Salivary and gastric secretion Flashcards

1
Q

What is the function of secretions?

A

•Lubricate, protect and aid digestion

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2
Q

What is the difference between endocrine and exocrine glands?

A
  • Exocrine glands (with duct) eg salivary glands, gastric glands
  • Endocrine glands (without duct) eg enteroendocrine cells in stomach and small intestine
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3
Q

What is the role of salivary secretions?

A

ØLubrication

ØProtection – oral hygiene

Initiate chemical digestion

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4
Q

What are the major salivary glands?

A

ØParotid

ØSubmandibular

ØSublingual

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5
Q

What are the dispersed salivary glands?

A

Ømucosa of the mouth and tongue (labial, buccal, palatal, lingual)

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6
Q

What do the major salivary glands secrete?

A
  • Parotid - Serous, watery secretions containing salivary amylase for starch digestion
  • Submandibular - Mixed serous and mucus
  • Sublingual - Mucus: thicker mucus dominant secretions for lubrication
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7
Q

Complete the diagram of the major salivary glands

A
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8
Q

What are the components of saliva?

A

Water (99.5%)

Electrolytes K+, HCO3-, Na+, Cl-, (PO4)3-

Enzymes

  • 1.a-amylase (ptyalin)
  • 2.Lysozyme
  • 3.Lingual lipase (serous salivary glands of tongue)
  • 4.Lactoferrin
  • 5.Kallikrein

Secretory IgA

mucin

Organics urea and uric acid

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9
Q

Complete the diagram on the components of saliva

A
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10
Q

Complete the diagram of a salivary gland

A
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11
Q

What are the properties of the acinar structure of a salivary gland?

A
  • Large volume of saliva produced compared to mass of gland
  • Low osmolarity
  • High K+ concentration
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12
Q

How is hypotonic saliva formed?

A

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
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13
Q

What are the electrolyte concentrations relative to plasma in saliva?

A
  • Na+ and Cl- < plasma
  • HCO3- and K+ > plasma
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14
Q

What saliva is produced at low rate of secretion?

A

•maximum reabsorption of electrolytes produces hypotonic saliva (lower concentration of osmotically active electrolytes)

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15
Q

What saliva is produced at high rate of secretion?

A

•reduced reabsorption of electrolytes produces alkaline, HCO3- rich saliva with increased osmolality closer to that of primary isotonic saliva

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16
Q

How is salivary secretions innervated?

A

Parasympathetic ANS regulation is dominant

  • Sight, thought, smell, taste (esp. sour acidic taste), tactile stimuli, 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
  • Increase salivary secretion, vasodilation, myoepithelial cell contraction
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17
Q

What are the inhibitors of salivary production?

A

•Inhibitors: fatigue, sleep, fear, dehydration

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18
Q

What effect does the sympathetic nervous system have on salivary secretions?

A
  • Overall slight increase in secretion
  • Produces a mucin and enzyme rich saliva
  • Activity is via superior cervical ganglion
  • Initial vasoconstriction (neurotransmitter noradrenaline stimulates a-adrenergic receptors)
  • Later vasodilation (salivary enzyme kallikrein action on blood plasma protein alpha-2 globulin to form vasodilator bradykinin)
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19
Q

What is Sjögren’s syndrome?

A
  • an autoimmune disease that destroys the exocrine glands
  • commonly affects tear and saliva production
  • dry eyes and dry mouth, known as sicca symptoms
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20
Q

What is xerostomia?

A

(dry mouth)

  • Patients lack adequate saliva
  • dental caries and halitosis common due to bacterial overgrowth
  • difficulty speaking or swallowing solid food due to inadequate lubrication
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21
Q

Gastric pits in the mucosa branch into which gastric glands?

A
  • Mucous neck cells – thin mucus
  • Parietal cells - HCl and intrinsic factor
  • Chief cells – pepsinogen (also rennin in neonates), gastric lipase
22
Q

What type of gland is gastric glands?

A

Exocrine gland cells (secrete gastric juice)

23
Q

What are the endocrine cells in the gastric glands?

