1- physiology of gastric secretion Flashcards

1
Q

what happens in stomach?

A
  • starting point for digestion of proteins (by pepsin + HCl) continues carb digestion (by salivary amylase)
  • mixes food with gastric secretions to produce semi-liquid chyme (solid mixed with liquid) = stores food before passing to small intestine as chyme
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2
Q

is there any absorption in stomach?

A

mostly in intestine but there is limited absorption in stomach

*think like more surface area = more absorption and small intestine has bigger surface area

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3
Q

what are the muscular contractions like in orad regions of stomach?

A

orad = near top

tonic low level background contraction that are weak (due to only thin layer of musculature)

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4
Q

what happens to orad region of stomach when swallowing?

A

relaxation driven by vagus occurs during swallowing (simultaneously opening the lower esophageal sphincter) permitting storage of ingested material

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5
Q

what is function of lower oesophageal sphincter?

A

allows food transit from oesophagus into stomach and prevents reflux of gastric contents back into oesophagus

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6
Q

how is contents moved from orad to caudad part of stomach?

A
  • contents propelled intermittently to caudad region by low amplitude tonic contractions of about 1 min duration – decrease stomach size as it empties
  • minimal mixing of contents for long (~1 hr) periods – allows for carbohydrate partial digestion by salivary amylase
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7
Q

what are muscular contractions like in caudad stomach?

A

phasic (more drastic, powerful contractions) - intermittent

slow waves occur continuously but only those reaching threshold elicit contraction

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8
Q

what is mechanism behind caudad region contractions in stomach?

A
  • phasic peristaltic contractions driven by suprathreshold slow waves progress from midstomach to gastroduodenal junction (antra wave, or pump) propelling the contents towards pylorus through which a very small volume of chyme flows into duodenum
  • velocity of contraction increases towards junction, overtaking the movement of chyme that rebounds against constricted distal antrum back into the relaxed body of the stomach – this is retropulsion
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9
Q

what is retropulsion?

A

movement that mixes gastric contents reducing chyme (‘grinding’ function) to small particles (~1 mm3) that pass through the pylorus
-backward movement of the bolus from the pylorus to the body = also aids in mechanical digestion

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10
Q

what controls of stomach emptying?

A

gastric factors + duodenal factors

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11
Q

what is the antrum region of stomach?

A

bottom bit - the antral wave/pump and opening of pyloric sphincter determines delivery to chyme to duodenum

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12
Q

what are gastric factors that influence control of stomach empyting?

A

= aspects related to stomach →volume + consistency of chyme, distension

*thin consistency better, large volume = empty faster

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13
Q

what is distension of stomach and how does it effect stomach emptying?

A

distension = stretching due to presence of food stimulating smooth muscle contraction and increased motility
(stimulation of intrinsic nerve plexuses and increased vagus nerve activity + gastrin release)

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14
Q

what is gastrin?

A

a peptide hormone (secreted by G cells) primarily responsible for enhancing gastric mucosal growth, gastric motility, and secretion of hydrochloric acid (HCl) into the stomach

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15
Q

what are duodenal factors that influence stomach emptying?

A

= must be ready to recieve chyme

can be delayed by: neuronal response and hormonal response (these are driven by fat, acid, hypertonicity, distension)

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16
Q

what is neuronal response?

A

delays emptying of stomach into duodenum
- it’s the enterogastric reflex = decreases antral activity by signals from intrinsic nerve plexuses and ANS

17
Q

what is hormonal response in duodenum that can delay stomach emptying?

A

it’s when release of enterogastrones (cholecystokinin CCK) from duodenum inhibits stomach contraction

18
Q

what is hypertonicity and why do i care about it in this context?

A

products of carbs + protein digestion are osmotically active and draw water into small intestine - this can be danger of reduced plasma volume + circulatory disturbances
- so hypertonicity can delay emptying of stomach into duodenum

19
Q

what are the 2 different gland areas of the stomach?

A
  1. oxyntic gland area = proximal stomach including fundus + body
  2. pyloric gland area = distal stomach, designated antrum
20
Q

what is gastric mucosa composed of?

A
  • a surface lining the stomach
  • pits, invaginations of the surface
  • glands, at the base of the pits responsible for several secretions

*know more detailed histology in different flashcard set

21
Q

what is gastric juice?

A

unique combo of HCl , lipase and pepsin

22
Q

what is function of HCl?

A
  1. activates pepsinogen to pepsin (breaks down proteins)
  2. denatures proteins (gastric acid does this)
  3. kills most (not all) microorganisms ingested with food
23
Q

what is function of intrinsic factor + gastroferrin?

A

bind vitamin B12 and Fe2+ respectively, facilitating subsequent absorption

24
Q

what is function of histamine?

A
  • stimulates HCl secretion
  • histamine receptors are target to reduce gastric acid secretion (as histamine stimulates so drugs can target receptors to block them and reduce secretion)
25
Q

what is function of mucous?

A
  • protective (over gastric pit - covers layer of enterocytes)
    • H.pylori infection interrupts mucous and allows interruption by gastric acid→ulceration
26
Q

what is function of gastrin?

A

stimulates gastric acid secretion

27
Q

what is function of somatostatin?

A

inhibits HCl secretion (histamine promotes, somatostatin inhibits)

28
Q

what secretes histamine?

A

enterochromaffin like cells in gastric glands, in response to acetylcholine

29
Q

what are the phases of gastric acid secretion?

A
  1. cephalic phase
  2. gastric phase
  3. intestinal phase
30
Q

what is cephalic phase?

A

= before food reaches stomach, vagus nerve kicks in sending signals to stomach

31
Q

what is gastric phase?

A

= food in stomach, both physical + chemical mechanisms

32
Q

what is intestinal phase?

A

= food left the stomach, weak stimulation of gastric acid, chyme entering the upper small intestine causes weak stimulation of gastric section via neuronal and hormonal mechanisms

33
Q

describe what happens in cephalic phase?

A

slight small taste of food or conditioned reflexes like chewing or swallowing →vagal activation which stimulates enteric neurons to:
1. release ACh which stimulates ECL cells, ECL cells increase histamine which act on parietal cells to increase gastric acid secretion
2. release ACh that acts directly on parietal cells to increase gastric acid secretion
3. release GRP causing release of gastrin from G cells which acts on parietal cells to increase gastric acid secretion
4. inhibit D cells to decrease the somatostatin release. decrease in somatostatin secretion reduces its inhibitory effect on other cells, particularly G cells

34
Q

describe what happens in process of gastric phase?

A

distension of stomach activates reflexes that cause acid secretion
- food buffers pH (controlling acidity as too acidic damages), D cells secrete somatostatin (which inhibits digestive processes) = acidity inhibits D cells so more G cell activity
- amino acids (tryptophan, phenylalanine) stimulate G cells - other stimulates like Ca2+, caffeine + alcohol

35
Q

how does cephalic phase stop?

A

vagal nerve activity decreases upon cessation of eating and following stomach emptying (pain, nausea and negative emotions also decrease vagal nerve activity (parasympathetic) and increase sympathetic activity that combined reduce gastric acid secretion)

36
Q

how does gastric phase stop?

A
  • antral pH falls when food exits stomach (due to decreased buffering of gastric HCl) – release of somatostatin from D cells recommences, decreasing gastrin secretion
  • prostaglandin E2 (PGE2) continually secreted by the gastric mucosa acts locally to reduce histamine- and gastrin-mediated HCl secretion
37
Q

how does intestinal phase stop?

A

The factors that reduce gastric motility also reduce gastric secretion (e.g. neuronal reflexes, enterogastrones)