Salivary and Gastirc Secretory Functions Flashcards
is saliva hyper or hypotonic
hypotonic
what type of control is saliva under
neuronal not hormonal
do hormones have an influence on saliva
they can modify it
what are the functions of saliva
taste, lubrication, protection, digestion, speech
What are the main components of saliva
water, mucus, alpha amylase, lingual lipase, ribonuclease, lysozyme, lactoferrin, lactoperoxidase, IgA, Bicarb
what are the functions of water and mucus in the saliva
dissolving, tasting and swallowing food. lubricaitons and makes a cohesive bolus
what is the function of alpha amylase in saliva
card digestion, breaks the alpha 1-4 bonds
What is the role of lingual lipase in saliva
fat digestion, hydrolysis of dietary lipid
what is the role of lysozyme in saliva
antibacterial, innate and aquired immunity
what is the role of lactoferrin in saliva
chelates iron
what is the role of bicarb in saliva
minimize tooth decay and neutralize refluxed gastric acid into lower esophagus
what is the primary secretory products of acini and duct cells
alpha amylase, mucus and ECF
What do acini cells secrete
saliva H2O na Cl K HCO3 and amylase
what is the role of myoepithelial cells in salivary glands
motile, contract to expel saliva
what is the role of ducta cells in salivary glands
modify secretion by modifying electrolytes
Na Cl reabsorbed
K HCO3 secreted
what is the role of the striated duct epithelium tight junction in salivary glands
H2O cannot leave duct
What is the ufunctional unit of the salivary gland
salivon
At low rates of secretion describe saliva
hypotonic, high K, low NaCl
at high secretion levels describe saliva
osmolality increases, high HCO3, high pH
Salivary duct cells produce a hypotonic fluid that usually has what composition of electrolytes
low NaCl
rich KHCO3
What are the steps for Na reabsorption in salivary glands
Na enters through epithelial Na Channels
NaK ATPase pump extrudes Na
What are the steps for Cl reabsorption in salivary glands
Cl enters through Cl HCO3 exchanger
Cl exits through basolateral Cl Channels
Where is HCO3 secreted by salivary glands
apical Cl-HCO3 exchanger
how is K secreted by salivary gland cells
uptake of K though Na K ATPase
Can water pass through epithelial cells of the salivary glands
no
Which parts of ANS controls flow of salivary gland secretions
SAN and PAN
Which branch of ANS has more control over salivary glands
PAN
Describe what SAN stimulate promotes in salivary glands
major B R so secrete protein, cAMP
minor alpha R to secrete fluid, IP3
describe what PAN stimulates in salivary gland
M3 R to secrete fluid, IP3
vasodilation to surrounding vessels
activation of acinar and duct cell transporter
What hormones have an effecton salivary composition
ADH and aldosterone can modify Na K levels
Kallikrein makes bradykinin (vasodilator)
What activates the ANS to salivary glands
taste, sound, smell
What inhibits ANS to salivary glands
sleep, fear, antidepreseant meds, dehydration, fatigue
how do you treat someone with excessive drooling
anticholinergics and surgical removal of sublingual glands
What is Xerostomia
dry mouth due to absence of saliva production
what can cause xerostomia
buccal infections, dental caries, drugs, radiation, autoimmune disease
What is Sjogrens syndrome
autoimmune to salivary and lacrimal glands resulting in decreased saliva and tear production
difficuly swallowing, speeech etc
How does cystic fibrosis affect salivary glands
elevated Na Ca and protein in saliva, sweat, pancreatic fluid and bronchial secretion
lack CFTR or chloride transporter
How does addisons affect salivary gland
increase Na in saliva, dereased reabsorption
how does Primary aldosteronism and Cushings affect salivary glands
decrease Na in salive, increased reabsorption (salivary NaCl is zero with increased K levels)
How can digoxin therapy affect salivary glands
increase Ca and K in saliva
How can parkinsons and tumors of the mouth and esophagus affect saliva
increased production due to unusual local reflexes and increased neuro stimulation
Is stomach fluid hypo, iso or hypertonic
isotonic
What does the proximal portion of the stomach secrete
HCl, Pepsinogen, IF, Mucus, HCO3, water
what does the distal portion of the stomach secrete
gastrin, somatostatin
Which part of the stomach has endocrine and paracrine actions
the distal
What are the types of secretory epithelial cells in the stomach
superficial, mucus neck cell, stem cell, parietal, chief and endocrine
What do the mucus neck cells in the stomach secrete
Mucus and bicarb
whar do the parietal cells in the stomach secrete
HCl, IF
What is IF required for in stomach
required for Vit B12 absorption in ileum
what is another name for Vit B12
cobalamine
What do the chief cells in the stomach secrete
pepsinogen and renin
what do the endocrine cells in the stomach secrete
enterochromaffin like cells secrete histamine
G cells- gastrin
D cells- somatostatin
Whey are Oxyntic glands in the stomach
fundus and body
What type of secretory cells are in the oxyntic glands
parietal (oxyntic)
peptic (chief, zymogenic)
mucus
what do parietal cells secrete
HCl for protein breakdown, pepsinogen
IF for vit B12 absorption
What do peptic,c hief cells secrete
Pepsinogen/zymogens- converted to pepsin
chymosin, gastric lipase
What do mucus cells secrete
mucus both thick and thin
where in the stomach can you find pyloric glands
antrum and pyloric region of stomach
What type of cells are in pyloric glands
G cells and Mucus cells
What do G cells secrete
Gastrin which stimulates parietal cells HCl and peptic cells (pepsinogen)
what do mucus cells secrete
mucus thin and thick
how often is the stomach mucosa replaced
every 3 days
What cells in the stomach are responsible for secretion in between meals
the non-parietal cells that maintain high NaCl and low H and K
what cells are responsible for stomach secretions after meals
