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GI > Physiology & pharmacology of gastric motility & secretion > Flashcards

Physiology & pharmacology of gastric motility & secretion Flashcards

1
Q

describe the shape and capacity of the stomach?

A

J shape

  • 50>1000ml capacity
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2
Q

how does the stomach relax and why?

A

RECEPTIVELY to accommodate food from oesophagus

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3
Q

what is the stomach the starting point for digestion of?

what does the stomach mix?

A

proteins (by pepsin and HCL continues carbohydrate digestion (by salivary amylase)

= mixes food with gastric secretions to produce semi-liquid chyme

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4
Q

the stomach stores food before passing it to where as what?

A

into small intestine as chyme for further digestion and absorption

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5
Q

how much does the stomach approximately secrete?

A

= approximately 2litres/day of gastric juice from gastric glands in gastric mucosa

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6
Q

what are the 2 mechanical activities of the stomach and what do they comprise?

What one is tonic and what one is phasic?

A

1) orad stomach
= fundus and proximal body

2) ciudad stomach
= distal body & antrum

Orad = tonic so is maintained 
Caudad = phasic so is intermittent
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7
Q

how is relaxation driven in the orad region?

A

= driven by vagus during a swallow (simultaneously with the opening of lower oesophageal sphincter) permitting storage of ingested material.

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8
Q

true or false.
Are there slow waves in the orad region?

what are there in replace?

A

no

  • tonic contractions which are weak due to relatively thin musculature
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9
Q

how are contents propelled intermittently to caudad region?

A

by low amplitude tonic contractions of about 1min duration = decreasing stomach size as it empties

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10
Q

why is their minimal mixing of contents for long period in orad region?

A

= allowing carbohydrate partial digestion by salivary amylase

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11
Q

what decreases contracts and hence rate of stomach emptying?

A

= gastrin

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12
Q

what happens in caudad region?

A

slow waves occur continuously but only those reaching threshold epic contractions

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13
Q

how are the phasic peristaltic contractions driven?

A

= by suprathreshold slow waves that progress from mid-stomach to gastroduodenal junction (the antral wave) propelling contents toward pylorus through which a small volume of chyme flows into duodenum

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14
Q

when does velocity of contractions in caudad region increase?
- what is retropulsion?

A

towards the junction, overtaking the movement of chyme that rebounds against constricted distal antrum back into relaxed body of stomach = retropulsion

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15
Q

what does retropulsion mix?

A

= gastric contents. reducing chyme (‘grinding’ function) to small particles that pass through pylorus

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16
Q

how is the strength of the antral wave determining escape of chyme through pyloric sphincter governed?

A

by;

1) gastric factors
2) duodenal factors

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17
Q

in gastric factors, what is the rate of emptying proportional to?

A

volume of chyme in stomach

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18
Q

why does distension increase motility?

A

due to;

(i) stretch of smooth muscle
(ii) stimulation of intrinsic nerve plexuses
(iii) increased vagus nerve activity and gastrin release

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19
Q

what does consistency of chyme play a crucial role in?

A

= emptying facilitated by thin liquid chyme

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20
Q

in duodenal factor, what delays emptying?

A

1) neuronal response
= enterogastric reflex
- decreases antral activity by signals from intrinsic nerve plexus and ANS

2) hormonal response
= release of enterogastrones (e.g. cholecystokinin, CKK) from duodenum inhibiting stomach contraction

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21
Q

what are the stimulus within the duodenum thats drives neuronal and hormone responses?

A

1) FAT - potent
= delays gastric emptying required for digestion & absorption in small intestine

2) acid
– time is required for neutralization of gastric acid by bicarbonate secreted from the pancreas – important for optimal function of pancreatic digestive enzymes

3) hypertonicity
- products of carbohydrate
& protein digestion are osmotically active & draw water into the small intestine – danger of reduced plasma volume and circulatory disturbances (e.g. ‘dumping syndrome’)

4) distension

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22
Q

for consideration of secretion of mucosa of stomach, how is it classed as and describe their location?

A

1) oxyntic gland area
= proximal stomach including fungus and body

2) pyloric gland area
= distal stomach
- designated the antrum

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23
Q

what is gastric mucosa composed of?

A

1) surface lining stomach
2) pits invaginations of surface
3) glands = at base of pits responsible for several secretions

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24
Q

in oxyntic mucosa, what gastric secretions are produced?

A

1) HCL
2) pepsinogen
3) intrinsic factor and gasttroferrin
4) histamine
5) mucus

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25
Q

what does HCL, pepsinogen, intrinsic factor & gastrogerrindo, histamine and mucus do?

