GIT Diseases – I

Hope this article is going to clear your concept about diseases of gastrointestinal tract.

Let’s start up with congenital abnormalities.

• Omphalocele- This happens when abdominal musculature is incomplete and the viscera herniate into ventral membranous sac.
  Imp note– 40% cases are related to birth defects.

• Mackel Diverticulum- We very well know that true diverticulum is a blind pouch leading off the alimentary tract and is lined by mucosa including all the layers of the bowel wall, mucosa, submucosa,muscularis.
  Imp note– Mackel Diverticula most commonly result from persistence of the vitelline duct.

• Tracheoesophageal Fistula(TOF)– It is an abnormal connection between the esophagus and trachea.

It is due to failed fusion of tracheoesophageal ridges after fourth week of embryological development.

 Imp note– In new born if you find symptoms like copious salivation associated with choking, coughing and cyanosis co incident with onset of feeding there may be chances of TOF .

• Congenital Hypertrophic Pyloric Stenosis.- Occurrence 1 in 500 births.

Complex polygenic inheritance pattern.May have association with Turner Syndrome and Trisomy 18.

Symptoms– Regurgitation, projectile vomiting within 3 weeks of birth, externally visible peristalsis and a palpable firm ovoid mass.

• Hirschsprung Disease – Also known as congenital aganglionic megacolon .

Results from arrested migration of neural crest cells into the gut resulting in formation of aganglionic segment lacking peristaltic contractions.

Imp note– Affected intestinal segment lack Meissner and Auerbach plexuses.

Present with neonatal failure to pass meconium or abdin distension with severely distended megacolon.

Diagnosis is confirmed by rectal biopsy.

Diseases of Esophagus/Oesophagus

Diverticula–  contain one or more wall layers.

It can accumulate food to present as a mass with food Regurgitation

Mucosal webs- These are protrusions of fibrovascular tissue and overlying epithelium.

Most common site is – upper Esophagus.

Esophageal Rings–  are similar to webs but are circumferential and thicker include mucosa, submucosa and occasionally hypertrophic muscularis propria.

Achlasia- Increase in lower esophageal tone (mainly due to cholinergic signaling) , esophageal aperistalsis, Incomplete relaxation of Lower esophageal signaling.

Boerhaave Syndrome– Rupture by all esophageal layers and associated with spillage of contents into the mediastinum .

Barrett Esophagus– Complication of chronic GERD. Characterized by intestinal metaplasia.There is change of squamous epithelium by intestinal columnar cell.

Diseases of Stomach

Lesion of stomach can be divided into

• Gastritis
• Gastropathies

Gastritis

• As suggested from one study in India gastritis affects 25-33% of the total population . People aged between 15-50 years are more at risk .
• Gastritis may be defined as inflammation of gastric mucosa .
• Morphology- Moderate edema and hyperemia occassionally with hemorrhage.
• Stress Gastritis- Occurs in patients with severe trauma, extensive burns, intracranial disease and major surgery.
• Characterized by multiple small erosions in entire stomach and most commonly present at fundus of stomach.

 Types of Gastritis

Acute Gastritis– cause by drugs like NSAIDS, heavy smoking, excessive alcohol intake, highly spiced food and severe stress.

Chronic Gastritis-

• H.pylori related ( Type B ) Mainly antral mucosa is affected.
• Autoimmune type ( Type A )- Mainly body- fundic mucosa is affected.
• Reflux Gastritis- Predominant in antral body region

   Acute Gastritis

• Defined as acute inflammation of the gastric mucosa

Pathogenesis-

• Gastropathy, acute gastritis, and chronic gastritis can occur when gastric mucosa protective mechanism is defective.
• Stress related gastric mucosal injury is most commonly due to local ischemia.
• Increased formation of inducible NO synthase and increased release of endothelin-1 contribute to ischemic gastric mucosal injury.
• Increase in gastric acid secretion due to brain injury .
• Systemic acidosis , hypoxia, and reduced splanchnic blood flow are contributory factors that may cause ulcers.

