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Drugs Affecting Gut Motility Flashcards

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1
Q

What happens when a wave of depolarisation occurs in myogenic control in the intestines?

A

Causes rhythmic contraction of smooth muscle forming

  • segmenting seen in small intestine
  • haustral shuttling in large intestine
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2
Q

Where does neural control come from?

A

Intrinsically - enteric plexus

Extrinsically

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3
Q

Effect of the sympathetic and parasympathetic nervous system on gut motility?

A

Sympathetic - reduces motility via adrenergic receptors

Parasympathetic - increases motility via cholinergic receptors and vagus nerve

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4
Q

Where does the plexus for intrinsic control lie?

A

Myenteric plexus lies between the circular and longitudinal muscle layers

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5
Q

What is the enteric nervous system? What plexuses is it made up of?

A

An autonomous collection of nerves within the gut wall

Myenteric - between circular and longitudinal muscle layers
Meissner’s - in submucosa
Henle’s
Cajal’s

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6
Q

What are the reflexes allowing extrinsic control of the gut?

A

Intestine-inhibitory reflex: distension of one intestinal segment causes complete intestinal inhibition

Anointestinal inhibitory reflex: distension of the anus causes intestinal inhibition

Gastrocolic and duodenocolic reflexes: stimulates motility after material has entered the stomach/duodenum

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7
Q

What are the hormones involved in the control of the gut and where are they secreted from?

A

Gastric: promotes acid secretion

Secretin: from the duodenum

CCK: from the small intestine

Motilin : from the small intestine

Paracrine: histamine, somatostatin, prostaglandins

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8
Q

Possible causes of constipation?

A 
Diabetes
Parkinson's
Dehydration
Pregnancy
Mechanical obstruction
Cancer
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9
Q

Which types of drugs are given for soft faeces? Examples?

A

Stimulant laxatives eg Senna, bisacodyl, glycerol

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10
Q

Which types of drugs are given for hard faeces in constipation? Examples?

A

Osmotic laxative eg Movicol

Bulk laxative eg Ispaghula

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11
Q

Non-pharmacological interventions for constipation?

A

Increase fluid intake
High fibre diet
Exercise

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12
Q

What can excessive use of laxatives lead to?

A

Hypokalaemia due to excessive enteral loss of potassium

This can then itself cause bowel inertia

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13
Q

How do bulk laxatives work?

A

Insoluble, non-absorbable substances which distend the gut

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14
Q

When can bulk laxatives be used?

A

To restore normal bowel habit in chronic or simple constipation

  • IBS
  • pregnancy
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15
Q

ADRs of bulk laxatives (eg Ispaghula)

A

Flatulence

Adhesions or ulceration that may cause intestinal obstruction

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16
Q

Name some fecal softeners

A

Arachis oil

Glycerol

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17
Q

How do faecal softeners work?

A

Lubricate and soften stools - safe but not always effective

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18
Q

Indications for faecal softeners?

A

Hard stools
Adhesions - no risk of obstruction
Anal fissures
Haemorrhoids

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19
Q

Name some osmotically active laxatives

A

Magnesium and sodium salts
Lactulose
Macrgols

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20
Q

How do magnesium and sodium salts work?

A

Cause way retention in the small and large bowel which increases peristalsis

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21
Q

How long does it take for Ispaghula to work?

A

A couple of days

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22
Q

How long does it take for magnesium and sodium salts to work?

A

Quickly and are severe

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23
Q

How are magnesium and sodium salts normally administered?

A

PR

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24
Q

When are magnsrium and sodium salts normally used?

