T1 L5 salivary and gastric secretions Flashcards
what is the function of salivary and gastric secretions
Lubricate, protect and aid digestion
how are salivary and gastric secretions secreted
Exocrine glands (with duct) eg salivary and gastric glands Endocrine glands eg enteroendocrine cells in stomach and small intestine
what is the role of salivary secretions
lubrication, protection (oral hygiene), initiate chemical digestion
how are salivary secretions secreted
Major salivary glands – parotid, submandibular, sublingual
Dispersed salivary glands – mucosa of mouth and tongue (eg labial, buccal palatal, lingual)
what are the major salivary glands
Parotid gland – serous, watery secretions containing salivary amylase for starch digestion
Submandibular gland – mixed serous and mucus
Sublingual gland – mucus (thicker mucus dominant secretions for lubrication)
what is the composition of saliva
water (99.5%)
Electrolytes (K+, HCO3-, Na+, Cl-, (PO4)3-)
Enzymes (a-amylase, lysozyme, lingual lipase, lactoferrin, kallikrein)
Secretory IgA
Mucin
Organic urea and uric acid
what is the role of water in saliva
solvent dissolves food components to aid taste, swallowing, initiating digestion, oral hygiene
what is the role of electrolytes in saliva
buffer for acidic food contents
what is the role of enzymes in saliva
amylase - breakdown starch
lysozyme - hydrolyse peptidoglycans
lingual lipase - TG to FA and diglycerides
what is the role of secretory IgA in saliva
prevent microbial attachment to epithelium
what is the role of mucin in saliva
lubrication
what is the role of organics urea and uric acid in saliva
waste product removal for excretion
what is the acing structure of salivary glands
Acinar – secrete primary saliva into duct lumen
Myoepithelial cells – surround acinar, contractile, drive secretions along duct
Ductal cells – modify saliva
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
how does the composition of saliva changes with flow rate
Electrolyte composition – Na+ and Cl- plasma
Low rate of secretion – maximum reabsorption of electrolytes produces hypotonic saliva (low concentration of osmotically active electrolytes)
High rate – reduced reabsorption of electrolytes produces alkaline, HCO3- rich saliva with increased osmolarity closer to that of primary isotonic saliva
how are secretions controlled parasympathetically
dominant
Sight, thought, smell, taste (esp sour acidic taste), tactile stimuli and 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
Increases salivary secretion, vasodilation, myoepithelial cell contraction
Inhibitor – fatigue, sleep, fear, dehydration
Sympathetic neural stimulation of secretions
Overall slight increase in secretion
Produces a mucin and enzyme rich saliva
Activity is via superior cervical ganglion
Initial vasoconstriction (NT NA stimulates B adrenergic receptors)
Later vasodilation (salivary enzyme kallikrein on blood plasma protein alpha 2 globulin to form vasodilator bradykinin)
Salivary gland dysfunction
Sjoren’s syndrome – an AI disease that destroys exocrine glands, commonly affects tear and saliva production, dry eyes and mouth (sicca symptoms)
Xerostomia (dry mouth) – lack adequate saliva, dental caries and halitosis common due to bacterial overgrowth, difficulty speaking or swallowing solid food due to inadequate lubrication
Gastric secretions - where do they come from
Gastric pits in mucosa branch into gastric glands
Exocrine gland cells (secrete gastric juice)
Mucous neck cells- thin mucus
Parietal cells- HCl and intrinsic factor
Chief cells- pepsinogen (also renin in neonates), gastric lipase
Endocine cells
G cells – hormone gastrin (antrum)
D cells – hormone somatostatin
Enterochromaffin-like (ECL) cells secrete histamine
Two major types of gastric glands
Body and fundus (80%)
Gastric/oxyntic glands – exocrine secretion of 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
what makes up gastric juice
water, electrolytes, mucus, pepsinogen pro-enzyme, renin in neonates, gastric lipase, HCL, IF
what allows parietal cells to secrete
Parietal cells have an intracellular branched canalicular structure and are packed with tubulovesicles in resting state
Contain enzymes carbonic anhydrase and H+/K+-ATPase for acid secretion
Stimulation of acid production tubulovesicles fuse with the canalicular membrane to form microvilli
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
What stimulates gastric acid secretion
Ach release from vagus
Gastrin from G cells
Histamine from ECL cells
Act via second messengers
What inhibits gastric acid secretion
Somatostatin from D cells (paracrine and endocrine): Inhibits adenylate cyclase (AC)
Mucosal prostaglandin antagonists for H receptor (NSAIDs inhibit prostaglandin formation and increase gastric acid secretion)
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
How does the hormone gastrin promote gastric digestion
Vagus, distension, peptide
Gastrin promotes – parietal cell secretion of HCl, chief cell secretion of pepsinogen, lower oesophageal sphincter contraction, increased motility of stomach, relaxation of pyloric sphincter
Three phases of gastric secretion
Cephalic – vagus stimulates parietal, chief cell production of gastric juice and hormone gastrin secretion
Gastric -stimulate 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, distension, protein breakdown products, hypo/hyper-osmotic products inhibit gastric secretions via cholecystokinin, secretin, gastric inhibitory polypeptide
Why is gastric mucosa not damaged
Surface mucosa glands secrete viscous mucus layer of mucopolysaccharides/proteins
Mucus viscosity generates mucosal barrier
Mucin has basic side chains
HCO3- secreted from surface epithelial cells
Both neutralise H+ ions
Tight junctions stop acid damaging underlying tissue
=unstirred layer of pH 7, pepsinogen not activated, prevents enzymatic and chemical damaged
Dysfunction of gastric mucosa
Gastritis (inflammation of gastric mucosa)
commonly caused by bacteria heliobacter pylori (primary cause of peptic ulcer disease)
Gram neg 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 process called restitution – rapid division of stem cells located in neck of gastric glands
Gastric parietal cell dysfunction
AI atrophic gastritis is an antibody mediated destruction of gastric parietal cells, caused hypochlorhydria (insufficient acid secretion) and a deficiency of intrinsic factor IF
The loss of IF = B12 malabsorption and pernicious anaemia
