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Sem 4, case 4 (bowel cancer) > cellular aspects of motility and interaction with commonly used drugs (lecture series) > Flashcards

cellular aspects of motility and interaction with commonly used drugs (lecture series) Flashcards

(80 cards)

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1
Q

Regulation of what mechanisms help maximise absorption of nutrients ?

A
  1. regulating motility
  2. controlling secretion of digestive juices in response to the presence of food
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2
Q

Is absorption of nutrients highly controlled or not ?

A

there is little control of absorption as the mechanisms are always active, rather than turned on in the presence of food

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3
Q

Which organ is considered the “largest sensory organ” in the body ?

A

intestinal epithelium

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4
Q

What do intestinal mechanoreceptors respond to ?

A

distention

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5
Q

What do intestinal osmoreceptors respond to ?

A

osmolality

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6
Q

What do intestinal chemoreceptors respond to ?

A
  • acidity
  • digestive products
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7
Q

What does activation of intestinal receptors (mechano, chemo…) result in ?

A
  • hormone release
  • reflexes (short and long)
  • paracrine transmission

all occurring together

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8
Q

What is paracrine transmission ?

A

cell to cell communication that alters the activity of neighbouring cells

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9
Q

What are the main sensory cells in the intestine called ?

A

enteroendocrine cells

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10
Q

What feature of enteroendocrine cells increase their SA ?

A

Microvilli

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11
Q

What do enteroendocrine cells contain ?

A

stored hormones and neurotransmitters that can be released into the blood of stimulated

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12
Q

Where is the majority of gastrin released in the GI tract ?

A

Antrum of the stomach

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13
Q

Where are the 3 places Gastrin is released from?

A
  • Antrum of stomach (main site)
  • Duodenum
  • Jejunum
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14
Q

Where is the majority of CCK released in the GI tract ?

A
  • Duodenum
  • Jejunum
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15
Q

Where are the 3 places CCK is released from?

A
  • duodenum (main site)
  • jejunum (main site)
  • ileum
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16
Q

Where is the majority of Secretin released in the GI tract ?

A
  • duodenum
  • jejunum
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17
Q

Where are the 3 places secretin is released from?

A
  • duodenum (main site)
  • jejunum (main site)
  • ileum
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18
Q

What are the 2 main places GIP is secreted in the GI tract ?

A
  • duodenum
  • jejunum
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19
Q

Where is the majority of GLP-1 released in the GI tract ?

A
  • ileum
  • colon
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20
Q

Where are the 4 places GLP-1 is released from?

A
  • duodenum (starts halfway through)
  • jejunum
  • ileum (main site)
  • colon (main site)
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21
Q

What are the 2 main places Motilin is secreted in the GI tract ?

A
  • duodenum
  • jejunum
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22
Q

What type of hormone are GIP and GLP-1 ?

A

Incretins

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23
Q

What is the main role of Incretins ?

A

enhance insulin release

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24
Q

What is the main role of GIP and GLP-1 ?

