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GI Physiology > Salivation and Gastric Function > Flashcards

Salivation and Gastric Function Flashcards

1
Q

how are GI hormones delivered?

A

they are secreted into capillaries, go through the liver and return in the systemic blood

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2
Q

what is paracrine signaling and what are the three main factors?

A

chemicals that act in the same tissue that secretes them
serotonin (excites ENS), somatostatin (inhibits pancreatic and gastric secretion and motility) and histamine (stimulates HCl secretion with H2 receptors)

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3
Q

what are neurocrine signals?

A

signaling molecules synthesized in ENS neurons and released with action potential (neurotransmitters)

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4
Q

where is gastrin secreted and what does it do?

A

secreted by antral mucosa (G cells)- distension and vagus

increases parietal cell action and mucosal growth

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5
Q

what is CCK secreted by and what does it do?

A

in duodenum and jejunal I cells- fats and protein

gall bladder contraction, increases pancreatic enzyme and bicarbonate secretion and inhibits gastric emptying

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6
Q

where is secretin secreted and what does it do?

A

duodenum (S cells)- acidic chyme

increases bicarb and fluid secretion, decreases gastric acid secretion (decreases gastrin), inhibits gastric empty

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7
Q

where is motilin secreted and what does it do?

A

small intestine mucosa (M cells) during fasting

promotes clearance of indigestible materials

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8
Q

where is glucose dependent insulinopic peptide (GIP) secreted and what does it do?

A

small intestine mucosa (K cells)- fat and carbohydrates

stimulates insulin secretion and inhibits HCl secretion

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9
Q

digestion of what materials is initiated in the mouth?

A

carbohydrates and lippids

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10
Q

what type of digestion occurs in the stomach?

A

protein and lipid (salivary amylase denatured by acid)

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11
Q

where are enzymes in the small intestine located?

A

secreted into the lumen or anchored to the brush border

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12
Q

what is the function of saliva?

A 
to lubricate (mucus)
protect (clear bacteria off teeth and substances that reduce bacterial growth)
digest (salivary amylase and lingual lipase)
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13
Q

what is secreted by acinar cells?

A

alpha amylase and watery substance

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14
Q

what is sjogren syndrome?

A

autoimmune disease that destroys salivary and lacrimal glands

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15
Q

what is xerostomia?

A

dry mouth

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16
Q

describe the secretions from salivary glands

A

basal flow rates: high in K and low in Na and Cl (reabsorbed)
high flow rates: saliva more like plasma with higher bicarb

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17
Q

what is the only agent that affects salivation?

A

aldosterone- stimulates Na reabsorption and K secretion

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18
Q

where is lingual lipase added to the saliva?

A

in the mouth

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19
Q

what controls salivary secretion

A

ANS (unaffected by GI hormones)
PNS increases and sustains secretion
SNS more transient stimulation

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20
Q

what types of mouthfeel stimulate salivation

A

smooth tactile stimuli- not rough

21
Q

responses to what GI upset causes salivation?

A

stomach and small intestine with irritation or nausea

22
Q

what does the activation of salivary glands cause?

A

release of kallikrein- results in bradykinin production

vasodilation of capillary increases filtration

23
Q

where are oxyntic glands located and what cell types do they contain?

A

in body and fundus

mucous neck cells (mucous), chief cells (pepsinogen and gastric lipase) and parietal cells (IF and HCl)

24
Q

what occurs when parietal cells are destroled?

A

achlorhydria and perinicious anemia

25
Q

what do pyloric glands do? where are they located?

A

secrete mucus for protenction, gastrin and somatostatin

;pcated om tje amtri,

26
Q

what do cardiac glands secrete and where are they?

A

mucus- near LES

27
Q

what stimulates oxyntic glands?

A

vagus and ENs

28
Q

what type of enzyme is pepsin and how is it made

A

endopeptidase

activated from pepsinogen by HCl (pH 3-5) by removing N terminal

29
Q

what does mucus do in the stomach?

A

prevents H+ and pepsin access to mucosa

traps bicarb to be a buffer to H+ and inactivate pepsin

30
Q

what occurs if H+ reaches the gastric mucosa

A

degranulation of mast cells increasing blood flow and mucous and bicarb production

31
Q

what is erosive gastritis and what is it caused by

A

decreases secretion of mucus and bicarbonate

chronic NSAID use that inhibits prostaglandin synthesis in stomach

32
Q

what is the main driving force for HCl secretion by parietal cell?

A

H+ K+ ATP ase in the luminal membrane
Cl follows by diffusion through channels
(targeted by proton pump inhibitors)

33
Q

where do the H+ ions come from in parietal cells?

A

CO2 enters the cell and becomes an acid- dissociates into H+ and bicarb
H+ transported into lumen and HCO3- transported into blood with Cl exchanger

34
Q

where is the vomiting center? what does it cause?

A

in the medulla

causes salivation, reverse peristalsis, relaxation of UES and expulsion of contents through the mouth

35
Q

name 4 stimuli that initiate vomiting

A

irritants in stomach or SI
systemic irritant sensed by 4th ventricle chemoreceptor
head injury
abnormal stimulation of vestibular organs

36
Q

what does prolonged vomiting cause?

A

dehydration, lakalosis, hypokalemia

37
Q

what are 6 stimulators of acid secretion?

A

vagus (direct and indirect), gastrin (acts on cell and triggers histamine), histamine, insulin, caffeine (increases proton pump) and stress

38
Q

what are inhibitors of acid secretion?

A

somatostatin (acts on G cells and parietal cells), GIP (acts on parietal cells) and secretin (acts on G cells)

39
Q

describe the action of ACh and gastrin on parietal cells.

A

activate G coupled receptors (separate)> activate phospholipase C> activates protein kinase C> increases intracellular Ca

40
Q

describe the action of histamine on parietal cells

A

binds to H2 receptor (g coupled) >activation of adenlyly cyclase> cAMP increase> PKA activation

41
Q

describe the action of somatostatin and prostaglandins on parietal cells

A

separate g linked receptors that oppose the action of histamine (decrease cAMP

42
Q

what do H2 receptor antagonists do?

A

OTC antacid agents, decrease HCl production

43
Q

what do proton pump inhibitors do?

A

block final common pathway of all secretagogues (more effective than histamine antagonists)

44
Q

describe the cephalic phase

A

smelling and tasting
vagus directly stimulates parietal cells
indirect stimulation by gastrin productions (gastrin releasing peptide)

45
Q

describe the gastric phase

A

distension of the stomach and presence of amino acids
direct and indirect vagal parietal stimulation
distension of antrum and AA> gastrin releasing reflex

46
Q

describe the intestinal phase

A

mediated by amino acids

only 10% of gastric acid secretion

47
Q

when is HCl secretion inhibited? what is the major mediator of this?

A

when it is no longer needed to activate pepsinogen

somatostatin through direct and indirect effects

48
Q

what does vagal stimulation of D cells do?

A

inhibits the release of somatostatin

49
Q

what are the negative and positive feedback mechanisms of HCl release?

A

luminal H+ causes release of somatostatin

protein digestion products stimulate gastrin secretion

GI Physiology (7 decks)

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