A

ØG cells - hormone gastrin (antrum)

ØD cell hormone somatostatin

ØEnterochromaffin-like (ECL) cells secrete histamine

24
Q

What gastric gland is found in the body and fundus?

A

Body and fundus (80%)

•gastric/oxyntic glands

25
Q

What gastric gland is found in the antrum

A

Antrum (20%)

•pyloric glands

26
Q

Complete the diagram

A
27
Q

What is the function of the gastric/oxyntic glands?

A

ØExocrine secretion of HCl, pepsinogen, intrinsic factor and mucus

Øparacrine ECL cell secretion of histamine, paracrine D cell secretion of somatostatin

28
Q

What is the function of the pyloric glands?

A

Ømucus and endocrine hormone gastrin

Øparacrine/endocrine somatostatin

29
Q

Complete the table

A
30
Q

What are the componenets of gastric juice?

A

Water and electrolytes

Mucus (glycoprotein mucin)

Pepsinogen pro-enzyme

Rennin in neonates only

Gastric lipase

HCl (pH 1-3)

Intrinsic factor(IF)

31
Q

How are parietal cells specialised to secrete HCl?

A
  • Parietal cells have an intracellular branched 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
32
Q

Which is the apical and basolateral side?

Which cell is this?

A

Gastric parietal cell

33
Q

How does HCL secretion occur?

A
  • 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

34
Q

What stimulates activation of gastric acid secretions?

A
  • ACh: acetylcholine release from vagus
  • Gastrin from G cells
  • Histamine from ECL cells
35
Q

What stimulates inhibition of secretion of gastric acid?

A
  • 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)
36
Q

How does the stimulation of gastric acid secretion occur?

A

PLC phospholipase C -> IP3 inositol triphosphate ->

AC adenylate cyclase

37
Q

What is omeprazole?

A

proton pump inhibitor inactivates H+/K+-ATPase

38
Q

What is cimetidene?

A

•H2 receptor antagonist inhibits stimulus for acid secretion

39
Q

What is atropine?

A

inhibits muscarinic receptors and vagal stimulation of acid secretion

40
Q

What is the secretion of gastrin stimulated by?

A
  • Vagus
  • Stomach distension
  • Peptide secretions
41
Q

What does gastrin promote?

A
  • parietal cell secretion of HCl
  • Chief cell secretion of pepsinogen
  • lower oesophageal sphincter contraction
  • Increased motility of stomach
  • Relaxation of pyloric sphincter
42
Q

What are the 3 phases of gastric secretion?

A
  • Cephalic:
  • Gastric:
  • Intestinal
43
Q

What happens during the cephalic phase of gastric secretions?

A

•Vagus stimulates parietal, chief cell production of gastric juice and hormone gastrin secretion

44
Q

What happens during the gastric phase of gastric secretions?

A

•stimulate parietal, chief, mucus secretion, antral G cells (gastrin stimulates parietal cells directly and indirectly via ECL histamine release)

45
Q

What are the excitory and inhibitory elements of the intestinal phase of gastric secretions?

A
  • Excitatory: Chyme with pH >3, peptides stimulates gastric secretions via vagus and gastrin
  • Inhibitory: Chyme with pH< 2, distention, protein breakdown products, hypo/hyper-osmotic products inhibit gastric secretions via cholecystokinin, secretin, gastric inhibitory polypeptide
46
Q

Complete the diagram on gastric secretions

A
47
Q

Why is the gastric mucosa not damaged?

A
  • 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
48
Q

What is the net result of gastric muscosa adaptations?

A

•Net result - unstirred layer is ~pH7, pepsinogen not activated, prevents enzymatic and chemical damage

49
Q

What is gastritis?

A

(inflammation of the gastric mucosa)

50
Q

What is gastritis caused by?

A
  • Most commonly caused by an infection by the bacteria Helicobacter pylori (Primary cause of peptic ulcer disease)
  • Gram negative bacteria produce urease which forms ammonia from urea, Ammonia neutralizes 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
51
Q

What is restitution?

A

•Following acute damage rapid regeneration is via a process called restitution - rapid division of stem cells located in the neck of gastric glands

52
Q

What is autoimmune atrophic gastritis?

A
  • Autoimmune atrophic gastritis is 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 anemia