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PBL SEM 4 > cellular aspects of motility and interaction with some commonly used drugs > Flashcards

cellular aspects of motility and interaction with some commonly used drugs Flashcards

1
Q

main role of the GIT and how is this achieved

A

to maximise absorption of nutrients

achieved by:
1. regulating motility
2. controlling secretion of digestive juices

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2
Q

what and how does the intestinal epithelium sense the lumen contents?

A
  1. distention — mechanoreceptors
  2. osmolality — osmoreceptors
  3. acidity — chemoreceptors
  4. digestive products — chemoreceptors
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3
Q

what are causes of receptor activation in the intestinal epithelium?

A
  1. hormones
  2. nerves — short and long reflexes
  3. paracrine transmission - eg. histamine secretion controlling acid production in the stomach

this is not either a 1 or 2 or 3 response but more 1 and 2 and 3 all together

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4
Q

enteroendocrine cells account for what % of mucosal cells?

A

1% - they are the main sensory cells

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5
Q

where is gastrin released?

A

mainly antrum, also duodenum and jejunum

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6
Q

where are CCK and secretin released?

A

mainly released in upper 1/3 of small intestine, also some in ileum

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7
Q

what is GIP?

A

used to be gastric inhibitory peptide, now glucose dependent insulinotropic polypeptide

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8
Q

where is GIP released?

A

duodenum and jejnunum

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9
Q

what is GLP-1?

A

glucagon-like peptide 1

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10
Q

where is GLP-1?

A

mainly in ileum and colon, also duodenum and jejunum

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11
Q

describe motilin

A

important in inter-digestive motility. stimulates migrating motor complex — clears the SI of any debris into the colon — episodic release 2/3 x day

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12
Q

where where is motilin released?

A

duodenum and jejunum

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13
Q

what is the migrating motor complex used for?

A

inter-digestive motility

The migrating motor complex (MMC) is a system of electrical waves that “migrate” throughout the small intestine, serving to propel luminal contents all the way from the stomach to the terminal ileum

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14
Q

what are GIP and GLP-1?

A

incretins which enhance insulin release by endocrine pancreas

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15
Q

describe GI hormones

A
  • all are short chain peptides
  • secreted by enteroendocrine cells found in the mucosa into the blood
  • target various regions of GI and glands
  • many have effects on nervous system
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16
Q

all neurons involved in the short reflex are part of what?

A

enteric nervous system = 100 million neurons in the myenteric and submucosal plexus

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17
Q

what excitatory substances are there in the ENS?

A

ACh, substance P, gastrin release peptide (GRP)

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18
Q

what inhibitory substances are there in the ENS?

A

nitric oxide and vasoactive intestinal peptide

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19
Q

extrinsic nerves (autonomic nervous system) - parasympathetic effect on GIT

A

preganglionic fibres synapse with ENS, which can release: ACh, SP, GRP, NO, VIP

— involved in long reflexes eg. vago-vagal (vagus = both afferent and efferent - 80% vagal fibres are sensory)

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20
Q

extrinsic nerves (autonomic nervous system) - sympathetic effect on GIT

A

postganglionic fibres —> NA = decreased motility and blood flow

no major role in “day to day” motility because we have inhibitory neurotransmitters in the ENS

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21
Q

what are the range of neurotransmitters released by enteric nerves?

A

ACh, SP, GRP, NO, VIP

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22
Q

what are the 2 ways CCK works?

A

works as a classic hormone and as a paracrine transmitter

23
Q

describe the signalling complexity of CCK on the gall bladder

A

classic hormone: CCK released from wall of duodenum and travels in blood to GB, and causes GB contraction

CCK also released as paracrine transmitter, locally stimulating nerves (vagal afferents) — vago-vagal long reflexes — some branches (vagal efferents) stimulate release of ACh on GB to cause GB contraction — some branch of PSNS go elsewhere to sphincter of Oddi. get release of NO and VIP — relaxation of sphincter of Oddi
—> so as GB contracts, the sphincter opens to allow bile to enter the duodenum

24
Q

what does the GB respond to?

A

presence of nutrients, peptides and fatty acids in duodenum

25
Q

what do enterochromaffin cells secrete?

A

serotonin

26
Q

what are 90% of enteroendocrine cells?

A

enterochromaffin cells

other 10% produce hormones such as CCK and secretin

27
Q

what does released 5-HT stimulate?

A

afferent neurons in the submucosa via 5-HT receptors

28
Q

cells contain enzymes which convert _______ to 5-HT

A

tryptophan

29
Q

what is 5-HT stored in?

