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Medsci305 > Lecture 21: drugs that regulate GI function > Flashcards

Lecture 21: drugs that regulate GI function Flashcards

1
Q

What cell types comprise the GIT?

A 
smooth muscle
blood vessels
glands
neuro network
and other specific cells
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2
Q

What is the GIT controlled by?

A

neural activity in the CNS (vagus nerve leads on to enteric nervous system)
GI hormones

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3
Q

Where are the majority of cells found in the stomach?

A

either in the fundus or antrum

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4
Q

Where are D cells and G cells found?

A

in the antrum

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5
Q

Which cells are found in the fundus?

A

parietal and mast cells

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6
Q

Are the mast cells in the stomach the same as those in the immune system?

A

they are slightly different.

Those in the stomach are now termed ECL cells

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7
Q

What does the enteric nervous system comprise of?

A

a lot of fleuxes:

  • neural networks run through the different layers (lumen and mucosa)
  • This innervation controls hormone release and motiliy
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8
Q

What are the two main different types of flexus?

A

myenteric flexus: mainly controls motility and contractions

submocusal flexus: one layer deeper and controls the secretions

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9
Q

What sorts of hormonal control regulates the GIT?

A
  • endocrine secretions released in the bloodstream which travel to the site of action
  • in the GIT gastrin is secreted from G cells in the antrum and move to surface at the fundus (food comes in from fundus)

paracrine secretions (local) from parietal cells. These release histamine which acts on ECL cells

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10
Q

How does the vagus nerve acts on the cells in the stomach?

A

via acetylcholine

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11
Q

What are the functions of the GIT?

A
  • vomiting,
  • formation and excretion of bile
  • motility of bowel and expulsion of faeces
  • gastric acid secretion
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12
Q

How is gastric acid normally secreted?

A
  • by parietal cells in the fundus.
  • HCl is triggered by hormone secretions and nervous system
  • proton pumps need to pump H+ across a concentration and electrical gradient
  • gastric secretion tightly controlled as we don’t want an empty stomach full of HCl.
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13
Q

What triggers HCl secretions?

A

hormonal and nervous stimuli

  • when you see/smell food, it can trigger ACh
  • presence of food in the mouth triggering saliva production also triggers gastric secretions
  • as food enters stomach, the distension also causes acid production
  • 80% of gastric secretion starts just by having food in the mouth
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14
Q

What are the main secretions that controls gastric acid?

A
  • histamine (main)
  • acetylcholine
  • gastrin
  • somatostatin (inhibitory)
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15
Q

What are the main characteristics of the parietal cell?

A
  • lots are dotted among the folds in the gut
  • they contain proton pumps within the caniculi
  • when the cell is not needed, there are lots of vesicles which contain proton pumps either resting or not fully assembled which lie in the basal membrane until they are triggered
  • there are also a lot of receptors which regulate the movement of pumps up to the canniculi
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16
Q

How does the proton pump work to form HCl?

A
  • proton pump pushes against a very high gradient
  • CO2 diffuses into cells of stomach where there is water already, to form carbonic acid
  • carbonic anhydrase catalyses this formation
  • the H is separated from the carbonic acid and quickly fired out by the proton pumps
  • proton pump also brings in a potassium
  • An alkali molecule (carbonate) is pumped out via an antiport (this causes alkaline tide a few minutes after your meal) which simultaneously brings in a Cl
  • The Cl forms HCl with the hydrogen
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17
Q

What is the role of somatostatin in the regulation of secretion?

A
  • somatostatin is released by delta cells and goes into the bloodstream
  • it acts both endocrine and paracrine as it can act closely on g cells as well as ECL cells
  • inhibits release of histamine from the ECL cell and the release of gastrin from parietal cells
18
Q

How does ACh regulate gastric secretions?

A
  • ACh is released from cholinergic neurons and acts on M1 in the ECL cell to increase histamine release
  • also acts on M3 whih is a GPCR on the parietal cell to increase H release
  • These receptors are Gq, so will activate protein kinase which acts on calcium channels and SR
  • Increase calcium causes translocation of pumps up to the caniculi membrane to increase production of gastric acid
  • Ach also acts on delta cells to inhibit somatostatin
19
Q

How does Gastrin regulate gastric secretions?

A
  • Gastrin is synthesised in the G cells and released by presence of food or stomach distension and vagal stimulation
  • There are also proteins which can act on G cells to release gastrin
  • Gastrin circulates through the bloodstream and binds to the CCK receptor
  • CCK receptors are also on the parietal cell. Gastrin binds here to increase H release
  • Gastrin also causes increased release of histamine
20
Q

How does histamine contribute to gastric acid secretion

A
  • There is a steady basal release of Histamine
  • this is increased by gastrin and Ach
  • H2 receptors in the stomach are Gs coupled and they activate AC which acts via cAMP to activate PKA
  • There are many proteins invovled in scaffolding and trafficking which causes these pumps to move up onto the surface
  • causes more insertion of proton pumps into apical membrane of parietal cell
  • more HCl produced
21
Q

What are the protective molecules in terms of gastric acid secretion?

