GI - med path test 2
Gastrointestinal Introduction
Description of the gastrointestinal tract (GIT)
A continuous hollow tube extending from the mouth to the anus
Accessory organs contributing to digestion and metabolic processes
FUNCTIONS
Digestion: Mechanical and chemical breakdown of food into absorbable molecules.
Absorption: Uptake of nutrients (carbohydrates, proteins, fats, vitamins, and minerals) into the bloodstream or lymph.
Motility: Coordinated muscular contractions (peristalsis and segmentation) propel and mix contents along the tract.
Secretion: Release of enzymes, acids, bile, and mucus to aid digestion and protect the mucosa.
Excretion: Elimination of undigested material and waste products.
ANATOMY BASICS
Composition of the GIT:
A tubular structure balancing digestion and absorption while maintaining a critical barrier against pathogens.
Distinct layers with specific roles:
Mucosa:
Epithelium: innermost layer for absorption and secretion, adapted to different GI segment functions.
Lamina Propria: connective tissue layer with blood vessels, lymphatics, and immune cells.
Muscularis Mucosae: thin smooth muscle layer managing mucosal movements.
Submucosa:
Dense connective tissue supporting the mucosa, containing blood vessels, lymphatics, and submucosal plexus (part of the enteric nervous system) for local neural control.
Muscularis Externa:
Two main layers of smooth muscle:
Inner Circular Layer: constricts the lumen.
Outer Longitudinal Layer: shortens GIT length.
Contains the myenteric plexus (Auerbach’s plexus) for motor control.
Serosa / Adventitia:
Serosa: mesothelium covered layer for intraperitoneal organs.
Adventitia: fibrous connective tissue for retroperitoneal organs anchoring them to surrounding structures.
CELLS IN THE GIT
Enterocytes:
Located in the small intestines (specifically jejunum), responsible for nutrient absorption.
Surrounded by microvilli (brush border) to increase absorption surface area.
Damage to brush border leads to malabsorption (e.g., in celiac disease).
Goblet Cells:
Present predominantly in colonic epithelium.
Responsible for secreting mucus to protect the mucosal lining, crucial in acidic environments.
A decrease in goblet cells can lead to increased inflammation and injury.
Enteroendocrine Cells:
Scattered in the epithelium, secrete hormones like gastrin, cholecystokinin (CCK), and secretin to regulate digestion and motility affecting acid, bile, and enzymes.
Paneth Cells:
Reside in the crypts of the small intestine secreting antimicrobial peptides and enzymes for protection against pathogens (innate immune defense).
Stem Cells:
Found at the base of intestinal crypts, renew endothelial lining, replacing enterocytes and goblet cells rapidly (vulnerable to chemo or radiation).
NEURAL + HORMONAL REGULATION BASICS
Mechanisms ensuring efficient absorption, digestion, and homeostasis.
NEURAL REGULATION
The GIT is referred to as the “second brain” due to its autonomous extensive neural network, the enteric nervous system (ENS).
ENS:
Located within the GIT walls with two major plexuses:
Myenteric Plexus: controls motility between muscular layers.
Submucosal Plexus (Meissner’s plexus): located in the submucosa; regulates secretion and local blood flow.
Capable of independent operations but influenced by the central nervous system (CNS).
Autonomic Nervous System (ANS):
Modulates the ENS affecting GI functions.
Parasympathetic: stimulates motility and secretion (rest-digest response), primarily via the vagus nerve and pelvic nerves.
Sympathetic: inhibits motility and secretion, redirecting blood from the GIT during stress (flight or fight).
BRAIN-GUT AXIS
Communication between the CNS and ENS involving neural, hormonal, and immunological pathways.
Impacts GI function, appetite regulation, and stress/emotional responses.
HORMONAL REGULATION
GI hormones secreted by enteroendocrine cells in response to nutrients and neural signals, modulating digestion and motility.
Gastrin:
Released by G cells in the stomach upon food arrival (triggered by protein/stomach stretching/vagal stimulation).
Stimulates acid secretion, preparing the stomach for digestion. Inhibits itself when pH drops sufficiently (negative feedback).
Secretin:
Released from S cells in the duodenum upon arrival of acid, stimulating bicarbonate (HCO3-) secretion to neutralize acid and protect the intestinal lining.
Cholecystokinin (CCK):
Released by I cells in the duodenum in response to fat and protein. Stimulates bile release from the gallbladder and pancreatic enzyme release, slowing gastric emptying to give time for fat/protein digestion.
Motilin:
Released by M cells during fasting, triggering migrating motor complex (MMC) for house-keeping contractions to clear undigested debris, bacteria, and leftover food.
