Major GI diseases, salivary gland secretions, gastric secretions, secretion of HCl and bicarbonate, integrity of GI wall, GERD, Barrett's esophagus, PUD

7 Pages
82 Views
Unlock Document

Department
Biomedical Science
Course
BMS 460
Professor
D.Rao Veeramachaneni
Semester
Fall

Description
9 October Overview of Major GI Diseases: A few facts The function depends on normal development and differentiation of the GI tract E.g., Megacolon or Hirschsprung Disease in which autonomic smooth muscle ganglia do not develop; aganglionic segment contracts but cannot relax GI tract is open-ended and thus readily accessible to pathogens and carcinogens Intestinal mucosa is an interface and a barrier between the internal and external milieu that is maintained actively (requires energy) and should be kept intact The GI tract is a tube that can dilate or become obstructed Obstruction may be anatomical or functional resulting in dilation of the lumen proximal to obstruction GI diseases may disturb one or more of the basic functions of GI tract E.g., Dysphagia (abnormal swallowing), Dyspepsia (abnormal digestion), Malabsorption The GI tract is an important source of biologically active substances Each portion produces unique enzymes, hormones, and immunoglobulins Abundant blood flow and superficial location of blood vessels in the mucosa make GI tract prone for hemorrhage or ischemia Disorders of Salivary Glands and Esophagus Sjögren’s syndrome, Warthin tumor Gastro-Esophageal Reflux Disease Hiatal Hernia Alterations in Integrity and Function of the GI Tract Wall Atrophic Gastritis Peptic Ulcer Disease Gastroenteritis Inflammatory Bowel Disease Ulcerative Colitis Crohn’s Disease Irritable Bowel Syndrome Alterations in Motility of GI Tract Achalasia Megacolon Hirschsprung Disease Malabsorption Mucosal Disorders Celiac Disease Tropical Sprue Neoplasms Esophageal, Gastric and SI Cancers Colonic Polyps and Colon Cancer Salivary Gland Secretions Two types of salivary glands: serous and mixed Serous glands (e.g., parotid), which are primarily composed of serous cells, secrete a nonviscous saliva containing water, electrolytes, and enzymes (amylase) Mixed glands (submandibular, sublingual), which are composed of serous and mucous cells, secrete a viscous saliva rich in mucin glycoproteins Regulation of salivation Salivation is mainly controlled by the autonomic nervous system Both branches of the autonomic nervous system stimulate salivation, but the parasympathetic nervous system does so much more strongly than the sympathetic nervous system Sjögren’s Syndrome An autoimmune disorder characterized by lymphocytic infiltration (blocks glands) of exocrine glands, mainly affecting the salivary and lacrimal glands Relatively common in people older than 40 yr; 9 of 10 are women Characterized by dry mouth (xerostomia) and dry eyes (keratoconjunctivitis sicca) Warthin Tumor Papillary cystadenoma lymphomatosum or adenolymphoma is a benign tumor of the salivary glands with a strong association with cigarette smoking Gastric Secretions Gastric secretion is under the influence of the vagus nerve, which directly or through its connectors stimulates parietal cells to secrete HCl. The dilation of the stomach by food initiates the vasovagal reflex, which further promotes the release of acetylcholine (Ach) from the terminal branches of the vagus nerve and the parasympathetic autonomic nerves in the stomach. ACh stimulates parietal cell to secrete HCl – acts on chief cell to produce pepsin The vagus nerve also stimulates the enterochromaffin-like cells (ECLs) to secrete histamine (H), enteroendocrine G cells to secrete gastrin (G), and delta (D) cells to secrete somatostatin (S). Gastrin stimulates the parietal cells. Somatostatin inhibits the secretion of gastrin and inhibits the secretion of HCl from parietal cells. HCl stimulates the chief cells to secrete pepsin via pepsinogen. The entry of food into the duodenum leads to a release of inhibitors of gastric secretion, such as secretin, cholecystokinin (CKK), somatostatin, and gastric inhibitory peptide (GIP). The entry of chime into the ileum leads to a release of peptide YY, which inhibits gastric emptying. Note: pancreatic islet cells also secrete some of these hormones. Pepsin cleaves proteins to amino acids, some of which, notably tryptophan and phenylalanine, stimulate G cells to release gastrin; this further promotes HCl production. When the gastric pH drops below pH 3 the secretion of gastrin stops. The acidity of the contents also has an inhibitory effect on the parietal cells, and when it drops <2, HCl production drops entirely. In atrophic gastritis, many of the glands containing acid-secreting parietal cells are destroyed, thereby limiting the extent of gastric acidification (achlorhydria). This lack of acid production causes a loss of feedback inhibition of gastrin secretion. As a result, hypergastrinemia often develops. Secretion of HCl and Bicarbonate Plasma CO is 2enerated within the parietal cells or diffuses into them, where it reacts - + + with water to from HCO and 3 ions. H ions are then secreted into the gastric lumen in exchange for K ions, and HCO diffuse3 from parietal cells into the plasma in exchange for chloride. This results in a brief “alkaline tide” after a meal. Bicarbonate enters into fenestrated capillary with blood flowing toward the surface epithelium; some of it diffuses into the mucous blanket to increase pH The release of H ions and Cl by the parietal cell involves the membrane fusion of the tubulovesicular system with apical membrane of canaliculus - These gastric secretions are counteracted by the secretion of HCO into the gu3 lumen by organs such as the pancreas and hence metabolic alkalosis is not precipitated following a large meal. The stomach secretes ~2L of HCl/day [H ] > 150 mM The role of mucus and prostaglandins in maintaining the integrity of GI wall Prostaglandins stimulate mucus production Mucosal blood flow is highly dependent on the local production of prostaglandins Protective gastric mucus blanket Mucous surface cells also produce bicarbonate Anti-inflammatory drugs can impair mucosal blood flow by inhibiting prostaglandin synthesis - This compromises the protective abilities of the mucosa (mucus and HCO 3 secretion) and can
More Less

Related notes for BMS 460

Log In


OR

Join OneClass

Access over 10 million pages of study
documents for 1.3 million courses.

Sign up

Join to view


OR

By registering, I agree to the Terms and Privacy Policies
Already have an account?
Just a few more details

So we can recommend you notes for your school.

Reset Password

Please enter below the email address you registered with and we will send you a link to reset your password.

Add your courses

Get notes from the top students in your class.


Submit