salivary & gastric secretions

Question 1

what are exocrine glands?

Answer 1

glads with a duct

Question 2

what are endocrine glands?

Answer 2

glands without a duct

Question 3

give some examples of exocrine glands

Answer 3

• salivary glands

- gastric glands

Question 4

give some examples of endocrine glands

Answer 4

enteroendocrine cells in stomach and small intestine

Question 5

what is the role of salivary secretions?

Answer 5

• lubrications
• protection (oral hygiene)
• imitate chemical digestion

Question 6

what are the 3 main salivary glands?

Answer 6

• parotid
• submandibular
• sublingual

Question 7

where are the salivary glands dispersed?

Answer 7

• mucosa of mouth and tongue

- labial, buccal, palatal, lingual

Question 8

what are the key features of parotid glands?

Answer 8

• serous

- watery secretions containing salivary amylase for starch digestion

Question 9

what are the key features of submandibular glands?

Answer 9

mixed serous and mucus

Question 10

what are the key features of sublingual glands?

Answer 10

mucus: thicker mucus dominant secretions for lubrications

Question 11

what are the unique properties of acinar structure of salivary glands?

Answer 11

• large volume of saliva produced compared to gland
• low osmolarity
• high potassium concentrations

Question 12

what are the 2 stages of hypotonic saliva formation?

Answer 12

1) acinar cells secrete isotonic saliva similar to blood plasma in electrolyte composition
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 13

how does the composition of saliva change with low rate of secretion?

Answer 13

maximum reabsorption of electrolytes produces hypotonic saliva

Question 14

how does the composition of saliva change with the high rate of secretion?

Answer 14

reduced reabsorption of electrolytes produce alkaline, HCO3- rich saliva with increased osmolarity closer to that of primary isotonic saliva

Question 15

how does the parasympathetic ANS regulation dominate the salivary & gastric secretions?

Answer 15

• sight, thought, smell, taste, tactile stimuli, nausea
• signal superior and inferior salivary 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, vasodilation, myoepithetlail cell contraction
• inhibitors: fatigue, sleep, fear, dehydration

Question 16

how does the sympathetic system stimuli neural system?

Answer 16

• overall slight increase in secretion
• produces mucin and enzyme rich saliva
• activity is via superior cervical ganglion
• initial vasoconstriction
• later vasodilation

Question 17

what is Sjogren’s syndrome?

Answer 17

• salivary gland dysfunciton
• an autoimmune disease that destroys the exocrine glands
• commonly affects tear and salivary production
• dry eyes and dry mouth, known as sick symptoms

Question 18

what is Xerostomia?

Answer 18

• salivary gland dysfunction
• dry mouth
• patients lack inadequate saliva
• dental caries and halitosis common due to bacterial overgrowth
• difficulty speaking or swallowing solid food due to inadequate lubrication

Question 19

what are the 2 types of gastric glands?

Answer 19

• body & fundus

- antrum

Question 20

what are the key features of body & fundus gastric glands?

Answer 20

• 80%
• gastric/oxyntic glands
• exocrine secretion of HCl, pepsinogen, intrinsic factor and mucus
• paracrine ECL cell secretion of histamine, paracrine D cell secretion of somatostatin

Question 21

what are the key features of antrum gastric glands?

Answer 21

• 20%
• pyloric glands
• mucus and endocrine hormone gastrin
• paracrine/endocrine somatostatin

Question 22

how is HCl secreted by parietal cells?

Answer 22

• parietal cells have an intracellular branched canalicular structure and are packet 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 23

how does HCl secretion occur?

Answer 23

• H+/K+-ATPase proton pump drives active secretion of H+
• carbonic anhydrase (CA) catalysed formation of HCO3- producing H+ ions
• HCO3- exchanged for Cl-
• Cl- diffuses into lumen

Question 24

what activates gastric acid secretion?

Answer 24

• ACh: acetylcholine release from vagus
• gastrin: from G cells
• histamine: from ECL cells

Question 25

what inhibits gastric acid secretion?

Answer 25

- somatostatin: from D cells which inhibits adenylate cyclase (AC) - mucosal prostaglandin antagonists for H receptor

Question 26

what are the pharmacological inhibitors of gastric acid?

Answer 26

- omeprazole: proton pump inhibitor inactivates H+/K+-ATPase - cimetidine: H2 receptor antagonist inhibits stimuli for acid secretion - atropine: inhibits muscarinic receptors and vagal stimulation of acid secretion

Question 27

what are the 3 phases of gastric secretion?

Answer 27

- cephalic - gastric - intestinal

Question 28

what happens in the cephalic phase of gastric secretion?

Answer 28

vagus stimulated parietal, chief cell production of gastric juice and hormone gastrin secretion

Question 29

what happens in the gastric phase of gastric secretion?

Answer 29

stimulate parietal, chief mucus secretion, antral G cells

Question 30

what happens in the intestinal phase of gastric secretion?

Answer 30

- 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, secretion, gastric inhibitory polypeptide

Question 31

why is the gastric mucosa not damaged?

Answer 31

- surface mucous 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 - net result: unstirred layer is around pH7, pepsinogen not activated, prevents enzymatic and chemical damage

Question 32

what are the key features of gastritis?

Answer 32

- dysfunction & inflammation of gastric mucosa - most commonly caused by an infection by the bacterial Helicobacter pylori - gram negative bacteria produce urease which forms ammonia from urea, ammonia neutralises bacterial acid and is toxic to mucosal barrier - also caused by smoking, alcohol, non-steroidal anti-inflammatory drugs, chronic stress - following acute damage, rapid regeneration is via a process caused restitution: rapid division of stem cells located in neck of gastric glands

Question 33

what is autoimmune atrophic gastritis?

Answer 33

- an antibody mediated destruction of gastric parietal cells, which causes hypochlorydria and a deficiency of intrinsic factor If - the loss of If results in vitamin B12 Mal-absorption and pernicious anaemia