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BIOM2009 > GIT > Flashcards

GIT Flashcards

1
Q

What is the main function of the stomach

A

Mechanical breakdown of food to produce chyme

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2
Q

What is a gastric mucous cell? What is the function of the mucous it secretes?

A

Gastric pit cell that secrete mucous. Mucous (controlled by prostaglandins) is slightly alkaline and can protect the stomach lining from the acidic environment.

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3
Q

How do NSAIDs lead to the formation of gastric ulcers?

A

NSAIDs act on prostaglandins, therefore reducing gastric mucous secretion. Insufficient mucous leads to ulcers

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4
Q

Describe function of parietal cells. How are secretions from parietal cells mediated?

A

Secrete HCl and intrinsic factor. Secretion is response to histamine release from ECL cells.

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5
Q

What is intrinsic factor? How does it relate to B12

A

Vitamin B12 is only taken up by the ileum when it is a complex with intrinsic factor. B12 is important for fatty acid metabolism and DNA synthesis

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6
Q

What are the 3 enteroendocrine cells and what do they secrete?

A

G - secretes gastrin, a hormone that promotes the release of histamine from ECL cells
A - secretes glucagon
D - secretes somatostatin

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7
Q

Function of chief cells?

A

Secretes pepsinogen, the precursor to pepsin (responsible for breaking down proteins)

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8
Q

Explain the release of H+ from the proton pump

A

Proton pump = active transporter. Pumps H+, K+ and Cl- into the lumen. H+ and Cl- come together in the lumen to form HCL

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9
Q

HCL function in stomach?

A
  • acidic environment allows for pepsinogen to be converted to pepsin
  • denatures proteins, exposing them to digestive enzymes
  • kills microbes
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10
Q

Name 3 receptors found in small intestine

A
  • muscarinic (ACh)

- alpha 1 and beta 2 (adrenoreceptors)

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11
Q

Gastrin and CCK inhibit gastric motility, whereas somatostatin and GIP (gastric inhibitory peptide) stimulate motility. True or false?

A

False. It is the opposite. Gastrin and CCK stimulate

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12
Q

Name 2 uses of prokinetic agents

A
  • relieve nausea due to overeating

- IBS

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13
Q

Explain the role of acetylcholine in gastric motility

A

ACh binds to muscarinic receptors on the smooth muscle cells. This activates the muscle and leads to contraction.

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14
Q

Compare the 5-ht 4 and 5-ht 3 receptors in the GIT

A

4 - stimulates motility by increasing ACh release

3- mediates nausea and abdominal pain

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15
Q

Explain how D2 and CB1 receptors inhibit gastric motility

A 
D2 = binding of agonist to D2 receptor blocks the releases of ACh 
CB1 = cannabinoids reduce gut motility ... effect on nervous system maybe?
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16
Q

Compare metoclopramide and domperidone

A

Metoclopramide = both an antagonist of D2 and agonist at 5-HT4

Domperidone = D2 antagonist
Both increase motility and are antiemetics

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17
Q

Explain the CTZ (chemoreceptor trigger zone) and how it leads to activation of the vomiting centre in the medulla.

A

CTZ is an area of the brain where the BBB is not developed. Allows brain to measure / detect what is in the blood stream. If opioids, chemo drugs, etc are detected, the vomiting reflex can be activated

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18
Q

Explain the process of the inner ear activating vomiting.

A

Labyrinth in the inner ear detects info about posture, movement, etc. it can induce vomiting when rapid movement (kinetosis) is detected = motion sickness. Info is carried to medulla via Cholinergic pathway (muscarinic receptors and ACh)

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19
Q

Why can’t dopamine antagonists be used for motion sickness?

A

No dopamine receptors in the labyrinth

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20
Q

What effect do dopamine antagonists have on vomiting and gastric motility?

A

Vomiting =antiemetic

Motility = increase

21
Q

List some side effects on dopamine antagonists?

A 
Extrapyramidal / Parkinson’s symptoms (like muscle dystopia, muscle stiffness, tremors)
Others:
Increased prolactin release 
Sedation 
Hypotension
22
Q

List 2 examples of a dopamine antagonist and muscarinic antagonist.