A

vesicles

30
Q

what removes 5-HT to terminate signal?

A

SERT

31
Q

what is PIEZO2 channel?

A

mechanosensor involved in 5-HT release

32
Q

what is PIEZO?

A

the principle mechanosensing channels in our body

PIEZO1 = touch in skin
PIEZO 2 = other areas of the body

33
Q

side effect of SSRIs?

A

diarrhoea

34
Q

what are SERT mutations linked to and why?

A

IBS - get inappropriate amounts of 5-HT floating around for longer than it should

35
Q

where are teh 5-HT reuptake transporters?

A

epithelial cells around the enteroendocrine cells

36
Q

what are currently in trials for IBS?

A

5-HT3 antagonists and 5-HT4 agonists

37
Q

how does the presence of food lead to food being pushed along?

A

presence of food = luminal stimulus —> distention —> 5-HT release —> stimulates afferent neurons in ENS —> stimulate efferent neurons which both excite and inhibit smooth muscle contractions —> contraction of food behind and relaxation ahead of food —> food pushed along

38
Q

where is the vomiting centre?

A

medulla

39
Q

how can toxins and cytotoxic drugs (eg in metastatic cancer, ionising radiation) cause vomiting?

A

cytotoxic drugs and toxins cause release of inappropriate amounts of 5-HT:

can damage the lining of the gut — release of lots of 5-HT from EE cells — stimulates ENS and vagal afferents via 5-HT3R — vagal afferents to vomiting centre in medulla

40
Q

what are used as useful anti-emetics in chemotherapy?

A

5-HT3 antagonists

41
Q

what stimulates vomiting? describe the vomiting process

A
  1. retrograde peristalsis from terminal ileum (peristalsis in wrong direction)
  2. contents of the intestine moved towards the stomach
  3. distention of upper tract re-enforces urge to vomit
  4. increase in intra-abdominal pressure (inspiration and contraction of abdominal muslces) — pushes diaphragm up = increased intra-thoracic pressure
  5. increased IA + IT pressure force stomach contents through oesophagus and U.O.S
  6. autonomic discharge — nausea, sweating, salivation, increased HR, ventilation
42
Q

what is the main site for sensing emetic stimuli? what acts on here?

A

CTZ / area postrema

  • toxins such as opiates, digoxin etc, and vestibular nuclei (input from labyrinth), and vagal afferents (convey signals from gut to brainstem)
43
Q

what acts on the vomiting centre?

A

vagal afferents (receive input from EC cells), area postrema, higher cortical centres (pain, repulsive sights, and smells and emotional factors)

44
Q

describe some anti-emetic drugs

A
  • H1 and M1 antagonists
  • D2 and 5-HT3 antagonists
  • 5-HT3 antagonists, NK1 antagonists (inhibits substance P) and nabilone (CB1 antagonist)
45
Q

what are opiates?

A

powerful analgesics for visceral pain in metastatic cancer

46
Q

what are the side effects of opiates?

A
  • vomiting in 30% of patients (vita CTZ)
  • dysphoria (agitation)
  • constipation (which needs to be managed as part of palliative care) (main SE affecting virtually everyone)
47
Q

opioid receptors : mechanism of action

A
  • u,d,k receptors expressed in GIT
  • u-receptors of paramount importance in GIT
  • receptor activation = G protein (Go) —> direct interactions with channel proteins
  • activates K+ channels
  • inhibits Ca++ channels
    ^^ decrease synaptic transmission
  • stimulates Gi —> decreases cAMP = decreased fluid secretion
48
Q

what is the main mechanism for analgesia and for decreased GI motility from opioids?

A

decreased synaptic transmission

49
Q

what does increased transit time in the colon lead to?

A

increased water absorbed = harder to move = viscous cycle

50
Q

opioids reduce ___________ and cause failure of _____________

A

reduce forward propulsion and cause failure of sphincters to relax

51
Q

what endogenous opioids are in the GIT?

A

enkephalins and endomorphins

52
Q

how do endogenous opioids affect motility?

A

decrease motility

53
Q

what is naloxene affect motility and intestinal secretion?

A

naloxene = opioid receptor antagonists — increase motility and intestinal secretion

54
Q

opioids as anti-diarrhoeal drugs?

A

mu-receptor agonists

  • loperamide = immodium
  • diphenoxylate + atropine = lomotil
    = peristalsis, decreases gastric emptying

PBL SEM 4 (50 decks)

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