Physiology and Pharmacology of Gastric Motility and Secretion Flashcards Preview

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

Flashcards in Physiology and Pharmacology of Gastric Motility and Secretion Deck (54)
1

What is stomach relaxation driven by?

vagus nerve

2

What is the starting point for digestion of proteins?

HCl and pepsin

3

What is produced by the stomach?

chyme

4

What are the rugae?

folds in the empty stomach

5

What is the fundus?

top of stomach, gas pocket, usually no food

6

What is the antrum?

next to duodenum - thick sm. muscle for contraction

7

How is food mixed in the stomach?

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

8

What size of food does the pyloric sphincter let through?

2mm or less

9

What governs the strength of the antral wave?

gastric factors and duodenal factors

10

What are the gastric factors mediating the antral wave?

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

11

What are the duodenal factors mediating the antral wave?

must be ready to recieve chyme and can delay emptying

12

How does the duodenum delay emptying of the stomach?

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

13

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

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

14

Where do secretions from the gastric glands come from?

Pyloric Gland Area
Oxyntic Mucosa

15

What is produced by the oxyntic mucosa?

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

16

What is produced by the pyloric gland area?

D cell - somatostatin - endocrine
G cell - gastrin - endocrine

17

What is the function of HCl?

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

18

What is the function of pepsinogen?

inactive precursor of peptidase - pepsin
pepsin is autocatalytic once formed

19

What is the function of Intrinsic Factor?

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

20

What is the function of histamine?

stimulates HCl secretion

21

What is the function of mucus?

protects stomach wall

22

What is the function of gastrin?

stimulates HCl secretions

23

What is the function somatostatin?

inhibits HCl secretion

24

What are the processes involved with secretion of HCl?

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

What converts CO2 and H20 to H2CO3?

carbonic anhydrase

26

What takes HCO3 out of the cell?

HCO3/Cl antiporter

27

How is H taken into the cannaliculus?

via H-K ATPase

28

Which cell produces HCl?

The parietal cell

29

How is H+ increased by the parasympathetic nervous system?

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

What inhibits the production of HCl?

somatostatin by inhibiting gastrin release
PGE2 inhibits all H2, M3 and CCK2 Receptors

31

Where are proton pumps found between meals?

tubulovesicles

32

What happens to the proton pumps when stimulated?

move to the apical membrane in extended microvilli

33

What are the 3 phases of Gastric Secretion?

Cephalic
Gastric
Intestinal

34

What happens in the cephalic stage?

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

What happens in the gastric stage?

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

36

What happens in the intestinal stage?

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

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

Muscarinic R Antagonists
H2R antagonists
Proton-pump inhibitors
NSAIDsn

38

What is the effect of Muscarinic Antagonists? Give an example

decrease HCl
Pirenzipine

39

What is the effect of H2R blockers? Give an example

decrease HCl
Ranitidine

40

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

decrease HCl
Omeprazole

41

What is the effect of NSAIDs? Give an example

increase HCl - blocks only negative control of pathway
Aspirin

42

What is the effect of NSAIDs? Give an example

increase HCl - blocks only negative control of pathway
Aspirin

43

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

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

44

What may result from taking NSAIDs?

gastric ulceration and bleeding

45

How might the effects of NSAIDs be counteracted?

taking PGE1 analogue such as misprostol or COX2 selective inhibitors

46

What does misoprostol do?

inhibits basal and food stimulated gastric acid formation
maintains secretion and mucus and HCO3

47

What does Helicobactor pylori do?

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

48

When are drugs that reduce acid secretion used?

Gastric ulcer
gastro-osophageal reflux
acid hypersecretion

49

What are some mechanisms of anti-secretory activity?

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

50

How do proton pump inhibitors work?

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

51

How are proton pump inhibitors delivered to the stomach?

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

52

How are proton pump inhibitors activated?

by accumulation they are converted to a sulfenamide

53

How do proton pump inhibitors inhibit the pump?

covalent modification of sulphydryl groups on the pumps

54

How often would you take a proton pump inhibitor?

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