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Module 104: Theme 1 > Salivary and gastric secretions > Flashcards

Salivary and gastric secretions Flashcards

1
Q

Major glands that secrete saliva

A

Submandibular

  • 70% of saliva
  • Saliva is mixed

Parotid:

  • 25% of saliva
  • Serous saliva

Sublingual

  • 5% of salvia
  • Mucous saliva
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2
Q

Structure of saliva glands

A

Blind ended acini that drain into major ducts

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3
Q

Functions of saliva

A

Lubrication: swallowing, speech, dissolving substances.

Protection: Oral bacteria, neuralisation of acid from oral bacteria, wash away bacteria, contains substances to inhibit bacterial growth

Digestion:

  • alpha amylase; breaks down carbs
  • lingual lipase; breaks down lipids
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4
Q

Alpha amylase

A

Also called ptyalin

Enzyme found in saliva that hydrolyses starch

It becomes denatured by gastric acid.

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5
Q

Lingual lipase

A

Enzyme in saliva that hydrolyses triglycerides.

Secreted from salivary glands on the tongue surface and remains active in the stomach.

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6
Q

Sjogren’s syndrome

A

An autoimmune disease that attacks exocrine glands; especially salivary and tear glands.

Symptoms: [sicca symptoms]
Dry mouth
Dry eyes

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7
Q

Xerostomia

A

A condition where a patient lacks adequate saliva.

Consequence:

  • Dental cavities due to loss of protection against bacteria.
  • Difficulty speaking
  • Difficulty swallowing
  • Halitosis (bad breath due to bacterial overgrowth).
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8
Q

Two types of salivary secretions

A

Serous:
Mainly composed of ptyalin which hydrolyses starch.

Mucous:
Mainly composed of mucin- lubricant

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9
Q

Primary saliva

A

The fluid firstly released from the acinar cells in the salivary glands.

It resembles acinar fluid.

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10
Q

First stage of salivary secretion: Primary fluid secretion

A

Acinar cells:
- Basolaterally, Na+, K+, 2Cl- cotransporter takes in Cl- ions.

  • Apically, Ca2+ activated Cl- channels release Cl- ions into acinar lumen.
  • Na+ enters the acinar lumen paracellularly through leaky tight junctions.
  • Water enters acinar lumen via aquaporin 5 or paracellularly
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11
Q

Second stage of salivary secretion: NaCl reabsorption and K+ secretion.

A

At the ductal cells:

  • Removal of Na+ ions. Apical Na+ channels take Na+ into duct cells.
    Na+ leaves ductal cell via basolateral Na+/K+ ATPase
  • Removal of Cl-.
    Cl- channels at the apical and basolateral membrane of the ductal cells.
  • Water not reabsorbed. Ductal cell tight junctions are not leaky.
    No aquaporins in apical membranes.
  • K+ secrete into ductal lumen via potassium proton exchangers at the apical membrane.
  • HCO3- secreted into ductal lumen via bicarbonate chloride exchanger at the apical membrane.

This forms hypotonic saliva.

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12
Q

Salivary flow rate

A

The greater the rate of secretion, the less hypotonic saliva is.

Slower rate of secretion= more time for the reabsorption of electrolytes.

Faster flow = more Na+ and Cl-

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13
Q

Electrolyte components in saliva

A

Na+ and Cl- less than in plasma

HCO3- and K+ greater than that in plasma

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14
Q

Central control of salivary secretions

A

Efferent nerves from salivary nuclei in the pons reach salivary glands;

  • Glossopharyngeal nerves
  • Facial nerves

AcH is released—> acts on muscarinic receptors

Parasympathetic and sympathetic stimulation.

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15
Q

What stimulates and inhibits saliva secretion centrally?

A

Secretion is stimulated by:

  • Thoughts
  • Smell
  • Taste
  • Nauseas

Secretion is inhibited by:

  • Dehydration
  • Fatigue
  • Fear
  • Sleep
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16
Q

Sympathetic stimulation of the salivary glands

A

Increases output of amylase

Reduces blood flow to glands = decreased rate of secretion.

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17
Q

Parasympathetic stimulation of the salivary glands

A

Increases blood flow to the glands

Promotes secretion of saliva- myoepithelial cells around acini and duct contracts to eject saliva.

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18
Q

Hormonal effect on saliva secretion

A

Superior cervical ganglion innervates the salivary glands.

Aldosterone is secretion to increase ductal Na+ absorption and K+ secretion.

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19
Q

Components of gastric juice

A

Water, electrolytes

HCl

Pepsin

Mucus: protects surface epithelial cells from acid and pepsin erosion

Intrinsic factor

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20
Q

Function of HCl in gastric juice

A

Hydrolyses fat and starch.

Antiseptic

Provides optimum pH for pepsin- converts pepsinogen to pepsin.

21
Q

Pepsin

A

Endopeptidase that leaves peptide bonds in proteins

Secreted as inactive pepsinogen- only activated at pH<5

22
Q

Origins of gastric secretions

A

Exocrine [ pepsin, IF, HCl] : fundus, corpus of the stomach.

Endocrine [secretes gastrin]: antrum

23
Q

Mucous cells

A

Cell found in the gastric gland that secretes mucus- protective barrier

24
Q

D cells

A

Endocrine cells that secretes somatostatin

Found in gastric glands

25
Q

Chief cells

A

Cells of the gastric glands that secrete pepsinogen

26
Q

Parietal/ oxyntic cells

A

Cells of the exocrine region in the stomach- fundus + corpus.