A

Resistant constipation

If urgent relief is required

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25
Mechanism of action of lactulose?
It is a disaccharide (galactose or fructose) Cannot be hydrolysed by digestive enzymes Fermented to lactulose by colon bacteria producing acetic and lactic acid They have an osmotic effect
26
How long does it take for lactulose to work?
48 hours
27
Indications for lactulose?
Liver failure to reduce ammonia production
28
How do macrogols such as Movicol work?
Osmotic laxative
29
How is macrogol administered?
A powder dissolved in fluid
30
How long does macrogol take to work?
Within hours | 2-4 days to get full relief
31
How do irritant/stimulant laxatives work?
Excite sensory nerve endings leading to water and electrolyte retention and therefore peristalsis
32
Indications for irritant/stimulant laxatives?
Soft faeces - rapid treatment eg in faecal impaction or surgical prep - colonic atony - hypokalaemia
33
How long do irritant laxatives take to have an effect and when are they given?
6-8 hours Before bed Taken orally
34
Examples of irritant/stimulant laxatives?
``` Castor oil Bisacodyl Anthraquinones -danthron -Senna -rhubarb roots ```
35
Why can anthraquinones not be used in intestinal obstruction?
Cause abdominal cramps
36
What is docusate sodium?
A faecal softener | -can be combined with danthron to give codanthraner
37
What can abuse of anthraquinones lead to?
Melanosis coli
38
Main types of anti-diarrhoeals?
Anti-motility Bulk-forming - fluid absorbents Fluid adsorbents
39
Name some anti-motility drugs
Opiate analgesics eg codeine | Opiate analogues eg loperamide (Imodium)
40
Mechanism of action of anti-motility drugs?
Act via opioid receptors in the bowel to - reduce bowel motility - increases time for fluid to reabsorption - increase anal tone and reduce sensory defacation reflex
41
Indications for anti-motility drugs?
Chronic diarrhoea
42
Contra-indications for anti-motility drugs?
IBD due to risk of toxic mega colon
43
Mechanism of action of bulk-forming drugs in diarrhoea (eg Ispaghula)
Absorb water
44
Indications for bulk-forming agents?
Patients with IBS - good for constipation and diarrhoea | Ileostomy
45
Name a fluid adsorbent
Kaolin
46
How does cholestyramine work?
It is a bike acid sequestration used for bile salt-induced diarrhoea seen in crohn's or post-vagotomy
47
What are pancreatic enzymes helpful for?
Diarrhoea
48
Symptoms of IBS?
``` Nausea Vomiting Belching Abdominal discomfort Frequent bowel actions Constipation No blood loss ```
49
What happens in IBS?
Chronic, re-lapsing condition where abdominal pain is associated with defacation or change in bowel habit Abnormal smooth muscle activity or visceral hypersensitivity
50
Treatment of IBS?
Mebeverine - anti spasmodic - anti-muscarinic - has direct effects on colonic hypermotility - relieves spasm of intestinal muscle
51
What is mebeverine normally combined with?
A bulk-forming agent - fybogel mebeverine
52
What are some other anti-spasmodics?
(Mebeverine) | Hyoscine
53
What happens in emesis?
Pyloric sphincter closes while the cardia and oesophagus relax Gastric contents propelled by contraction of abdominal wall and diaphragm Glottis closes with elevation of the soft palate to prevent entry of vomit into the trachea or nasopharynx
54
Preliminary signs of vomiting?
``` Nausea Dilated pupils Increased salivation Sweating Retching Paleness ```
55
Where is the vomiting centre?
In the ependymal cells (postrema) on the floor of the fourth ventricle in the brain
56
What can activate the vomiting centre?
``` Medications Pregnancy Toxins Pain Irritation Smell Touch (gag) Raised ICP Stomach inflammation Rotation ```
57
Neurotransmitters involved in vomiting?
Vestibular apparatus - Ach and histamine (H1) Medullary centre - Ach, H1, 5-HT Vomiting centre - dopamine
58
What drugs are used to prevent vomiting
Dopamine receptor D2 antagonists - eg metoclopramide or domperidone 5-HT3 receptor antagonists eg ondansteron Anti-muscarinics H1 receptor antagonists eg cyclizine, promethazine Others eg cannabinoids, benzodiazepines
59
Mechanism of action of domperidone?
Acts on postrema on floor of fourth ventricle Acts on stomach to increase gastric emptying Antagonises dopamine
60
Administration of domperidone?
Administered orally
61
Indications for domperidone?
Acute nausea and vomiting episode | -especially if induced by L-DOPA or dopamine agonists
62
ADRs of domperidone?
Excessive prolactin release causing galactorrhoea | Occasionally dystonia
63
When is 5-HT released into the GI tract and from where?
Released when there are poisonous compounds, bacterial toxins, drugs etc From enterochromaffin cells lining the GI tract
64
Where does the vomiting centre receive signals from?
5-HT triggering vagal afferents Vestibular apparatus which receives input from labyrinth Medullary centre which senses emetic stimuli Higher cortical centres - pain, sights, smells, emotional factors Medullary centre also receives input from those three
65
Mechanism of action of 5-HT antagonists
Effective in the postrema of the fourth ventricle, against vagal afferent nerves in the GI, medullary centre
66
Indications for 5-HT antagonists?
Radiation therapy | Chemotherapy
67
Administration of 5-HT antagonists?
IV IM Orally
68
What can enhance the anti-emetic effect of 5-HT antagonists?
A single dose corticosteroid
69
ADRs of 5-HT antagonists?
Headache Constipation Flushing (IV)
70
Mechanism of action of metoclopramide?
D2 antagonist via fourth ventricle Has anticholinergic effects (GI tract) Blocks vagal afferent 5-HT (GI)
71
Indications for metoclopramide?
GI cause of nausea and vomiting Migraine Post-op
72
Routes of administration of metoclopramide?
Oral IM IV
73
Half-life of metoclopramide?
4 hours
74
ADRs of metoclopramide?
Extra-pyramidal reactions (dystonia) - so avoid in Parkinson's Galactorrhoea due to release of prolactin
75
Mechanism of action of hyoscine? (Anti-emetic)
Ach antagonist
76
Indications for hyoscine?
Prevention and treatment of motion sickness
77
Administration and half life of hyoscine?
Oral or latch | 2 hours
78
ADRs of hyoscine?
Systemic anti-cholinergic effects such as - bradycardia - dry mouth
79
Mechanism of cyclizine?
H1 antagonist
80
Indications for cyclizine?
Acute nausea and vomiting
81
Administration of cyclizine?
Oral IV IM
82
ADRs of cyclizine?
Prolonged QT, reducing cardiac index in myocardial ischaemia | Sedative as can cross BBB
83
What are the pacemaker cells of myogenic control of the gut?
Interstitial cells of cajal act as pacemakers by producing slow waves of depolarisation which travel thought the smooth muscle across gap junctions

Pharmacology (23 decks)

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