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Physiology > GI Gastric Morility And Gastric Acid Secretion > Flashcards

GI Gastric Morility And Gastric Acid Secretion Flashcards

1
Q

What is the stand the starting point for

A

Digestion of proteins (via pepsin and HCl)

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2
Q

What does the stomach do

A

Mixes the food with gastric secretions to products chyme

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3
Q

What is the absorption like in the stomach

A

Limited amount

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4
Q

How much gastric juice is approx prod by stomach a day

A

2litre/day

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5
Q

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

A 
Fundus
Cardia 
Body 
Rugae
Pylorus
Antrim 
Lesser and greater curvature
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6
Q

What so the mixing like in the stomach

A

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

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7
Q

What determines the escape of chyme through the pyloric sphincter

A

The strength of the Antral wave

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8
Q

What is the strength of the Antral wave governed by

A

Gastric factors originating in stomach

Duodenal factors originating in duo

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9
Q

What are the gastric factors influencing gastric emptying

A

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

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10
Q

What are the duodenal factors which influence gastric emptying

A

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

Stimuli which duodenum drives the neuronal and hormonal responses

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11
Q

How can the duo delay the stomach emptying

A

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

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12
Q

How does fat influence the duodenal hormonal and neural responses

A

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

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13
Q

Howes acid affect the duodenal hormonal and neuronal repsonse

A

Only small mount added

Time required for neutralisation by bicarbonate sec from pancreas

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14
Q

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

A

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

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15
Q

What does a g cell in the gastric pit release

A

Gastrin

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16
Q

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

A

Somatostatin.

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17
Q

What does a parietal cell release

A

HCl and intrinsic factor

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18
Q

What does an enterochromaffinlike cell prod

A

Histamine

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19
Q

What does a chief cell produce

A

Pepsinogen

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20
Q

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

A

Pyloric gland area in the Antrum

Oxcyntic mucosa in the fungus and body

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21
Q

What fuels are found in the pyloric gland area pastric pit

A

D cells and g cells

22
Q

What cell homes are found in the oxcyntic mucosa gastric pits

A

Parietal
Enterochromaffinlike cell
Chief cell

23
Q

What does an oxcyntic gland produce

A 
HCl 
Pepsinogen 
Histamine 
Mucus
Intrinsic factor
24
Q

What does a pyloric area gland produce

A

Gastrin
Somatostatin
Mucus

25
Q

He hat does HCl from the oxcyntic mucosagastric pit do

A

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

26
Q

What does pepsinogen from the oxcyntic do

A

Inactive preserver for pepsin for protein digestion

27
Q

What does intrinsic factor from oxcyntic do

A

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

28
Q

What does the histamine and mucus do form the oxcyntic do

A

Histamine - stim HCl sec

Mucus - protective pord in gastric pits and epi, stops apical attack of epi cells

29
Q

What does gastrindo form the pyloric do

A

Stimulate HCl sec

30
Q

What’s does somatostatin do form pyloric

A

inhibits HCl sec between meals

Counter regulation to Gastrin

31
Q

What is the resting state of the parietal cell

A

Hydrogen and pottasium ATPase largely in cyto tubulovesicles

32
Q

What so the stim state of the parietal cell

A

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

33
Q

What are the 3 phases of gastric sec

A

Cephalic
Gastric
Intestinal

34
Q

What is the cephalic phase of gastric sec

A

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

35
Q

What is the gastric phase of gastric secs

A

When food is In the stomach

36
Q

What is the intestinal phase of gastric sec

A

After food left stomach chyme acid sec off

Includes factors from small intestine

37
Q

What does muscarinic receptor antagonists do and an example

A

Block acid sec competitively

38
Q

What does h2 histamine receptor antagonists do and an example

A

Block acid sec competitively

Ranitidine

39
Q

What do proton pump inhibitors do and an example

A

Block acid sec by covalent modification

Omeprazole

40
Q

What do non steroidal anti inflammatory drugs do and an examole

A

Block acid sec irreversibly

Aspirin

41
Q

What protects the mucosa form HCl attack and pepsin

A

Locally produced prostaglandins.

42
Q

What do locally produced prostaglandins do

A

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

43
Q

What is a peptic ulcer

A

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

44
Q

What so th development of a peptic ulcer associated with

A

A shift in balance between mucosal damaging and mucosal protecting mechanisms

45
Q

What do NSAIDs do

A

Reduce prostaglandin formations - COX1 Inhibition which may trigger

Gastric ulceration
Bleeding

46
Q

How can longer term gastric damage due to NSAIDs be treated

A

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
Q

What is the origination of a peptic ulcer form

A

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
Q

What do drugs used to treat peptic ulcers aim to do

A

Decrease acid sec.
Increasing mucosl resistance
Eradicating h pylori

49
Q

What are drugs used to reduce gastric acid used for

A

Peptic ulcers
Gastric oesophageal reflux disease
Acid hypersecrtion

50
Q

What are mechanisms of antisec activity

A

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

51
Q

What is the stomach driven by (nerve)

A

Vagus

Physiology (28 decks)

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