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Gastrointestinal Block > L24 - Pharm of GIT motility > Flashcards

L24 - Pharm of GIT motility Flashcards

1
Q

Drugs affecting motility of the GI tract

A

1) Antiemetic drugs

  • H1 receptor antagonists
  • Muscarinic receptor antagonists
  • 5HT3 receptor antagonists
  • Dopamine D2 receptor antagonists

2) Motility stimulants

  • 5HT4 receptor agonists
  • Dopamine D2 receptor antagonists

3) Laxatives

  • Bulk laxatives
  • Osmotic laxatives
  • Faecal softeners
  • Stimulant laxatives

4) Antidiarrhoeal agents

  • Oral rehydration therapy
  • Opioid receptor agonists
  • Adsorbents

5) Antispasmodic agents

  • Muscarinic receptor antagonists

6) Drugs for Irritable bowel syndrome

  • Depends on symptoms:
  • spasm: antispasmodic agents
    • pain, nausea*: 5HT3 receptor antagonists
  • constipation: bulk & osmotic laxatives
  • diarrhoea: opioid receptor agonists
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2
Q

Stimuli of vomiting

A

1) Pain, repulsive sights & smells, emotional factors
2) Motion sickness
3) Endogenous toxins, drugs (e.g. chemotherapy, surgery anaesthetics, food poisoning)
4) Stimulus in pharynx or stomach (e.g. finger in throat, eating too much)

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3
Q

Mechanism of vomit due to Pain, repulsion & emotion

A

1) Stimuli: Pain, repulsive sights & smells, emotional factors
2) Input: these feelings transmitted via sensory afferents
3) Integration: Signals processed in the higher centers of CNS, then directed to the vomiting center
4) Output: Vomiting center send signals via nerves to somatic & visceral receptors, leading to vomiting

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4
Q

Mechanism of vomit due to motion sickness

A

1) Stimuli: motion information perceived in the labyrinth of the ear (and the contradicting inactivity information perceived by the visual receptors)

2) Input: the above stimuli are perceived by the labyrinth

3) Integration: Cerebellum (H1 & mACh receptors) receive and process the contradictory information; and signals will be sent to vomiting center

4) Output: Vomiting center send signals via nerves to somatic & visceral receptors, leading to vomiting

[note: motion sickness is greater when eyes closed or vehicle does not have a window to allow view of movement]

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5
Q

Mechanism of vomit due to endogenous toxins and drugs

A

1) Stimuli: endogenous toxins & drugs (e.g. high level of alcohol, chemtherapy drugs, surgery anaesthetics, food poisoning, etc.)

2) Input:

i) endogenous toxins & drugs may directly travel through blood to the chemoreceptor trigger zone (CTZ)
ii) endogenous toxins & drugs may stimulate the release of emetogenic agents (5HT, prostanoids, free radicals). These emetogenic agents may enters CTZ directly
iii) endogenous toxins & drugs may stimulate the release of emetogenic agents (5HT, prostanoids, free radicals). These emetogenic agents may stimulate the Extrinsic primary afferent nerves (EPAT; contains 5HT3 receptors), which will send signals to the CTZ & nucleus of solitary tract in brain stem

3) Integration:

i) Chemreceptor Trigger Zone (CTZ; contains D2 & 5HT3 receptors) will be stimulated by:
- endogenous toxins & drugs in blood
- emetogenic agents
- signals from EPAT

and send signals to the vomiting center

ii) Nucleus in solitary tract (contains H1, mACh, D2 & 5HT3 receptors) will be stimulated by signals from EPAT, and send signals to the vomiting center

4) Output: Vomiting center send signals via nerves to somatic & visceral receptors, leading to vomiting

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6
Q

Mechanism of vomit due to stimulus in pharynx and stomach

A

1) Stimuli: stimulus in pharynx and stomach (e.g. finger in throat, stomach distension due to eating too much)

2) Input: the sensory signals will stimulate the Extrinsic primary afferent nerves (EPAT; contains 5HT3 receptors), which will send signals to the Chemoreceptor Trigger Zone & nucleus of solitary tract in brain stem