Secretes acid and intrinsic factor

27
Q

Histamine cells

A

Cells of the exocrine region in the stomach.

Secretes histamine which stimulates gastric secretion.

28
Q

Endocrine G cells

A

Cells of the endocrine region in the stomach that produces gastrin.

29
Q

Protection against self digestion and mechanical damage

A

Secretion of mucus layer by mucous cells.

Mucin and HCO3- released neutralise H+ ions.

Tight junctions between cells prevent acid from entering underlying tissue.

The mucosal barrier has a pH of around 7, prevents the activation of pepsinogen— prevents enzymatic damage.

30
Q

Gastritis

A

Inflammation of the gastric mucosa.

Most commonly bacterial cause.

Can also be caused by:

  • smoking
  • alcohol
  • NSAIDs
  • chronic stress
31
Q

Regeneration of gastric cells

A

When the surface epithelium is damaged, stem cells at the neck of gastric glands rapidly divide.

This is called restitution- helps to heal gastritis

32
Q

Acid secretion from oxyntic cell

A

Tubulovesicular membrane contains H+/K+- ATPase that causes acid secretion.

When stimulated, tubulovesicular membrane fuses to form canalicular membrane- increased SA.

Fusion causes more K+/H+- ATPasee to be inserted into canalicular membrane.
- K+ and Cl- channels also inserted

33
Q

Formation of acid in oxyntic cells

A

H+ and HCO3- generated via H2CO3 breakdown via carbonic anhydrase.

H+ pumped into lumen via H+/K+ ATPase

HCO3-/ Cl- exchanger in the basolateral membrane brings Cl- into the cell.

Cl- leaves cell via Cl- channel, down its concentration gradient.

34
Q

Postprandial alkaline tide

A

State where the gastric blood becomes alkaline due to the entry of HCO3- during acid production.

HCO3- is exchanged for Cl- basolaterally.

35
Q

Proton pump inhibitors

A

Drugs that inhibit H+/K+- ATPase on the luminal surface of oxyntic cells.

Example: Omeprazole

36
Q

Stimulators of acid secretion

A

Gastrin- from antral G cells.

Histamine- mast cells

AcH- postsynaptic vagal fibres innervating gastric mucosa.

37
Q

Paracrine inhibitors of gastric acid secretion

A

Somatostatin- antral and oxyntic D cells.
- Pancreatic cells

Prostaglandins- mucosal cells

38
Q

Gastrin and AcH stimulation

A

Both stimulants of acid secretion.

Stimulation is triggered by an increase in intracellular Ca2+.

39
Q

Histamine

A

Acid secreting stimulant released by mast cells.

Binds to H2 receptors on oxyntic cells.

Stimulates acid secretion by increasing intracellular cAM.

40
Q

Prostaglandin E2

A

Molecule produced in the stomach.

Antagonist of histamine - inhibits intracellular production of cAMP

This inhibits acid secretion.

NSAIDs inhibits prostaglandin E2

41
Q

Atrophic gastritis

A

Autoimmune condition where antibodies attack gastric parietal cells.

Causes hypochlorhydria and IF deficiency- leads to pernicious anaemia.

42
Q

Hypochlorhydria

A

Condition that describes insufficient acid secretion.

43
Q

Cephalic controlled gastric secretion

A

This accounts for 35% control of secretion.

Triggered by sight, smell, taste, chewing.

This stimulates the vagus nerve to secrete AcH at the synapse of gastric cells.

This increases intracellular Ca2+ and stimulates the secretion of gastrin from G cells.

Acts on parietal cells and causes the release of HCl and pepsin.

44
Q

Gastric regulation of gastric secretion

A

This accounts for controlling 60% of gastric secretions.

  1. Distension of the stomach stimulates vago-vagal and local reflexes.
  2. This stimulates the release of ACh at nerve endings.
  3. Stimulates release of gastrin from G cells of the stomach.
  4. Gastrin acts on parietal cells to stimulate release of HCl and Pepsin
45
Q

Intestinal regulation of gastric secretion

A

This accounts for 5% of gastric secretion regulation.

  1. Amino acids from protein digestion in the duodenum is detected.
  2. Stimulates G cells in the intestines to stimulate parietal cells.
  3. This stimulates gastric secretions.

Inhibitory effects:

  • Protein digestion detected stimulates CCK (cholecystokinin) and GIP (gastric inhibitory polypeptide).
  • CCK and GIP inhibit the secretion of gastrin and inhibits gastric parietal cells.
46
Q

Gastrin

A

A hormone released from the G cells in the pylorus and duodenum.
- Acts on CCK2 receptors

Secretion is stimulated by the release of amino acids and peptides in the stomach.

Secretion is inhibited by low pH.

47
Q

Histamine

A

Molecule released by ECL cells close to parietal cells.

ECL cells stimulated by gastrin and ACh cause the release of histamine.

Histamine acts on parietal cells to stimulate gastric secretions.

48
Q

GRP

A

Gastrin releasing peptide

Stimulated by vagal stimulation

Released from G cells to stimulate gastrin release.

Inhibits the release of somatostatin from D cells.

Module 104: Theme 1 (18 decks)

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