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Semester 4 > Case 2 - gastric acid production > Flashcards

Case 2 - gastric acid production Flashcards

1
Q

what is the pH of the stomach

A

1.55-3.5

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2
Q

what is HCl produced by in the stomach

A

the parietal cells

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3
Q

what is the first step to produce hydrochloric acid

A

water and carbon dioxide combine within the parietal cell cytoplasm to produce carbonic acid

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4
Q

what is the carbonic acid catalysed by

A

carbonic anhydrase

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5
Q

what happens to the carbonic acid after it has been catalysed

A

spontaneously dissociates into a hydrogen ion and a bicarbonate ion

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6
Q

where is the hydrogen ion transported to and via what?

A

transported into the stomach lumen via the H+/K+ ATPase ion pump.

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7
Q

what does this pump use for the exchange of ions

A

this pump uses ATP as an energy source to exchange potassium ions into the patietal cells of the stomach with H+ ions

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8
Q

how is the bicarbonate ion transported out of the cell into the blood

A

via a transporter pump called anion exchanger which transports the bicarbonate ion out of the cell in exchange for a chloride ion.

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9
Q

what happens to this chloride ion

A

it is then transported into the stomach lumen via a chloride channel

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10
Q

what is the result of the Cl going into the stomach lumen via a chloride channel

A

result in both the hydrogen and chloride ions being present within the stomach lumen.

their opposing charges leads to them associated with each other to form hydrochloric acid

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11
Q

how is the production of gastric acid controlled

A

as a result, the number of H+/K+ ATPases present within the parietal cell membrane is minimal. the rest are sequestered within tubulovesicles in the parietal cell

upon stimulation the vesicles fuse with the cell membrane, hence allowing for the increases movement of hydrogen ions into the stomach thus increasing acid production

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12
Q

explain the mechanism to increase gastric acid production via ACH

A

ACh is released form the vagus nerve.

this is released firstly during the cephalic phase of digestion, which is activated upon seeing or chewing food, leading to direct stimulation of parietal cells via the vagus nerve

it is also produced during the gastric phase of digestion when intrinsic nerves detect distension of the stomach, stimulating the production of ACh by the vagus nerve

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13
Q

explain how gastric acid production is increased via gastrin

A

the main regulation pathway involves the hormone gastrin which is secreted by G cells in the stomach.

G cells are activated by the vagus nerve, gastrin related peptide and by peptides in the stomach lumen produced via protein digestion.

activation of the G cells leads to the production of gastrin which is released into the blood and travels through the blood until it reaches the parietal cells.

Gastrin binds to CCK receptors on parietal cells which also elevates calcium levels causing increased vesicular fusion

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14
Q

how is gastric acid production increased via histamine

A

enterochromaffin like cells in the stomach secrete histamine which binds to H2 receptors on the parietal cells. these cells release histamine in response to the presence of gastrin and ACh. this leads to increased fusion however it is via the secondary messenger cAMP as opposed to calcium in the other methods

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15
Q

how is gastric acid production decreased - important and long but learn all of it

A

Via the accumulation of acid in the empty stomach between meals. This increase in acid leads to a lower pH within the stomach, which inhibits the secretion of gastrin, via the production of somatostatin from D cells.

Once food has been broke down into chyme, it passes into the duodenum, triggering the enterogastric reflex.

This reflex can be stimulated by distension of the small bowel, if there is excess acid in the upper intestine, the presence of protein breakdown products as well as excess irritation to the mucosa

Inhibitory signals are sent to the stomach via the enteric nervous system, as well as signals to medulla - reducing vagal stimulation of the stomach

The enterogastric reflex, is important in slowing down gastric emptying when the intestines are already filled

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16
Q

what does the presence of chyme within the duodenum also stimulate

A

stimulates entero-endocrine cells to release cholecystokinin and secretin, both of which play a variety of important roles in completing digestion, but also inhibit gastric acid secretion

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17
Q

what is secretin release by and when

A

released by the S cells of the duodenum when there is excessive acid production in the stomacb

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18
Q

what other hormones work to decrease acid production in the stomach

A

Other hormones including glucose dependent insulinotropic peptide and vasoactive intestinal polypeptide

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19
Q

what are the two mai drugs used to prevent excessive acid formation

A

H2 antagonists and protein pump inhibitors

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20
Q

how do H2 antagonists work and give an example

A

H2 antagonists such as ranitidine bind to the H2 receptors preventing the binding of histamine and thus reduce acid secretion

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21
Q

how do protein pump inhibitors work and give an example

A

protein pump inhibitors (PPIs) such as omeprazole bind to the H+/K+ ATPase pump, hence preventing the transportation of hydrogen ions into the stomach lumen. PPIs completely prevent stomach acid formation due to hydrogen ions not being able to react with chloride ions in the stomach.