3) Integration:

i) Chemreceptor Trigger Zone (CTZ; contains D2 & 5HT3 receptors) will be stimulated by signals from EPAT and send signals to the vomiting center
ii) Nucleus in solitary tract (contains H1, mACh, D2 & 5HT3 receptors) will be stimulated by signals from EPAT, and send signals to the vomiting center

4) Output: Vomiting center send signals via nerves to somatic & visceral receptors, leading to vomiting

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7
Q

Types of Antiemetics

A

1) histamine H1 receptor antagonist
2) muscarinic receptor antagonist
3) 5HT3 receptor antagonist
4) Dopamine D2 receptor antagonist

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8
Q

histamine H1 receptor antagonists

A

Antiemetics

Example: Dimenhydrinate

Mechanism:

  • blocking the histamine H1 receptors found in cerebellum & the nucleus of the solitary tract, thus preventing signals to vomiting center from these two sites
  • effective against vomiting caused by motion sickness (exclusively integrated by cellubellum)
  • not as effective against vomiting caused by endogenous toxins & drugs and pharngeal- gastric stimuli as CTZ is not blocked

ADR:

  • Dizziness, sedation, confusion (conterindicative of machine operation)
  • Not very specific, thus can inhibit muscarinic receptors as well (i.e. causing dry mouth, blurred vision, urinary retention, constipation, tachycardia)
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9
Q

Muscarinic receptor antagonist (antiemetics)

A

Antiemetics, antispasmodic agents

Example: Hyoscine

Mechanism:

  • blocking the muscarinic mACh receptors in cerebellum & nucleus of the solitary tract, thus preventing signals to vomiting center from these two sites
  • effective against vomiting caused by motion sickness (exclusively integrated by cellubellum)
  • not as effective against vomiting caused by endogenous toxins & drugs and pharngeal- gastric stimuli as CTZ is not blocked

ADR:

  • Drowsiness
  • dry mouth
  • blurred vision
  • urinary retention
  • constipation
  • tachycardia
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10
Q

5HT3 receptor antagonist (antiemetics)

A

Antiemetics, drugs for IBS

Example: Ondansetron

Mechanism:

  • blocking the 5HT3 receptors found in CTZ, Nucleus of solitary tract, & EPAN, thus preventing stimulation of vomiting centers from these sites
  • effective against vomiting caused by endogenous toxins & drugs (e.g. chemo, surgery, food poison) and pharngeal- gastric stimuli as CTZ, nucleus of solitary tract & EPAN are blocked
  • not effective against vomiting caused by motion sickness (as cerebellum is not blocked)

ADR:

  • Headache, dizziness, and constipation
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11
Q

Dopamine D2 receptor antagonist (antiemetics)

A

Antiemetics, prokinetics

Example:

  • Metoclopamide
  • Domperidone

Mechanism:

  • blocking the dopamine D2 receptors found in CTZ & Nucleus of solitary tract, thus preventing stimulation of vomiting centers from these sites
  • effective against vomiting caused by endogenous toxins & drugs (e.g. chemo, surgery, food poison) and pharngeal- gastric stimuli as CTZ & nucleus of solitary tract are blocked
  • not effective against vomiting caused by motion sickness (as cerebellum is not blocked)

ADR:

  • Headache, dizziness

**Metoclopamide can pass through BBB, thus blocks dopamine receptors elsewhere in the CNS; resulting in extrapyrimidal symptoms (e.g. parkinsonian features, dystonias and tardive dyskinesia)

** Domperidone does not penetrate BBB, thus less side effects

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12
Q

CTZ location

A

On the blood side of blood-brain barrier

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13
Q

Extrinsic primary afferent nerves

A

Receptor: 5HT3 receptors

Transmission:

  • to CNS (i.e. Chemoreceptor trigger zone, nucleus of the solitary tract)

Output: nausea, vomiting and abdominal pain

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14
Q

Intrinsic primary afferent nerves

A

Receptor:

  • 5HT1P receptor at dendrite
  • 5HT4 receptor at axon

Transmission:

