Esophagus: 3-second delay at the entrance to the stomach; cardiac sphincter is important for GERD.
Stomach: Fundus, body, pyloric portion with the pyloric sphincter.
Pyloric sphincter: Marks the boundary between stomach and duodenum.
Duodenum: Shortest segment of the small intestine but most important.
Linked with pancreas and gallbladder/liver.
Receives bile from the liver/gallbladder and pancreatic juice from the pancreas.
Pancreatic duct merges with the bile duct.
Sphincter of Oddi: Controls the release of pancreatic juice and bile.
Jejunum and Ileum.
Ileocecal valve: Boundary between small and large intestine.
Cecum: Blind spot at the beginning of the ascending colon, leads to the appendix.
Colon: Ascending, transverse, descending, pelvic or sigmoid colon.
Rectum: Follows the sigmoid colon.
Anal canal and anus: Last segment of the rectum.
Peritoneal Position
Small intestine (except duodenum) is intraperitoneal.
Colon: Some segments are intraperitoneal (transverse, sigmoid), others are retroperitoneal.
Motility of the GI Tract
Coordinated contraction of smooth muscle to remove luminal contents.
Resting membrane potential.
Smooth muscle cells are fusiform and lack striations (no sarcomere).
Actin and myosin filaments facilitate contraction.
Neighboring cells contract or dilate simultaneously due to electrical signals passing through the cells.
Sphincters
Tonic contractions: Sphincters are usually in contraction.
Pyloric sphincter: Controls movement of processed food from stomach to duodenum.
Ileocecal valve and anal canal sphincter: Operate similarly.
Abnormal relaxation of sphincters leads to diarrhea or incontinence.
Ionic Constituents of Fluid
Sodium, potassium, chloride, and bicarbonate levels vary throughout the intestines.
Significant changes between the stomach/duodenum and the small/large intestine.
Absorption
Transcellular (through cells) and paracellular (between cells) routes.
Intestinal epithelium: Simple epithelium (one layer) with crowded cells.
Passive vs. active transport: Differ based on ATP requirement.
Diffusion: Passive transport.
Channels: Proteins in plasma membrane for polar molecule transport.
Facilitated diffusion: Requires protein transporters.
Active transport: Requires ATP (e.g., sodium-potassium ATPase).
Secondary active transport: Dependent on primary active transport.
Defense Mechanisms of the GI Tract
Exposed surface: Requires defense against acid and infection.
Defense from Acid
Mucus: Prevents direct contact of acid with epithelium.
Bicarbonate: Neutralizes acid (made by Brunner glands in duodenum).
Prostaglandins: Influence hydrochloric acid production (cyclooxygenase 1 and 2).
Tight junctions: Prevent epithelial breach.
Bicarbonate from pancreas: Neutralizes acid.
Defense from Infection
Immune system.
Secretory immune system (MALT: mucosa-associated lymphoid tissue).
Epithelial replication: Replaces dead or damaged cells rapidly.
Normal colonic microbiota: Group of microorganisms/bacteria in the GI tract.
Stomach acid: Kills organisms.
Immune Defense Details
Aggregates of lymphoid cells (Peyer's patches in distal small intestine).
Innate defense: Cells making hydrochloric acid.
Goblet cells: Make mucus.
Paneth cells: Offer defense against microorganisms.
Lymphocytes (B and T cells), plasma cells, macrophages, mast cells, and eosinophils present.
Villi/vilus enhance the absorption area.
Peyer's patches: Lymphocyte collection that picks up information and activates the system in the lymph node to make specialized plasma cells, that are able to go to other organs for surveillance.
Stratified squamous epithelium (skin) vs. esophagus:
Skin is keratinized, esophagus is not (keratin in esophagus indicates cancer).
Skin has dermis, esophagus does not.
Dermis contains sebaceous and pseudoepherous glands (not in esophagus).
Lamina propria: mast cells, eosinophils.
Muscularis mucosa is and muscularis propria are different layers.
Eosinophilic Esophagitis
Eosinophilic esophagitis: Inflammatory reaction with many eosinophils.
Diagnosis: Typical esophageal symptoms and esophageal mucosal biopsies.
Alternative etiologies of esophageal eosinophilia include GERD, drug hypersensitivity, connective tissue disorders, hyper eosinophilic syndrome, Crohn's disease, and infection.
Some populations are more prone to this reaction that others (antigen sensitization of susceptible individuals).
Natural History: Unclear, but there is an increased risk of esophageal stricture parallel in the duration of untreated disease.
Found often in kids: Abdominal pain, nausea, vomiting, food aversion, chest pain, heartburn.
Atopic history of food allergy, asthma, eczema, allergy, rhinitis.
Also having endoscopy and biopsy report very important.
Esophagitis on Endoscopy:
Eosinophilic esophagitis
Candida (white patches)
Giant ulcer associated with HIV (immunocompromised patients, clear borders)
Schatzky ring (constriction due to long-term esophagitis)