Gastrointestinal Pathophysiology

Gastrointestinal Pathophysiology

Structure:

The gastrointestinal tract is composed of 4 layers:

• Mucosa: The innermost layer, responsible for nutrient absorption and secreting mucus to protect the mucosa.

• Submucosa: Contains a network of capillaries that nourish the mucosa and transport substances.

• Smooth muscle: Responsible for mixing and moving food.

• Serosa: The outermost layer, reduces friction and prevents adhesion.

Function:

• Contraction: Moves food along the gastrointestinal tract.

• Secretion: Secretes enzymes, acids, and mucus to help digest food.

• Absorption: Absorbs nutrients into the bloodstream.

• Excretion: Eliminates waste.

Secretion:

• Gastric glands: Secrete mucus, acid, intrinsic factor, pepsinogen, and histamine.

• Pyloric glands: Secrete gastrin, somatostatin, histamine, and mucus.

• Regulation of gastric juice secretion: Controlled by the nervous and endocrine systems.

Gastric pathology:

• Disorders of secretion:

• Gastric ulcers: Due to an imbalance between aggressive factors (acid, pepsinogen) and protective factors (mucus, HCO3-, mucosal regeneration).

• Achlorhydria: Decreased gastric acid secretion.

• Disorders of motility: Affects food mixing and movement.

Histology:

• Fundic mucosa: Primarily exocrine glands.

• Pyloric mucosa: Primarily endocrine glands.

• Terminal vagus nerve: Contains two nerve networks:

• Meissner’s plexus: Located in the submucosa, controls secretion.

• Auerbach’s plexus: Located in the muscle layer, controls contraction.

Cells involved in secretion:

• Mucous cells: Secrete mucus to protect the mucosa.

• Parietal cells: Secrete HCl acid and intrinsic factor.

• Chief cells: Secrete pepsinogen.

• Stem cells: Replace damaged cells.

• ECL cells: Secrete histamine, which stimulates acid secretion and gastric smooth muscle contraction.

• D cells: Secrete somatostatin, which inhibits HCl secretion.

• G cells: Secrete gastrin.

Regulation of acid secretion:

• Parietal cells: The only cells that produce HCl acid.

• Vagus nerve: Stimulates the secretion of acetylcholine, gastrin, somatostatin, and histamine.

Stimulators of secretion: Acetylcholine, gastrin, histamine.

Inhibitors of secretion: Somatostatin.

Regulation of gastric secretion by the nervous system:

• Unconditioned reflex: Food in the mouth stimulates the vagus nerve.

• Conditioned reflex: The smell of food stimulates secretion due to the signal of food appearing in the brain.

Secretion during a meal:

• Early phase: By nervous mechanisms.

• Late phase: By humoral mechanisms.

Secretion during fasting:

• Basal secretion: Secretion outside of meals.

Gastric juice secretion tests:

• Basal acid output (BAO): Measures the amount of acid secreted without stimulation.

• Peak acid output (PAO, MAO): Using gastrin or GRP.

• BAO/PAO ratio: Used for diagnosis and prediction of acid secretion status.

• Blood pepsinogen levels: Reflects gastric juice secretion.

• Blood gastrin levels: Induces strong acid secretion.

Pathology of peptic ulcers:

• Imbalance between aggressive and protective factors:

• Aggressive factors: Acid, pepsinogen.

• Protective factors: Mucus, HCO3-, mucosal regeneration.

Pylorus is prone to ulcers because:

• The amount of food passing through is less, but acid is abundant.

• H.P. virus often exists in the pyloric region.

• The alkaline environment of the proximal duodenum cannot tolerate gastric acid.

Zollinger-Ellison syndrome:

• Occurs after surgery: Reduced protective factors, increased aggressive factors, especially acid.

Protective factors:

• Mucus: Protects the mucosa from acid.

• Mucosal epithelial cells: Rapid regeneration when damaged.

• Rich blood supply: Removes H+ from the mucosa.

• Prostaglandins: Amplify and coordinate protective factors.

Aggressive factor Pepsinogen:

• Causes ulcers but is dependent on acid.

• Helps acid amplify and reach the epithelium.

