salivary and gastric secretion

Question 1

what do secretions do?

where do they come from? 2

Answer 1

• lubricate, protect and aid digestion
• exocrine glands (with duct)
• endocrine glands (without duct)

Question 2

what is the role of salivary secretions? 3

Answer 2

• lubrication
• protection (oral hygiene)
• initiate chemical digestion

Question 3

what are the major salivary glands? 3

Answer 3

• parotid (under ear, back of jaw)= serous, watery solution containing amylase for starch digestion
• submandibular (under tongue, closer to oesophagus)= mixed serous and mucus
• sublingual (under tongue, closer to lips)= mucus, thicker mucus dominant secretions for lubrication

Question 4

what are dispersed salivary glands? 5

Answer 4

• mucosa of the mouth and tongue
• labial
• buccal
• palatal
• lingual

Question 5

what is the composition of saliva and role? 6

Answer 5

• water (99.5%)= solvent dissolves food components to aid taste, swallowing, ignition of digestion and oral hygiene
• electrolytes (K+, HCO3-, Na+, Cl-)= buffer for acidic food contents
• enzymes (different functions)
• secretory IgA= prevents microbial attachment to the epithelium
• mucin= lubrication
• organics urea and uric acid= waste product removal for excretion

Question 6

what are the different enzymes in salvia and their role? 5

Answer 6

• alpha amylase (ptyalin)= hydrolysis of alpha-1,4 glycosidic bonds in starch to disaccharide maltose, trisaccharide maltose and alpha-dextrin
• lysozyme= hydrolysis of peptidoglycan in wall of gram-negative bacteria
• lingual lipase (serous salivary glands of the tongue)= hydrolysis of lipid triglycerides to fatty acid and diglycerides (optional in acidic pH)
• lactoferrin= chelates iron to prevent microbial manipulation
• kallikrein= converts plasma protein alpha-2-globulin into bradykinin

Question 7

describe the acinar structure of salivary glands? 3

Answer 7

• Acinar cells: serous or mucin secreting
• Myoepithelial cells: around the acinar cells and are contractile in nature to help move the secretions through the duct
• Ductal cells: columnar, line the salivary gland duct and modify the primary saliva

Question 8

what are the unique properties of a salivary gland? 3

Answer 8

• Large volume of saliva produced compared to the mass of the gland
• Low osmolarity
• High K+ concentration

Question 9

describe the 2 stage formation of hypotonic saliva? 2

Answer 9

• 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. This produces HCO3- and K+ rich hypotonic saliva

Question 10

describe how the composition of saliva can change? 4

Answer 10

• with flow rate
• Electrolyte composition= Na+ and Cl-plasma
• Low rate of secretion= maximum reabsorption of electrolytes produced hypertonic saliva (lower concentration of osmotically active electrolytes)
• High rate of secretion= reduced absorption of electrolytes produces alkaline HCO3- rich saliva with increases osmolality closer to that of the primary isotonic saliva

Question 11

what normally regulates the secretions of saliva? 7

Answer 11

• parasympathetic ANS regulation is dominant
• Simulation= sight, thought, smell tase, tactile stimuli, nausea
• Signal superior and inferior salivatory nuclei in the medulla
• Via cranial nerve VII (facial nerve) for the sublingual and submandibular gland
• Via cranial nerve IX (glossopharyngeal nerve) for the parotid gland
• Increase salivary secretion, vasodilation, myoepithelial cell contraction
• Inhibitors= fatigue, sleep, fear, dehydration

Question 12

describe the sympathetic neural stimulation for the secretion of saliva? 5

Answer 12

• Overall slight increase in secretion
• Produces a mucin and enzyme 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)

Question 13

name 2 salivary gland dysfunctions and 3 things about each?

