Stomach and duodenum Omar - PowerPoint Presentation

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Stomach and duodenum

Omar alnoubani MD,MRCS

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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 .

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The organs that commonly abut the stomach are the liver,

colon, spleen, pancreas, and occasionally the kidneyThe lesser curvature is tethered to the liver by the

hepatogastric

ligament

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the

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

The

antrior

to liver ,hepatoduodenal ligament as ant. N. of laterjetThe post. To celiac plexus .The Ns of laterjet terminate near the angularis

incisura

as crow’s foot

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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

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Parietal

: • Location: Body • Function: secrete acid and intrinsic factor

Mucus:

Location: Body,

Antrum Function: mucus production Chief: Location: Body Function: produce Pepsin

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Surface epithelium:

Location: Diffuse Function: produce mucus, bicarb, prostaglandins

ECL:

Location: Body

Function: Histamine production G cells: Location: Antrum Function: Gastrin production

Other cells ….

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Acid Secretion

Two forms: Basal Acid Secretion Stimulated Acid Secretion

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Stimulated Acid Secretion

Three Phases: Cephalic phase Gastric phase Intestinal Phase These phases occur concurrently NOT consecutively.

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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.

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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.

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Intestinal Phase

Poorly understood. initiated by chyme entering the small bowel.

Accounts for ~10% of acid production.

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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

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Gastric Hormones

Gastrin Somatostatin Gastrin-releasing peptide (GRP)

Histamine

Leptin

Ghrelin

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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

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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.

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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

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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

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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

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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

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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.

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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.

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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.

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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.

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Pathophysiology and Etiology

No acid no ulcer

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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.

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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 gastritisHave a role in gastric lymphoma

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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.

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Gastric ulcers

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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 .

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Nonsteroidal

Anti-Inflammatory Drugs in Peptic UlcerDiseaseChronic 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

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Indications of acid suppression in patients taking NSAIDs

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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

.

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Medical management

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Surgical Treatment of Peptic Ulcer Disease

Indications :BleedingPerforationObstructionIntractability or

nonhealing

Malignancy .

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Mainly

oversewing of the bleeders and patch closure for perforating .The use of vagotomy is increasingly uncommon because of PPI.

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Before PPI !!!

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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 .

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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%.

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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

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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

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Intractable or

Nonhealing Peptic UlcerShould 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.

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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.

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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

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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.

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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

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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%.

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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

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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.

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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

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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.

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MALIGNANT NEOPLASMS OF THE STOMACH

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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.

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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).

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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.

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Genetics

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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.

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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.

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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

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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%.

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Gross Morphology and Histologic Subtypes

polypoid, fungating, ulcerative, and scirrhousIn 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.

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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.

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WHO and Ming classification

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

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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

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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

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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 .

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Physical exam

Signs of wt loss and malnutrition Virchow’s node ,Irish node, Krukenberg’s tumor , Sister Joseph’s nodule ,Blumer’s shelf

ascites

.

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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.

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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

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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

.

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Extent of

Lymphadenectomy D1 vs D2D1 lymphadenectomy in total gastrectomy requires dissection of stations 1 through 7 and in D2, from 8a to 12a too.

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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 .

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Endoscopic Resection

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

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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 .

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Gastrointestinal Stromal Tumor

Arise from (ICC) . Prognosis depends mostly on size , mitotic

count, and

metastasis.

hematogenous spreadExpress 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

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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

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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.

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Type

II gastric carcinoids are associated with MEN1 and ZES. Type III gastric carcinoids are sporadic tumors

the most aggressive .

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BENIGN GASTRIC NEOPLASMS

Leiomyoma : umbilicated appearance , Asymptomatic Lipoma : small , asymptomatic .

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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 .

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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 .

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Volvulus

Associated with hiatus hernia Borchardt's triadOrgano-axial from a line connected the cardia to pylorus

Mesntro

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

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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” .

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Diarrhea

.Gastric Stasis.Bile Reflux Gastritis and Esophagitis .Roux Syndrome

.

Weight Loss

.Anemia .Bone Disease Gallstones .

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Thank you