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
Name for serotonin antagonists is ____
Setrons
26
Setrons are used to treat acute ekes is caused by xxx and xxx
Radiotherapy / chemotherapy or post op
27
Example of setrons used as antiemetic?
Ondansetron (note suffix)
28
3 treatment options for hyperemesis gravidarum?
Severe vomiting during pregnancy 1. IV rehydration 2. D2 antagonists (metoclopramide) 3. Ondansetron
29
Explain MOA of bulk laxatives
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
Example of bulk laxative
Methylcellulose | Psyllium
31
Describe MOA of osmotic laxatives
Non-absorbable sugars which increase the stool osmolarity, which draws fluid in. Onset usually 1-3 days. Can cause bloating or cramping
32
Describe osmotic laxatives II MOA
More intense osmotic laxatives. Used before surgery. Works in 1-3 hours
33
Give examples of both osmotic and osmotic II laxatives
Osmotic - lactulose - sorbitol Osmotic II - epsom salt
34
Explain MOA of stimulant laxatives
Directly stimulate the myenteric plexus to promote peristalsis and defecation E.g. senna
35
Which laxative can lead to dependence with frequent use?
Senna - stimulant laxatives
36
Explain MOA of faecal softeners
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
Compare the 3 different types of diarrhoea. Secretory, osmotic and exudative
``` 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
Describe MOA of loperamide
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
Compare D2 and 5-HT4 receptors in GIT
Agonist @ D2 = decreased motility due to block of ACh release Agonist @ 5-HT = increased motility due to increased ACh release
40
Describe MOA of metoclopramide. Which receptors does it act on
Increases motility by encouraging ACh release. | Agonist at 5ht4 and antagonist at D2
41
Do cannabinoids increase or decrease gut motility?
Decrease
42
What does CRTZ stand for
Chemoreceptor trigger zone
43
Describe the CRTZ
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
Name 4 different sources of input into the vomiting centre of the medulla
- labyrinth - higher cortical centres - CRTZ - stomach
45
Dopamine agonists increase motor control, therefore describe some of the extrapyrimidal side effects of dopamine antagonists
Tremors, muscle stiffness, dystonia (uncontrolled contractions), etc
46
Name 2 dopamine antagonists and their use
Metoclopramide and promethazine. | Used as anti-emetics. Increases ACh release
47
Describe MOA of scopolamine and hyoscine, including which receptors they bind to and systemic side effects
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
How do setrons suppress nausea
Block 5-ht3 receptors in gut and vomiting centre