parietal cells to maintain high H Cl
and low Na K
Describe “alkaline tide” of stomach
increased pH of venous blood leaving stomach after a meal because H+ has increased secretion into the lumen so HCO3 is secreted to maintain neutrality
What are the 3 mechanisms of direct stimulation of parietal cells
ACh releaed from vagus binds M3 R
Histamine recleased binds H2 R
Gastrin released binds CCKb R
Describe the indirect stimulatroy mechanisms of parietal cells
ACh released from vagus binds M3R on ECL and release histamine
Gastrin released bund to CCKb on ECL to released histamine
Histamine released then binds H2 R on parietal cells
Which agonist of the parietal cells is most potent
gastrin
What are some inhibitors of parietal cells and how do they block the cells
somatostatin and PGs
somatostatin binds to SST T
PGs ving to PGs R
The release of Ach to parietal cells is controlled by what
neuronal
the release of gastrin on parietal cells is controlled how
hormonally
the release of histamine on parietal cells is controlled by
paracrine
What stim and inhibits release of somatostatin
pH dependent
inhibited by vagal stimulation
What is the effect of Gastric inhibitory peptide
inhibits gastrin and acid in duodenum and jejunum
What is natures antacid
secretin, inhibits gastrin and acid release in duodenum
What cells secrete CCK
I cells of SI
What cells secrete secretin
S cells in SI
What cells release GIP
K cells in duodenum and jejunum
What cells secrete Somatostatin
D cells of stomach and duodenum
and cells in pancreatic islets
What are the stimuli for decrease in gastric secretions
distension of stomach ad it empties
accumulation of acid in the antrum and duodenum
fat acid hypertonicity and distension in duodenum
What are the 3 phases of gastric secretions
Cephalic phase
Gastric Phase
Intestinal Phase
What phase does most of the gastric secretion take place
gastric phase
What is a vagotomy and what it it used for
cutting of vagus
inhibit gastric secretion and used to Tx peptic ulcers
side effects are diarrhea and delay in gastric emptying
What is selective vagotomy
cutting vagal nn supplying parietal cells only
What are the 3 hormones in the duodenum that inhibit acid secretion
secretin
GIP
CCK
What structural component is responsible for peptic ulvers
damaged gastric mucosal barrier from over load of H+
What are the 2 main signals for pepsinogen secretion
vagal by Ach
direct response to gastric acid
How does IF help with vit B 12 absorption
bind into a complex and then bind to cubulin in the terminal ileum for R mediated endocytosis
What could result from defective Vit B 12 absorption, or absent IF
defective RBC production,, pernicious anemia
What is the function of the mucus secreted by surface cells
acts as diffusion barrier for H and pepsin, also traps HCO3 to titrate H and innactivate pepsin
What happens if H penetrates into gastric epithelium
destorys mast cells and so histamine is released and there is great damage from inflammation PAFs LTs
What are some substances that can lead to mucosal damage
alcohol
salicylates
H. pylori
Bile acids
What does pepsin digest
proteins
What is the prmiary stimulus for secretin release
acidic chym
what are the general actions of secretin
increased HCO3 secretion
increase biliary and SI buffer system
What is the main action of CCK
increase pancreatic enzyme secretion to break down small peptides and amino acids and fats
What hormone increases pancreatic insulin secretion
GIP
What is the main cause of peptic ulcers
H pylori
How can aspirin cause ulcers
NSAID inhibit Cox-1 which forms PGs, so no protective PGs in gastric mucosa
it is a weak acid that is easily absorbed in low pH of stomach adn then causes histamine release and disruption of mucosal layer
What is more common gastric ulcers of duodenal
duodenal
What pathologies cause increased gastrin secretion
gastrinoma or zollinger-Ellison
What is used to test gastric acid levels
pentagastrin challenge
describe the difference between gasttrionmas and H pylori chornic infection on gastrin release
increase acid release in gastrinomas and decrease gastric acid release in chronic inflammation
how does pernicious anemia affect gastrin secretion
lack of IF decreases H+ and somatostatin so now there is no inhibition of gastrin release so this increases while there is no H+
What type of bacterium is H pyloric
gram negative
What are the actions of H pylori on gut
high urease activity to neutralize acid and dmage epithelium
these damaged cells now increase acid secretion
results in inflammation and mucosal degredation
t/F everyone iwth a gastric ulcer is caused by h pylori or has it too
True
What factors strenghten the mucosal barrier
mucuc HCO3 gastrin PGs epidermal growth factor
What are types of antacids
NaHCO3 (alka-seltzer) or KHCO3
what are H2 R blockers
rantidine (zantaz) and cimetidine (tagamet)
What are proton pump inhibitos
omeparazole (prilosec)
What are antibiotics used for H pylori infection
clarithromycin and cymxicillin or metronidazole
What are surgical Tx for ulcers
vagotomy and anterctomy
What are long term effects of proton pump inhibitors
pneumonia
clostridium difficile in gut
osteoporosis
What is the drug dicyclomine and why don’t we use it
blocks Ach R, however no specific so does this everywhere in body
Where is the primary saliva produced and where is it modified
produced in the end pieces called acini and is modified through th ducts
does the saliva become hypotonic or hypertonic as it moves throughducts
more hypotonic
All regulatroy control of salivation is from what
ANS
What allows parietal cells to secrete acid
H K pump ATPase on apical side
During the cephalic phase of secretion are the parietal cells directly or indirectly stimulate and how?
directly via Ach and gastrin release
When the pH in the luminal contents of stomach drop below 3 what happens
somatostatin is released from D cells in antrum and oxyntic gland area