A

HCL

  • activates pepsinogen to pepsin
  • denatures protein
  • kills most (not all) micro-organisms ingested with food

Pepsinogen

  • inactive precursor of peptidase, pepsin
  • pepsin once formed activates pepsinogen (autocatalytic)

histamine
- stimulates HCL secretion

Mucus
- protective

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26
Q

in pyloric gland area what gastric secretions are produced and what do they do?

A

1) gastrin = stimulates HCL secretion
2) somatostatin = inhibits HCL secretion
3) mucus = protection

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27
Q

what secretes HCL?

A

= gastric parietal cells

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28
Q

describe receptors and signal-transduction pathways Modulating Acid Secretion from the Gastric Parietal Cells?

A

Stimuli for secretion of H+ act by both PLC - IP3 (gastrin, ACh) and cAMP - PKA (histamine) signalling pathways

Stimuli for inhibition of secretion of H+ act by cAMP - PKA (somatostatin, prostaglandins) signalling pathways

Note the opposing effects of histamine (stimulation) and somatostatin and prostaglandins (inhibition) upon adenylate cyclase

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29
Q

what does secretagogues cause?

A

= trafficking of H+/K+ATPase

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30
Q

how is the rate of gastric secretion controlled?

A

by stimulatory & inhibitory mechanisms that occur in 3 overlapping phases;

1) cephalic phase - in head
= before food reaches stomach preparing it stomach to receive food
- driven directly and indirectly by CNS and vagus nerve (CN X)

2) gastric phase - when food is in stomach
= involves both physical and chemical mechanisms

3) intestinal phase - after food has left stomach
= chyme entering the upper small intestine causes weak stimulation of gastric section via neuronal and hormonal mechanisms

31
Q

in the cephalic phase, the vagus stimulate enteric neurones that do what?

A
  • release ACh directly activating parietal cells (neurotransmitter action)
  • via release of GRP causes release of gastrin from G cells in to systemic circulation that activates parietal cells (endocrine action)
  • via release of histamine from ECL cells that locally activates parietal cells (paracrine action)
  • via inhibition of D cells decreases the inhibitory effect of ss on G-cells
32
Q

in the gastric phase, what does distension of stomach activate?

A

= reflexes that cause acid secretion

33
Q

in the gastric phase, what causes gastrin release to be decreased?

A
  • food buffers pH, D cell inhibition via ss of gastric release
34
Q

in gastric phase what do amino acids stimulate?

A

G cell

- other stimulants include Ca2+, caffeine, alcohol

35
Q

what does inhibition of gastric acid secretion involve?

A
  • cephalic, gastric and intestinal phases.
36
Q

what does the cephalic phase involve?

A

vagus nerve activity decreases upon cessation of eating & following stomach emptying

37
Q

in gastric phase, when does antral pH fall?

A

when food exists stomach (due to decreased buffering of gastric HCL) = releasing somatostatin from D cells recommences, decreasing gastrin secretion

38
Q

what is continually released from gastric mucosa in gastric phase and what does it do?

A

= prostaglandins I2 (PGE2) acts locally to reduce histamine & gastrin mediated HCL secretion

39
Q

in the intestinal phase, what do factors that reduce gastric motility also reduce?

A

= gastric secretion (e.g. neuronal reflex, enterogastrones)

40
Q

what are 4 drug classes influencing acid secretion?

A

1) muscarinic receptor antagonists (e.g. pirenzepine) block competitively

2) proton pump inhibitors
(e. g. omeprazole) block covalent modification

3) NSAIDS e.g. aspirin blocks irreversibly
4) H2 histamine receptor antagonists (e.g. ranitidine) blocks competitvely

41
Q

what protects mucosa from attack by HCL and pepsin?

A

= locally produced prostaglandins (PGE2 and PGI2)

  • reduce acid secretion
  • increase mucus & bicarbonate secretion
  • increase mucosal blood flow
42
Q

what is an important factor for peptic ulcers?

A

= chronic infection of gastric antrum with bacterium, Helicobacter pylori

43
Q

how does drug treatment of peptic ulcer aim to promote ulcer healing by?

A
  • reducing acid secretion
  • increasing mucosal resistance
  • eradication H. Pylori
44
Q

what is a peptic ulcer?

A

= any ulcer in an area where the mucosa is exposed to HCL and Pepsin (Stomach or duodenum)

45
Q

what is development of peptic ulcer associated with?

A
  • shit in the balance between mucosal damaging and protecting mechanisms
46
Q

give an example of a NSAID drug and what they do?

