Ulceroinflammatory Disorders of

the GIT

Dr. Mehzabin Ahmed

 TOPICS
 Common symptoms & terminology
 Disorders of :
 Mouth: Ulcers, Premalignant lesions

 Pharynx: Infections, Tumors

 Salivary gland: Inflammations, Tumors

 Esophagus: Hiatus hernias, Barrett esophagus

 Stomach: Peptic ulcers

 Intestines: Inflammatory bowel disease (Crohn

disease & ulcerative colitis) and Malabsorption
syndromes
 The gastrointestinal tract extends from the mouth to the
anus and includes the oral cavity and salivary glands,
pharynx, oesophagus, stomach, small and the large
intestines.

 The main function of the GIT is digestion, absorption

and assimilation of the food consumed.
1. Dysphagia: Difficulty in swallowing.
Causes :
 Acute infections of the pharynx or tonsils, or

 Obstruction by foreign bodies or tumors (in the oesophagus

or outside it producing compression) or

 Impaired neuromuscular function (as in achalasia cardia or

multiple sclerosis)

2. Leukoplakia: is a term used to describe the white patches of

keratosis (increased keratinization) resulting due a chronic
irritation. It is characterized by
 Hyperkeratinization and hyperplasia of the squamous
epithelium
 Dysplasia in some cases and in these situations it is

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

 Mallory Weis syndrome (oesophageal mucosal tears in

chronic alcoholic occurring due to retching and vomiting
b) Melena: passage of altered blood in the stools.
the blood lost may originate from
- Upper GI:. It occurs in ulcers and tumors of the stomach and
duodenum
- Lower GI: the blood in the stools appears fresh and red. It occurs
in ruptures anal fissures, hemorrhoids (piles), or ulcers and
tumors of the colorectum.
6. Weight loss: it may be due
· Impaired food intake: as in eating disorders
· Malabsorption syndromes
· Increased catabolism a/w a malignant tumor.

7. Anaemia: it may be due to blood loss or due to impaired absorption of

iron, folic acid or B12 (either due to a mucosal abnormality eg.
pernicious anaemia or to a defect in the transport proteins)

8. Diarrhoea: Causes: an impaired absorption (usually due to an infective

cause as in cholera, shigellosis and are called infective diarrhoeas) or
excessive secretion of fluid (osmotic diarrhoea- as in lactose
intolerance)

9. Steatorrhoea: due to impaired absorption of fat either because of

reduced lipase secretion or reduced absorption area or due to lymphatic
obstruction.
 Mouth
 Ulcers: The oral mucosa is commonly affected by ulcers.
These may be
 infectious (herpes virus, candida albicans) or

 non infectious (aphthous ulcers- due to an

immunological imbalance, or associated with Crohn’s
disease- usually self limited).

 Leukoplakia: premalignant lesion resulting from a chronic

irritation- if untreated leads to squamous cell carcinoma.
 Aphthous
ulcers

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

 important because of their complications, like rheumatic

fever and its complications, glomerulonephritis, and
vascultis.

 Tumors: Ebstein Barr virus is implicated in the development of

Nasopharyngeal carcinoma.
 Salivary glands
 Inflammations of the salivary glands is called sialedinitis.
 It may be due to bacterial/ viral infections or autoimmune
reaction.
 Bacterial infections can act as a nidus for stone formation,
resulting in duct obstruction.
 Tumors:
 the most common tumor of the salivary gland is the mixed
tumor or the pleomorphic adenoma.
 The adenoid cystic carcinoma is a malignant tumor of the
salivary glands that involves the parotid gland, and commonly
extends and infiltrates into the facial nerve leading to
paralysis.
 Esophagus
 Congenital conditions like
 Atresia (failure to canalize/ absence of the lumen)

 Diverticula (formation of outpouchings in the wall)

 Tracheoesophageal fistula (fistula-abnormal connections between

two hollow organs) may be seen.

 Hiatus hernia is the presence of a part of the stomach above the
diaphragmatic orifice. It may be due to
 a congenital shortening of the esophagus, or

 in aged patients due to increased abdominal pressure coupled with a

decreased diaphragmatic muscle tone.

 Achalasia is a condition when the contractility of the lower esophagus is
lost and failure of relaxation of the sphincter. It may be due to
 destruction or degeneration of the myentric plexus as in neurotropic

infection like Chaga’s disease or

 due a congenital absence of the ganglion cells of the myentric plexus.
Esophageal atresia

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,

 severe stress as in burns/trauma/surgery (Curling’s ulcers),

 irradiation,

 ingestion of acids/ alkali,

 systemic infection and

 ischemia and shock.

 Depending on the severity there may be lesions ranging from

 vasodilatation and edema to

 erosions and hemorrhage. Erosion is a partial loss of mucosa whereas an

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)

 Clinically the patient presents with a burning pain, which is

worse at night and 1-3 hours after meals, nausea, vomiting,
bloating, belching, and weight loss.

 Complications of the ulcers include hemorrhage, anemia,

extension and perforation of the ulcers, and obstruction due to
healing by fibrosis.
 Intestines
Congenital abnormalities include atresia, stenosis, diverticula and
Hirschsprung’s disease (absence of ganglion cells in the large
intestine (rectum and sigmoid colon).

Malabsorption: The sub optimal absorption of nutrients

(carbohydrates, proteins, fats, vitamins, electrolytes and
minerals) and water. It is classified as due to
 Defective digestion: due to deficiency of enzymes
 Mucosal cell abnormalities: results in defective terminal
digestion and/or defective transport of the nutrients
 Reduced small intestinal surface area: Celiac sprue or
Iatrogenic: post surgical resection
 Lymphatic obstruction: due to lymphoma or tuberculosis:
resulting in deficient fat absorbtion
 Infections: tropical sprue, parasites, and Whipple’s disease.
 The clinical consequences of
malabsorption syndromes
• Alimentary tract: diarrhea, pain, weight loss, passage of bulky,
greasy stools
• Hematopoietic system: causes anemia, bleeding
• Musculoskeletal system: osteopenia and tetany (hypocalcemia)
• Endocrines: amenorrhea, impotence, infertility and
hyperparathyroidism
• Skin: purpura, petechia, edema, dermatitis
• Nervous system: peripheral neuropathy
 Idiopathic inflammatory bowel disease

It includes Crohn’s disease and ulcerative colitis

Crohn’s disease is a granulomatous disease affecting any portion of
the gut but most often the small intestine and colon.
Ulcerative colitis is a non-granulomatous inflammatory disorder
involving the colon.

Both the diseases are unexplained (idiopathic) but some

etiological factors are implicated like:
Genetic (familial clustering is noted), infectious agent may be the
cause (as there is inflammation), or abnormal host
immunoreactivity.
 Feature Crohn’s disease Ulcerative colitis

Site Throughout the GIT The colon starting from the

rectum
Distribution Skip lesion Continuous lesion

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

Ulcers Deep and linear Superficial

Fistulas Present Absent

Pseudopolyps Absent Present

Granulomas Present Absent

Extra intestinal Arthritis, Ankylosing Occur but to a lesser extent

manifestations spondylitis Uveitis,
Cholangitis and Erythema
nodosum
Malignant potential & Definite risk Present but rarer
Prognosis Poor prognosis Good prognosis
Fat & vitamin malabsorption Present Absent