Gastric secretions Flashcards

1
Q

function of stomach

A

secretes hydrogen, pepsinogen, mucus, bicarbonate and intrinsic factor

muscular contractions to mix contents

releases humoral factors

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2
Q

function of acid secreted

A

denature proteins, aid digestion

promotes truncation of pepsinogen to form active enzyme pepsin

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3
Q

which cells secrete HCL?

A

Parietal cells

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4
Q

intrinsic factor function

A

aids B12 absorption

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5
Q

mechanism of acid secretion

A
  1. intracellular carbonic anhydrase catalyses the hydration of carbon dioxide to yield carbonic acid that then dissociates into hydrogen and bicarbonate ions
  2. hydrogen potassium ATPase pumps out hydrogen ions at apical membrane in exchange for potassium
  3. potassium recycles out of the cell through apical potassium channels
  4. bicarbonate ions exit basolateral membrane then enter blood to act as a buffer
  5. chloride diffuses through apical channel to form HCL in lumen
  6. water follows via aquaporins
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6
Q

alkaline tide definition

A

alkalinisation of blood during acid secretion

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7
Q

Where is the ATPase located in inactive cells?

A

within vesicles

ATPase is inside out, pumping hydrogen ions to the lumen and potassium out

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8
Q

three molecules that induce acid secretion

A

ACh, gastrin and histamine

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9
Q

explain stimulation of ACh and actions

A
  1. vagus releases ACh that binds to M3 receptors
  2. activate PLC which conerts PIP2 to IP3 and DAG
  3. IP3 releases calcium, DAG activates PKC
  4. PKC phosphorylates parietal cell proteins, including H/K pump
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10
Q

explain gastrin mechanism of action

A
  1. Binds to CCKb receptors

2. GqPCR- PKC and IP3

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11
Q

explain release of gastrin

A
  1. vagus nerve/ protein digestion products in the lumen stimulate GRP-releasing neurones
  2. GRP-releasing neurones release gastrin related peptide which binds to G cells
  3. G cells then release gastrin
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12
Q

histamine precursor

A

histamine

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13
Q

where is histamine released from?

A

ECL cells in stomach

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14
Q

Histamine mechanism of action

A
  1. binds to H2 receptors
  2. activate cAMP–> PKA
  3. PKA phosphorylates H/K ATPase
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15
Q

how is histamine released?

A

gastrin and ACh bind to M3 CCK receptors on the ECL cells to induce histamine release

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16
Q

common mediator definition

A

gastrin and ACh affect histamine which induces gastric acid release

17
Q

evidence for common mediator

A

Ranitidine, a H2 antagonist, is a strong inhibitor of gastric acid secretion

18
Q

ulcer definition

A

an area of dead epithelium

19
Q

peptic ulcer definition

A

area of necrosed lining of the stomach, proximal duodenum or oesophagus caused by gastric secretions

20
Q

common causes of peptic ulcers

A

Helicobacter pylori bacteria or long term use of NSAIDS

21
Q

explain NSAID adverse action

A

acidic molecules directly irritate gastric mucosa and inhibit COX-1 and COX2, reducing levels of prostaglandins

increases gastric acid secretion, diminishes bicarbonate and mucus secretion

22
Q

common therapy for peptic ulcers

A

antacids

23
Q

what are antacids?

A

reduce the problem of too much acid by neutralising them with an alkali

24
Q

examples of antacids

A

aluminium hydroxide, magnesium hydroxide, trisilicate

25
Q

side effects of antacids

A

diarrhea

26
Q

two other treatments for peptic ulcer

A

H/K pump blocker, H2 antagonists

27
Q

example of H/K pump blocker

A

omeprazole

28
Q

prostaglandin functions

A

secretion of mucus is mediated by prostaglandins E and I-2

29
Q

evidence for H.pylori involvement

A

eradication of bacteria reduces the risk of peptic ulcer recurrence

30
Q

what is being used against H.pylori?

A

chemotherapy