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Small Animal Final Year > NSAIDs > Flashcards

NSAIDs Flashcards

1
Q

Define pharmacokinetics

A

What the body does to the drug

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2
Q

Define pharmacodynamics

A

What the drug does to the body

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3
Q

What is the therapeutic window of NSAIDs?

A

Narrow

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4
Q

What do NSAIDs block?

A

Prostaglandins

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5
Q

Where do NSAIDs act? (2)

A
  • Periphery
  • Spinal cord
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6
Q

Where do steroids act in the pathway? What is the negative of this?

A

At phospholipase, which is one stage higher than NSAIDs and you therefore get more side effects

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7
Q

Where do NSAIDs act in the pathway?

A

Cyclooxygenase

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8
Q

Name 5 things NSAIDs have been shown to inhibit in horses (7)

A

–Inflammation

–Fever

–Oedema

–‘Endotoxaemia’ (??)

–Ileus

–Adhesion formation

–(thrombosis formation)

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9
Q

Which NSAID can we use in inflammatory visceral disease in equine?

A

Flunexin

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10
Q

What can occur with poor IV administration of phenylbutazone?

A

Thrombophlebitis and necrosis

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11
Q

What must you do if you give a horse phenylbutazone?

A

Sign the horse passport out of the food chain

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12
Q

What should you do if you want to give phenylbutazone but there is no passport available?

A

Use meloxicam as this can go into food chain

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13
Q

Compared with opioids, what is NSAIDS:

A) Better for?

B) Less good for?

A

A) MSK Pain

B) Visceral pain

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14
Q

Name 2 reasons we would rather use NSAIDs than opioids in horses?

A

Side effects

Don’t want to dispense too many opioids (horse owners are dodge)

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15
Q

Name 7 pracitcal considerations when it comes to NSAID use (9)

A
  • Non-scheduled (still POM-V)
  • Cheaper vs opioids
  • Effective per-os
  • Little long-term decrease in efficacy
  • Longer duration of action
  • Side effects
  • Compliance (owner)
  • Cost
  • Co-morbidities
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16
Q

Where are NSAIDs metabolised?

A

Liver

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17
Q

Where are NSAIDs excreted?

A

Kidneys

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18
Q

What is the protein binding of NSAID?

A

High

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19
Q

What is the volume of distribution of NSAIDs?

A

Low

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20
Q

What is the wash out period?

A

–If you want to change from one NSAIDs to another. There is advice to allow a number of half life wash out before we start the next one. May need bridging medication to tide them over e.g. adjuncts – paracetamol. Not currently done in horses.

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21
Q

What should you do if you have a problem with an NSAID?

A

Yellow form or online reporting to VMD

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22
Q

What is the “housekeeping” pathway?

A

Cox 1 - constitutive

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23
Q

What is the inflammatory pathway?

A

COX 2 - inducible

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24
Q

Why can NSAIDs cause problems with the kidneys?

A
  • Renal blood flow mediated by prostaglandins (PG) in medullary circulation (Therefore PG inhibition by NSAIDS can cause problems)
  • Hypotension + NSAID = renal damage hence concern peri-operatively
25
Q

What is the effect of prostaglandins in the GIT?

A

They are cytoprotective

–Decrease the volume, acidity and pepsin content in the stomach

–Stimulate bicarbonate secretion

–Promote mucosal blood flow and repair and turnover of cells

26
Q

Name 5 side effects of NSAIDs (7)

A

–Vomiting (small ans)

–Colic

–Inappetance

  • D++

–PLE

-2° anaemia,

–Ulceration

–Death

27
Q

What are young horses more susceptible to with NSAIDs?

A

Gastric ulceration

28
Q

What are adult horses with NSAIDs more susceptible to?

A

Right dorsal colitis

29
Q

What is the relative ulcerogenicity with:

Flunixin

Phenylbutazone

Ketoprofen?

A

Phenylbutazone > flunixin > ketoprofen

30
Q

Name 2 long term adaptations of the GI tract to NSAIDs (3)

A
  • Increased mucosal blood flow
  • Increased mucosal cell regeneration
  • Decreased inflammatory cell infiltrate
31
Q

How many days on NSAIDs does it take for there to be long term adaptation?

32
Q

What is enterohepatic recycling?

A

Excretion into intestine from bile – repeated exposure of the duodenum to drug

33
Q

What does enterohepatic recycling directly correlate to?

34
Q

Name 4 ways GI safety with NSAIDs can be improved (6)

A

–Protective strategy – case by case basis

–Sucralfate (sucrose aluminum sulphate)

–H2 antagonists

–Proton pump-inhibitors

–? Newer Coxibs ?

