T1 L5 salivary and gastric secretions

Question 1

what is the function of salivary and gastric secretions

Answer 1

Lubricate, protect and aid digestion

Question 2

how are salivary and gastric secretions secreted

Answer 2

Exocrine glands (with duct) eg salivary and gastric glands 
Endocrine glands eg enteroendocrine cells in stomach and small intestine

Question 3

what is the role of salivary secretions

Answer 3

lubrication, protection (oral hygiene), initiate chemical digestion

Question 4

how are salivary secretions secreted

Answer 4

Major salivary glands – parotid, submandibular, sublingual

Dispersed salivary glands – mucosa of mouth and tongue (eg labial, buccal palatal, lingual)

Question 5

what are the major salivary glands

Answer 5

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)

Question 6

what is the composition of saliva

Answer 6

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

Question 7

what is the role of water in saliva

Answer 7

solvent dissolves food components to aid taste, swallowing, initiating digestion, oral hygiene

Question 8

what is the role of electrolytes in saliva

Answer 8

buffer for acidic food contents

Question 9

what is the role of enzymes in saliva

Answer 9

amylase - breakdown starch
lysozyme - hydrolyse peptidoglycans
lingual lipase - TG to FA and diglycerides

Question 10

what is the role of secretory IgA in saliva

Answer 10

prevent microbial attachment to epithelium

Question 11

what is the role of mucin in saliva

Answer 11

lubrication

Question 12

what is the role of organics urea and uric acid in saliva

Answer 12

waste product removal for excretion

Question 13

what is the acing structure of salivary glands

Answer 13

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

Question 14

Two stage formation of hypotonic saliva

Answer 14

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

Question 15

how does the composition of saliva changes with flow rate

Answer 15

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

Question 16

how are secretions controlled parasympathetically

Answer 16

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

Question 17

Sympathetic neural stimulation of secretions

Answer 17

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)

Question 18

Salivary gland dysfunction

Answer 18

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

Question 19

Gastric secretions - where do they come from

Answer 19

Gastric pits in mucosa branch into gastric glands

Question 20

Exocrine gland cells (secrete gastric juice)

Answer 20

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

Question 21

Two major types of gastric glands

Answer 21

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

Question 22

what makes up gastric juice

Answer 22

water, electrolytes, mucus, pepsinogen pro-enzyme, renin in neonates, gastric lipase, HCL, IF

Question 23

what allows parietal cells to secrete

Answer 23

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

Question 24

How does HCl secretion occur

Answer 24

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

Question 25

What stimulates gastric acid secretion

Answer 25

Ach release from vagus
Gastrin from G cells
Histamine from ECL cells
Act via second messengers

Question 26

What inhibits gastric acid secretion

Answer 26

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)

Question 27

Pharmacological inhibition of gastric acid

Answer 27

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 28

How does the hormone gastrin promote gastric digestion

Answer 28

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

Question 29

Three phases of gastric secretion

Answer 29

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

Question 30

Why is gastric mucosa not damaged

Answer 30

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

Question 31

Dysfunction of gastric mucosa

Answer 31

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

Question 32

Gastric parietal cell dysfunction

Answer 32

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