Salivary and Gastric Secretion Flashcards
Secretion
Lubricate, protect and aid digestion
Exocrine glands (with duct) - salivary glands, gastric glands
Endocrine glands (without duct) - enteroendocrine cells in stomach and small intestine
Saliva secretions - 1500 ml/day
Gastric Secretions - 2000 ml/day
Salivary Secretions
Role: lubrication, protection (oral hygiene), initiate chemical digestion
Major salivary glands: parotid (serous, watery secretions containing salivary amylase for starch digestion), submandibular (mixed serous and mucus), sublingual (mucus - thicker mucus dominant secretions for lubrication)
Dispersed Salivary glands: mucosa of mouth and tongue (labial, buccal, palatal, lingual)
Saliva Composition and Role
Water: 99.5% - dissolves food components
Electrolytes: K+, HCO3-, Na+, Cl-, (PO4)3- - buffer for acidic food
Enzymes: alpha amylase (hydrolysis of 1,4- glycosidic bonds in starch), lysozyme (hydrolysis of peptidoglycans), lingual lipase (hydrolysis of lipid triglycerides to fatty acid and diglycerides), lactoeferrin, kallikrein
Secretory IgA - prevents microbial attachment to epithelium
Mucin - lubrication
Organics urea and uric acid - waste production removal for excretion
Acinar Structure of Salivary Glands
Unique properties: large volume of saliva produced compared to mass of gland, low osmolarity, high K+ concentration
Two stage formation of hypotonic saliva
Stage 1: acinar cells secrete isotonic saliva, similar to blood plasma in electrolyte composition
Stage 2: ductal cells secrete HCO3- and K+ ions with reabsorption of NaCl and limited movement of water by osmosis; produces HCO3- and K+ rich hypotonic saliva
Composition of saliva changes with flow rate
Electrolyte composition:
Na+ and Cl- < plasma
HCO3- and K+ > plasma
Low rate of secretion - maximum reabsorption of electrolytes produces hypotonic saliva (lower concentration of osmotically active electrolytes)
High rate - reduced absorption of electrolytes produces alkaline, HCO3- rich saliva, with increased osmolarity closer to that of primary isotonic saliva
Parasympathetic ANS regulation is dominant
Sight, smell, thought, taste (especially sour acidic taste), tactile stimuli, nausea
Signal superior and inferior salivatory nuclei in the medulla
Via cranial nerve VII (facial nerve) for the sublingual and submandibular gland
Cranial nerve IX (glossopharyngeal nerve) for the parotid gland
Increase salivary secretion, vasodilatio, myoepithelial cell contraction
Inhibitors: fatigue, sleep, fear, dehydration
Sympathetic Neural Stimulation
Overall, slight increase in secretion
Produces a mucin and enzume rich saliva
Activity is via superior cervical ganglion
Initial vasoconstriction (neurotransmitter noradrenaline stimulates beta adrenergic receptors)
Later vasodilation (salivary enzyme kallikrein action on blood plasma protein alpha-2 globulin to form vasodilator bradykinin)
Salivary gland dysfunction
Sjogren’s syndrome: an autoimmune disease that destroys the exocrine glands; commonly affects tear and saliva production; dry eyes and dry mouth, known as sicca symptoms
Xerostomia (dry mouth): patients lack adequate saliva; dental caries and halitosis common due to bacterial overgrowth; difficulty speaking or swallowing solid food due to inadequate lubrication
Gastric Glands
Gastric pits in mucosa branch into gastric glands - mucous neck cells (thin mucus); parietal cells (HCl and intrinsic factor); chief cells (pepsinogen - also rennin in neonates - gastric lipase); endocrine cells: G cells (hormone gastrin (antrum)), D cell hormone somatostatin, enterochromaffin-like (ECL) cells secrete histamine
2 types of gastric gland
Body and Fundus (80%) - gastric/oxyntic glands: exocrine secretion of HCl, pepsinogen, intrinsic factor and mucus; paracrine ECL secretion of histamine, paracrine D cell secretion of somatostatin.
