Salivary and Gastric Secretory Functions (choudhury) Flashcards
under what control is saliva?
neuronal
hormones just modify
what are some functions of saliva
taste lubrication protection digestion speech not essential for life
what is the composition of parotid salivary gland secretions
serous thin saliva
25 percent of saliva
what is the compostion of submandibular saliva
serous/mucous (thick)
70 percent
what is the composition of sublingual saliva
serous/mucous
5 %
what is the function of water in saliva
facilitates speech
dissolving and tasting food
swallowing
what is the function of kallikrein in saliva
activates bradykinin - dilates arterioles, constricts veins and increases flow to secretory glands
what is the function of bicarb in saliva
minimizes tooth decay
neutralizes refluxed gastric acid into lower esophagus (heartburn)
what tonicity is saliva and why
saliva is hypotonic so that food can dissolve into int and we can TASTE
cannot taste proteins
what is the function of myoepithelial cells
motile, contracts and expels saliva
what is the function of ductal cells
modifies secretion by modifying electrolytes
Na, Cl- reabsorbed
K and HCO3- are secreted
what is the function of striated duct epithelium tight junctions
H20 cannot leave duct
making it hypotonic
what do acini secrete
saliva (H20, Na, Cl, K, HCO3-, amylase)
what is the relationship between salivary rate of secretion and composition
at low rates of secretion –> saliva is hypotonic (high K+, low Na and Cl-)
at higher rates of secretion –> osmolality increases (High HCO3- conc and high pH = alkaline)
what is the major receptor for the sympathetic stimulation of saliva
minor?
Beta receptors –> leads to protein secretion
minor is alpha receptors –> leads to fluid secretion
which on (para or symp) exerts more control over salivary gland secretion?
parasympathetic
what receptor does the parasympathetic NS use and what is its effect
M3 receptors
fluid secretion
what hormones are involved in the hormonal control of saliva secretion
and what are there effects
ADH and aldosterone
- decrease Na conc and increase K + conc.
Kallikrein
-produces bradykinin which vasodilates
increases blood flow
increase salivary secretions
what is the effect of antidepressents on saliva
decreases salviary secretions and can lead to decreased bicarb –> rotting teeth
what occurs in drooling
what is the cause and treatment
excessive salivation due to increase nervous stimulation
treatment: anticholinergics and surgical removal of sublingual glands
what occurs in xerostomia and what are some causes
dry mouth due to absence of saliva production
(drugs, radiation treatment, autoimmune disease)
buccal infections/dental caries
Note lacrimal glands are fine
what is sjogren’s syndrome
what are the outcome s
autoimmune process-targets salivary and lacrimal glands
glandular atrophy and decreased saliva production (xerostomia)
difficulty in chewing, swallowing and speech.
dry oral mucosa, superficial ulceration, poor dentition
(dental caries, fractures, loss of teeth)
what is the problem with cystic fibrosis and saliva
elevated Na+, Ca2+ and protein in saliva, sweat, pancreatic fluid & bronchial secretion
CF patients lacks CFTR or chloride transporter
what is addison’s disease
increase Na+ in saliva (↓ Na+ reabsorbed), hypertonic saliva possibly
what happens to saliva with primary aldosteronism and cushing’s
decrease Na+ in saliva (↑ Na+ reabsorbed), salivary NaCl is zero, increase K+ levels
what occurs with digoxin therapy to saliva
increase Ca and K in saliva
what occurs to saliva with parkinson’s or tumors of mouth/esophagus
increased saliva (drooling) production due to unusual local reflexes and increase neurological stimulation
what is the composition of stomach secretion
isotonic
what are the three cell types of the oxyntic glands in the body and fundus region of the setomach
The parietal (oxyntic) cells secrete
- HCl (protein breakdown, pepsinogen
activation, kills most microbes)
- intrinsic factor (IF) (necessary for
the absorption of vit. B12 by the ileum)
- Peptic (chief, zymogenic) cells secrete
- Pepsinogen/zymogens- converted to pepsin
- Chymosin, gastric lipase
- Mucous cells (mucus)
what are the two cells of the pyloric glands in the pyloric and antrum region of the stomach
G cells
- Gastrin (hormone) – stimulates
parietal cells (HCl) & peptic cells
(pepsinogen) *cancer of antrum would mean too many G cells –>
- Mucous cells secrete
- Mucous (thick/thin mucous)
how often is the entire stomach mucosa replaced
every 3 days
what do surface epithelial cells secrete
thick viscous alkaline mucous
what do mucous neck cells secrete
thin water mucus
what is the relationship between gastric secretion rate and composition
Non-parietal cells responsible for basal (low rate) secretion (between meals)
- high in Na + and Cl -
- low in H + and K +
Parietal cells responsible for stimulated (high rate) secretion (after a meal)
(stimulated by gastrin & histamine)
- high in H + and Cl -
- low in Na + and K +
what is the alkaline tide
Secretion of H+ into the lumen is balanced by secretion of an equal amount of HCO3- into blood
Increased pH of venous blood leaving stomach following a meal is alkaline & referred to as alkaline tide
what are the mechanisms of direct stimulation of parietal cells (3) and what is the result
ACh released from vagus nerve binds to M3 receptors
- Histamine released from ECL cell binds to H2 receptors
- Gastrin released from G cell binds to CCKB receptors
All three agonists synergistically stimulate and
potentiate acid secretion from parietal cell
what are the mechanisms of indirect stimulation of parietal cells (3) and what is the results
ACh released from vagus nerve binds to M3
receptors on ECL cell and release histamine
-Gastrin released from G cells binds to CCKB
receptors on ECL cell to release histamine