22
Q

what is achlorhydria

A

state where there is a decrease in volume of stomach acid produced

can result in an increased risk of salmonella and chloera

23
Q

what are the two types of tubular glands found in the stomach mucosa

A

oxyntic glands and pyloric glands

24
Q

what are oxyntic glands

A

acid forming glands composed of three types of cells:
- mucous neck cells - secrete mucus
- peptic (chief) cells - large quantities of
pepsinogen
- pariental (oxytnic cells) - HCL and
intrinsic factor

These are located on the inside surfaces of the body and fundus of the stomach, constituting the proximal 80% of the stomach

25
Q

what are pyloric glands

A

secrete mainly mucus for protection of the pyloric mucosa from the stomach acid and they also secrete the hormone gastrin
These are located in the antral portion of the stomach, the distal 20% of the stomach

26
Q

what do the parietal cells contain

A

large branching intracellular canaliculi

27
Q

what is the relationship between HCl and these canaliculi

A

The HCL is formed at the villus like projections inside these canaliculi and is then conducted through the canaliculi to the secretory end of the cell (the apical end)

28
Q

step one of mechanism of HCL secretion

A

Cl- ions are actively transported from parietal cell cytoplasm into the limen of the canaliculus via a chloride pump. Na+ ions are actively transported out of the canaliculus into the cytoplasm of the parietal cell via a sodium pump. This creates a negative potential (-40 to -70) in the canaliculus. This causes K+ ions to enter the canaliculus from the cytoplasm. Thus, in effect, mainly KCl and smaller amounts of NaCl enter the canaliculus.

29
Q

step two in the mechanism of HCL secretion

A

Water dissociates into hydrogen ions and hydroxyl ions in the cytoplasm. H+ ions are actively secreted into the canaliculus in exchange for K+ ions. This is catalysed by the K+/H+ ATPase pump. Also, Na+ ions are actively reabsorbed by a separate sodium pump. Therefore, the Na+ ions and K+ ions that were initially secreted into the canaliculus have been reabsorbed, whilst H+ ions have been added to the canaliculus. This gives us the HCl in the canaliculus

30
Q

step three in the mechanism of HCL secretion

A

Water passes into the canaliculus by osmosis because of the increased ionic concentration in the canaliculus. The final secretion from the canaliculus contains water, HCl, KCl and small amounts of NaCl.

31
Q

step four in the secretion of HCL mechanism

A

OH- combines with CO2 under the influence of carbonic anhydrase to form bicarbonate ions. These diffuse into the extracellular fluid in exchange for Cl- ions.

32
Q

what do ECL cells secrete

A

histamine which binds to H2 histamine receptors on parietal cells

33
Q

what does histamine do to parietal cells

A

activates the parietal cells to form and secrete HCL

34
Q

what is the rate of formation and secretion of HCL dependent on

A

the amount of histamine secreted by ECL cells

35
Q

how are ECL cells activated:

A

gastrin
acetylcholine
hormonal substances secreted by the enteric nervous system of the stomach wall

36
Q

gastrin activating ECL cells:

A

when G cells of the antral mucosa come into contact with amino acids, they pass gastrin to ECL cells through the digestive juices, which in turn secrete histamine

37
Q

what is acetycholine released from

A

stomach vagal nerve endings

38
Q

where are the G cells located in the stomach

A

located in the antral mucosa (pyloric glands)

39
Q

what are the two forms in which gastrin is secreted

A

G-34 = this contains 34 amino acids
G-17 = this contains 17 amino acids (and is more abundant)

40
Q

what does chyme do to gastric secretion

A

chyme initially increases gastric acid secretion

however, later chyme inhibits gastric acid secretion

41
Q

what is the first way in which chyme inhibits gastric acid secretion

A

presence of food in the small intestine initiates a reverse enterogastric reflex, transmitted through the myenteric nervous system and vagus nerves, that inhibits stomach secretion. this reflex can be initiated by distending the small bowel, by the presence of acid in the upper intestine, by the presence of protein breakdown products, or by irritation of the mucosa

42
Q

what is the other way in which chyme inhibits gastric secretion

A

The hormone secretin is secreted as a result of the presence of… (listed above). It is important in the control of pancreatic secretion. Secretin opposes stomach secretion. Other hormones have a slight effect on inhibiting gastric secretion - GIP, vasoactive intestinal polypeptide and somatostatin

43
Q

what is the inhibition of gastric secretion by intestinal factors for

A

to slow passage of chyme from the stomach when the small intestine is already filled or already overactive

44
Q

what does somatostain do

A

inhibits G cells, ECL cells and if there is an excess of acid in the duodenum, it inhibits the parietal cells

45
Q

what happens during the indigestive period

A

the stomach secretes gastric juice in the indigestive period

this is a non-oxyntic secretion consisting mainly of mucus, but little pepsi and almost no acid

emotional stimuli increase indigestive gastric secreiton.

46
Q

what is the main cause of GERD

A

incompetence of the anti-reflux barriers at the oesophogastric junction

47
Q

what does gastric pepsin duodenal contents do

A

exacerbate the action of acid and deleterious effect on the production of oesophagitis

48
Q

what are the two sphincter mechanisms of the anti reflux barriers

A

the lower oesophageal sphincter and the crural diaphragm that functions as an external sphincter

49
Q

when does gastroesophageal reflux occur

A

when LES pressure is lower than intragastric pressure such as in LES hypotension, increased frequency of transient lower osesophageal sphincter relaxation when the intragastric presure increases

50
Q

when does the severity of GERD increase

A

increases progressively with reflux that is mainly in the postprandial period to that in the upright posture, to that in the supine or that is bipositional reflux
Night time reflux leads to severe GERD

51
Q

what are the mechanisms from which a hiatal hernia results

A

associated with a decreased LES presure, decreased acid clearance, increased reflux and more severe oesophagitis

Semester 4 (80 decks)

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