Answer 13

• 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 syndromes
• .
• Xerostomia (dry mouth)
• Patients lack adequate saliva
• Dental caries and halitosis common due to bacteria overgrowth
• Difficulty speaking or swallowing solid food due to inadequate lubrication

Question 14

describe gastric glands? 9

Answer 14

-gastric pits in the mucosa branch into gastric pits

• Exocrine gland cells (secrete gastric juice):
• 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

Question 15

what are the two major types of gastric gland and 3 subcategories of each?

Answer 15

• 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

Question 16

what are the components of gastric juice and what they do? 7

Answer 16

• Water and electrolytes= medium for action of acids and enzymes, digestion or organic substances
• Mucus (glycoprotein mucin) (mucus neck) = protects surface epithelium from acid/pepsin
• Pepsinogen pro-enzyme (chief) = active pepsin form is an endopeptidase that cleaves peptide bonds (protein to make smaller peptides)
• Rennin in neonates only (chief) = coagulation of milk through casein proteolysis
• Gastric lipase (chief)= triglycerides to fatty acid and diglycerides
• HCl (pH1-3) = converts pro-enzyme pepsinogen to pepsin, denatures proteins, kills microorganisms
• Intrinsic factor (parietal) = vitamin B12 absorption in the ileum, erythropoiesis in bone marrow, absence= pernicious anaemia

Question 17

describe HCl secretion by parietal cells? 4

Answer 17

• Parietal cells have in intracellular branches canalicular structure and are packed with tubulovesicles in resting 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

Question 18

how does HCl secretion occur? 4

Answer 18

• H+/K+ ATPase proton pump drives active secretion of H+
• Carbonic anhydrase catalyses formation of HCO3- producing H+ ions
• HCO3- exchanged for Cl- (alkaline tide – gastric venous blood becomes more alkaline postprandially)
• Cl- diffuses into the lumen

Question 19

what activates gastric acid secretion? 3

Answer 19

• Ach=acetylcholine release from vagus
• Gastrin from G cells
• Histamine from ECL cells

Question 20

what inhibits gastric acid secretion? 2

Answer 20

• Somatostatin from D cells (paracrine and endocrine): inhibits adenylate cyclase (AC)
• Musical prostaglandin antagonists for H receptor (NSAIDS inhibit prostaglandin formation and increase gastric acid secretion)

Question 21

what stimulates the parietal cell to secrete acid? 3

Answer 21

• PLC phospholipase C
• IP3 inositol triphosphate
• AC adenylate cyclase

Question 22

describe pharmalogical inhibition of gastric acid? 3

Answer 22

• 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

Question 23

what hormone promotes gastric secretion, how does it do this? 6

Answer 23

• gastrin (promoted by the vagus, distention of the stomach and peptide)
• Promotes:
• Parietal cell secretion of HCl
• Chief cell secretion of pepsinogen
• Lower oesophageal sphincter contraction
• Increased motility of the stomach
• Relaxation of pyloric sphincter

Question 24

what are the 3 phases of gastric secretion?

Answer 24

• 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 stimulate gastric secretions via vagus and gastrin
• inhibitory: chyme with pH<2, distention, protein breakdown produces, hypo/hyper-osmotic products inhibit gastric secretions via cholecystokinin, secretin, gastric inhibitory polypeptide

Question 25

why is the gastric mucosa not damaged? 4

Answer 25

• Surface mucous glands secrete viscous mucus layer of mucopolysaccharides/proteins
• Mucous viscosity generates a mucosal barrier= Mucin has basic side chains and HCO3- secreted from surface epithelial cells both neutralise H+ ions
• Tight junctions stop acid damaging underlying tissue
• Net result= unstirred layer of pH7, pepsinogen not activated, prevents enzymatic and chemical damage

Question 26

describe a dysfunction of the gastric mucosa? 5

more specific type of this? 3

Answer 26

• Gastritis (inflammation of gastric mucosa)
• Most commonly causes by an infection by the bacteria Helicobacter pylori (primary cause of peptic ulcer disease)
• Gram negative bacteria produced urease which forms ammonia from urea, ammonia neutralizes bactericidal acid and is toxic to the 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
• Autoimmune atrophic gastritis
• 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