYMPTOMS

• Obstruction,

• Ulceration, bleeding

DIAGNOSTIC TESTS

• UGIS, EGD, CT scan

TREATMENT

• Enzyme therapy (papain, cellulase, acetylcysteine)

• Endoscopic disruption and removal

• Surgical removal

MALLORY WEISS LESION

• Longitudinal tear in the mucosa of the GE junction

• Caused: forceful vomiting &/or retching

• Commonly seen in alcoholics

• Boehaave’s syndrome (esophageal rupture): vomiting, ches

pain, subcutaneous emphysema

• EGD: confirm diagnosis and

• Control bleeding

• 90% of patients stop bleeding spontaneously

• Other options:

– Balloon tamponade

– Angiographic embolization

– Selective infusion of vasopressin

– Systemic vasopressin, and operation

– Surgery: oversew

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END OF TRANX

1.3b Stomach

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