GI Gastric Morility And Gastric Acid Secretion Flashcards Preview

Physiology > GI Gastric Morility And Gastric Acid Secretion > Flashcards

Flashcards in GI Gastric Morility And Gastric Acid Secretion Deck (51):
1

What is the stand the starting point for

Digestion of proteins (via pepsin and HCl)

2

What does the stomach do

Mixes the food with gastric secretions to products chyme

3

What is the absorption like in the stomach

Limited amount

4

How much gastric juice is approx prod by stomach a day

2litre/day

5

What are the structural elements that make up the j shaped bag stomach

Fundus
Cardia
Body
Rugae
Pylorus
Antrim
Lesser and greater curvature

6

What so the mixing like in the stomach

Direction of peristaltic move from funds to pylorus forces food to sphincter
If sphincter open this is emptying to duo
If closed retropulsion of chyme allowing mix

7

What determines the escape of chyme through the pyloric sphincter

The strength of the Antral wave

8

What is the strength of the Antral wave governed by

Gastric factors originating in stomach
Duodenal factors originating in duo

9

What are the gastric factors influencing gastric emptying

Rate of emptying proportional to volume of chyme in stomach
- as vol increases the greater distension of wall of stomach

Consistency of chyme
- rotting facilitated by finely divided thick liquid chyme so can fit through pyloric sphincter

10

What are the duodenal factors which influence gastric emptying

Duodenum must be ready to receive chyme and can delay this emptying

Stimuli which duodenum drives the neuronal and hormonal responses

11

How can the duo delay the stomach emptying

Neuronal - enterogastric reflex, when duo senses chyme sends signal to decrease Antral peristalsis via intrinsic nerve plexuses and autonomic neurones

Homonal - release enterogastrones( secretin, cck) from endocrine cells in duo inhibit stomach contraction thoug GPCR's

12

How does fat influence the duodenal hormonal and neural responses

Potent delay in emptying required for digestion and abs in small intestine
Difficult to digest as insol water
Digested v slow

13

Howes acid affect the duodenal hormonal and neuronal repsonse

Only small mount added
Time required for neutralisation by bicarbonate sec from pancreas

14

How does hyper tonicity affect the hormonal and neuronal factors of the duo

Products of carb and protein digestion are osmotically active and draw water into small intestine
Danger of reduced plasma vol and circulatory disturbances

15

What does a g cell in the gastric pit release

Gastrin

16

What's does a d cell in a gastric pit release

Somatostatin.

17

What does a parietal cell release

HCl and intrinsic factor

18

What does an enterochromaffinlike cell prod

Histamine

19

What does a chief cell produce

Pepsinogen

20

What are the two oes of gastric pits and where are they found

Pyloric gland area in the Antrum
Oxcyntic mucosa in the fungus and body

21

What fuels are found in the pyloric gland area pastric pit

D cells and g cells

22

What cell homes are found in the oxcyntic mucosa gastric pits

Parietal
Enterochromaffinlike cell
Chief cell

23

What does an oxcyntic gland produce

HCl
Pepsinogen
Histamine
Mucus
Intrinsic factor

24

What does a pyloric area gland produce

Gastrin
Somatostatin
Mucus

25

He hat does HCl from the oxcyntic mucosagastric pit do

Activates pepsinogen to pepsin for proetin digestion
Denatures protein breaks tertiary and secondary structures
Kills most micor ORGS ingested in food

26

What does pepsinogen from the oxcyntic do

Inactive preserver for pepsin for protein digestion

27

What does intrinsic factor from oxcyntic do

Binds vit b12 allowing abs in terminal ileum only thing essential for life

28

What does the histamine and mucus do form the oxcyntic do

Histamine - stim HCl sec
Mucus - protective pord in gastric pits and epi, stops apical attack of epi cells

29

What does gastrindo form the pyloric do

Stimulate HCl sec

30

What's does somatostatin do form pyloric

inhibits HCl sec between meals
Counter regulation to Gastrin

31

What is the resting state of the parietal cell

Hydrogen and pottasium ATPase largely in cyto tubulovesicles

32

What so the stim state of the parietal cell

Hydrogen and pottasium ATPase traffics to apical mem taking residence in extended Microvilli

33

What are the 3 phases of gastric sec

Cephalic
Gastric
Intestinal

34

What is the cephalic phase of gastric sec

Before foods reaches stomach, anticipatory phase causes increases parasymp flow to stomach and sec acid to prep for digestion of meal

35

What is the gastric phase of gastric secs

When food is In the stomach

36

What is the intestinal phase of gastric sec

After food left stomach chyme acid sec off
Includes factors from small intestine

37

What does muscarinic receptor antagonists do and an example

Block acid sec competitively

38

What does h2 histamine receptor antagonists do and an example

Block acid sec competitively
Ranitidine

39

What do proton pump inhibitors do and an example

Block acid sec by covalent modification
Omeprazole

40

What do non steroidal anti inflammatory drugs do and an examole

Block acid sec irreversibly
Aspirin

41

What protects the mucosa form HCl attack and pepsin

Locally produced prostaglandins.

42

What do locally produced prostaglandins do

Reduce acid sec
Increase mucus and bicarbonate sec
Increase mucosal blood flow

43

What is a peptic ulcer

Any ulcer in an area where the mucosa is exposed to HCl and pepsin (stomach, duo)

44

What so th development of a peptic ulcer associated with

A shift in balance between mucosal damaging and mucosal protecting mechanisms

45

What do NSAIDs do

Reduce prostaglandin formations - COX1 Inhibition which may trigger

Gastric ulceration
Bleeding

46

How can longer term gastric damage due to NSAIDs be treated

With pge1 analogue misoprostol

Inhib basal and food stim gastric acid formation
Maintains secretion of mucus and bicarbonate
Compensates for loss prostaglandins when cox1 inhib

47

What is the origination of a peptic ulcer form

Imp factor H.pylori motile bacteria which burrows into mucosal barrier where it is protected by gel but caused inflammation and breakdown mucosal barrier expo the mucosal mem to HCl and pepsin

48

What do drugs used to treat peptic ulcers aim to do

Decrease acid sec.
Increasing mucosl resistance
Eradicating h pylori

49

What are drugs used to reduce gastric acid used for

Peptic ulcers
Gastric oesophageal reflux disease
Acid hypersecrtion

50

What are mechanisms of antisec activity

Inhibition of proton pump
Competitive antagonisms if histamine h2 receptors
Competion antagonism of muscarinic m1 and m2 ACh receps
Antagonism of Gastrin receps

51

What is the stomach driven by (nerve)

Vagus