Salivary and gastric secretions Flashcards
Major glands that secrete saliva
Submandibular
- 70% of saliva
- Saliva is mixed
Parotid:
- 25% of saliva
- Serous saliva
Sublingual
- 5% of salvia
- Mucous saliva
Structure of saliva glands
Blind ended acini that drain into major ducts
Functions of saliva
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
Alpha amylase
Also called ptyalin
Enzyme found in saliva that hydrolyses starch
It becomes denatured by gastric acid.
Lingual lipase
Enzyme in saliva that hydrolyses triglycerides.
Secreted from salivary glands on the tongue surface and remains active in the stomach.
Sjogren’s syndrome
An autoimmune disease that attacks exocrine glands; especially salivary and tear glands.
Symptoms: [sicca symptoms]
Dry mouth
Dry eyes
Xerostomia
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).
Two types of salivary secretions
Serous:
Mainly composed of ptyalin which hydrolyses starch.
Mucous:
Mainly composed of mucin- lubricant
Primary saliva
The fluid firstly released from the acinar cells in the salivary glands.
It resembles acinar fluid.
First stage of salivary secretion: Primary fluid secretion
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
Second stage of salivary secretion: NaCl reabsorption and K+ secretion.
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.
Salivary flow rate
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-
Electrolyte components in saliva
Na+ and Cl- less than in plasma
HCO3- and K+ greater than that in plasma
Central control of salivary secretions
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.
What stimulates and inhibits saliva secretion centrally?
Secretion is stimulated by:
- Thoughts
- Smell
- Taste
- Nauseas
Secretion is inhibited by:
- Dehydration
- Fatigue
- Fear
- Sleep
Sympathetic stimulation of the salivary glands
Increases output of amylase
Reduces blood flow to glands = decreased rate of secretion.
Parasympathetic stimulation of the salivary glands
Increases blood flow to the glands
Promotes secretion of saliva- myoepithelial cells around acini and duct contracts to eject saliva.
Hormonal effect on saliva secretion
Superior cervical ganglion innervates the salivary glands.
Aldosterone is secretion to increase ductal Na+ absorption and K+ secretion.
Components of gastric juice
Water, electrolytes
HCl
Pepsin
Mucus: protects surface epithelial cells from acid and pepsin erosion
Intrinsic factor
Function of HCl in gastric juice
Hydrolyses fat and starch.
Antiseptic
Provides optimum pH for pepsin- converts pepsinogen to pepsin.
Pepsin
Endopeptidase that leaves peptide bonds in proteins
Secreted as inactive pepsinogen- only activated at pH<5
Origins of gastric secretions
Exocrine [ pepsin, IF, HCl] : fundus, corpus of the stomach.
Endocrine [secretes gastrin]: antrum
Mucous cells
Cell found in the gastric gland that secretes mucus- protective barrier
D cells
Endocrine cells that secretes somatostatin
Found in gastric glands
Chief cells
Cells of the gastric glands that secrete pepsinogen
Parietal/ oxyntic cells
Cells of the exocrine region in the stomach- fundus + corpus.
Secretes acid and intrinsic factor
Histamine cells
Cells of the exocrine region in the stomach.
Secretes histamine which stimulates gastric secretion.
Endocrine G cells
Cells of the endocrine region in the stomach that produces gastrin.
Protection against self digestion and mechanical damage
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.
Gastritis
Inflammation of the gastric mucosa.
Most commonly bacterial cause.
Can also be caused by:
- smoking
- alcohol
- NSAIDs
- chronic stress
Regeneration of gastric cells
When the surface epithelium is damaged, stem cells at the neck of gastric glands rapidly divide.
This is called restitution- helps to heal gastritis
Acid secretion from oxyntic cell
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
Formation of acid in oxyntic cells
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.
Postprandial alkaline tide
State where the gastric blood becomes alkaline due to the entry of HCO3- during acid production.
HCO3- is exchanged for Cl- basolaterally.
Proton pump inhibitors
Drugs that inhibit H+/K+- ATPase on the luminal surface of oxyntic cells.
Example: Omeprazole
Stimulators of acid secretion
Gastrin- from antral G cells.
Histamine- mast cells
AcH- postsynaptic vagal fibres innervating gastric mucosa.
Paracrine inhibitors of gastric acid secretion
Somatostatin- antral and oxyntic D cells.
- Pancreatic cells
Prostaglandins- mucosal cells
Gastrin and AcH stimulation
Both stimulants of acid secretion.
Stimulation is triggered by an increase in intracellular Ca2+.
Histamine
Acid secreting stimulant released by mast cells.
Binds to H2 receptors on oxyntic cells.
Stimulates acid secretion by increasing intracellular cAM.
Prostaglandin E2
Molecule produced in the stomach.
Antagonist of histamine - inhibits intracellular production of cAMP
This inhibits acid secretion.
NSAIDs inhibits prostaglandin E2
Atrophic gastritis
Autoimmune condition where antibodies attack gastric parietal cells.
Causes hypochlorhydria and IF deficiency- leads to pernicious anaemia.
Hypochlorhydria
Condition that describes insufficient acid secretion.
Cephalic controlled gastric secretion
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.
Gastric regulation of gastric secretion
This accounts for controlling 60% of gastric secretions.
- Distension of the stomach stimulates vago-vagal and local reflexes.
- This stimulates the release of ACh at nerve endings.
- Stimulates release of gastrin from G cells of the stomach.
- Gastrin acts on parietal cells to stimulate release of HCl and Pepsin
Intestinal regulation of gastric secretion
This accounts for 5% of gastric secretion regulation.
- Amino acids from protein digestion in the duodenum is detected.
- Stimulates G cells in the intestines to stimulate parietal cells.
- 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.
Gastrin
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.
Histamine
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.
GRP
Gastrin releasing peptide
Stimulated by vagal stimulation
Released from G cells to stimulate gastrin release.
Inhibits the release of somatostatin from D cells.
