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GI exam 1 > Salivary and Gastric Secretory Functions (choudhury) > Flashcards

Salivary and Gastric Secretory Functions (choudhury) Flashcards

1
Q

under what control is saliva?

A

neuronal

hormones just modify

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2
Q

what are some functions of saliva

A 
taste
lubrication
protection
digestion
speech
not essential for life
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3
Q

what is the composition of parotid salivary gland secretions

A

serous thin saliva

25 percent of saliva

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4
Q

what is the compostion of submandibular saliva

A

serous/mucous (thick)

70 percent

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5
Q

what is the composition of sublingual saliva

A

serous/mucous

5 %

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6
Q

what is the function of water in saliva

A

facilitates speech
dissolving and tasting food
swallowing

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7
Q

what is the function of kallikrein in saliva

A

activates bradykinin - dilates arterioles, constricts veins and increases flow to secretory glands

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8
Q

what is the function of bicarb in saliva

A

minimizes tooth decay

neutralizes refluxed gastric acid into lower esophagus (heartburn)

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9
Q

what tonicity is saliva and why

A

saliva is hypotonic so that food can dissolve into int and we can TASTE

cannot taste proteins

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10
Q

what is the function of myoepithelial cells

A

motile, contracts and expels saliva

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11
Q

what is the function of ductal cells

A

modifies secretion by modifying electrolytes

Na, Cl- reabsorbed
K and HCO3- are secreted

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12
Q

what is the function of striated duct epithelium tight junctions

A

H20 cannot leave duct

making it hypotonic

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13
Q

what do acini secrete

A

saliva (H20, Na, Cl, K, HCO3-, amylase)

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14
Q

what is the relationship between salivary rate of secretion and composition

A

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)

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15
Q

what is the major receptor for the sympathetic stimulation of saliva

minor?

A

Beta receptors –> leads to protein secretion

minor is alpha receptors –> leads to fluid secretion

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16
Q

which on (para or symp) exerts more control over salivary gland secretion?

A

parasympathetic

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17
Q

what receptor does the parasympathetic NS use and what is its effect

A

M3 receptors

fluid secretion

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18
Q

what hormones are involved in the hormonal control of saliva secretion

and what are there effects

A

ADH and aldosterone
- decrease Na conc and increase K + conc.

Kallikrein
-produces bradykinin which vasodilates
increases blood flow
increase salivary secretions

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19
Q

what is the effect of antidepressents on saliva

A

decreases salviary secretions and can lead to decreased bicarb –> rotting teeth

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20
Q

what occurs in drooling

what is the cause and treatment

A

excessive salivation due to increase nervous stimulation

treatment: anticholinergics and surgical removal of sublingual glands

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21
Q

what occurs in xerostomia and what are some causes

A

dry mouth due to absence of saliva production

(drugs, radiation treatment, autoimmune disease)

buccal infections/dental caries

Note lacrimal glands are fine

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22
Q

what is sjogren’s syndrome

what are the outcome s

A

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)

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23
Q

what is the problem with cystic fibrosis and saliva

A

elevated Na+, Ca2+ and protein in saliva, sweat, pancreatic fluid & bronchial secretion

CF patients lacks CFTR or chloride transporter

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24
Q

what is addison’s disease

A

increase Na+ in saliva (↓ Na+ reabsorbed), hypertonic saliva possibly

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25
what happens to saliva with primary aldosteronism and cushing's
decrease Na+ in saliva (↑ Na+ reabsorbed), salivary NaCl is zero, increase K+ levels
26
what occurs with digoxin therapy to saliva
increase Ca and K in saliva
27
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
28
what is the composition of stomach secretion
isotonic
29
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) 2. Peptic (chief, zymogenic) cells secrete - Pepsinogen/zymogens- converted to pepsin - Chymosin, gastric lipase 3. Mucous cells (mucus)
30
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 --> 2. Mucous cells secrete - Mucous (thick/thin mucous)
31
how often is the entire stomach mucosa replaced
every 3 days
32
what do surface epithelial cells secrete
thick viscous alkaline mucous
33
what do mucous neck cells secrete
thin water mucus
34
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 +
35
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
36
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
37
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
38
what is the source of CCK
I cells of duodenum and jejunum | neurons in ileum and colon
39
what is the source os secretin
s cells in small intestine
40
what is the source of VIP
ENS neurons
41
what is the source of GIP
K cells in duodenum and jejunum
42
what is the source of neurotensin
endocrine cells in ileum
43
what is the source of peptide YY
endocrine cells in ileum and colon
44
what is the source of somatostatin
D cells of stomach and duodenum cells of pancreatic islets
45
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)
46
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
47
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
48
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
49
what is a selective vagotomy
cutting only vagal nerves supplying parietal cells only
50
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
51
what are 4 agents that cause mucosal damage
Alcohol Salicylates (Aspirin) H.pylori- breaks down bicarb layer Bile acids- Breaks down lipid bilayer
52
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
53
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
54
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 production ```
55
what 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
56
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
57
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
58
what is atrophic gastritis
lack of parietal cells crhonic inflammation of gastric mucosa due to h.pylori --> decrease in gastric acid
59
what are examples of antacids
alka seltzer | Na HCO3 or KHCO3
60
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
61
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
62
what antibiotics are used for h pylori
clarithromycin | cymoxicillin (metronidazol)
63
what are the surgical intervention in the stomach
vagotomy | antrectomy
64
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

GI exam 1 (11 decks)

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