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104 Theme 1 - The Alimentary System > Salivary and gastric secretion > Flashcards

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
What gastric gland is found in the antrum
Antrum (20%) •pyloric glands
26
Complete the diagram
27
What is the function of the gastric/oxyntic glands?
ØExocrine secretion of HCl, pepsinogen, intrinsic factor and mucus Øparacrine ECL cell secretion of histamine, paracrine D cell secretion of somatostatin
28
What is the function of the pyloric glands?
Ømucus and endocrine hormone gastrin Øparacrine/endocrine somatostatin
29
Complete the table
30
What are the componenets of gastric juice?
Water and electrolytes Mucus (glycoprotein mucin) Pepsinogen pro-enzyme Rennin in neonates only Gastric lipase HCl (pH 1-3) Intrinsic factor(IF)
31
How are parietal cells specialised to secrete HCl?
* 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
Which is the apical and basolateral side? Which cell is this?
Gastric parietal cell
33
How does HCL secretion occur?
* 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
What stimulates activation of gastric acid secretions?
* ACh: acetylcholine release from vagus * Gastrin from G cells * Histamine from ECL cells
35
What stimulates inhibition of secretion of gastric acid?
* 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
How does the stimulation of gastric acid secretion occur?
PLC phospholipase C -\> IP3 inositol triphosphate -\> AC adenylate cyclase
37
What is omeprazole?
proton pump inhibitor inactivates H+/K+-ATPase
38
What is cimetidene?
•H2 receptor antagonist inhibits stimulus for acid secretion
39
What is atropine?
inhibits muscarinic receptors and vagal stimulation of acid secretion
40
What is the secretion of gastrin stimulated by?
* Vagus * Stomach distension * Peptide secretions
41
What does gastrin promote?
* parietal cell secretion of HCl * Chief cell secretion of pepsinogen * lower oesophageal sphincter contraction * Increased motility of stomach * Relaxation of pyloric sphincter
42
What are the 3 phases of gastric secretion?
* Cephalic: * Gastric: * Intestinal
43
What happens during the cephalic phase of gastric secretions?
•Vagus stimulates parietal, chief cell production of gastric juice and hormone gastrin secretion
44
What happens during the gastric phase of gastric secretions?
•stimulate parietal, chief, mucus secretion, antral G cells (gastrin stimulates parietal cells directly and indirectly via ECL histamine release)
45
What are the excitory and inhibitory elements of the intestinal phase of gastric secretions?
* 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
Complete the diagram on gastric secretions
47
Why is the gastric mucosa not damaged?
* 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
What is the net result of gastric muscosa adaptations?
•Net result - unstirred layer is ~pH7, pepsinogen not activated, prevents enzymatic and chemical damage
49
What is gastritis?
(inflammation of the gastric mucosa)
50
What is gastritis caused by?
* 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
What is restitution?
•Following acute damage rapid regeneration is via a process called restitution - rapid division of stem cells located in the neck of gastric glands
52
What is autoimmune atrophic gastritis?
* 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

104 Theme 1 - The Alimentary System (17 decks)

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