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GI > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

what do mucous cells secrete and why?

A

mucous and bicarbonate to create a protective layer

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2
Q

what do parietal cells secrete and why?

A

hydrochloric acid, to begin digestion of proteins

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3
Q

what do chief cells secrete and why?

A

pepsinogen, to be converted to pepsin to being digestion of proteins

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4
Q

what do enterochromaffin-like cells secrete and why?

A

histamine, to regulate the amount of HCl released

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5
Q

what do G cells secrete and why?

A

gastrin, to regulate the amount of HCl/gastric acid released from parietal cells

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6
Q

what do D cells secrete?

A

somatostatin, to regulate the amount of gastric acid/HCl secretion from parietal cells

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7
Q

what cells are present in the gastric crypts/glands? (6)

A

mucous cells, chief cells, parietal cells, enterochromaffin-like cells, G cells, D cells

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8
Q

Describe how HCl is secreted from gastric parietal cells.

A

Cl- part:

  • Cl- enters the cell from the blood plasma while bicarbonate is removed - via a chloride bicarbonate exchanger.
  • Cl- is transported across the cell and secreted into the gastric lumen by a chloride potassium symporter (K ions leave at the same time).

meanwhile in the cytopplasm of the cell carbonic anhydrase is present which converts CO2 + H2O into carbonic acid which quickly dissociates to HCO3- and H+ ions.
The HCO3- is used to bring in Cl- (see above)
The H+ ions are secreted into the gastric lumen via the proton pump (K in, H+ out)

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9
Q

What effect does histamine have on gastric parietal cells?

A

increases gastric acid secretions

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10
Q

Describe the action of histamine on gastric parietal cells.

A

Histamine is secreted by enterochromaffin-like cells into the blood plasma.
This is stimulated by acetylcholine.
Histamine binds to H2 receptors of the parietal cell.
This activates adenylyl cyclase.
This increases the cAMP which increases the number of proton pumps, increasing the gastric acid secretion

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11
Q

what is cAMP?

A

a derivative of adenosine triphosphate used for intracellular signalling

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12
Q

describe the action of gastrin on gastric parietal cells.

A

Gastrin is released by G cells into the blood plasma.
It binds to CCK2 receptors on parietal cells.
This activates PLC.
Causing an increase in intracellular Ca2+, which increases the number of proton pumps, increasing the gastric acid secretion from parietal cells

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13
Q

what would a histamine antagonist do?

A

bind to H2 receptors decreasing secretion of gastric acid.

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14
Q

which part of the nervous system is responsible for stimulation of release of histamine from enterochromaffin-like cells?

A

parasympathetic (as it is stimulated by acetylcholine and histamine increases digestion)

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15
Q

describe the action of acetylcholine in reference to gastric parietal cells.

A

ACh is released by para cholinergic neurons.
ACh binds to muscarinic (M3) ACh receptors on parietal cells.
This activated PLC.
This increases intracellular Ca2+ ions, increasing the number of proton pumps, increasing gastric acid secretion from parietal cells.

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16
Q

what effect does somatostatin have on parietal and enterochromaffin-like cells?

A

On parietal cells: causes decreased gastric acid secretion.

On enterochromaffin-like cells it reduces the amount of histamine reduced, leading to decreased gastric acid secretion from parietal cells.

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17
Q

Describe the action of somatostatin in the stomach.

A

Somatostatin is secreted by D cells into the blood plasma.

In parietal cells:
It binds to SST2R receptors.
This inhibits adenylyl cyclase.
This causes a decrease in cAMP, resulting in decreased secretion of gastric acid.

In enterochromaffin-like cells:
It binds to SST2R receptors on these cells resulting in decreased histamine secretion, further decreasing the gastric acid secretion from parietal cells.

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18
Q

Give examples of antacids.

A

gaviscon and peptac

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19
Q

what do antacids do and how?

A

reduce the symptoms of excessive gastric acid secretion by buffering HCl with NaHCO3 and CaCO3

20
Q

what are NSAIDs?

A

non-steroidal anti-inflammatories

21
Q

what effect do NSAIDs have on the action of prostaglandins?

A

they disrupt the production of prostaglandins by inhibiting COX-1

22
Q

describe the effect of NSAIDs on gastric parietal cells.