  • releases acetylcholine (ACh) & calcitonin gene-related peptide (CGRP), which stimulates neurons of Enteric Nervous System, which will release ACh to stimulate GIT muscle walls

Output:

  • Increase the tone of lower oesophageal sphincter
  • stimulation of gastric emptying
  • stimulation of peristalsis
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15
Q

Stimulation of EPAN & IPAN

A

when stimulated, enterochromaffin cells will release 5HT that stimulates the 5HT receptors on EPAN & IPAN

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16
Q

Oesophageal reflux mechanism

A
  • Incompetence of the lower esophageal sphincter (LES)
  • Transient LES relaxation
  • Delay in gastric emptying

Medication:

  • prokinetics
  • Gastric acid inhibitor for oesophageal reflux (e.g. proton pump Inhibitors, H2 antagonists)
17
Q

Gastroparesis

A

Disorder of gastric emptying

Mechanism: Occurs when vagal nerves are damaged and the muscles of the stomach and intestines do not work normally

Medication: prokinetics

18
Q

Diseases that require prokinetics

A
  • Oesophageal reflux
  • Gastroparesis
19
Q

Types of prokinetics

A

1) 5HT4 receptor agonist
2) Dopamine D2 receptor antagonist

20
Q

5HT4 receptor antagonist

A

Prokinetics

Example: cisapride

Mechanism:

  • Stimulation of 5HT4 receptors on axon of IPAN
  • increase the release of acetylcholine and calcitonin gene-related peptide (CGRP), thus stimulating ENS neurons, which in turn stimulate GIT muscle walls
  • increases tone of lower oesophageal sphincter, gastric emptying and gut motility

ADR:

  • Diarrhoea, abdominal cramp

** long QT syndrome, which predisposes to arrhythmias (therefore in US & HK cisapride withdrawn; had its indications limited as an alternative when dopamine receptor antagonist failed)

21
Q

Dopamine D2 antagonist (prokinetics)

A

Antiemetics, prokinetics

Example:

  • Domperidone
  • Metoclopamide

Mechanism:

  • Normally, dopamine will act on dopamine D2 receptors on ENS neurons to inhibit ACh release
  • D2 receptor antagonist can block these receptors, thus Increase the release of acetylcholine from postganglionic cholinergic ENS neurons, which stimulates GIT muscle walls

ADR:

  • Headache, dizziness

**Metoclopamide can pass through BBB, thus blocks dopamine receptors elsewhere in the CNS; resulting in extrapyrimidal symptoms (e.g. parkinsonian features, dystonias and tardive dyskinesia)

** Domperidone does not penetrate BBB, thus less side effects

22
Q

Constipation durgs

A

Laxatives

23
Q

Types of laxatives

A

1) Bulk laxatives
2) Osmotic laxatives
3) Faecal softeners
4) Stimulant laxatives

24
Q

Bulk laxatives

A

Laxative

Examples: Methylcellulose

Mechanism:

  • They increase faecal mass which stimulates peristalsis (cannot be digested by humans)
  • Drink plenty of water so that the bulk laxatives can work efficiently (by absorbing water and forming bulk)

ADR:

  • Flatulence (bacteria may digest methyl cellulose and release gases)
  • abdominal distension
25
Q

Osmotic laxatives

A

Laxative

Example: Lactulose

Mechanism: They increase the amount of water in the large bowel, either by drawing fluid from the body into the bowel or by retaining the fluid they were administered with

ADR: Flatulence, abdominal distension

26
Q

Faecal softeners

A

Laxative

Examples:

  • Docusate sodium (ingested)
  • Glycerol (applied in anus)
  • Liquid paraffin (applied in anus)

Mechanism: They soften stool materials by acting as a detergent, which permits water and lipids to penetrate

Docusate sodium and glycerol are also weak stimulant laxatives that encourage peristalsis

ADR:

  • Paraffin may lead to seepage as it is liquid
  • Anal irritation after prolong use (glycerol & paraffin)
27
Q

Stimulant laxatives

A

laxative

Example:

  • Bisacodyl
  • Senna

Mechanism:

