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NSAIDs Flashcards

1
Q

Name the 3 properties of NSAID?

A
  • antiinflammatory
  • antipyretic
  • analgesic
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2
Q

Name 4 adverse effects of NSAIDs?

A
  • gastrointestinal: anorexia, diarrhoea, vomiting, lethargy
  • renal toxicity
  • hepatic toxicity
  • decreases platelet aggregation

veterinary­ approved, NSAID­ induced GI adverse effects are usually mild and self­limited –> ulceration/perforation when label recommendations are not followed or CI ignored

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3
Q

Name 8 relative contraindications for NSAIDs?

A
  1. History of GI disease
  2. NSAID intolerance
  3. uncontrolled renal or hepatic disease
  4. Anaemia
  5. Coagulopathy
  6. Hypovolemia or dehydration
  7. Hypotension
  8. Hypoproteinemia or Hypoalbuminemia
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4
Q

Name 7 common reasons for development of serious adverse effects?

A
  1. concurrent corticosteroid administration
  2. concurrent or recent administration of other NSAIDs
  3. Higher than recommended dose
  4. Higher than recommended frequency of administration
  5. Continued administration in the presence of GI signs
  6. Lack of close patient monitoring
  7. Owner’s inability to report or identify clinical signs
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5
Q

How long should the wash-out period after aspirin be and why?

A

9-11 days due to platelet lifespan

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6
Q

How long should the wash-out period be between 2 different NSAIDs according to clinical experience?

A

2-3 days

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7
Q

What is the general mechanism of action of NSAIDs?

A

act in cell membranes by inhibiting the expression of cyclo­- oxygenase (COX) enzymes that are essential in the biosynthesis of prostaglandins

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8
Q

Name two types of prostaglandins and their associated COX enzyme?

A

Constitutive prostaglandins = COX-1
- gastroprotection via secre­tion of gastric mucus and production of bicarbonate
- renal perfusion under hypotensive conditions
- vascular homeostasis via throm­boxane and prostacyclin production
- expression also during inflammation

Inducable prostaglandins = COX-2
- overexpressed after tissue injury
- production of inflammatory mediators (e.g. endotoxins, cytokines, growth factors responsible for sensitizing peripheral nociceptors)
- ulcer healing

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9
Q

Why may selective COX­2 inhibitors (coxibs) induce adverse effects in small animals when dosage regimens are not appropriate?

A

prostaglandins via COX­2 activity may have physiological func­ tions in several tissues and in ulcer healing

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10
Q

Do preferential and selective COX­2 inhibitors have a superior safety profile when compared with nonselective COX-­inhibitors?

A

yes

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11
Q

Where can COX-3 be found and what is it?

A
  • canine and human cerebral cortex
  • COX­3 is a subform of COX­1
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12
Q

How do COX3 inhibitors mediate their analgesic effect?

A
  • decrease PGE2 synthesis
  • suggesting central mechanisms of analgesia
  • e.g. acetaminophen (paracetamol), met­amizole
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13
Q

How are NSAIDs metabolised?

A

primarily via cyto­chrome P­450 enzymes either via glucuronidation (e.g., phenolic compounds) or oxidation (e.g., oxicam group) into inactive or less active metabolites

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14
Q

Why may cats be more susceptible to some NSAID toxicity?

A
  • Cats have deficient glucuronidation which is important for metabolisation of some NSAIDs
  • e.g. acetaminophen (paracetamol), carprofen (slow elimination and longer half-life than in dogs)
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15
Q

Why is acetaminophen contraindicated in cats?

A

Cats have deficient glucuronidation which is important for metabolisation of acetaminophen

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16
Q

How are NSAIDs exrected?

A

predominantly biliary (fecal) and urine

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17
Q

What is the most common predisposing factor for GI ulceration and perforation in dogs? What is the difference to cats?

A

NSAID therapy

NSAID ­related GI ulceration in cats is uncommon.

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18
Q

What is the reported mortalitiy rate in dogs with GI perforation?

A

37% to 69%

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19
Q

Hunt JR reported the frequency of reported adverse events associated with NSAID administration in dogs and cats in the United Kingdom in Vet J 2015. What were the findings?

A
  • no differ­ences in terms of frequency of NSAID­ induced adverse effects between dogs and cats
  • reported frequency of adverse effects higher after coxibs than non­coxibs (could reflect their increased usage in comparison with non­coxibs + increased reporting in general)
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20
Q

What clinical consequence does COX1-inhibition have on the GI tract?

A
  • decreased local gastric blood flow
  • suppression of bicarbonate secretion
  • decreased mucus production

some NSAIDs (e.g., aspirin) might cause direct damage to the GI mucosa

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21
Q

What clinical consequence does COX2-inhibition have on the GI tract?

A
  • impaired tissue healing

some NSAIDs (e.g., aspirin) might cause direct damage to the GI mucosa

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22
Q

Discuss the mechanism of NSAID inducsed lower GI toxicity?

A
  • enterohepatic recycling and consequent prolonged and repeated exposure of the intestinal mucosa to the drug and its compounds
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23
Q

Discuss co-administration of NSAIDs and PPIs in people and dogs/cats? What recommendations are made by ACVIM consensus statement?

