GIT Disorders
GIT Disorders
GIT Disorders
the GIT
multiple sclerosis)
premalignant.
4. Abdominal pain: it can originate in the
a) Viscera: due to spasm or colic of the muscular layer of the gut
b) Peritoneum: due to irritation or inflammation
5. Blood loss: it may be as
a) Hematemesis: Vomiting of blood- usually due to an upper GI
bleeding, due to:
Oesophagus: ruptured blood vessels (oesophageal varices) r
Stomach: due to
an erosion by an ulcer
Leukoplakia- hyperkeratosis
PHARYNX
Most infections of the pharynx are due to a
viral infection like influenza, measles, rhinovirus, infectious
mononucleosis.
Bacterial infections due to streptococcus
A B C
A,B-Tracheoesophageal fistulas
C- Esophagela atresia with fistula
Oesophageal varices are dilated veins of the lower esophagus,
which serve as shunts when portal venous flow through the liver
is impaired. It is a cause for massive hematemesis. Other sites of
varices are around the anus and the umbilicus.
Reflux esophagitis is a chronic inflammation in the esophagus
occurring as a result of the regurgitation of the acidic gastric
contents. It produces heartburn
Barrett’s esophagus is a metaplastic change in the mucosal
lining of the lower esophagus, from stratified nonkeratinized
epithelium to columnar epithelium, occurring as a result of
longstanding reflux. Its significance lies in the fact that it is
premalignant.
Tumors involving the oesophagus could be benign like the
leiomyoma (smooth muscle tumor) or carcinoma (squamous cell
carcinoma or the adenocarcinoma).
Stomach
Congenital pyloric stenosis is the hypertrophy of the circular
muscle coat of the pyloric sphincter leading to an outflow
obstruction.
Acute gastritis:
It is the acute inflammation of the stomach in response to an
irritant chemical like drugs or alcohol.
The principal drugs implicated are the nonsteroidal anti-
inflammatory drugs (NSAIDs), notably aspirin.
These agents result in exfoliation of the surface epithelial cells
and decrease the secretion of the mucus.
Inhibit the prostaglandin synthesis.
Other causes include
excessive alcohol ingestion,
heavy smoking,
cancer chemotherapy,
irradiation,
ulcer is a full thickness loss. Erosions in acute gastritis are usually multiple
and frequently bleed causing hemorrhage.
Chronic gastritis is frequently due to Helicobacter pylori infection, or may
be autoimmune (associated with vitamin B12 deficiency resulting in
megaloblastic anemia- pernicious anemia) or chemical injury due to NSAIDs,
chronic bile reflux or alcohol, radiation, post surgery, obstruction, and
chronic granulomatous conditions like Crohn’s disease.
Peptic ulceration
Ulcers are a breach in the continuity of the mucosal epithelial
lining of the alimentary tract extending through the muscularis
mucosa into the submucosa or deeper, arising as a result of the
acid and pepsin attacks on the mucosa.
Normally these attacks are counteracted by the defense
mechanism like
the mucus- bicarbonate barrier,
increased mucosal blood flow,
increased regenerative capacity of the epithelium and
prostaglandin secretion by the epithelium.
Ulcers result when the mucosal defenses are weakened or when
the damaging forces are increased.
This occurs in:
Helicobacter pylori infection-
releases enzymes (digests the mucosal lining) and
lipopolysaccharides (attract the inflammatory cells which
release digestive enzymes) and
a platelet activating factor that promotes the thrombotic
occlusion of the surface capillaries (promotes ischemic
damage)
Chronic use of NSAIDs- these suppress the prostaglandin
secretion
Increased gastric acidity as in gastrinomas (increased gastrin
secretion)- Zollinger Ellison syndrome.
Chronic smoking, alcohol ingestion, corticosteroid
administration are other causes.
Major sites include first part of the duodenum, junction of the
antrum and the body of the stomach, distal oesophagus, at the
gastro enterostomy stoma (post partial gastrectomy patients) and
in Meckles diverticula (sac like out pouching from the intestinal
wall)
Stricture & Fibrosis Occurs early in the disease Rare/ occurs late as fibrosis
due to marked fibrosis is to a lesser degree
Wall Thickened Thin & Dilated