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.