A

prostaglandins E2 and I2

  • synthesised by COX I
  • inhibits gatric acid secretion
  • there are PG receptors on the ECL cells which inhibit histamine release as well as having other functions directuly on mucous cells to stimulate mucin and bicarbonate secretion
22
Q

What is a peptic ulcer?

A
  • lesions more than half a cm

- opening of stomach lining resutling in degradation of mucous, canniular membranes and outside layers

23
Q

What is the result of a peptic ulcer?

A

Pepsin beings to have contact in places it shouldn’t, causing holes

24
Q

What is the difference between duodenal ulcers and gastric ulcers?

A 
duodenal= in SI
gastric = in stomach
25
Q

What are ulcers caused by?

A
  • more acid than normal
  • defect in barrier of mucosal layer
  • H pylor infection (80% of cause)
  • Drug induced like NSAID, steroid, aspirin (10% cause)
26
Q

How does H. pylori cause gastric ulcers?

A
  • H. pylori is a bacteria with a flagellum that allows it to burrow into the stomach
  • has urease enzyme which breaks down urea and produces cloud of ammonia to neutralise the pH
  • It then penetrates through the mucous layer to be protected from the acid
  • It has a helical shape which allows it to screw itself into the mucous wall
  • releases cag-a which changes adherence junctions and changes epithelial cells into migratory cells. This disrupts the structure and integrity of stomach lining leading to ulcers
27
Q

How can drugs induce peptic ulcers?

A
  • these inhibit cox I which damages the mucous cells

- results in loss of integrity of mucous layer

28
Q

How are peptic ulcers treated?

A
  • as bacterial infection is main cause, antibiotic treatment is one form of therapy
  • triple therapy (amox, larithromycin and PPI) this kills bacteria and decreases the stomach acid to repair the ulcer
29
Q

What is zollinger ellison syndrome?

A

gastrin producing tumour

30
Q

What are the main classes of drug treatments for peptic ulcers?

A
  • drugs which block the secretion of histamine
  • drugs which block acid secretion
  • drugs which neutralise the acid
31
Q

What are histamine H2 antagonists?

A

e. g. cimetidine, ranitidine
- competitive antagonists at H2 receptors
- inhibit cAMP and PK to reduce gastric secretion
- taken more often and work more quickly, but duration is not as long

32
Q

What are proton pump inhibitors?

A

e. g. omeprazole, pantoprazole
- pro drugs which have a low pka (4)
- higher concentration in active state and can selectively bind directly onto the pump
- cause long term inhibition of gastric acid release
- takes longer to work (several days or a week before effect)

33
Q

Which drugs can neutralise the stomach acid?

A

gastric antacids
-divided into

1) systemic
2) non systemic

34
Q

What is the rationale for using systemic gastric antacids?

A

-absorbs into the blood and acts rapidly

35
Q

What are the limitations with using systemic antacids?

A
  • can cause electrolyte imbalance

- may not be suitable to all patients e.g. sodium bicarbonate not suitable for cv risk patients due to high Na content

36
Q

What are examples of non systemic antacids?

A
  • aluminium OH, magnesium OH, calcium carbonate
  • these cations are not well absorbed in the GIT and complex with excess acid
  • the precipitate into the stomach and are excreted
  • neutralises gastric acid and increases gastric pH
37
Q

What are the limitations with non systemic antacids?

A
  • they can chelate with other meds like folate and iron
  • may have specific problems e.g. calcium carbonate releases carbon dioxide -> belching and flatulence
  • Mg at higher doses has laxative effect
  • hence, Mg and Al often blended together
38
Q

What drugs protect the mucosa?

A
  • Bismuth chelate
  • sucralfate
  • misoprostol
39
Q

What is bismuth chelate?

A
  • may be used in combination with antibiotic and PPI treatments
  • coats the ulcer like a polymer and binds to certain cells above the ulcer
  • absorbs pepsin and enhances local PG synthesis (good for mucous cells)
  • stimulates more bicarbonate secretion
40
Q

What is a side effect of bismuth chelate?

A
  • bad taste
  • black stools
  • black tongue
41
Q

What is sucralfate?

A
  • used for duodenum ulcers
  • complex of Al(OH)3 and sulfated sucrose
  • forms bandage across ulcer
  • stimulates bicarbonate secretion and PG production
42
Q

What is misoprostol?

A
  • analogue of PGE1
  • inhibits activation of pumps and increases production of mucous
  • basically reducing gastric acid secretion and protecting the gut and mucosa

Medsci305 (17 decks)

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