A

enhance insulin release

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25
Are GI hormones long or short chain peptides?
short chain peptides
26
What type of cell secretes the GI hormones ?
**enteroendocrine cells** in the mucosa of the epithelium
27
Between which layers of the GI epithelium does the myenteric plexus lie ?
- longitudinal muscular layer *myenteric plexus* - circular smooth muscle layer
28
Between which layers of the GI epithelium does the submucosal plexus lie ?
- circular smooth muscle layer *submucosal plexus* - mucosa
29
Which 2 plexuses make up the enteric nervous system ?
- myenteric plexus - submucosal plexus
30
Are enteric neurones excitatory or inhibitory ?
Both !
31
What is the main excitatory neurotransmitter released by the enteric NS ?
Acetylcholine
32
Name the 3 main excitatory neurotransmitters released by the enteric NS …
- acetylcholine - substance P - GRP (gastric releasing peptide)
33
Name the 2 main inhibitory neurotransmitters released by the enteric NS …
- **NO** (nitric oxide) - **VIP** (vasoactive intestinal peptide)
34
What is a short reflex?
a reflex where **all neurones involved** are part of the **enteric NS**
35
What kind of extrinsic nerve fibres synapse with the enteric NS ?
preganglionic **parasympathetic** fibres from the autonomic NS **VAGAL NERVE FIBRES** *release the same neurotransmitters as the enteric NS*
36
Which type of reflex are parasympathetic nerve fibres involved in, with regards to the GI tract ?
Long reflexes
37
Are vagal fibres the efferent or afferent leg of GI tract long reflexes ?
both
38
What % of vagal fibres are sensory ?
80%
39
What are vago-vagal reflexes an example of ?
long reflexes
40
What do sympathetic nerve fibres release that has minor impact on gut motility ?
noradrenaline *slight reduction in motility and blood flow*
41
Which neurotransmitter reduces motility and blood flow in the gut ?
**noradrenaline** via sympathetic fibres
42
Which GI hormone primarily controls gall bladder function ?
CCK *Cholecystokinin*
43
How does CCK control gall bladder function ?
**1. ‘hormonal control’** - presence of nutrients in duodenum causes release of CCK into blood - CCK travels to gall bladder and causes contraction **2. ‘paracrine transmission’** - presence of nutrients in duodenum causes release of CCK into blood - CCK stimulates local afferent vagal nerves - Dorsal vagal complex stimulates vago-vagal (long) reflexes …. **2a. Long reflexes (contraction)** - dorsal vagal complex in brain stimulated - causes efferent vagal nerves to release Ach onto gall bladder - causes contraction **2b. Long reflexes (relaxation)** - dorsal vagal complex in brain stimulated - causes efferent vagal nerves to release NO + VIP onto sphincter of Oddi - relaxes the sphincter, opening it to allow bile to enter duodenum
44
What % of enteroendocrine cells are enterochromaffin cells ?
90%
45
What type of cells are the main mechano/chemo-sensory cells of the GI tract ?
enterochromaffin cells
46
Which neurotransmitter do enterochromaffin cells secrete ?
serotonin *5-HT*
47
How do enterochromaffin cells show up on a histological stain ?
Small dark brown dots (like moles)
48
What % of all serotonin in the body is found in the GI tract ?
95% !!
49
What feature of enterochromaffin cells increases their SA ?
microvilli
50
What feature of enterochromaffin cells enhances their sensitivity ?
microvilli
51
What type of neurone does 5-HT stimulate when released from enterochromaffin cells ?
afferent neurones
52
How do neighbouring epithelial cells stop the action of 5-HT released by enterochromaffin cells ?
The surrounding membrane contains **SERT** that removes 5-HT from the junction
53
Why is diarrhoea a side effect of some SSRIs ?
- 5-HT stimulates motility in the gut via afferent neurones - there are SERT proteins in neighbouring cell membranes that terminate this signal - if the termination is inhibited then the gut will be continually stimulated = diarrhoea
54
What is a potential cause of IBS that is linked to 5-HT ?
**SERT mutations**, so serotonin action in the GI tract is not terminated sufficiently
55
How does 5-HT stimulate motility/peristalsis in the gut ?
- food in the lumen **stimulates enterochromaffin cells** - **5-HT released** - stimulates **afferent neurones** in the enteric NS - these **act on efferent neurones** - some have excitatory effects via **Ach/SP** (behind the food bolus), others are inhibitory via **NO/VIP** (in front of the bolus) - causing muscle to both **contract and relax in a wave-like pattern = peristalsis**
56