Bisacodyl acts by stimulating sensory nerve endings in gut directly, leading to enhanced peristalsis

Anthraquinones are released from senna after hydrolysis by bacteria. Anthraquinones then stimulate the myenteric plexus, leading to enhanced peristalsis

ADR: Diarrhea, abdominal clamp

28
Q

Treatment of diarrhoea

A

1) Oral rehydration solution
2) Antidiarrhoeal agents
- Opioid agonists
- Adsorbents

[Note: Usually only ORT os prescribed but not antidiarrhoeal agents, as diarrhoeaa will eliminate toxins and pathogens and is protective. Drugs are given when diarrhoea must be controlled for convenience e.g. work]

29
Q

Oral rehydration therapy

A

Treatment of diarrhoea

Components:

  • Sodium
  • Potassium
  • Chloride
  • Citrate: as a basic salt that can reduce effect of acidosis caused by diarrhoea
  • Glucose: help to enhance sodium absorption via glucose-sodium co-transporter
  • ** Formula must be slightly hypo-osmolar to prevent the possible induction of osmotic diarrhoea*
  • ** Bicarbonate not used because not stable - will decompose to water & CO2 naturally*

Mechanism:

  • Replace the electrolyte deficit adequately
  • Enhance the absorption of water and electrolytes

Clinical considerations:

  • The amount of rehydration that is needed depends on the size of the individual and the degree of dehydration.
  • Rehydration is generally adequate when the person no longer feels thirsty and has a normal urine output.

Home-made ORT:

+ 1 level teaspoon of salt
+ 8 level teaspoons of sugar
+ 1 litre of clean drinking water

30
Q

Opioid receptor agonists

A

Antidiarrhoeal agent

Examples:

  • Codeine
  • Loperamide
  • Diphenoxylate

Mechanism:

  • They stimulate opioid receptors in ENS neurons, which will inhibit the release of ACh from ENS neurons
  • that in turn decrease peristalsis of gut, thus increasing colonic transit time
  • increase faecal water absorption will decrease diarrheoa
  • Codeine and loperamide have antisecretory actions as well.

ADR:

  • Drowsiness, dizziness
  • constipation, paralytic ileus can also occur.
31
Q

Adsorbents

A

Antidiarrhoeal agent

Examples:

  • Kaolin
  • Pectin

**Mechanism: **

  • claim to bind toxins and bacteria
  • But there is no good evidence to show their effectiveness

Notes:

  • no side effects
  • very cheap
32
Q

Intestinal pain & spasm treatment

A

Antispasmodic drugs e.g. muscarinic receptor antagonist

33
Q

Muscarinic receptor antagonist (antispasmodic agent)

A

Antiemetics, antispasmodic agent

Example: Hyoscine

Mechanism:

  • Normally, both neurons from ANS (parasympathetic) & ENS will release ACh that act on muscarinic receptors of GIT smooth muscle cells for contraction
  • By blocking muscarinic receptors in intestinal smooth muscle cells, intestinal smooth muscle will relax, thus decreasing peristasis and basal tone, hence reducing spasm

ADR:

  • Drowsiness
  • dry mouth
  • blurred vision
  • urinary retention
  • constipation
  • tachycardia
34
Q

irritable bowel syndrome

A
  • An idiopathic chronic disorder

Clinical presentation:

  • Abdominal discomfort (pain, bloating, distension, nausea)
  • Alteration in bowel habits (diarrhoea, constipation, or cycle of both)
35
Q

Therapies for IBS

A

Therapies for irritable bowel syndrome are directed at relieving abdominal pain and discomfort

  • For patients with predominant diarrhoea, opioid agonists (e.g. loperamide) are used.
  • For patients with predominant constipation, bulk laxatives or osmotic laxatives are used.
  • For intestinal spasm, antispasmodic agents (i.e. muscarinic receptor antagonist) are used
  • **For unpleasant visceral sensation (e.g. nausea, bloating and pain), 5HT3 receptor antagonists will be used by blocking the 5HT3 receptors of EPAN, preventing sensory signalling to CNS

Gastrointestinal Block (24 decks)

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