A

NSAIDs disrupt the production of prostaglandins.
This reduced availability results in histamine secretion from enterochromaffin-like cells, increasing HCl secretion from parietal cells.

23
Q

what is misoprostol used for?

A

treatment of NSAID induced peptic ulcers.

24
Q

how does misoprostol work?

A

acts as an agonist at prostaglandin receptors, increasing the amount of prostaglandins produced, decreasing the levels of histamine. Therefore reducing gastric acid secretion

25
Q

what can NSAIDs cause in the GI tract and why?

A

peptic ulcers, due to the increase in histamine secretion to already damaged epithelium?

26
Q

what are the adverse effects of misoprostol?

A

abdominal pain, diarrhoea, induces labour

27
Q

describe how proton pump inhibitors work.

A

they irreversibly bind to the proton pump inhibiting H+ ion secretion into the lumen, therefore reducing HCl secretion

28
Q

what do proton pump inhibitors do?

A

act as antagonists to reduce HCl secretion

29
Q

what are the adverse effects of proton pump inhibitors?

A

increased stomach pH (reducing GI defence against pathogens)

30
Q

give examples of some proton pump inhibitors.

A

lansoprazole
omeprazole
pantoprazole

31
Q

what are proton pump inhibitors indicated for?

A

benign gastric acid ulceration AND NSAID-associated gastric ulceration, gastro-oesophageal reflux and Zollinger-Ellison syndrome.

32
Q

describe the action of histamine H2 receptor antagonists.

A

acts as a histamine H2 receptor antagonist which blocks the H2 receptor, preventing histamine binding to it. This eventually reduces HCl secretion.
(note: complete block will give a more rapid effect)

33
Q

what are histamine H2 receptor antagonists used for?

A

benign gastric acid ulceration and NSAID-associated gastric ulceration.

34
Q

what causes peptic ulcers?

A

H. pylori infeciton

35
Q

describe how peptic ulcers occur.

A

H. pylori gets into the GI tract. It infects and kills the mucous cells. This causes a gradual destruction of the mucous layer as mucous and bicarbonate secretion is decreased. This damages the protective coat, lowering the pH and gastric acid will influx into the damaged area resulting in ulceration

36
Q

how do you treat a peptic ulcer (aiming to eradicate H.pylori)?

A

proton pump inhibitors and antibiotics (clarithromycin and amoxicillin OR metronidazole)

37
Q

what is vomiting?

A

a defence mechanism triggered by the vomiting/emetic centre located in the brainstem

38
Q

what is the chemoreceptor trigger zone?

A

the main site for sensing emetic stimuli - located in brainstem

39
Q

what is the chemoreceptor trigger zone (CTZ)?

A

the main site for sensing emetic stimuli - located in brainstem

40
Q

what do antihistamines act on?

A

H1 receptors

41
Q

what does hyoscine act on?

A

M1 receptors

42
Q

what is hyoscine used to treat?

A

motion sickness and postoperative nausea and vomiting

43
Q

what role do enterochromaffin cells play in vomiting?

A

they sense toxic chemical or toxins in the gut

44
Q

what 3 centres are located in the medulla that are important in vomiting?

A

chemoreceptor trigger zone, vomiting centre, vestibular nuclei

45
Q

where does the vomiting centre receive inputs from?

A

the chemoreceptor trigger zone, vagal afferents (from the GI tract) and from higher cortical centres

46
Q

describe how the vomiting centre works.

A

enterochromaffin cells sense toxicity in the gut sending a vagal afferent to the brainstem (either directly to the vomiting centre, or via the CTZ)

OR vestibular nuclei can get input from the labyrinth signalling to the vomiting centre via the CTZ

OR the higher corical centres can sense pain, repulsive sight and smells and emotional factors sending signals straight to the vomiting centre.

The vomiting centre then integrates these signal and coordinates emesis

47
Q

describe how the vomiting centre works - referring to signals

A

enterochromaffin cells sense toxicity in the gut releasing 5-HT which transmit signals via vagal afferents to the brainstem (either directly to the vomiting centre, or via the CTZ)

OR vestibular nuclei can get input from the labyrinth signalling to the vomiting centre via the CTZ

OR the higher corical centres can sense pain, repulsive sight and smells and emotional factors sending signals straight to the vomiting centre.

The vomiting centre then integrates these signal and coordinates emesis

GI (11 decks)

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