-Histamine released from ECL cell (by the action of
Ach and gastrin) binds to H2 receptors on parietal cell
what is the source of CCK
I cells of duodenum and jejunum
neurons in ileum and colon
what is the source os secretin
s cells in small intestine
what is the source of VIP
ENS neurons
what is the source of GIP
K cells in duodenum and jejunum
what is the source of neurotensin
endocrine cells in ileum
what is the source of peptide YY
endocrine cells in ileum and colon
what is the source of somatostatin
D cells of stomach and duodenum
cells of pancreatic islets
what happens during the cephalic phase
- conditioned reflexes (thought, smell, taste, hypoglycemia chewing, swallowing, hypoglycemia) send impulses to medulla oblangata which stimulates vagus nerve (parasympathetic): -ACh acts on parietal cells to release acid -ACh acts on ECL cells to release histamine H2 on parietal cells
- ENS stimulate G cells to release gastrin -Chief cells release pepsinogen -Inhibits D cells, reduce release of somatostatin (somatostatin inhibits gastrin release)
what happens during the gastric phase
-food distends gastric mucosa (inside the stomach!) -vagus & ENS reflexes activated -increase in acid and pepsinogen secretion –peptides (peptones) & a.a stimulate gastrin release
what happens during the intestinal phase
peptides in duodenum stimulates gastrin secretion -chyme containing lipids or acid (pH 2) inhibits impulses from medulla oblangata and decrease vagal nerve stimulation, decrease acid secretion -duodenum releases 3 hormones-inhibits acid secretion -Secretin –released when too much acidic food , release a lot of bicarb from pancreas -GIP (gastric inhibitory peptide) -CCK (cholecystokinin)- fatty food comes along, CCK is released, causes lots of release of pancreas juice. CCK effects liver as well
what is a vagotomy and what are the side effects
Vagotomy (cutting of vagus nerve):
- inhibits gastric acid secretion - used to treat peptic ulcers - side effects: delay in gastric emptying, diarrhea
what is a selective vagotomy
cutting only vagal nerves supplying parietal cells only
what causes Pernicious anemia
absence of intrinsic factor
b/c IF is needed for Vitamin B12 absorption
and vit B12 absorption is needed for erythrocyte production
what are 4 agents that cause mucosal damage
Alcohol
Salicylates (Aspirin)
H.pylori-
breaks down
bicarb layer
Bile acids-
Breaks down lipid bilayer
what is the function of mucus secretion by surface cells
what happens if this layer is defected
acts as a diffusion barrier for H+ & pepsin
allows stomach to contain acid without injuring itself
-mucus layer traps HCO3- alkaline soln
HCO3- titrates H+ & inactivates pepsin
If H+ penetrates into gastric epithelium:
-it destroys mast cells-histamine released-inflammation
-severe damage-histamine, PAF, LTs, TXs, etc release
-tissue damage-H+ back diffusion
what is the mechanism by which ulcer formation occurs?
Acid and pepsin break through mucosal barrier
Acid stimulates histamine release
Histamine stimulates parietal cells to release acid
Acid diffuses through broken barrier
Vicious cycle continues
how does aspirin cause ulcers
Aspirin (a weak acid) is easily
absorbed in low pH of the
stomach
Once absorbed it acts by acid
stimulating histamine release
and disruption of local mucosa
Aspirin suppresses protective
mucosal barrier productionwhat occurs with a pentagastrin test with gastrinoma or zollinger-ellison syndrome
with gastrinoma there is already a large increase in gastrin secretion and subsequent gastric acid secretion both at rest and after a meal
so after a pentagstrin test the acid output doesn’t significantly increase because it is already elevated
what happens with pernicocious anemia during pentagstrin testing and what are the serum gastrin levels
this is an autoimmune condition where antibodies against parietal cells and/or IF are produced
if there are attacks on parietal cells then both gastric acid secretions are low AND IF secretions are low
acid secretions are the stimulus for secretion of somatostatin so if there is no acid to stimulate there will be low/no somatostatin
if there is no somatostatin to inhibit gastrin, there is going to be a high serum gastrin level
however, there is going to be zero gastric acid secretion both before and after pentagastrin
without IF –> no Vitamin B12 absorption and this can lead to neurological disorders
what are the lab values like for a duodenal ulcer compared to normal?
serum gastrin is elevated but not extremly high
basal acid output is similar (or slightly above) normal acid output before a meal
and acid output after pentagastrin stimulus, the acid out put is similar in values to normal
what is atrophic gastritis
lack of parietal cells
crhonic inflammation of gastric mucosa due to h.pylori –> decrease in gastric acid
what are examples of antacids
alka seltzer
Na HCO3 or KHCO3
what are the H2 blockers used and what is there mechanism
rantidine (zantac)
cimetidine (tagamet)
Histamine potentiates effects of gastrin & ACh on parietal cells via H2 to release acid
Inhibiting H2 will decrease H+ release in the stomach
what are the Proton Pump inhibtors
what is the mechanims
what are the long term side effects of PPI usage
omeprazole (prilosec) (H pump ATPase inhibitor)
PPIs inhibits proton pump and decreases H+ release, increases gastric pH (alkaline)
Long term side effects of PPIs usage are:
Pneumonia??
Clostridium difficle growth in gut
Osteoporosis
what antibiotics are used for h pylori
clarithromycin
cymoxicillin (metronidazol)
what are the surgical intervention in the stomach
vagotomy
antrectomy
what is the muscarinic antagonist used in stomach problems and why is this not used often
dicyclomine
this is not used because there are many many locations for muscarinic receptors throughout the body and can cause harmful side effects