Clinical Features

Most critically ill patients will have some evidence of gastric mucosal injury.

After removal of the injurious factors, healing with complete re- epithelialization is the norm.

Chronic Gastritis

• Characterized by ongoing mucosal inflammation with mucosal atrophy.
• Symptoms are less severe but more persistent .
• TypeB gastritis mainly related to H.pylori .
• Autoimmune related Type gastritis is the second most common cause after H.pylori infection.

Pathogenesis

H.pylori commonly cause antral gastritis.

It’s features are increased acid production and disrupting the normal mucosal protection mechanism.

Virulence factors include-

• Motility via flagella.
• Urease production buffering gastric acid.
• Adhesins that enhance bacterial adherence to surface foveolar cells.
• Toxins

Clinical features

H.pylori can be diagnosed by :-

• AST(Antibody serologic test).
• Urea breath test .
• Bacterial culture.
• Serology(ELISA) is the best non-invasive investigation is to diagnose the presence of H.pylori.
• Rapid urease test is the best invasive investigation to diagnose the presence of H.pylori.

Imp Note:- H.pylori infection is a risk factor for-

• Peptic Ulcer disease.
• Gastric Adenocarcinoma.
• Gastric Lymphoma.

Autoimmune related Type A Gastritis:-

• It will affect body and fundus predominantly.
• Etiology is autoimmune and usually associated with hypergastrinemia.

    Clinical features

• Gastric atrophy progression occurs over 20-30 years.
• Symptoms of Anaemia may be found.
• Vitamin B 12 deficiency may also be found.
• Autoimmune Gastritis is associated with other autoimmune disease such as Hashimoto thyroiditis ,Type1 Diabetes and Addison disease.

Complication of Chronic Gastritis

PUD( Peptic Ulcer Disease)- It is a chronic mucosal ulceration affecting duodenum or stomach.

Almost all peptic ulcers are mainly associated with H.pylori infection, NSAIDS or cigarette smoking.

Common sites of PUD

• Duodenal peptic ulcers are most commonly located within first 2.5 cm of duodenum.
• Gastric peptic ulcers are most commonly located along the lesser curvature.

Pathogenesis

• Caused due to imbalances in mucosal damage and defenses.
• Hyperacidity in PUD can be caused by infection, parietal cell hyperplasia and increased gastrin production.
• Cigarette smoking impairs mucosal blood flow and healing.

Imp Note– Blood group O is most prone for PUD.

Blood group A is more prone for stomach carcinoma.

Clinical Features

• Classic symptoms include epigastric gnawing, burning, or aching pain, worse at night and 1-3 hours after meals.
• Nausea, vomiting, bloating, belching and weight loss can also occur.
• Most common complication of PUD is- Perforation in case of “Gastric ulcers”.
• Bleeding in case of “Duodenal ulcers”.
• Bleeding is seen due to – Erosion of gastroduodenal arteries in case of duodenal ulcers.
• Erosion of Left Gastric Artery in case of Gastric ulcers.

Imp note– Most common cause of death in peptic ulcer is due to bleeding.

Hypertrophic Gastropathies

• Giant enlargement of gastric regal folds due to epithelial hyperplasia.
• It is due to excessive growth factor production.

Menetrier’s Disease-

• Mostly males are affected between 40-60 years of age.
• It is due to overexpression of transforming growth factor-alpha.
• Characterized by giant cerebriform rugal folds.
• Diffuse foveolar cell hyperplasia associated with a protein losing enteropathy causing systemic hypoproteinemia.

Zollinger- ellison Syndrome

• Cause by gastrin secreting tumors in the small bowel or pancreas
• Present with multiple duodenal ulcers and chronic diarrhoea.
• 60-90% of gastronemias are malignant.
• Elevated gastrin levels are seen.

Imp note– mortality of PUD- Perforated PUD is a serious condition with an overall reported mortality of 5%-25% rising to as high as 50% with age.

Contributor- Medico Rohan Barnwal