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Principles of Science BVetMed 3 > GIT drugs > Flashcards

GIT drugs Flashcards

1
Q

When might it be inappropriate to use anti-emetic therapy? 3

A
  • GIT infections (may prolong infections, especially bacterial)
  • GIT obstruction (may increase gastric motility leading to perforations)
  • GIT toxicity (may prevent elimination of toxin)
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2
Q

What structures feed into the vomitting centre? (6)

A
  • Higher CNS (pain, fear smell)
  • vestibular (motion sickness, inner ear infection)
  • Nucleus tractus solitarius (integration)
  • Peripheral receptors (GIT, abdominal organs)
  • toxins
  • CRTZ
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3
Q

How do cats and dogs differ in terms of anti-emetics?

A

The receptors they have differ in terms of importance of receptors in emesis.

  • D2-R in dog CRTZ most important (targetted with apomorphine)
  • alpha2-adrenergic receptors more important in felin CRTZ (xylazine more potent in dog v cat, prochlorperazine more useful than metclopramide (DA antagonist) in cats)
  • Histamine is a potent emetic in the dog, not cat
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4
Q

Name the 6 classes of anti-emetic drugs

A
  • NK1 antagonists
  • Metclopramide
  • Phenothiazines
  • Antihistamines
  • 5HT3 antagonists
  • Anti-cholinergics
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5
Q

What is maropitant?

A

General name of a NK1 antagonist (a class of anti-emetic)

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6
Q

Where/how does maropitant act?

A

Selective antagonist of substance P at NK1 receptor at the nucleus tractus solitarius (where final common pathway leading to vomiting centre are integrated therefore very potent). Effective against peripheral and central stimuli

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7
Q

Uses of maropitant (3)

A

Canine anit-emetic (acute gastroenteritis, cytotoxic-induced vomitting, motion sickness).

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8
Q

Considerations when using maropitan (4)

A
  • v effective so take care
  • use symptomatically only
  • invetigate thoroughly before re-prescribing
  • don’t use if suspicious of GI obstruction
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9
Q

How does metoclopramide work?

A
  • Antagonist (D2 dopaminergic and 5HT3 serotonergic. Acts on both of these in the CRTZ and the peripheral receptors)
  • Peripheral pro-cholinergic effect (i.e. increases GIT motility)
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10
Q

Inidcations - metoclopramide

A
  • Various emesis-inducing disorders (central or peripheral)
  • cancer chemotherapy
  • gastroesophageal refluc
  • decreased gastric emptying (associated with inflammatory GIT disorders, gastric ulcers, gastric neoplasia, autonomic neuropathy - DM, pyloric stenosis, postop gastric volvulus, hypokalaemia, abnormal gastric motility)
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11
Q

How do phenothiazines work? (6) Where?

A

Antagonise:

  • a1 and a2 (vomiting centre) adrenergic receptors
  • D2 dopaminergic receptors (vestibular and CRTZ and peripheral receptors)
  • H1 and H2 histaminergic receptors (CRTZ)
  • muscarinic hcolinergic (vestibular)
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12
Q

Indications - phenothiazines

A

Any central or peripheral cause

Not UK veterinary registered therefore few UK indications for use

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13
Q

Name 2 antihistamines (general names)

A

Diphenhydrinate and diphenhydramine

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14
Q

Where do anti-histamines work as anti-emetics?

A

H1 and H2 receptors in CRTZ (for canine motion sickness - CRTZ connected with the vestibular system , cats suffer less from this).
Off label use in UK

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15
Q

Examples of 5HT3 antagonists

A

Dolasetron (Anzemet -trade name)
Ondansatron (Zofran - trade name)
Cisplatin - used to control cytotoxic drug-induced emesis

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16
Q

2 considerations of 5HT3 antagonists

A

Better than metoclopramide (efficacy-wise)

Expensive

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17
Q

Where do 5HT3 antagonists act? (2)

A

CRTZ and peripheral receptors

18
Q

Name 4 anti-cholinergics

A

atropine, butylscopolamine, propantheline and isoproamide

19
Q

Advantage/disadvantage of anti-cholinergic anti-emetics:

A

+ effective for motion sickness due to antagonism of M1 receptors in vestibular apparaus
- also acts on M2 receptors resulting in potential for delayed gastric emptying and ileus.

