salivary and gastric secretion Flashcards
1
Q
what do secretions do?
where do they come from? 2
A
- lubricate, protect and aid digestion
- exocrine glands (with duct)
- endocrine glands (without duct)
2
Q
what is the role of salivary secretions? 3
A
- lubrication
- protection (oral hygiene)
- initiate chemical digestion
3
Q
what are the major salivary glands? 3
A
- parotid (under ear, back of jaw)= serous, watery solution containing amylase for starch digestion
- submandibular (under tongue, closer to oesophagus)= mixed serous and mucus
- sublingual (under tongue, closer to lips)= mucus, thicker mucus dominant secretions for lubrication
4
Q
what are dispersed salivary glands? 5
A
- mucosa of the mouth and tongue
- labial
- buccal
- palatal
- lingual
5
Q
what is the composition of saliva and role? 6
A
- water (99.5%)= solvent dissolves food components to aid taste, swallowing, ignition of digestion and oral hygiene
- electrolytes (K+, HCO3-, Na+, Cl-)= buffer for acidic food contents
- enzymes (different functions)
- secretory IgA= prevents microbial attachment to the epithelium
- mucin= lubrication
- organics urea and uric acid= waste product removal for excretion
6
Q
what are the different enzymes in salvia and their role? 5
A
- alpha amylase (ptyalin)= hydrolysis of alpha-1,4 glycosidic bonds in starch to disaccharide maltose, trisaccharide maltose and alpha-dextrin
- lysozyme= hydrolysis of peptidoglycan in wall of gram-negative bacteria
- lingual lipase (serous salivary glands of the tongue)= hydrolysis of lipid triglycerides to fatty acid and diglycerides (optional in acidic pH)
- lactoferrin= chelates iron to prevent microbial manipulation
- kallikrein= converts plasma protein alpha-2-globulin into bradykinin
7
Q
describe the acinar structure of salivary glands? 3
A
- Acinar cells: serous or mucin secreting
- Myoepithelial cells: around the acinar cells and are contractile in nature to help move the secretions through the duct
- Ductal cells: columnar, line the salivary gland duct and modify the primary saliva
8
Q
what are the unique properties of a salivary gland? 3
A
- Large volume of saliva produced compared to the mass of the gland
- Low osmolarity
- High K+ concentration
9
Q
describe the 2 stage formation of hypotonic saliva? 2
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. This produces HCO3- and K+ rich hypotonic saliva
10
Q
describe how the composition of saliva can change? 4
A
- with flow rate
- Electrolyte composition= Na+ and Cl-plasma
- Low rate of secretion= maximum reabsorption of electrolytes produced hypertonic saliva (lower concentration of osmotically active electrolytes)
- High rate of secretion= reduced absorption of electrolytes produces alkaline HCO3- rich saliva with increases osmolality closer to that of the primary isotonic saliva
11
Q
what normally regulates the secretions of saliva? 7
A
- parasympathetic ANS regulation is dominant
- Simulation= sight, thought, smell tase, tactile stimuli, nausea
- Signal superior and inferior salivatory nuclei in the medulla
- Via cranial nerve VII (facial nerve) for the sublingual and submandibular gland
- Via cranial nerve IX (glossopharyngeal nerve) for the parotid gland
- Increase salivary secretion, vasodilation, myoepithelial cell contraction
- Inhibitors= fatigue, sleep, fear, dehydration
12
Q
describe the sympathetic neural stimulation for the secretion of saliva? 5
A
- Overall slight increase in secretion
- Produces a mucin and enzyme rich saliva
- Activity is via superior cervical ganglion
- Initial vasoconstriction (neurotransmitter noradrenaline stimulates beta-adrenergic receptors)
- Later vasodilation (salivary enzyme kallikrein action on blood plasma protein alpha-2-globulin to form vasodilator bradykinin)
13
Q
name 2 salivary gland dysfunctions and 3 things about each?
A
- Sjogren’s syndrome:
- An autoimmune disease that destroys the exocrine glands
- Commonly affects tear and saliva production
- Dry eyes and dry mouth, known as sicca syndromes
- .
- Xerostomia (dry mouth)
- Patients lack adequate saliva
- Dental caries and halitosis common due to bacteria overgrowth
- Difficulty speaking or swallowing solid food due to inadequate lubrication
14
Q
describe gastric glands? 9
A
-gastric pits in the mucosa branch into gastric pits
- Exocrine gland cells (secrete gastric juice):
- Mucous neck cells= thin mucus
- Parietal cells= HCl and intrinsic factor
- Chief cells= pepsinogen (also rennin in neonates), gastric lipase
- .
- Endocrine cells:
- G cells= hormone gastrin (antrum)
- D cell= hormone somatostatin
- Enterochromaffin-like (ECL) cells secrete histamine
15
Q
what are the two major types of gastric gland and 3 subcategories of each?
