UNIT FIVE

ALTERATION IN GIT FUNCTION

Peptic ulcer disease (PUD)
Ulcers are breaches in the mucosa that

extend into the submucosa or deeper.

Peptic ulcer
Definition: ulcers of the distal stomach and

proximal duodenum caused by gastric

secretions (hydrochloric acid and pepsin) and
impaired mucosal defenses
 Etiology
 Chronic NSAID and aspirin use

 Steroids

 Smoking

 H. pylori infection

 Major locations
 Duodenum

 Gastric

 Morphology
 All peptic ulcers (gastric or duodenal) are identical in appearance.

 Gross:
 clean, sharply demarcated lesions that are slightly elevated at the
edges
 Microscopic:

 four layers: necrotic debris; inflammation, with neutrophils

predominating; granulation (repair) tissue; fibrotic tissue

Duodenal peptic ulcer

More common than gastric ulcers

Associations

 H. pylori (~1O0%)
 Increased gastric acid secretion
 Increased rate of gastric emptying
 Blood group 0
  Multiple endocrine neoplasia (MEN) type I and Zollinger-
Ellisonsyndromes
 Cirrhosis and COPD

Location:

 anterior wall of the proximal duodenum

Pathogenesis
 Defective mucosal barrier due due to H. pylori
 Increased acid production (increased parietal cell mass)

Classic presentation:

 burning epigastric pain 1-3 hours after eating, which is

relieved by food
Gastric peptic ulcer
Associated with H. pylori (75%)

Location:
 lesser curvature of the antrum

Gross
 Small «3 cm), solitary ulcers
 Round or oval shape
 Sharply demarcated, "punched-out" ulcers
 Overhangingmargins
 Radiatingmucosalfolds
Pathogenesis

 Defective mucosal barrier due to H. pylori

 Mucosal ischemia (reduced PGE), bile reflux,
delayed gastric emptying

Classic presentation:

 burning epigastric pain, which worsens with eating

Gastric Carcinoma
Among the malignant tumors that occur in the
stomach, carcinoma is overwhelmingly the most
important and the most common (90% to 95%).
Epidemiology and Classification.
 Gastric carcinoma is a worldwide disease with a

widely varying incidence.

 Japan, Colombia, Costa Rica, and Hungary have a

particularly high incidence.

 Nevertheless, in most countries there has been a

steady decline in both the incidence and the

mortality of gastric cancer.
Gastric cancers exhibit two morphologic types
 intestinal and

 diffuse

The intestinal variant

 is thought to arise from gastric mucous cells that have
undergone intestinal metaplasia in the setting of chronic
gastritis.
 This pattern of cancer tends to be better differentiated
and is the more common type in high-risk populations.
 Intestinal-type carcinoma is the pattern that is
progressively diminishing in frequency in the United
States.
The diffuse variant
 is thought to arise de novo from native gastric

mucous cells, is not associated with chronic gastritis,

 Tends to be poorly differentiated.

 Most importantly, diffuse gastric carcinoma has not

significantly changed in frequency in the past 60

years and now constitutes approximately half of
gastric carcinomas in the United States.
 Whereas the intestinal-type carcinoma occurs

primarily after age 50 years with a 2:1 male

predominance, the diffuse carcinoma occurs at an
earlier age with no male predominance
 Risk factors
 Dietary factors
 Smoked fish and meats
 Pickled vegetables
 Nitrosamines
 Benzpyrene
 Decreased intake of fruits and vegetables .
 H. pylori infection

 Chronic atrophic gastritis

 Smoking

 Blood type A

 Bacterial overgrowth in the stomach

 Prior subtotal gastrectomy

Presentation
Often (90%) asymptomatic until late in the course

 Weight loss and anorexia

Epigastric abdominal pain mimicking a peptic ulcer

 Early satiety

Occult bleeding and iron deficiency anemia

Location:
lesser curvature of the antrum
 Gross and microscopic findings:

 Intestinal type
 polypoid, ulcerated appearance

 Early lesions are confined to the mucosa an submucosa.

 Advanced lesions extend into the muscle wall.

 Diffuse type
 Characterized by diffuse infiltration of the stomach wall
(linitis plastica) and no peristalsis;
 composed of "signet-ring" cells (mucin-filled neoplastic

cells with the nucleus pushed to the periphery)

 Hematogenous spread, causing bilateral Krukenberg

tumors in ovaries
Intestinal Obstruction
 Intestinal Obstruction exists where there is any pathogenic
impediment to the normal flow of intestinal contents
through the intestinal tract.

