GASTRO INTESTINAL
DISORDERS
PREPARED BY MR. ABHIJIT DAS
GASTRO OESOPHAGEAL REFLUX DISEASE
DEFINITION
GERD is when stomach acid flows back into the
esophagus due to a weak
lower esophageal sphincter (LES).
ETIOPATHOGENESIS
1. Weak lower
esophageal sphincter (LES).
2. Delayed stomach emptying.
3.
Obesity
4. Pregnancy (increased abdominal pressure).
5.
Smoking and alcohol.
CLINICAL
MANIFESTATIONS
1. Heartburn and chest pain.
2. sour or bitter taste.
3. Difficulty swallowing (dysphagia).
4. Chronic cough
5. laryngitis.
NON-PHARMACOLOGICAL
MANAGEMENT
1. Avoid trigger foods (spicy, fatty, caffeine, alcohol).
2. Eat smaller meals and maintain a healthy weight.
3. Avoid lying down after meals for at least 3 hours.
4. Quit smoking
5. Avoid tight clothing around the waist.
PHARMACOLOGICAL
MANAGEMENT
1. Proton pump inhibitors (PPIs): Reduce acid (e.g., omeprazole).
2. H2 blockers:
Decrease acid production (e.g., ranitidine).
3. Antacids:
Neutralize stomach acid (e.g., calcium carbonate).
4. Prokinetic agents: Strengthen LES and aid stomach emptying (e.g., metoclopramide).
PEPTIC ULCER
DEFINITION
Peptic ulcer is a sore in
the lining of the stomach, duodenum, or esophagus caused by stomach acid.
ETIOPATHOGENESIS
1. H. pylori infection: Major cause of gastric and duodenal ulcers.
2. NSAIDs:
Damage the stomach lining.
3. Acid and pepsin:
Damage the mucosal wall.
4. Smoking:
increases acid.
5. Alcohol:
Causes mucosal damage and acid secretion.
CLINICAL
MANIFESTATIONS
1. Burning pain in the upper abdomen (epigastric pain).
2. Nausea, vomiting, and loss of appetite.
3. Bleeding (vomiting blood).
4. Anemia from chronic blood loss.
NON-PHARMACOLOGICAL
MANAGEMENT
1. Avoid spicy, fatty, and acidic foods.
2. Quit smoking and manage stress.
3. Eat smaller, frequent meals.
4. Limit NSAIDs
5. Maintain a healthy weight.
PHARMACOLOGICAL MANAGEMENT
1. PPIs:
Reduce acid (e.g., omeprazole).
2. H2 blockers:
Lower acid (e.g., ranitidine).
3. Antacids:
Neutralize acid (e.g., calcium carbonate).
4. Antibiotics:
Eradicate H. pylori (e.g., amoxicillin).
5. Cytoprotective agents: Protect stomach lining (e.g., sucralfate).
ALCOHOLIC LIVER DISEASE
DEFINITION
ALD is liver damage caused by prolonged excessive alcohol
use, ranging from fatty liver to hepatitis.
ETIOPATHOGENESIS
1. Alcohol metabolism: Produces toxic byproducts like acetaldehyde, damaging liver cells.
2. Oxidative stress: Alcohol generates harmful reactive oxygen species (ROS).
3. Inflammation:
Cell damage triggers liver inflammation.
4. Genetics:
Certain genes increase susceptibility to ALD.
CLINICAL
MANIFESTATIONS
1. Fatigue, weakness, and weight loss.
2. Abdominal pain, nausea, and jaundice.
3. Swelling in legs.
NON-PHARMACOLOGICAL
MANAGEMENT
1. Quit Alcohol:
Stop drinking.
2. Nutrition:
Eat a protein-rich, balanced diet to prevent malnutrition.
3. Weight management: Lose excess weight through diet and exercise.
4. Hepatitis prevention: Vaccinate against hepatitis.
PHARMACOLOGICAL
MANAGEMENT
1. Corticosteroids:
Reduce liver inflammation (e.g., prednisolone).
2. Pentoxifylline:
reduces inflammation.
3. N-acetylcysteine: Reduces oxidative stress.
CROHN’S DISEASE
DEFINITION
Crohn's disease is a chronic inflammatory bowel disease (IBD)
affecting any part of the gastrointestinal tract, most commonly the small
intestine and colon.
ETIOPATHOGENESIS
1. Genetics:
Family history and specific genes increase risk.
2. Abnormal immunity: Immune system mistakenly attacks gut bacteria or food, causing
inflammation.
3. Environmental triggers: Smoking, infections, and diet may exacerbate
symptoms.
CLINICAL
MANIFESTATIONS
1. Abdominal pain (often in the lower right side).
2. Chronic diarrhea with mucus, blood, or pus.
3. Weight loss and malnutrition.
4. Fatigue and anemia.
5. Intestinal obstruction causing severe pain and
vomiting.
NON-PHARMACOLOGICAL
MANAGEMENT
1. Dietary changes:
Avoid trigger foods (spicy, fatty, alcohol, high-fiber).
2. Stress reduction: Use relaxation techniques like yoga or meditation.
3. Exercise:
Improves overall health and symptoms.
4. Quit smoking:
Reduces disease severity and complications.
5. Stay hydrated:
Prevents dehydration from diarrhea.
PHARMACOLOGICAL
MANAGEMENT
1. Aminosalicylates: Reduce inflammation (e.g., mesalamine).
2. Corticosteroids:
Treat inflammation (e.g., prednisone).
3. Immunomodulators: Suppress immune response (e.g., azathioprine).
4. Biologics:
Target specific immune proteins (e.g., infliximab).
5. JAK inhibitors:
Block enzymes causing inflammation (e.g., tofacitinib).
ULCERATIVE COLITIS
DEFINITION
A chronic inflammatory bowel
disease causing inflammation and ulcers in the colon and
rectum.
ETIOPATHOGENESIS
1. Genetics:
Inherited factors increase risk.
2. Immune dysfunction: Immune system attacks the colon lining.
3. Environmental triggers: Stress, diet, infections may worsen symptoms.
4. Microbiome changes: Imbalance in gut bacteria may contribute.
CLINICAL
MANIFESTATIONS
1. Abdominal pain, cramping.
2. Diarrhea, sometimes with blood.
3. Rectal bleeding.
4. Urgent need for bowel movements.
5. Fatigue, weight loss, anemia.
NON-PHARMACOLOGICAL
MANAGEMENT
1. Balanced diet, avoid trigger foods.
2. Stress management (yoga, meditation).
3. Regular exercise.
4. Adequate rest and sleep.
5. Probiotics for gut health.
PHARMACOLOGICAL
MANAGEMENT
1. Aminosalicylates: Reduce colon inflammation.
2. Corticosteroids:
Control severe inflammation.
3. Immunosuppressants: Lower immune overactivity.
4. Biologics:
Target inflammation-causing proteins.
5. Antibiotics:
Manage infections.
6. Anti-diarrheals:
Relieve symptoms like diarrhea.