• Works with acid to damage ulcers when the mucus layer is broken.

Aggressive factor HCl:

• The strongest, penetrates deep into the mucosal layer.

Risk factors for ulcers:

• Blood group O: More prone to ulcers than blood group A.

• Susceptible genes: HLA genes.

• Habits: Spicy food, alcohol, coffee.

NSAIDs and Corticosteroids:

• NSAIDs (non-steroidal anti-inflammatory drugs): A leading risk factor for ulcers.

• Mechanism: Penetrates the mucus layer, releases acid causing inflammation and ulcers.

Risk factors for NSAIDs:

• Previous history of ulcers.

• Concurrent use with corticosteroids.

• High dose.

• Combined use of multiple NSAIDs.

• Concurrent use with anticoagulants.

• Patients with severe systemic disease.

Gastritis due to H.P.:

• Mechanism: H.P. secretes urease to produce ammonia and CO2, damaging the mucosa.

• Transmission: Through the digestive tract.

Identifying H.P.:

• Endoscopy, tissue biopsy: Detects bacteria in tissue.

• Breath test: Drink a carbon isotope tablet, detect H.P. through exhaled CO2.

Causes of decreased acid secretion – achlorhydria:

• Hypoacidity: BAO significantly decreased.

• Achlorhydria: Only reaches 10% of maximal stimulation with gastrin.

• Causes:

• Extra-gastric: Dehydration, malnutrition, psychological stress.

• Gastric: Acute gastritis, chronic gastritis, cancer, pernicious anemia.

Disorders of motility:

• Tone: Gastric capacity changes in response to food volume.

• Peristalsis: Moves food along the stomach.

• Controlling factors: Vagus nerve, histamine.

Functional bowel pathophysiology:

• Disorders of secretion:

• Bile: Decreased fat absorption, deficiency of vitamins A, D, E, K.

• Pancreas: Causes digestive disorders, malnutrition.

• Disorders of motility: Causes diarrhea, constipation, irritable bowel syndrome (IBS).

Disorders of bile secretion:

• Causes: Liver insufficiency, bile duct obstruction, duodenal disease.

Disorders of pancreatic secretion:

• Causes: Stones, worms blocking the Vater ampulla.

• Pancreatic insufficiency: Causes digestive disorders, malnutrition.

Pancreatitis:

• Symptoms: Pain in the upper abdomen behind the back.

• Treatment: Supplementation of nutrition via intravenous route.

Pathology related to motility:

• Increased contraction: Diarrhea, watery stools, IBS.

• Decreased contraction: Constipation.

Diarrhea syndrome:

• Stools contain a lot of water.

• Acute/chronic diarrhea:

• Causes: Enteritis, toxins, allergies, enzyme deficiency, intestinal tumors, peritonitis, appendicitis.

• Mechanism:

• Increased secretion: Watery stools.

• Increased motility: Food moves quickly, not fully digested.

Intestinal obstruction syndrome:

• Causes: Mechanical obstruction (stricture, volvulus, intussusception, hernia, worm infestation) and functional obstruction (intestinal paralysis, sympathetic hyperactivity).

• Progress: Cramps, flatulence, intestinal paralysis, shock.

• Consequences: Dehydration, acidosis, poisoning.

Constipation:

• Difficulty or inability to defecate: Due to hard stools.

• Mechanism: Mechanical obstruction, decreased colonic tone, habit of withholding defecation, diet.

• Consequences: Hemorrhoids, infection, rectal prolapse, anal fissures.

Malabsorption in the intestines – maldigestion:

• Requires good motility and secretion for nutrient absorption.

• Conditions for absorption: Food exists in an absorbable form, intestinal mucosa is intact, good blood supply, good general condition.

• Malabsorption syndrome: Maldigestion.

Etiology – pathogenesis of malabsorption:

• Gastrointestinal causes: Enteritis, enzyme deficiency, gastric, liver, and pancreatic diseases.

• Extra-intestinal causes: Gastrointestinal diseases, endocrine diseases.

Consequences of decreased absorption:

• Malnutrition, vitamin deficiency, micronutrient deficiency.