A

e.g. aspirin
= reduce prostaglandins formation (COX 1 inhibition) and may:
- trigger gastric ulceration
- cause bleeding

47
Q

How can gastric damage due to long term NSAIDS treatment be prevented and how does this work?

A

with a stable PGE1 analogy (i.e. misoprostol, but has adverse effects)

Mechanism of action;

  • inhibits basal and food stimulated gastric acid formation
  • maintains (or increases) secretion & mucus & bicarbonate
48
Q

what are drugs that reduce gastric acid secretion used too treat?

A

1) peptic ulcers

2) gastro-oesophageal reflux disease (GORD)
= inappropriate relaxation of lower oesophageal sphincter allowing reflux of acid gastric contents into oesophagus and subsequent tissue damage (oesophagitis)

3) and hyper-secretion
= e.g. Zollinger ellison syndrome (rare, gastric producing tumor), Cushings ulcers (heightened vagal tone)

49
Q

what are mechanisms of anti-secretory activity?

A

1) irreversible inhibition of the proton-pump (H+/K+ ATPase
2) competitive antagonism of histamine H2 receptors
3) competitive antagonism of muscarinic M1 and M3 ACh receptors (mostly obsolete)
4) antagonism of gastrin (CCK2) receptors (not utilized clinically)

50
Q

Give an example of a proton pump inhibitor?

A

= omeprazole

51
Q

how do PPI work?

A

= inhibit the active (i.e. membrane inserted) H+/K+-dependent ATPase (proton-pump)

52
Q

what type of drugs are PPI?

A

= basic prodrugs that are inactive at neutral pH, but which change conformation in a strongly acidic environment

53
Q

how are PPI absorbed and delivered?

A

absorbed from GI tract and delivered via systemic circulation to secretory canaliculi of stomach where accumulation, activation and covalent modification of lumen sulphydryl groups of membrane inserted proton pump occurs

54
Q

in PPI drugs, describe the relationship between inhibition of acid secretion and plasma half life?

A

= inhibition of acid secretion (typically 10-14 hr duration after a single dose before breakfast) greatly exceeds plasma half-life [for most PPIs e.g. lansoprazole, pantoprazole, rabeprazole 1 to 1.5 hr – tenatoprazole is an exception].

55
Q

why is timing of dosing important in PPI drugs?

A

drug must be present in plasma at an effective concentration whilst proton pumps are active

56
Q

when are PPI drugs effective?

A

= orally once daily
as a capsule containing enteric-coated granules). However, not all pumps are inactivated and nocturnal acid breakthrough (NAB) may occur

57
Q

when is full effect only achieved with PPI drugs?

A

= after repeated dosing

58
Q

when are PPi drugs used?

A

treatment of peptic ulcers (particularly when associated with H. pylori), GORD and are the drugs of choice in Zollinger-Ellison syndrome

59
Q

given 2 examples of histamine H2 receptor antagonists?

A
  • ranitidine

- cimetidine

60
Q

how do H2 receptor antagonists work?

A

= competitive (reversible) antagonists of H2 receptors

  • completely block the histamine-mediated component of acid secretion and reduce secretion evoked by gastrin and ACh
61
Q

what are H2 receptor antagonists effect against?

A

basal and stimulated gastric acid production

62
Q

when are H2 receptor antagonists effected?

A

once/twiice daily by oral admin

63
Q

what are H2 receptor antagonists used?

A

treatment of

  • peptic ulcers
  • reflux oesophagitis
64
Q

give an example of a muscarinic ACh receptor antagonist?

A

e.g. pirenzepine

65
Q

give an example of gastrin receptor antagonists?

A

e.g. progleumide

66
Q

what are 2 examples of mucosal strengtheners and what are they?

A

1) sucralfate
= complex of aluminium hydroxide and sulphate sucrose

2) bismuth chelate

67
Q

what do sucralfate require?

A

= an acid environment for activation, releasing aluminium to acquire strong negative charge

68
Q

what do sucralfate bind to?

A

ulcer base (+ charged proteins) and forms complex gels with mucus = providing a mucosal barrier against acid and pepsin

69
Q

what do sucralfate result in?

A
  • increased mucosal blood flow, mucus, bicarbonate and prostaglandin production
70
Q

how are sucralfate administered?

A

= orally

71
Q

what do bismuth chealate has mucosal strengthening action similar tot

A

sucralfate

72
Q

what is bismuth chealate toxic towards?

A

= towards H. pylori (used in combo with antibiotics and histamine H2 antagonists (ranitidine) to promote eradication of bacterium and ulcer healing

73
Q

how are bismuth chealate administered?

A

orally (in combo with ranitidine)

GI (43 decks)

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