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MONOGASTRIC GI > 5.1b – Salvia and Gastric Secretions II > Flashcards

5.1b – Salvia and Gastric Secretions II Flashcards

1
Q

What does distension of the stomach wall do to gastric secretion (neural control)?

A

-activates reflexes that stimulate acid secretion from parietal cell
*signals are contained within the ENS

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2
Q

What is another way for gastric secretion to be activated by neural control by vagus nerve?

A

-afferent nerves receive sensory information from the duodenum
>trigger responses that travel to the stomach to activate parietal cells

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3
Q

What happens to gastric secretion (neural control) with a gastric vagotomy?

A

-decreases basal and distension induced acid secretion

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4
Q

What does atropine do on vagal activation induced acid secretion?

A

-reduced by 70%

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5
Q

Gastrin:

A

-gastric acid stimulating hormone
-produced by G cell of the antrum
*increased synthesis with AA and Ca+

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6
Q

Where are gastrin receptors found?

A

-basolateral membrane of parietal cells

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7
Q

Histamine is synthesized by:

A

-histidine decarboxylase in the ECL cells in the corpus gastric glands

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8
Q

What activates histamine release?

A

-activated by circulating gastrin via CCK2R

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9
Q

What suppresses histamine release?

A

-somatostatin

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10
Q

What does histamine act via?

A

-H2 histamine receptor
>H2R

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11
Q

Which cells express G-coupled H2 receptors?

A

-parietal cells
>increase intracellular cAMP to stimulate acid secretion via cAMP dependent protein kinases

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12
Q

What produces ghrelin?

A

-X cells of stomach corpus

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13
Q

Ghrelin circulating levels:

A

-circadian rhythm
>increased by fasting

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14
Q

What inhibits ghrelin?

A

-SCFA
-LCFA
-AA
-etc.

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15
Q

Motilin:

A

-same family as ghrelin
-released during interdigestive period

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16
Q

Somatostatin:

A

-entereoendocrine D cells
-reduces feeding or gastrin-stimulated gastric acid secretion

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17
Q

GLP-1 and PYY:

A

-GLP: glucagon like peptide
-PYY: peptide tyrosine-tyrosine
*responsible for ‘ileal brake’ primarily in response to FAs in lumen

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18
Q

Parietal cells hormonal control of gastric secretion:

A

-produce gastric acid in response to histamine, ACh, and gastrin

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19
Q

Enterochromaffin-like cells (ECL) hormonal control of gastric secretion:

A

-produces Histamine, in vicinity of parietal cells
-stimulated by gastrin, ACh, and gastrin
*histamine and gastrin act synergistically on parietal cells
-inhibited by serotonin

20
Q

Luminal regulators:

A

-stimulate gastrin secretion indirectly
*major trigger is the presence of protein in the antrum

21
Q

What can increase acid output (luminal regulators)?

A

-short peptides
-AAs (especially aromatic AA)
-alcohol
-coffee (including decaffeinated)
-dietary Ca
*not all mechanisms are known

22
Q

What can decrease acid output (luminal regulation?

A

-dietary lipids

23
Q

Helicobacter pylori:

A

-association between it and gastric disease
-chronic infection with different strains leads to hypersecretion or hyposecretion

24
Q

What is hypersecretion associated with? (helicobacter pylori)

A

-duodenal ulcers

25
Q

What is hyposecretion associated with? (helicobacter pylori)

A

-risk of gastric cancers

26
Q

What protects the wall of the stomach?

A

-mucous (physical barrier)
-bicarbonate (chemical)
*H+ would be able to damage epithelium

27
Q

How does the mucous protect the epithelium?

A

-forms an unstirred layer adjacent to the epithelium
>HCO3 becomes trapped and will neutralize H+ ions
>further from the mucus layer the pH decreases as HCO3 decreases

28
Q

Where does HCO3 and mucous come from?

A

-secretory epithelial cell via carbonic anhydrase
-‘non-parietal mucus secreting cell’
*activated by prostaglandins and ANS

29
Q

What do chief cells secret?

A

-pepsinogen
-rennin (proteolytic enzyme)
>digestion of milk

30
Q

Pepsinogen:

A

-precursor (proenzyme) to the enzyme pepsin
-cleaved to pepsin by HCl in the gastric glands and the lumen

31
Q

What regulates chief cells?

A

-ANS and gastric hormones (gastrin, etc.)
>similar to parietal cell

32
Q

What is the source of HCl and its functions?

A

-parietal
*hydrolysis
*activation of zymogens

33
Q

What is the source of intrinsic factor and its function?

A

-parietal cells (humans and pigs)
-exocrine pancreas
>major source in dogs
>exclusive source in cats
*VitB12 absorption

34
Q

What is the source of pepsinogen and its function?

A

-chief cell
*protein digestion

35
Q

What is the source of mucus, bicarbonate and their function?

A

-surface mucus cells
*gastric production

36
Q

What is the source of histamine and its function?

A

-ECL cells
*regulation of gastric secretion

37
Q

What is the source of gastrin and its function?

A

-G cells
*regulation of gastric secretion

38
Q

What is the source of somatostatin and its function?

A

-D cells
*regulation of gastric secretion

39
Q

What is the source of ACh and its function?

A

-nerves
*regulation of gastric secretion

40
Q

What are the 3 phases of gastric acid secretion?

A

-cephalic phase
-gastric phase
-intestinal phase

41
Q

Cephalic phase of gastric acid secretion:

A

-30% stimulated by anticipation of eating, smell or taste
-neuronal stimulation (ACh)
-gastrin-releasing peptide (GRP)

42
Q

Gastric phase of gastric acid secretion:

A

-60% stimulated by stomach distension and digested proteins (G cells)

43
Q

Intestinal phase of gastric acid secretion:

A

-10% stimulated when chyme enters SI
>SI distension (S cells)
-starts out stimulatory and then inhibits as gastrin levels increase
>especially as CCK is released from I cells

44
Q

What are some categories of anti-ulcer drugs?

A

-receptor antagonists
-receptor agonists
-pump inhibitors

45
Q

Receptor antagonists (anti-ulcer drugs):

A

-histamine H2-receptor antagonists

46
Q

Receptor agonists (anti-ulcer drugs):

A

-Prostaglandin E receptor
-somatostatin receptor (ex. octreotide (sandostatin))

47
Q

Pump inhibitors (anti-ulcer drugs):

A

-H+/K+ proton pump inhibitors
Ex. omeprazole

MONOGASTRIC GI (24 decks)

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