Antrum (20%) - pyloric glands: mucus and endocrine hormone gastrin; paracrine/endocrine somatostatin
Gastric Juice
Water and electrolytes: medium for action of acid and enzymes, digestion
Mucus: protects surface epithelium from acid/pepsin
Pepsinogen pro-enzyme: active pepsin form is an endopeptidase that cleaves peptide bonds, triglycerides to FAs and diglycerides
HCl: converts pro-enzyme pepsinogen to pepsin, denatures proteins, kills microorganisms
HCl Secretion by Parietal Cells
Parietal cells have an intracellular branched canalicular structure and are packed with tubulovesicles in restinc state
These contain enzymes carbonic anhydrase and H+/K+ - ATPase for acid secretion
On stimulation of acid production tubulovesicles fuse with the canalicular membrane to form microvilli
HCl is formed at these microvilli and secreted
How does HCl secretion occur?
H+/K+-ATPase proton pump drives active secretion of H+ Carbonic anhydrase (CA) catalyses formation of HCO3- producing H+ ions HCO3- exchanged for Cl- (alkaline tide - gastric venous blood becomes alkaline postprandially) Cl- diffuses into lumen
Stimulation of gastric acid secretion and parietal cell acid secretion
Activation: Ach- release from Vagus; gastrin from G cells; histamine from ECL cells
Inhibition: somatostatin from D cells (paracrine and endocrine) - inhibits adenylate cyclase (AC); mucosal prostaglandin antagonists for H receptro (NSAIDS inhibit prostaglandin formation and increase gastric acid secretion)
Parietal cell acid secretion: PLC phospholipase C, IP3 inositol triphosphate; AC adenylate cyclase
Pharmacological Inhibition of Gastric Acid
Omeprazole: proton pump inhibitor inactivates H+/K+ ATPase
Cimetidine - H2 receptor antagonist inhibits stimulus for acid secretion
Atropine: inhibits muscarinic receptors and vagal stimulation of acid secretion
Gastrin promotes gastric digestion
Parietal secretion of HCl Chief cell secretion of pepsinogen Lower oesophageal sphincter contraction Increased motility of stomach Relaxation of pyloric sphincter
3 phases of gastric secretion
Cephalic: Vagus stimulates parietal, chief cell production of gastric juice and hormone gastrin secretion
Gastric: stimulates parietal, chief, mucus secretion, antral G cells (gastrin stimulates parietal cells directly and indirectly via ECL histamine release)
Intestinal: excitatory - chyme with pH>3, peptides stimulates gastric secretions via vagus and gastrin; inhibitory - chyme with pH<2, distention, protein breakdown products, hypo/hyper-osmotic products inhibit gastric secretions via cholecystokinin, secretin, gastric inhibitory polypeptide
Why is the gastric mucosa not damaged?
Surface mucous glands secrete viscous mucus layer of mucopolysaccharides/proteins
Mucus viscosity generates mucosal barrier - mucin has basic side chains, HCO3- secreted from epithelial cells, both neutralise H+ ions
Tight junctions stop acid damaging underlying tissue
Net result - unstirred later is ~pH7, pepsinogen not activated, prevents enzymatic and chemical damage
Dysfunction of gastric mucosa
Gastritis (inflammation of gastric mucosa)
Most commonly caused by and infection by bacteria Helicobacter pylori (primary cause of peptic ulcer disease) - gram negative bacteria produce urease which forms ammonia from urea; ammonia neutralises bactericidal acid and is toxic to mucosal barrier
Also caused by smoking, alcohol, nonsteroidal anti-inflammatory drugs (NSAIDS) (inhibit cyclooxygenase to reduce protective prostaglandin synthesis), chronic stress
Following acute damage rapid regeneration is via a process called restitution - rapid division of stem cells located in the neck of gastric glands
Gastric Parietal Cell Dysfunction
Autoimmune atrophic gastritis is an antibody mediated destruction of gastric parietal cells, which causes hypochlorhydria (insufficient acid secretion), and a deficiency of intrinsic factor IF
The loss of IF results in vitamin B12 mal-absorption and pernicious anaemia
