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
where is intrinsic factor produced
parietal cells
26
intrinsic factor function
vitamin B12 absorption - intrinsic factor/B12 complex is absorbed from the ileum
27
what does a defect in the production of intrinsic factor cause
pernicious anaemia (failure of erythrocyte maturation)
28
what is the role of gastric mucus
CYTOPROTECTIVE role 1. protects mucosal surface from mechanical injury 2. neutral pH (HCO3) - protects against gastric acid corrosion and pepsin digestion
29
How does the gastric mucus protect against corrosion
High bicarbonate content – protects – makes pH around 7 at cell surface Acid buffered and neutralised by bicarbonate as it enters mucus layer
30
what is interesting about when acid is neutralised in the stomach
only neutralised on the way IN to the stomach - not on the way out
31
Describe the processes that occur during the cephalic stage of acid production
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
Describe the processes that occur during the gastric phase of acid production
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
what are the two indicators that stop acid production
1. acid in the duodenum | 2. fat in the duodenum
34
how does acid in the duodenum stop acid production
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
how does fat in the duodenum stop acid production
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
what are enterogastrones
hormones released from gland cells in duodenal mucosa - act collectively to prevent further acid build up
37
name the three enterogastrones
1. secretin 2. cholecystokinin (CCK) 3. GIP (Gastro-inhibitory peptide)
38
when are enterogastrones released
in response to acid or hypertonic solutions (mainly secretin) and fatty acids or monoglycerides (mainly GIP) in the duodenum
39
what are the two strategies by which enterogastrones work
1. inhibit gastric acid secretion | 2. reduce gastric emptying (inhibit motility/contract pyloric sphincter)
40
what is the name of the inactive form of an enzyme precursor (eg pepsinogen)
zymogen
41
where is pepsinogen secreted
chief cells
42
what determines secretion of pepsinogen
low pH (<3) - causes secretion of pepsinogen which is then converted to pepsin
43
what kind of feedback mechanism does pepsin production use
positive feedback - i.e. presence of pepsin makes more pepsin
44
how is the pepsin reaction stopped
by raising the pH - inactivated at neutral pH