–Different formulation of NSAIDs sometimes

35
Q

What is the effect of some NSAIDs on cartilage and what is the mechanism of this?

A

Worsen cartilage degeneration in arthritic animals – decreased GAG synthesis

36
Q

What is the effect of carprofn on equine cartilage cells? (2)

A
  • Increased GAG at therapeutic doses
  • Increase proteoglycan metabolism
37
Q

What type of reactions happen with NSAIDs causing hepatotoxciity?

A

Type 1 and type 3

38
Q

What is the breed predisposition of dogs getting hepatotoxcity with NSAIDs?

A

There isn’t one

39
Q

What is the difference between cats and dogs having NSAIDs?

A

They have a lower clearance of salicylates

40
Q

Name 5 of the possible effects cats may get with NSAIDs (7)

A
  • Hyperthermia
  • Respiratory alkalosis
  • Metabolic acidosis
  • Methaemoglobinaemia
  • Haemorrhagic gastro-enteritis
  • Renal failure
  • Hepatic injury
41
Q

What is Robenacoxib (onsior)?

A

A tissue selective NSAID

42
Q

Name 5 guidelines for safe use of NSAIDs? (7)

A

–No hypovolaemia (but what about colic sx?)

–No concurrent administration of another NSAID OR a steroid – possibly allow washout (4-5 half lives?? in dogs), but this is not performed in horses..

–No hepatic or renal insufficiency

–Dog – high confidence in absence of renal failure

–Cats – no margin of safety !

–Routine biochemistry? For long term use? YES

–Screening biochemistry? Before starting in some cases of long term therapy? YES IF POSSIBLE

43
Q

What is acetaminophen?

A

Paracetamol

44
Q

Where is paracetamol licensed?

45
Q

When is paracetamol most commonly used?

A

As a bridgng mechanism

46
Q

Where is sodium salicylate licensed?

A

Catlle and pigs

47
Q

What is the mechanism of paracetamol action?

A

–Unknown mechanism of action – central ?, 5-HT3, TPRV1, Cox, cannabinoid pathways possibly involved?

48
Q

Where should you look for off licence use of NSAIDs?

A

BSAVA formulary

49
Q

What is the issue of using NOAH for drugs?

A

Not all drugs are in there - companies have to pay to be in there

50
Q

Name 4 licensed NSAIDs in horses (6)

A
  • Phenylbutazone,
  • Suxibuzone,
  • Flunixin,
  • Meloxicam,
  • Vedaprofen,
  • Firocoxib
51
Q

Name 3 licensed NSAIDs in cats (4)

A
  • Meloxicam,
  • Robenacoxib,
  • Ketoprofen,
  • Tolfenamic acid
52
Q

Name 7 licensed NSAIDs in dogs (10)

A
  • Meloxicam,
  • Carprofen,
  • Robenacoxib,
  • Mavacoxib,
  • Paracetamol (with codeine),
  • Tolfenamic acid,
  • Ketoprofen, (tepoxalin - expired )
  • Firocoxib,
  • Phenylbutazone,
  • Cimicoxib
53
Q

Name 4 licensed NSAIDs in pigs (6)

A
  • Ketoprofen,
  • Meloxicam,
  • Tolfenamic acid,
  • Flunixin,
  • Salicylic acid,
  • Paracetamol
54
Q

Name 3 licensed NSAIDs in cows (4)

A
  • Ketoprofen,
  • Meloxicam,
  • Flunixin,
  • Salicylic acid
55
Q

Name licensed drugs in sheep and goats

A

Nothing licensed – use cascade as for other food producing animals

56
Q

What is the benefit of mavacoxib?

A

Duration up to a month

57
Q

Name 6 therapeutic decsions of using NSAIDs (8)

A
  • Consider Efficacy
  • Consider Safety
  • Address compliance (see suggestions in the OA NSAID booklet for improvements)
  • Consider the formulation – route of admin
  • Cost ?
  • Duration of action
  • Support packages?
  • EBM
58
Q

Name 8 “other” therapies to NSAIDs for MSK disease (10)

A
  • Exercise management
  • Weight control & diet (may need additional analgesics
  • Modifications to lifestyle (ramps, rugs, claws)
  • Hydrotherapy & physiotherapy
  • Chondroprotectives
  • Joint replacement
  • IRap
  • Stem cell therapies
  • Other ‘drugs’ :Isoxsuprine hydrochloride (Navilox), vegetable tablets, garlic & fenugreek, sodium hyaluronate (Hyonate), prednoleucotropin (PLT)
  • EP4 receptor blockers (galliprant –USA only, UK 2018/19)

Small Animal Final Year (317 decks)

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