A

Dopamine =

  • metoclopramide
  • promethazine

Muscarinic =

  • scopolamine
  • hyoscine
23
Q

How do muscarinic antagonists work as antiemetics

A

Block muscarinic receptors in vomiting centre and reduce nausea associated with kinetosis (motion sickness)
Can be given transdermally to minimise systemic effects (sludge-bbb)

24
Q

What does SLUDGE-BBB stand for? Side effects of activating muscarinic receptors.

A

Salivation, lacrimation, urination, defecation, gastroEmesis, bronchorrhea, bronchospasm, bradycardia
Antagonist of M receptors = opposite effects.

25
Q

Name for serotonin antagonists is ____

A

Setrons

26
Q

Setrons are used to treat acute ekes is caused by xxx and xxx

A

Radiotherapy / chemotherapy or post op

27
Q

Example of setrons used as antiemetic?

A

Ondansetron (note suffix)

28
Q

3 treatment options for hyperemesis gravidarum?

A

Severe vomiting during pregnancy

  1. IV rehydration
  2. D2 antagonists (metoclopramide)
  3. Ondansetron
29
Q

Explain MOA of bulk laxatives

A

Contains non-absorbable carbs and fibre supplements are aren’t digested. They swell with water, and the presence of the large bulk promotes peristalsis and initiates defecation reflex.

30
Q

Example of bulk laxative

A

Methylcellulose

Psyllium

31
Q

Describe MOA of osmotic laxatives

A

Non-absorbable sugars which increase the stool osmolarity, which draws fluid in. Onset usually 1-3 days. Can cause bloating or cramping

32
Q

Describe osmotic laxatives II MOA

A

More intense osmotic laxatives. Used before surgery. Works in 1-3 hours

33
Q

Give examples of both osmotic and osmotic II laxatives

A

Osmotic

  • lactulose
  • sorbitol

Osmotic II
- epsom salt

34
Q

Explain MOA of stimulant laxatives

A

Directly stimulate the myenteric plexus to promote peristalsis and defecation
E.g. senna

35
Q

Which laxative can lead to dependence with frequent use?

A

Senna - stimulant laxatives

36
Q

Explain MOA of faecal softeners

A

Anionic surfactant that lowers the surface tension of the stool, making it easier to pass. Typically combined with other laxative types as it s quite weak alone
E.g. docusate

37
Q

Compare the 3 different types of diarrhoea. Secretory, osmotic and exudative

A 
Secretory = stimulating substance have increased secretions. 
Osmotic = poor absorption of water in the colon 
Exudative = caused by inflammation or infection. Mucous present in stool. Due to reduction in contact time with the Small intestine, meaning not enough time to extract water
38
Q

Describe MOA of loperamide

A

Blocks the action of ACh on smooth muscle cells, leading to reduced GIT motility. By slowing down GIT, more time available for water absorption.

39
Q

Compare D2 and 5-HT4 receptors in GIT

A

Agonist @ D2 = decreased motility due to block of ACh release

Agonist @ 5-HT = increased motility due to increased ACh release

40
Q

Describe MOA of metoclopramide. Which receptors does it act on

A

Increases motility by encouraging ACh release.

Agonist at 5ht4 and antagonist at D2

41
Q

Do cannabinoids increase or decrease gut motility?

A

Decrease

42
Q

What does CRTZ stand for

A

Chemoreceptor trigger zone

43
Q

Describe the CRTZ

A

area of the brain located near 4th ventricle where the BBB is not developed, allowing the brain to measure / sense what is in the blood stream. When chemotherapy drugs, opioids, etc, are detected, the vomiting reflex can be activated.

44
Q

Name 4 different sources of input into the vomiting centre of the medulla

A
  • labyrinth
  • higher cortical centres
  • CRTZ
  • stomach
45
Q

Dopamine agonists increase motor control, therefore describe some of the extrapyrimidal side effects of dopamine antagonists

A

Tremors, muscle stiffness, dystonia (uncontrolled contractions), etc

46
Q

Name 2 dopamine antagonists and their use

A

Metoclopramide and promethazine.

Used as anti-emetics. Increases ACh release

47
Q

Describe MOA of scopolamine and hyoscine, including which receptors they bind to and systemic side effects

A

Bind to muscarinic receptors in the vomiting centre.
They reduce nausea associated with motion sickness
Given transdermal to avoid side effects. (Opposite of sludge-bbb)

48
Q

How do setrons suppress nausea

A

Block 5-ht3 receptors in gut and vomiting centre

BIOM2009 (13 decks)

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