Gastric secretions Flashcards

1
Q

How much gastric juice does the stomach secrete every day?

A

2L

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2
Q

Where are mucosal gland cells found?

A

gastric pits

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3
Q

How is the stomach split in terms of regions?

A

oxyntic mucosa - fundus and body

pyloric gland area - antrum

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4
Q

what are the secretions of:

Chief cells? Parietal Cells? Mucous Neck cells? Surface epithelial cells?

A

chief - pepsinogen
partietal - HCl and intrinsic factor (for B12)
mucus- mucus
sufrace - mucus

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5
Q

Explain the process by which HCL secretion happens. How is K+ recycled? What happens to the HCO3-?

A

CO2 and water in parietal cell
Carbonic anhydrase reaction CO2 + H2O -> H2CO3 (Carbonic ion)
Dissociates into bicarbonate and hydrogen ions
Bicarbonate moves to capillaries and goes to other cells in stomach
H+ secreted into the gastric lumen
H+ exchanges with potassium ions
Bicarbonate moves back into plasma in exchange for Cl-
Cl- transported into the gastric lumen

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6
Q

what extra thing do parietal cells release?

What does the acid in the stomach help?

A

IF
binds to vit B12 to enable re-absorption

HCl helps to activate pepsin

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7
Q

How is pepsinogen converted to pepsin?

A

acidic environment causes catalysis, breaking down pepsinogen into pepsin

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8
Q

What is the first phase of gastric secretion – before food enters stomach?
What nerve is involved?
What stimulates this phase?

A

cephalic phase
vagus n
thought or expectation of food

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9
Q

Explain the whole process of parasympathetic control of HCL secretion
What neurotransmitter stimulates the parietal cells? What are the receptor type?

A

parietal cells receive direct innervation by parasympathetic nn (ACh) stimulates M receptors on parietal cells = changes Ca ion conc and then secretion of HCl

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10
Q

Role of Enterochromaffin-like cells? What receptor involved?

A

contain histamine and innervation of PS: activated by M receptor. histamine interacts w H2 receptors=chnage in Ca level = secretion of HCl

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11
Q

Antral G-cell? What do they secrete and what NT activates them?

A

secretes gastrin, activated by PS (GRP neurotransmitter). interacts with CCK-2 receptors = histamine release and increase HCl

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12
Q

What receptor activated by gastrin on what cells?

A

CCK-2

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13
Q

Antral region contains what special cell? What does the cell release? What happens with parasympathetic activation?

A

D-cells
somatostatin (decreases gastrin release)

when stimulated = release less ss so less inhibition

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14
Q

What are the other 2 phases of gastric secretion?

Gastric phase – what triggers release (2 things)?

A

gastric phase
intestinal phase

mechanical stimulation (no CNS)
gastrin release from G-cells = positive feedback
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15
Q

what does VIP do? What’s the other mechanism?

What’s the CO of resting stomach and active stomach?

A

cause vasodilation

peptide release?

resting: 0.5%
active: >10%

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16
Q

how is gastric secretion inhibited (4)?

A

removal of peptide fragments
removal of food leads to decrease in pH - G-cells inhibited

distention of duodenum or presence of acid/food in chyme = releases enterogastrone: inhibits gastrin
gastric secretion influenced by cephalic factors such as fear or depression

17
Q

what are the 4 mechanisms by which the stomach protects itself from digestion?

A

luminal cells of gastric mucosal cells are impermeable to H+ions
negative feedback (pH or D-cells)
mucous released from surface epithelial cells
rapid repair of damaged mucosa

18
Q

Why do NSAIDs increase gastric bleeding?

A

Prostaglandins are important for this process as well – localised vasodilation, which gives the cells the bicarbonate ions that maintain the neutral pH
Prostagalndins produces by COX – explaining why NSAIDs damage the stomach