20
Q

Where do anti-cholinergic anti-emetics work?

A

M1 - vestibular and CRTZ

M2 - peripheral receptors

21
Q

5 classes of anti-ulcer drugs:

A
  • nonsystemic antacids
  • H2 receptor antagonists
  • sucralfate
  • misoprostol
  • omeprazole
22
Q

Why use/not use non-systemic antacids? (4)

A

Cheap
Oral (problematic if vomiting)
Frequent administration (at least every 4 hour)
Treats but doesn’t prevent

23
Q

Name 2 H2-receptor antagonists

A

Cimetidine (veterinary licensed)

Ranitidine and famotidine (not veterinary licensed)

24
Q

Uses of H2-receptor antagonists

A
  • treating gastric ulceration (from variety of disorders - NSAIDs and uraemia)
  • Equally effective at promoting ulcer healing (different potencies affect dosage not efficacy)
  • Consider that is it is cheap, convenience for owner? concurrent drug therapy?
25
Q

How does sucralfate work?

A

Sticks to ulcer, prevents further acid damage. By oral administration

26
Q

Uses - sucralfate.

A

Symptomatic treatment of gastric ulceration from a variety of causes.

27
Q

What is misoprostol?

A

Synthetic PGE1

28
Q

Use - misoprostol?

A

Main indication is management or prevention of NSAID toxicity

29
Q

Danger of misoprostol?

A

Causes abortion (humans) - big owner safety issues in terms of who should handle it

30
Q

How does omeprazole work?

A

Proton pump inhibitor (v effective)

31
Q

Use of omeprazole

A
  • Small animal vet med (increasingly common but off label for ulcers or oesophagitis refractory to other anti-ulcer treatments or for ulcers associated with gastrinomas or mast cell tumour)
  • equine medicine (GastroGard - treatment and prevention of gastric ulcers)
32
Q

Why use electrolyte solutions for small animals?

A

Enhance fluid absorption from gut - depends on active absorption of glucose and aminoacetic acid in the SI, directly linked with water and sodium movement. Does no harm - pleases owner as something to do (!)

33
Q

Indications for opiods

A

Motility modifying drugs - increase segmental contractions (random and multi-directional to prolong intestinal transit time theoretically to allow a greater time for fluid to be absorbed). Can be an effective symptomatic treatment (relieve abdominal pain and tenesmus, reduce the frequency of defecation). Overall = rarely required.

34
Q

How do anti-cholinergics affect motility modifying drugs?

A

Decrease peristalsis (bad thing - you don’t want this!)

35
Q

How do acute and chronic diarrhoea differ in their treatments?

A

Acute - usually self-limiting with appropriate symptomatic treatment
Chronic - doesn’t usually respond to symptomatic therapy but requires a definitive diagnosis

36
Q

Uses of anti-cholinergics?

A
  • Little use in management of diarrhoea (cats and dogs)
  • May be justified in short term (symptomatic relief of pain and tenesmus associated with large bowel inflammatory disease).
  • Used to manage spasmodic colic in horses
37
Q

Why isn’t a reduction in peristalsis not desirable?

A

Causes delayed gastric emptying and ileus.

38
Q

How much evidence supports adsorbents and protectants?

A
  • clinical efficacy unproven
  • no evidence they reduce GI fluid or electrolyte loss (Kaolin may even increase faecal sodium loss)
  • also messy to administer but gives owner something to do (!)
39
Q

What is bismuth salicylate an example of?

A

An adsorbent and protectant

40
Q

How does bismuth salicylate work? (2) Contraindications (2)?

A
  • May inhibit prostaglandin action.
  • May reduce gastrointestinal secretion in acute secretory diarrhoea
  • (unknown efficacy and avoid in cats)
41
Q

On what grounds can probiotics be used in small animals?

A

Little clinical efficacy shown in pets (unlike humans), not all products th esame, evidence of acitivity at cellular level in the gut, do no harm, more research needed, gives owners something to do (!)

Principles of Science BVetMed 3 (110 decks)

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