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Flashcards in Drugs Deck (68)
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1

Describe the mechanism of action of NSAIDs

Block production of prostaglanding by blocking COX conversion of arachidonic acid to PGG2

2

Compare COX 1 and 2

- COX1: constitutive, always present, maintain turnover cells, required for life
- COX2: inducible, active in response to inflammatory stimulus, invoke production of PGs that are not usually there (PGE2)

3

Where are COX1 found?

- Intestines
- Platelets
- Stomach
- Kidney

4

Where are COX2 found?

- Macrophages
- Leukocytes
- Fibroblasts
- Endothelial cells

5

Outline some equine specific problems with NSAIDs

- Thrombophlebitis wih pheynbutazone if have perivascular injection
- Prescription of phenylbutazone only done when this can be entered into passport immediately

6

Give examples of suggested equine specific effects of NSAIDs that have

Inhibit:
- Inflammation
- Pyrexia
- Oedema
- Endotoxaemia
- Ileus
- Adhesion formation (tenuous evidence)
- Thrombosis

7

Discuss the effect of NSAIDs on wound healing

- Some compromise to healing
- However pain has more significant impact on wound healing so administration of NSAIDs still positive

8

Outline the pharmacokinetics of NSAIDs

- Hepatic metabolism and renal excretion
- High protein binding, low vol of distribution
- Significant individual variation in response and susceptibility to toxicity
- Effects often outlive the plasma half life

9

Compare the risks of NSAIDs in ponies and horses

Ponies more susceptible to phenylbutazone toxicity than horses

10

Explain the adverse effects of NSAIDs regarding the kidney

- Reduce renal blood flow as this is mediated by prostaglandins in the medulla
- Hypotension + NSAID = renal damage
- Some concern regarding pre/peri-operative use bu several NSAIDs licensed for this

11

Explain the adverse effects of NSAIDs regarding the GI system

- Prostaglandins cytoprotective in the GIT
- GI side effects most common with chronic use
- Direct irritation and PG inhibition are the cause of these signs
- Some require administration with food, others on empty stomach

12

List the serious GI side effects of NSAIDs

- Vomiting (small animals)
- Colic
- Inappetance
- Diarrhoea
- Protein losing enteropathy (PLE), secondary anaemia
- Ulceration
- Death

13

Explain the role of prostaglandins in the GIT

- Cytoprotective
- Decrease volume, acidity and pepsin content in the stomach
- Stimulate bicarbonate secretion
- Promote mucosal blood flow and repair and turnover of cells

14

Compare the adverse effects of NSAIDs on the GI system of young and adult hoses

- Young: more susceptible to gastric ulceration
- Adults: more susceptible to right dorsal colitis

15

Describe the long term adaptation of the GI system to NSAID use

- Increased mucosal blood flow
- Increased mucosa cell regeneration
- Decreased inflammatory cell infiltrate
- From 14 days

16

Explain the role of enterohepatic recycling in the GI safety of NSAIDs

- Excretion into intestine from bile
- Leads to repeated exposure of the duodenum to the drug
- Directly correlates to toxicity

17

Give examples of ways in which the GI safety of NSAIDs can be improved

- Protective strategy
- Sucralfate sucrose (aluminium sulphate)
- H2 agonists
- Protein pump inhibitors
- Newer coxibs
- Different formulation of NSAIDs sometimes tolerated better by different individuals

18

How does hepatotoxicity occur as a consequence of NSAID use?

Type I and type III reactions

19

List the adverse effects of NSAID use in cats

- Hyperthermia
- Respiratory alkalosis
- Metabolic acidosis
- Methaemoglobinaemia
- Haemorrhagic gastro-enteritis
- Renal failure
- Hepatic injury

20

Which NSAID is particularly dangerous in cats?

Carprofen

21

Outline the dosing and frequency of administration of NSAIDs in cats

- Titrate to lowest effective dose
- Dose to lean/ideal body weight in obese animals
- Reduce dose but maintain frequency when titrating down
- Intermittent therapy i.e. 2-3 times a week rather than daily better than nothing
- Liquids more easily measured

22

Describe the screening recommended prior to commencing treatment with NSAIDs in cats

- Thorough history and physical examintion esp. looking at conditions that may impact on NSAID therapy e.g. blood pressure
- Blood biochem to asses renal and hepatic function
- Plasma proteins and haematocrit may be markers of GI bleeding and/or mucosal damage
- Abnormalities may not preclude NSAID use but must be evaluated and discussed with owner

23

List the NSAIDs licensed for systemic use in cats

- Caprofen (once only)
- Ketoprofen
- Meloxicam
- Robenacoxib
- Tolfenamic acid
- Acetylsalicyclic acid

24

Describe the suggested minimum monitoring parameters for long term NSAID use in cats

- History
- Full clinical exam
- Haematocri
- Urea, creatinine, ALT, ALP
- Specific gravity
- Dipstick biochem

25

Out;line guidelines for the safe use of NSAIDs in chronic MSK disease

- Ensure no hypovolaemia
- No concurrent administration of another NSAID or steroid
- No hepatic or renal insufficiency
- Regular (every 3-6 months) monitoring with serum biochem and haematology

26

Explain the risk of paracetamol use in cats

- OD and toxicity common
- Low feline capacity for glucoronidation of paracetamol, rely on sulfation
- When saturated, switches to P450 door detox, creates highly reactive metabolite NAPQI
- overwhelms glutathione availability and result is oxidative injury

27

For which species is paracetamol particularly useful?

- Dogs: adjunct in refractory long term arthritis
- Rodents/rabbits
- Pigs

28

Discuss the use of Mavacoxib

- 1 month duration in dogs
- Good for some owners
- No additional risk of problems in surgery over other NSAIDs
- May need to consider addition of gastroprotectants

29

Outline a therapeutic plan for the use of NSAIDs

- Initial course of NSAIDs, re-check 4 weeks later
- Improvement: continue and reassess q1-2 months
- Little or no improvement: check owner compliance
- Poor compliance: consider reason, consider different formulation
- Good compliance: switch to another NSAID while observing wash out period
- Improvement after switch: continue and reassess q1-2 months
- No/little improvement after switch: reassess diagnosis, consider individual variation, re-evaluate complementary techniques, consider additional of adjunct, seek referral

30

Outline other therapies other than NSAIDs used in the treatment of OA

- Exerise management
- Weight control and diet
- Modification to lifestyle e.g. ramps
- Hydrotherapy and physio
- Chrondroprotectives
- Joint replacement
- IRap (interleukin-1 receptor antagonist protein)
- Stem cell therapies
- Other "drugs": isoxsuprine hydrochloride, vegetable tablets, PLT
- Neutraceuticals