A
- Body and fundus (80%):
- Gastric/oxyntic glands
- Exocrine secretion of HCl, pepsinogen, intrinsic factor and mucus
- Paracrine ECL secretion of histamine, paracrine D cell secretion of somatostatin
- .
- Antrum (20%)
- Pyloric glands
- Mucus and endocrine hormone gastrin
- Paracrine/endocrine somatostatin
16
Q
what are the components of gastric juice and what they do? 7
A
- Water and electrolytes= medium for action of acids and enzymes, digestion or organic substances
- Mucus (glycoprotein mucin) (mucus neck) = protects surface epithelium from acid/pepsin
- Pepsinogen pro-enzyme (chief) = active pepsin form is an endopeptidase that cleaves peptide bonds (protein to make smaller peptides)
- Rennin in neonates only (chief) = coagulation of milk through casein proteolysis
- Gastric lipase (chief)= triglycerides to fatty acid and diglycerides
- HCl (pH1-3) = converts pro-enzyme pepsinogen to pepsin, denatures proteins, kills microorganisms
- Intrinsic factor (parietal) = vitamin B12 absorption in the ileum, erythropoiesis in bone marrow, absence= pernicious anaemia
17
Q
describe HCl secretion by parietal cells? 4
A
- Parietal cells have in intracellular branches 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
18
Q
how does HCl secretion occur? 4
A
- H+/K+ ATPase proton pump drives active secretion of H+
- Carbonic anhydrase catalyses formation of HCO3- producing H+ ions
- HCO3- exchanged for Cl- (alkaline tide – gastric venous blood becomes more alkaline postprandially)
- Cl- diffuses into the lumen
19
Q
what activates gastric acid secretion? 3
A
- Ach=acetylcholine release from vagus
- Gastrin from G cells
- Histamine from ECL cells
20
Q
what inhibits gastric acid secretion? 2
A
- Somatostatin from D cells (paracrine and endocrine): inhibits adenylate cyclase (AC)
- Musical prostaglandin antagonists for H receptor (NSAIDS inhibit prostaglandin formation and increase gastric acid secretion)
21
Q
what stimulates the parietal cell to secrete acid? 3
A
- PLC phospholipase C
- IP3 inositol triphosphate
- AC adenylate cyclase
22
Q
describe pharmalogical inhibition of gastric acid? 3
A
- Omeprazole= proton pump inhibitor inactivates H+/K+ ATPase
- Cimetidine= H2 receptor antagonist inhibits stimulus for acid secretion
- Atropine= inhibits muscarinic receptors and vagal stimulation of acid secretion
23
Q
what hormone promotes gastric secretion, how does it do this? 6
A
- gastrin (promoted by the vagus, distention of the stomach and peptide)
- Promotes:
- Parietal cell secretion of HCl
- Chief cell secretion of pepsinogen
- Lower oesophageal sphincter contraction
- Increased motility of the stomach
- Relaxation of pyloric sphincter
24
Q
what are the 3 phases of gastric secretion?
A
- Cephalic= vagus stimulates parietal, chief cell production of gastric juice and hormone gastrin secretion
- Gastric= stimulates parietal, chief, mucus secretion, antral G cells (gastrin stimulates parietal cells directly and indirectly via ECL histamine release)
- Intestinal=
- excitatory: chyme with pH>3, peptides stimulate gastric secretions via vagus and gastrin
- inhibitory: chyme with pH<2, distention, protein breakdown produces, hypo/hyper-osmotic products inhibit gastric secretions via cholecystokinin, secretin, gastric inhibitory polypeptide
25
Q
why is the gastric mucosa not damaged? 4
A
- Surface mucous glands secrete viscous mucus layer of mucopolysaccharides/proteins
- Mucous viscosity generates a mucosal barrier= Mucin has basic side chains and HCO3- secreted from surface epithelial cells both neutralise H+ ions
- Tight junctions stop acid damaging underlying tissue
- Net result= unstirred layer of pH7, pepsinogen not activated, prevents enzymatic and chemical damage
26
Q
describe a dysfunction of the gastric mucosa? 5
more specific type of this? 3
A
- Gastritis (inflammation of gastric mucosa)
- Most commonly causes by an infection by the bacteria Helicobacter pylori (primary cause of peptic ulcer disease)
- Gram negative bacteria produced urease which forms ammonia from urea, ammonia neutralizes bactericidal acid and is toxic to the mucosal barrier
- Also caused by smoking, alcohol, nonsteroidal anti-inflammatory drugs (NSAIDS) (inhibit cyclooxygenase to reduce protective prostaglandin synthesis), chronic stress
- Following acute damage, rapid regeneration is via a process called restitution= rapid division of stem cells located in the neck of gastric glands
- Autoimmune atrophic gastritis
- 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 anaemia
