T1 - Salivary and gastric secretions Flashcards

1
Q

what type of glands are the salivary and gastric glands?

A

exocrine

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2
Q

what are the main endocrine cells in the stomach and SI?

A

enteroendocrine cells

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3
Q

what is the volume and tonicity of salivary secretions?

A

high volume and hypotonic

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4
Q

where does the duct from the parotid gland enter the oral cavity?

A

above the second molar

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5
Q

what type of secretions does the parotid gland release and what enzyme does it contain?

A

serous/water secretions that contains salivary amylase

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6
Q

what type of secretions does the submandibular gland produce?

A

mixed serous and mucus secretions

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7
Q

what type of secretions does the sublingual gland produce?

A

viscous/thicker secretions for lubrication

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8
Q

which two glands produce 90% of saliva?

A

parotid and sub mandibular

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9
Q

what are five substances found in saliva and what do they do?

A

1) alpha amylase - digests starches by hydrolysis 1,4 glycosidic bonds
2) lysozyme - hydrolyses peptidoglycan in the wall of gram negative bacteria
3) lingual lipase - initiates hydrolysis of triglycerides and is active at an acidic pH
4) lactoferrin - antimicrobial properties and chelates iron to stop microbes multiplying
5) kalikrein - converts plasma protein alpha 2 globulin to bradykinin

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10
Q

what molecule is released when constriction of salivary glands is required?

A

kallikrein which converts plasma alpha 2 globulin to bradykinin which causes vasoconstriction

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11
Q

which cells secrete the predominant components of saliva?

A

acinar cells

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12
Q

what cells surround the acinar cells and what is their function?

A

myoepithelial cells which contract to push secreted contents into the duct

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13
Q

how is hypotonic saliva produced?

A
  • ion exchange: K+ and HCO3- in and NaCl out
  • NKCC1 brings Na, Cl and K in through acinar cells
  • Na is exchanged out for K+ in
  • Cl- is exchanged out for HCO3-
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14
Q

what happens to proportions of ions in the saliva when secretion increases (Na, HCO3-, CL and K)

A
  • HCO3- and K+ stay the same

- NaCl concentrations increase (still stays hypotonic)

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15
Q

which cranial nerves stimulate salivary secretion and via which glands?

A
  • cranial nerve VII (facial) to the sublingual and submandibular
  • cranial nerve IX (glossopharyngeal) to parotid gland
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16
Q

what effect does parasympathetic input have on saliva flow?

A
  • increases amylase and mucin containing watery saliva
  • vasodilation
  • increased saliva flow
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17
Q

what effect does sympathetic input have on saliva production and what is this via?

A
  • inhibits saliva production
  • signals via the superior cervical ganglion
  • vasoconstriction
18
Q

what is the effect of sympathetic input on amylase content on the saliva?

A
  • increased amylase content but decreased overall saliva production
19
Q

what is stoorgrens syndrome?

A

autoimmune condition that destroys exocrine glands

- reduced saliva production and dry eyes and mouth

20
Q

what is xerostomia?

A

lack of saliva production, decreased lubrication and hard to speak/swallow

21
Q

what are the three exocrine gland cells in the gastric pits?

A

1) mucus neck cells
2) chief cells
3) parietal cells

22
Q

what does each exocrine gland cell release?

A

mucus neck cells release mucus
parietal cells release Hcl and IF
chied cells release pepsinogen in adults and rennin/gastric lipase in neonates

23
Q

what are the endocrine cells of the gastric glands and what do they secrete?

A
  • G cells secrete gastrin
  • D cells secrete somatostain
  • enterochromaffin cells secrete histamine
24
Q

what does gastrin cause and what is it stimulated by?

A

causes gastric digestion

- stimulated by distention of stomach and presence of partially digested fragments

25
what cells does gastrin act on?
parietal and chief cells to increase secretion of acid and pepsinogen - also causes lower oesophageal contraction to allow mixing in the stomach
26
what three things do chief cells secrete?
pepsinogen pro-enzyme and rennin/gastric lipase in neonates
27
what do parietal cells secrete?
Secretes HCl and intrinsic factor
28
what three things can stimulate gastric acid secretion?
1) vagal innervation (each release which increases H+ secretion) 2) gastrin 3) histamine (H2 receptors on parietal cells)
29
what second messenger pathway does histamine work vi to increase gastric acid secretion?
adenylate cyalase
30
what second messenger pathway does Ach and gastrin work via to increase acid secretion?
PLC and Ip3
31
name two molecules that inhibit gastric acid secretion and how?
- somatostatin inhibits adenylate cylase | - mucosal prostaglandin inhibits the H2 receptor
32
what effects do NSAIDs have on gastric secretion?
increase it by inhibiting prostaglandin formation | PGs usually inhibit the H2 receptor which decreases gastric secretion
33
what does the cephalic phase of gastric secretion activate and what is it stimulated by?
stimulated by vagal stimulation (thought, smell, sight) | - activates chief and parietal cells
34
what stimulates the gastric stage of gastric secretion?
- bolus hitting the stomach - local nervous secretory reflexes - vagal reflexes - gastrin and histamine
35
what is excitatory to the intestinal phase of gastric secretion? (chyme entering the duodenum)
chyme with a pH >3 - stimulates gastric secretion
36
what inhibits secretion from stomach to duodenum?
- chyme pH <2 | - CCK, secretin, GIP
37
what two molecules form the viscous mucus layer that protects the gastric mucosa?
mucopolysaccharide and mucin
38
how does mucin stop acid damage of the mucosa?
has basic side chains
39
what condition results from dysfunction of the gastric mucosa and what is the most common cause?
gastritis - most common cause is helicobacter pylori which produces urease - urease produces ammonia which damages the mucosal barrier
40
what is restitution?
rapid regeneration of the damaged gastric mucosa due to stem cells in the neck of the gastric glands
41
what cells are dysfunctional in auto immune atrophic gastritis?
parietal cells
42
what is the mechanism of autoimmune atrophic gastritis?
autoimmune destruction of gastric parietal cells - gastric mucosa loses ability to produce acid - intrinsic factor deficiency - B12 malabsorption - pernicious anaemia