How do toxins and cytotoxic drugs cause vomiting ?
They damage the lining which stimulates enterochromaffin cells to **release excessive 5-HT** causes: - excessive efferent gut motility/churning - excessive afferent vagal stimulation of vomiting centre in medulla
57
Which type of 5-HT receptors are found on the afferent vagal neurones that extend to the vomiting centre in the medulla ?
5-HT**3** receptors
58
What is the MOA of antiemetic drugs used in chemotherapy ?
5-HT**3** receptor antagonists *= target the receptors found on afferent vagal neurones that extend to the vomiting centre in the medulla*
59
What physiological change normally instigates vomiting ?
**retrograde** (backwards) **peristalsis** in the terminal ileum **moves contents back towards stomach**
60
What is the physiology of vomiting ?
- retrograde peristalsis - food moves back towards stomach - causes distention in upper GI tract … - stimulates reflexes that urge vomiting the reflexes: - increase intra-abdominal pressure which pushes up diaphragm - causes increased intra-thoracic pressure - increased pressure forces stomach contents up into oesophagus - autonomic systems kick in to increase HR, ventilation, salvia, sweating …
61
What are the 3 main cytotoxic drugs used as antiemetics ?
- 5-HT3 antagonists - NK1 antagonists - CB1 agonist
62
What are the 2 main drugs used as antiemetics for motion sickness ?
- H1 antagonists (antihistamines) - M1 antagonists
63
What are the 2 main drugs used as antiemetics for nausea that is **not** caused by toxins or motion ?
- D2 antagonists - 5-HT3 antagonists
64
which drugs are used to treat the pain of metastatic cancer ?
Opiates
65
What are the main side effects of opiates ?
- **constipation** (main side effect) - **vomiting** (in 30% of patients) - **dysphoria** (agitation)
66
Which pathway do opiates affect that causes nausea ?
The **vagal afferent neurones to the CTZ** (vomiting centre in the medulla)
67
Which are the 3 receptor types that opiates act on in the GI tract ?
- μ opioid receptor - δ opioid receptor - κ opioid receptor
68
Which opioid receptor is the most important in controlling GI function ?
**μ** opioid receptor
69
How do opiates inhibit synaptic transmission in the gut ?
- μ receptor activated by opiates - activate G proteins which - directly interact with channel proteins (activates K channels / inhibits Ca channels) - causes inhibition of synaptic transmission *MOA for analgesia*
70
How do opiates inhibit fluid secretion in the gut ?
- μ receptor activated by opiates - activate G proteins which - stimulates Gi protein to decrease cAMP - causes decreased fluid secretion
71
Which effect of opiates is the main mechanism behind their analgesic properties ?
**decreased synaptic transmission** *- μ receptor activated by opiates - activates K channels - inhibits Ca channels - causes inhibition of synaptic transmission*
72
Which action of opiates is the main mechanism behind their inhibitory effect on GI motility ?
**decreased synaptic transmission** *- μ receptor activated by opiates - activates K channels - inhibits Ca channels - causes inhibition of synaptic transmission*
73
How do opiates cause constipation ?
- act on μ receptors - causes inhibition of synaptic transmission = **reduced gut motility** - **increases transit time in colon** - allows for **more water absorption** = harder stool that isn’t as easy to move
74
How do opioids interfere with gut motility ? (MOA)
- opiates **bind to μ receptors** in gut - causing **decreased synaptic transmission in the 5-HT peristalsis pathway** - via primarily **impacting the inhibitory efferent neurones** that normally relax muscle infront of food to propel it forwards **= opioids reduce forward propulsion of food and cause failure of sphincters to relax**
75
What is the impact of opioids on food propulsion through the gut ?
opioids **reduce forward propulsion** of food and **cause failure of sphincters to relax** *causing constipation*
76
What are the 2 main families of endogenous opioids ?
1. Enkephalins 2. Endomorphins *both present in GI tract*
77
What is the function of endogenous opioids in the GI tract ?
reduce gut motility
78
Due to their side effect of constipation, what could opioids be used as a drug treatment for ?
anti-diarrhoea drugs
79
What is the target receptor of opioids when used as anti-diarrhoea medications?
μ opioid receptors
80
What are 2 examples of anti-diarrhoea opioid drugs ?
- Imodium *(loperamide)* - Lomotil *(diphenoxylate + atropine)*

Sem 4, case 4 (bowel cancer) (2 decks)

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