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BSMS 104 > T1 - Salivary and gastric secretions > Flashcards

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
Q

what cells does gastrin act on?

A

parietal and chief cells to increase secretion of acid and pepsinogen
- also causes lower oesophageal contraction to allow mixing in the stomach

26
Q

what three things do chief cells secrete?

A

pepsinogen pro-enzyme and rennin/gastric lipase in neonates

27
Q

what do parietal cells secrete?

A

Secretes HCl and intrinsic factor

28
Q

what three things can stimulate gastric acid secretion?

A

1) vagal innervation (each release which increases H+ secretion)
2) gastrin
3) histamine (H2 receptors on parietal cells)

29
Q

what second messenger pathway does histamine work vi to increase gastric acid secretion?

A

adenylate cyalase

30
Q

what second messenger pathway does Ach and gastrin work via to increase acid secretion?

A

PLC and Ip3

31
Q

name two molecules that inhibit gastric acid secretion and how?

A
  • somatostatin inhibits adenylate cylase

- mucosal prostaglandin inhibits the H2 receptor

32
Q

what effects do NSAIDs have on gastric secretion?

A

increase it by inhibiting prostaglandin formation

PGs usually inhibit the H2 receptor which decreases gastric secretion

33
Q

what does the cephalic phase of gastric secretion activate and what is it stimulated by?

A

stimulated by vagal stimulation (thought, smell, sight)

- activates chief and parietal cells

34
Q

what stimulates the gastric stage of gastric secretion?

A
  • bolus hitting the stomach
  • local nervous secretory reflexes
  • vagal reflexes
  • gastrin and histamine
35
Q

what is excitatory to the intestinal phase of gastric secretion? (chyme entering the duodenum)

A

chyme with a pH >3 - stimulates gastric secretion

36
Q

what inhibits secretion from stomach to duodenum?

A
  • chyme pH <2

- CCK, secretin, GIP

37
Q

what two molecules form the viscous mucus layer that protects the gastric mucosa?

A

mucopolysaccharide and mucin

38
Q

how does mucin stop acid damage of the mucosa?

A

has basic side chains

39
Q

what condition results from dysfunction of the gastric mucosa and what is the most common cause?

A

gastritis

  • most common cause is helicobacter pylori which produces urease
  • urease produces ammonia which damages the mucosal barrier
40
Q

what is restitution?

A

rapid regeneration of the damaged gastric mucosa due to stem cells in the neck of the gastric glands

41
Q

what cells are dysfunctional in auto immune atrophic gastritis?

A

parietal cells

42
Q

what is the mechanism of autoimmune atrophic gastritis?

A

autoimmune destruction of gastric parietal cells

  • gastric mucosa loses ability to produce acid
  • intrinsic factor deficiency
  • B12 malabsorption
  • pernicious anaemia

BSMS 104 (6 decks)

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