Gastric Secretion Flashcards

1
Q

Fundus function

A

Storage

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2
Q

Body of stomach function

A

Storage, mucus, HCl, Pepsinogen, Intrinsic factor

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3
Q

Antrum function

A

mixing/grinding, gastrin

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4
Q

HCl function in stomach

A

marinating

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5
Q

What is pepsinogen the inactive form of

A

pepsin - a proteolytic enzyme

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6
Q

why is pepsin stored in its inactive form

A

so as to not erode the stomach

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7
Q

chyme definition

A

mixed food as it leaves the antrum

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8
Q

gastrin definition

A

hormone released in antrum from G-cells and secreted into the circulation - acts on cells of body

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9
Q

what is the cellular composition of a gastric gland

A

Gastric Pit -
1.surface mucous cells

Gastric Gland -

  1. mucous neck cells
  2. parietal cells
  3. chief cells
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10
Q

Mucous neck cells secrete

A

mucus

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11
Q

parietal cells secrete

A

HCl, intrinsic factor

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12
Q

chief cells secrete

A

pepsinogens

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13
Q

Why are the junctions between cells very tight

A

to stop stomach acid entering

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14
Q

How is HCl made in the stomach

THIS IS A VERY LONG ANSWER

A
  1. CO2 into cell – combines with water – makes carbonic acid – made faster by carbonic anhydrase – H2CO3 doesn’t last long – immediately dissociates to form H ions and bicarbonate
  2. H ions pumped out (need ATP) – works similar to NaK pump – one H out, one K in
    HCO3 – pumped out on exchange protein – HCO3 out, – HCO3 out causes temporary alkalisation
  3. Cl in (through cell and out the other side-joins with the other H and water to make the HCl in the stomach)
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15
Q

when is the only time HCl is produced in the stomach

A

when eating

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16
Q

What three molecules control acid production

A
  1. Gastrin
  2. Histamine
  3. Acetylcholine
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17
Q

What controls the switch off mechanism for acid production

A

prostaglandins

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18
Q

how does gastrin work

A

Binds to its receptor – g-protein coupled receptor – causes a rise in Ca – acts through protein kinase C to increase turn around of K/H proton pump

19
Q

how does histamine work

A

stomach has a unique histamine receptor – H2 receptor – coupled with Gs

20
Q

how does acetylcholine work

A

neurotransmitter – acts on muscarinic cholinergic receptros (M3) – g protein coupled – rise in Ca – rise in turn around of H/K

21
Q

How do prostaglandins inhibit acid production

A

Gi – inhibitor protein – coupled with that prevents reaction taking place – take away stimulus – turn pump off

22
Q

what three mechanisms is gastric acid section controlled by

A
  1. Neurocrine - (vagus/local reflexes)
  2. Endocrine (gastrin)
  3. Paracrine (histamine)
23
Q

What are the two phases of acid secretion

A
  1. cephalic - anticipation of food

2. gastric - food reaching stomach

24
Q

What is the only essential (non-compensated) function of the stomach

A

the production of intrinsic factor

25
Q

where is intrinsic factor produced

A

parietal cells

26
Q

intrinsic factor function

A

vitamin B12 absorption - intrinsic factor/B12 complex is absorbed from the ileum

27
Q

what does a defect in the production of intrinsic factor cause

A

pernicious anaemia (failure of erythrocyte maturation)

28
Q

what is the role of gastric mucus

A

CYTOPROTECTIVE role

  1. protects mucosal surface from mechanical injury
  2. neutral pH (HCO3) - protects against gastric acid corrosion and pepsin digestion
29
Q

How does the gastric mucus protect against corrosion

A

High bicarbonate content – protects – makes pH around 7 at cell surface

Acid buffered and neutralised by bicarbonate as it enters mucus layer

30
Q

what is interesting about when acid is neutralised in the stomach

A

only neutralised on the way IN to the stomach - not on the way out

31
Q

Describe the processes that occur during the cephalic stage of acid production

A
  1. anticipation of food stimulates vagus nerve = release of ACh
  2. vagus nerve stimulation casues stimulation of G-cells = release of Gastrin
  3. With both Gastrin and ACh present ECL cells are stimulated = release of histamine
  4. With ACh, gastrin and histamine all present -Parietal cells are activated
32
Q

Describe the processes that occur during the gastric phase of acid production

A
  1. arrival of food in stomach takes over for stimulating vagus nerve = release of ACh
  2. Peptides present in lumen take over for stimulation of G-cells = release of gastrin
  3. With both Gastrin and ACh present ECL cells continue to be stimulated = release of histamine
  4. With ACh, gastrin and histamine all present -Parietal cells are activated
33
Q

what are the two indicators that stop acid production

A
  1. acid in the duodenum

2. fat in the duodenum

34
Q

how does acid in the duodenum stop acid production

A
  1. stimulates enterogastric (splanchnic) reflex
  2. stimulates secretin release
  3. both of these processes lead to a decease in gastrin secretion which causes a decease in the stimulation of parietal cells
35
Q

how does fat in the duodenum stop acid production

A
  1. causes release of GIP

2. leads to a decrease in gastrin secretion which leads to a decrease in HCl secretion from parietal cells

36
Q

what are enterogastrones

A

hormones released from gland cells in duodenal mucosa - act collectively to prevent further acid build up

37
Q

name the three enterogastrones

A
  1. secretin
  2. cholecystokinin (CCK)
  3. GIP (Gastro-inhibitory peptide)
38
Q

when are enterogastrones released

A

in response to acid or hypertonic solutions (mainly secretin) and fatty acids or monoglycerides (mainly GIP) in the duodenum

39
Q

what are the two strategies by which enterogastrones work

A
  1. inhibit gastric acid secretion

2. reduce gastric emptying (inhibit motility/contract pyloric sphincter)

40
Q

what is the name of the inactive form of an enzyme precursor (eg pepsinogen)

A

zymogen

41
Q

where is pepsinogen secreted

A

chief cells

42
Q

what determines secretion of pepsinogen

A

low pH (<3) - causes secretion of pepsinogen which is then converted to pepsin

43
Q

what kind of feedback mechanism does pepsin production use

A

positive feedback - i.e. presence of pepsin makes more pepsin

44
Q

how is the pepsin reaction stopped

A

by raising the pH - inactivated at neutral pH