Two types of process can impede the flow.

 Mechanical-
 There is an intraluminal obstruction or mural obstruction from
pressure on the intestinal walls.
 Examples Polypoid tumors, stenosis, stricture, adhesions,
hernias and abscess.
 Paralytic-
 The intestinal musculature is unable to propel the contents
along the bowel.
 Example-Diabetes mellitus, Parkinson’s disease and after
surgery-paralytic illeus.
 Etiology
 Adhesions
 from previous surgery

 Hernia:
 small bowel trapped in indirect hernia sac; second most common cause
of obstruction in adults

 Intussusception
 Occurs most often in children
 Terminal ileum telescopes into the cecum, causing a combination of
obstruction and ischemia as well as colicky pain with bloody diarrhea.

 Meconium ileus:
 complication in newborns with cystic fibrosis

 Volvulus:
 bowel twists around mesenteric root, resulting in obstruction and
strangulation.
 Obstruction of the small bowel:
 Small-bowel (jejunoileal) obstruction is

 commonly caused by incarceration in hernias or by adhesions

 less commonly caused by tumors (primary or metastatic),
obturation by foreign bodies, a Meckel's diverticulum, or Crohn's
disease.
 Ascaris infestation is rare in the USA but occurs in some tropical
countries.
 Volvulus of the midgut is rare.
 Intussusception
 in adolescents and adults is almost always caused by tumors.
 In infants, it is usually caused by meconium ileus, volvulus of a
malrotated gut, atresia, and intussusception
 Obstruction of the duodenum:

 Duodenal obstruction is usually caused by cancer, primarily in the duodenum

or head of the pancreas.

 In neonates, duodenal obstruction is most commonly caused by atresia,

volvulus, bands, congenital esophageal webs, and annular pancreas.

 In rare instances, congenital webs persist into adult life and lead to deformities

(eg, the so-called intraluminal diverticula associated with obstruction).

 Obstruction of the large bowel:

 Large-bowel obstruction is caused by tumors, diverticulitis, volvulus, and fecal

impaction.
 Tumors include cancer that blocks the lumen and rare benign lesions (eg,

lipomas, large polyps) that can lead to intussusception.

 Obstructing cancer occurs most often at the splenic and sigmoid flexures,

diverticulitis usually obstructs in the sigmoid, and volvulus is most common in

the sigmoid or cecum
 Pathophysiology
 In simple mechanical obstruction,
 blockage occurs without vascular or neurologic compromise.

 Ingested fluid and food, digestive secretions, and gas accumulate in

excessive amounts if obstruction is complete.
 The proximal bowel distends, and the distal segment collapses.

 The normal secretory and absorptive functions of the mucous membrane

are depressed, and the bowel wall becomes edematous and congested.
 Severe intestinal distention is self-perpetuating and progressive,
intensifying the peristaltic and secretory derangements and increasing
the risks of dehydration, ischemia, necrosis, perforation, peritonitis, and
death.
In strangulating obstruction,
infarction of the bowel is most commonly associated with

hernia, volvulus, intussusception, and vascular occlusion.

Strangulation usually begins with venous obstruction,

which may be followed by arterial occlusion, resulting in

rapid ischemia of the bowel wall.
The bowel becomes edematous and infarcted, leading to

gangrene and perforation.

 Clinical presentation

 Obstruction of the small bowel:

 Diagnosis of simple obstruction is based on a triad of symptoms:
 (1) Abdominal cramps are centered around the umbilicus or in the
epigastrium; if cramps become severe and steady, strangulation probably
has occurred.
 (2) Vomiting starts early with small-bowel and late with large-bowel
obstruction.
 (3) Obstipation occurs with complete obstruction, but diarrhea may be
present with partial obstruction.

 Strangulating obstruction
 occurs in nearly 25% of cases of small-bowel obstruction and can
progress to gangrene in as little as 6 h;
 it is manifested by steady, severe abdominal pain from the outset or
beginning a few hours after the onset of crampy pain.
Obstruction of the large bowel:
 Symptoms usually develop more gradually than with small-

bowel obstruction.
 Increasing constipation leads to obstipation and abdominal

distention.
 If the ileocecal valve is competent, there may be no vomiting;

if it allows reflux of colonic contents into the ileum, vomiting

may occur (usually several hours after onset of symptoms).
 Lower abdominal cramps unproductive of feces are present.