Ghrelin:
Released by oxyntic (X/A) cells in the stomach when empty, signaling hunger to the hypothalamus and stimulating growth hormone release from the pituitary gland.
MOTILITY BASICS
Refers to coordinated contraction and relaxation of smooth muscles in the GIT for propulsion and mixing of contents.
Peristalsis:
Sequential, wave-like contractions propelling food from the esophagus to intestines.
Segmentation:
Alternating contractions in the small intestine enhancing mixing of bowel contents with digestive enzymes.
Migrating Motor Complex (MMC):
Cyclic wave-like contraction occurring during fasting every 90-120 mins, responsible for cleaning undigested materials from the intestines. Consists of:
Phase I: Quiescent period with minimal contractions.
Phase II: Intermittent contractions indicating activity increase.
Phase III: Intense rhythmic contractions (the housekeeping wave) pushing debris down and out of intestines.
Clinical note: Constant eating can inhibit MMC, causing bacterial overgrowth and bloating.
MOTILITY PHASES
Phase 1 – Filling:
Upon food arrival, the orad region relaxes (receptive relaxation), and the lower esophageal sphincter (LES) opens to let food into the stomach.
Phase 2 – Mixing:
Stomach muscles mix food with gastric acid and digestive enzymes, creating chyme. Retropulsion enhances mixing by forcing chyme back into the stomach for thorough mixing.
Phase 3 – Emptying:
Intense contractions push chyme through the pyloric sphincter into the duodenum. Gastric emptying is regulated by hormones (CCK, leptin, glucagon, insulin) and by the nutritional content of the food (fat/protein, acidity).
SECRETIONS
Gastric Acid (HCl):
Secreted by parietal cells in the stomach; it converts pepsinogen to pepsin and denatures proteins for easier enzyme digestion.
Mucus:
Produced by goblet cells; coats the stomach lining to prevent self-digestion by acid and enzymes.
Bile:
Synthesized by the liver, stored in the gallbladder, and released into the duodenum for fat emulsification.
Pancreatic Enzymes:
Amylase for carbohydrates, lipase for fats, proteases (like trypsin) for proteins released in response to CCK.
Bicarbonate:
Neutralizes gastric acid entering the duodenum, allowing enzymes to function properly and maintaining the intestinal pH.
PH REGULATION
pH Levels:
Saliva → 6.5
Gastric Juice → 1.5
Bile, Pancreatic juices, Membrane enzymes → 7-8
SECRETIONS IN THE STOMACH
Phases of Gastric Secretion:
Phase 1 – Cephalic Phase: Occurs before food reaches the stomach, triggered by sight, smell, thought, leading to vagus nerve stimulation.
Phase 2 – Gastric Phase: Initiated once food is in the stomach; local reflexes, vagal stimulation, and gastrin-release increase acid secretions.
Phase 3 – Intestinal Phase: Chyme enters the small intestine, modulating gastric secretions to prevent overload of the intestinal tract.
DIGESTION & ABSORPTION
CARBOHYDRATES
Digestion involves:
First breaking down complex carbohydrates into disaccharides via amylase (saliva + pancreas).
Brush border enzymes in the small intestine further break down disaccharides into monosaccharides for absorption.
Absorption: Via SGLT-1, a co-transporter bringing glucose and sodium into enterocytes (intestinal cells).
PROTEINS
Digestion begins with pepsin in the stomach, followed by pancreatic proteases in the small intestine, reducing proteins to amino acids and small peptides.
Absorption: Occurs in the small intestine via specific transporters.
LIPIDS
Emulsification of fats is achieved in two steps:
Emulsification: Bile salts wrap around fat globules, increasing surface area for enzyme access.
Micelle Formation: Fatty acids packaged into micelles for transport through the intestinal wall to enterocytes where they are reassembled into triglycerides and released into the lymphatic system.
MICRONUTRIENTS
Fat-soluble Vitamins (A, D, E, K): Absorbed along with lipids; malabsorption leads to deficiencies.
Water-soluble Vitamins (e.g., B12): Require intrinsic factor produced by parietal cells for terminal ileum absorption.
Iron & Calcium: Absorbed in the duodenum and small intestine, regulated by Vitamin D.
IMMUNE FUNCTION IN GIT BASICS
Balancing immune tolerance to microbiota while defending against pathogens is crucial to prevent conditions like food allergies and inflammatory bowel diseases (IBD).
GALT (Gut-Associated Lymphoid Tissue): Includes Peyer's patches and mesenteric lymph nodes, with IgA antibodies neutralizing pathogens.
MALT (Mucosal-Associated Lymphoid Tissue): Mucosal immune tissues spread across the gut, lungs, mouth, and urinary tract.
Barrier Function: Tight junctions in epithelial cells prevent permeability and regulate flow to prevent infection.