GI pharmacology Flashcards

1
Q

Describe the layout of the enteric nervous system

A

Myenteric plexus
Submucosal plexus

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2
Q

Describe the neuronal control of the GIT

A

Parasympathetic from vagus
- cholinergic and excitatory
Sympathetic fibres are post-ganglionic to:
- BVs
- smooth muscle
- glands
- inhibit acetyl choline release from plexuses

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3
Q

Describe the hormonal control of the GIT

A

Endocrine - peptides from mucosa (gastrin, CCK)
Paracrine - local regulatory peptides (+ histamine)

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4
Q

What is gastric secretion made up of?

A

acid
bicarbonate
mucous

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5
Q

In what ways can gastric secretion be modified?

A

Neutralisation
Mucosal protection
Absorbents
Histamine antagonists
Proton pump inhibitors
Misoprostol

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6
Q

What can be used to neutralise stomach acid?

A

Weak bases:
- Magnesium hydroxide and trisilicate
- Aluminium hydroxide gel
- Alginates and simeticone

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7
Q

What conditions can be managed by neutralising gastric secretion?

A
  • ruminal acidosis
  • gastritis
  • oesophagitis
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8
Q

What can be used for mucosal protection in gastric secretion modification - what is the clinical relevance of this?

A

Sucralfate (disaccharide)
- may prevent uptake of other drugs

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9
Q

What is the function of adding absorbents to gastric secretion?

A

Coating actions
Bind bacteria and toxins

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10
Q

What absorbents can be added to gastric secretion?

A

Activated charcoal
Bismuth
Kaolin (aluminium silicate)/pectin

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11
Q

What is the action of adding histamine antagonists in gastric secretion

A

Inhibits gastrin, histamine and acetylcholine stimulated secretion
Pepsin secretion falls (less volume of fluid)
Get a rebound increase on withdrawal

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12
Q

What histamine antagonists can be added to gastric secretion?

A

Ranitidine
Cimetidine

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13
Q

what is the action of adding proton pump inhibitors to gastric secretion?

A

irreversibly bind to ATPase
Inhibits basal and stimulated release

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14
Q

What proton pump inhibitors can be added to gastric secretion?

A

omeprazole
lansprazole

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15
Q

What is the action of misoprostol when added to gastric secretion?

A

inhibits acid secretion
increases mucosal blood flow
Increases uterine contraction (don’t use in pregnant animals)

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16
Q

What are the 2 centres that control emetics?

A

chemo receptor trigger zone (CRTZ)
Vomiting centre in brainstem

17
Q

what is the function of the chemo receptor trigger zone (CRTZ)?

A

chemical stimuli
BBB is permeable in area of CRTZ
Gets input from vestibular apparatrus (motion sickness)
Sends impulses to vomiting centre in brainstem

18
Q

What is the function of the vomiting centre in the brainstem?

A

coordinates and integrates vomiting

19
Q

Describe the pathophysiology of vomiting

A

Impulse to vomiting centre via central, peripheral pathways or vestibular apparatus => substance P (neurotransmitter) binds to NK-1 receptors at cell membrane => signal travels via vagus nerve to abdominal muscles + diaphragm => vomiting

20
Q

What substances are emetics?

A

Apomorphine:
- dopamine agonist
Alpha-2 agonists:
- xylazine)
Syrup of Ipecac:
- direct irritant
- causes cardiotoxicity in high doses

21
Q

what are some dopamine antagonists?

A

Phenothiazine derivatives e.g., chloropromazine
Metaclopramid
Domperidone

22
Q

Describe the action of metaclopramide and domperidone

A

Dopamine antagonists
Short action so need to infuse IV
Metaclopramide - centrally acting (CRTZ)
Domperidone - peripherally acting
Increase gastric emptying and increased motility
Do not use if vomiting due to obstruction (sends obstruction further down GIT)

23
Q

what are some anti-emetics drugs?

A

Dopamine antagonists
Cerenia (maropitant)
Anti-histamines
Anticholinergics
Cannabinoids

24
Q

Describe the action of cerenia (maropitant)

A

NK-1 antagonist
Competes with substance P

25
Q

How is diarrhoea managed?

A

maintenance of fluid balance:
- IV fluid therapy (Hartmann’s solution)
- oral fluids
- anti-infectives e.g., zinc = immune stimulant

26
Q

why may you want to modify intestinal motility?

A

reduce pain
increase transit time and re-absorption ‘window’

27
Q

What are the 2 main classes of spasmolytics (antimotility) drugs?

A

Opiates e.g., morphine, codeine and loperamide (immodium)
Muscarinic antagonists e.g., atropine, hyoscine (buscopan)

28
Q

What is the action of morphine as a spasmolytic drug?

A

increases intestinal contractions but decreases propulsion
increased large intestinal tone
=> constipation

29
Q

What is the action of muscarinic antagonists as spasmolytic drugs?

A

neuronal control
inhibit acetylcholine stimulatory effects from vagus nerve

30
Q

what classes of drugs improve GIT motility?

A

Prokinetics - cisapride
Laxatives

31
Q

What are some laxatives?

A

Saline and hyperosmotic agents
Bulk producing agents
irritants

32
Q

What is bulk and how does it improve aid intestinal motility

A

Methylcellulose
Polysaccharide polymers not easily digested => forms hydrated bulk in gut
Holds water and promotes peristalsis

33
Q

How do osmotic laxatives aid intestinal motility?

A

Poorly absorbed solutes
Lactulose - broken down to lactic acid => lower pH => traps ammonia and water in gut => softens faeces => eases motility

34
Q

What is the pharmacological intervention used in idiopathic inflammatory bowel disease?

A

Anti-inflammatory steroids e.g., prednisolone sulphasalazine

35
Q

what is a pro-drug?

A

drug that is broken down into the active substance in the liver

36
Q

What is the treatment for frothy bloat in ruminants?

A

antifoaming agents
Surfactants/detergents cause bubbles to break down

37
Q

what causes frothy bloat in ruminants?

A

clover