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Human Epithelial Biology > Physiology and Pharmacology of Gastric Motility and Secretion > Flashcards

Physiology and Pharmacology of Gastric Motility and Secretion Flashcards

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1
Q

What is stomach relaxation driven by?

A

vagus nerve

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2
Q

What is the starting point for digestion of proteins?

A

HCl and pepsin

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3
Q

What is produced by the stomach?

A

chyme

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4
Q

What are the rugae?

A

folds in the empty stomach

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5
Q

What is the fundus?

A

top of stomach, gas pocket, usually no food

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6
Q

What is the antrum?

A

next to duodenum - thick sm. muscle for contraction

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7
Q

How is food mixed in the stomach?

A

peristalic wave forces chyme down and back against pyloric sphincter which causes retropulsion

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8
Q

What size of food does the pyloric sphincter let through?

A

2mm or less

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9
Q

What governs the strength of the antral wave?

A

gastric factors and duodenal factors

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10
Q

What are the gastric factors mediating the antral wave?

A

rate of emptying is proportional to volume of chyme in stomach
distension increases motility due to stretch of smooth muscle, stimulation of intrinsic nerve plexus and increased vagal nerve activity and gastrin increase
consistency of chyme

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11
Q

What are the duodenal factors mediating the antral wave?

A

must be ready to recieve chyme and can delay emptying

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12
Q

How does the duodenum delay emptying of the stomach?

A

neuronal response - enterogastric reflex decreases antral peristalic wave from intrinsic nerve plexuses and ANS
hormonal response - release of secretin and CCK

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13
Q

What are the stimuli that drive the neuronal and hormonal responses of the duodenum?

A

fat - particularly potent as time required for digestion
acid - time needed for neutralisation by HCO3
hypertonicity - products of carbohydrate/ protein digestion are osmotically active and draw water into the sm. intestine
distension

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14
Q

Where do secretions from the gastric glands come from?

A

Pyloric Gland Area

Oxyntic Mucosa

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15
Q

What is produced by the oxyntic mucosa?

A

enterochromaffin cells - histamine - paracrine
chief cells - pepsinogen
parietal cell - HCl, Intrinsic factor

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16
Q

What is produced by the pyloric gland area?

A

D cell - somatostatin - endocrine

G cell - gastrin - endocrine

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17
Q

What is the function of HCl?

A

activates pepsinogen -> pepsin
denatures protein
kills most micro-organisms ingested

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18
Q

What is the function of pepsinogen?

A

inactive precursor of peptidase - pepsin

pepsin is autocatalytic once formed

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19
Q

What is the function of Intrinsic Factor?

A

binds vitB12 - allowing absorption in the terminal ileum - essential as only found in stomach

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20
Q

What is the function of histamine?

A

stimulates HCl secretion

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21
Q

What is the function of mucus?

A

protects stomach wall

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22
Q

What is the function of gastrin?

A

stimulates HCl secretions

23
Q

What is the function somatostatin?

A

inhibits HCl secretion

24
Q

What are the processes involved with secretion of HCl?

A

Conversion of CO2 and H20 to HCO3 + H
HCO3 exiting the cell and bringing Cl into the cell
H being extruded into the cannaliculus
Cl being extruded into the cannaliculus

25
Q

What converts CO2 and H20 to H2CO3?

A

carbonic anhydrase

26
Q

What takes HCO3 out of the cell?

A

HCO3/Cl antiporter

27
Q

How is H taken into the cannaliculus?

A

via H-K ATPase

28
Q

Which cell produces HCl?

A

The parietal cell

29
Q

How is H+ increased by the parasympathetic nervous system?

A

ACh stimulates M3 on parietal cells and M1 on ECL cells
Gastrin activates CCK2Rs on parietal and ECL cells
Hitamine generated from M1 and CCK activates H2R on parietal

30
Q

What inhibits the production of HCl?

A

somatostatin by inhibiting gastrin release

PGE2 inhibits all H2, M3 and CCK2 Receptors

31
Q

Where are proton pumps found between meals?

A

tubulovesicles

32
Q

What happens to the proton pumps when stimulated?

A

move to the apical membrane in extended microvilli

33
Q

What are the 3 phases of Gastric Secretion?

A

Cephalic
Gastric
Intestinal

34
Q

What happens in the cephalic stage?

A

Vagal activation of enteric neurons
ACh stimulates D cell which stops release of somatostatin and increases Gastrin release
ACh increases Gastrin Releasing Peptide and increases G cell activity and gastrin
Ach stimulates the parietal cell to produce HCl
Ach stimulates the ECL cell to produce histamine which stimulates the parietal cell to produce HCl

35
Q

What happens in the gastric stage?

A

distension stimulates mechanoreceptors which stimulate G cell and increase gastrin and HCl
Protein digestion products also stimulate the release of gastrin

36
Q

What happens in the intestinal stage?

A

the same factors that reduce gastric motility reduce gastric secretion
as the stomach empties the stimulus for secretion is less intense
secretion of somatostatin resumes

37
Q

What are some of the drug classes that influence acid secretion?

A

Muscarinic R Antagonists
H2R antagonists
Proton-pump inhibitors
NSAIDsn

38
Q

What is the effect of Muscarinic Antagonists? Give an example

A

decrease HCl

Pirenzipine

39
Q

What is the effect of H2R blockers? Give an example

A

decrease HCl

Ranitidine

40
Q

What is the effect of Proton-pump inhibitors? Give an example

A

decrease HCl

Omeprazole

41
Q

What is the effect of NSAIDs? Give an example

A

increase HCl - blocks only negative control of pathway

Aspirin

42
Q

What is the effect of NSAIDs? Give an example

A

increase HCl - blocks only negative control of pathway

Aspirin

43
Q

What is the function of prostaglandins in the mucosa of the stomach?

A

reduce acid secretion
increase mucus and HCO3 secretion
increase mucosal blood flow

44
Q

What may result from taking NSAIDs?

A

gastric ulceration and bleeding

45
Q

How might the effects of NSAIDs be counteracted?

A

taking PGE1 analogue such as misprostol or COX2 selective inhibitors

46
Q

What does misoprostol do?

A

inhibits basal and food stimulated gastric acid formation

maintains secretion and mucus and HCO3

47
Q

What does Helicobactor pylori do?

A

burrows into the mucosal gel and secretes agents that cause persistent inflammation weakening the mucosal barrier

48
Q

When are drugs that reduce acid secretion used?

A

Gastric ulcer
gastro-osophageal reflux
acid hypersecretion

49
Q

What are some mechanisms of anti-secretory activity?

A

inhibition of the H-pump
competitive antagonism of H2R
competitive antagonism of M1,M3Rs
antagonism of gastrin receptors CCK2R

50
Q

How do proton pump inhibitors work?

A

inhibit the active, membrane inserted form of H-K-ATPase

51
Q

How are proton pump inhibitors delivered to the stomach?

A

absorbed in GI tract and transported via systemic circulation to secretory cannaliculi

52
Q

How are proton pump inhibitors activated?

A

by accumulation they are converted to a sulfenamide

53
Q

How do proton pump inhibitors inhibit the pump?

A

covalent modification of sulphydryl groups on the pumps

54
Q

How often would you take a proton pump inhibitor?

A

once daily, more if there is a nocturnal acid break through

Human Epithelial Biology (20 decks)

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