A

People:
- PPI­ induced alterations of the intestinal microbiome –> - coadministration lead to decreased upper GI adverse events but increased lower GI adverse events

dogs/cats:
- no clear evidence of increased NSAID toxicity with the coadministration of PPIs;

ACVIM consensus:
- intestinal dysbiosis is a possible sequela and may further contribute to complications from NSAID therapy.
- PPIs should NOT be indiscriminately administered to dogs receiving NSAID therapy
- PPIs should be restricted to patients with increased risk of GI toxicity

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24
Q

Name COX enzymes expressed in the kidney?

A

COX1 + COX2

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25
Q

Discuss the role of prostaglandines on the level of the kidneys?

A

PGE2 + PGI2:
- promote vasodilation
- promote inhibition of Na+ reabsorption with a protective function of the kidneys

Thromboxane A2:
- modulates renin production + vaso­constriction

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26
Q

What effect does Thromboxane A2 mediate on the level of the kidneys?

A

modulates renin production + vaso­constriction

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27
Q

What effect does PGE2 mediate on the level of the kidneys?

A
  • promote vasodilation
  • promote inhibition of Na+ reabsorption with a protective function of the kidneys
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28
Q

What effect does PGI2 mediate on the level of the kidneys?

A
  • promote vasodilation
  • promote inhibition of Na+ reabsorption with a protective function of the kidneys
29
Q

Discuss how administration of NSAIDs that inhibit prostaglandin production produces adverse renal effects in sick animals?

A
  • interfering with the autoregulation of renal perfusion pressure
  • supression of PGE2 + PGI2 mediated vasodilation
  • supression of PGE2 + PGI2 mediated inhibition of Na+ reabsorption with a protective function of the kidneys
30
Q

Discuss renal adverse effects of normal NSAID use in normovolemic patients (even with hypotension or under GA)?

A
  • NSAID ­induced renal adverse effects are not expected in normo­volemic patients
  • Studies failed to demonstrate a significant associa­tion between the administration of NSAIDs and increases in renal enzymes or decreases in GFR
  • carprofen, meloxicam, or tepoxalin in healthy dogs undergoing GA and with hypotension did not result in clinically important renal effects (urinalysis, GFR)
31
Q

Monteiro B et al studied long­term use of NSAIDs in cats with CKD (JSAP 2019). What were the findings?

A

administration of NSAIDs was safe and beneficial in cats with concomitant chronic pain and stable IRIS I and II CKD

32
Q

Discuss the effect of COX1 activity on coagulation?

A

produces thromboxane A2:
- platelet aggregation
- vasoconstriction

33
Q

Discuss the effect of COX2 activity on coagulation?

A

produces prostacyclin:
- anticoagulant effects
- vasodilation

34
Q

Discuss the effects of NSAIDs on hemostasis and aspirin on hemostasis? What recommendations can be made?

A
  • Evidence is controversial
  • Most studies failed to demonstrate an association (BMBT, platelet function analysis + aggregation testing, TEG, PT)
  • Studies in dogs (ketoprofen + OHE or meloxicam + ortho Sx): decrease in platelet aggregation + increase in aPTT - but values still remained within RR; BMBT did not change
  • NSAID­ induced coagulation effects may only be of concern in patients with exist­ing coagulation disorders.

Aspirin (nonpreferential COX inhibitor) irreversibly binds to the COX complex, potentially impairing platelet ag­gregation throughout their lifespan (9–11 days)

SACCM recommendation:
Patients that are thrombocytopenic, coagulopathic, or at high risk of bleeding should not be administered NSAIDs.

35
Q

Discuss hepatic side effects and their mechanism of action in NSAIDs? What breed may be predisposed to this side effect?

A
  • Hepatotoxicity is rarely reported in dogs
  • idiosyncratic reaction
  • clini­cally important changes in liver enzymes have not been observed in dogs or cats after long­term NSAID therapy
  • increases in liver enzymes and acute liver toxicosis may be observed after NSAIDs in preexisting liver disease

Labrador Retrievers may be more likely to develop hepatocellular toxicosis after carprofen therapy (true predisposition has not yet been validated)

36
Q

Discuss the mechanism of action of grapiprant and its role as an analgesic?

A
  • Piprants are EP4 prostaglandin receptor antagonists
  • Grapiprant selectively blocks the EP4 receptor
  • EP4 receptor is involved in the PGE2­ induced inflammation + sensitization of peripheral nociceptors
  • 2 mg/kg PO every 24 hours: canine osteoarthritis
  • grapiprant vs. placebo in dogs: improved pain scores + increased frequency of adverse effects in grabiprant (but generally well tolerated)
  • reported side effects: vomiting, diarrhea, soft stools, anorexia, decreased appetite
37
Q

Name 3 properties of acetaminophen (paracetamol)?

A
  • analgesic
  • antipyretic effects
  • only weak antiinflammatory
38
Q

Discuss the mechanism of action of acetaminophen (paracetamol)?

A
  • COX3-inhibition (subtype of COX1)
  • inhibition of PGE2 synthesis in the CNS
39
Q

Discuss the role of acetaminophen (paracetamol) as an analgesic in dogs?

A
  • No evidence of analgesic efficacy for the oral administration (when combined with hydro­codone or codeine)
  • Parenteral administration has been anecdotally reported
40
Q

Name adverse effects of acetaminophen (paracetamol) toxicity?

A
  • hepatotoxicity
  • methemoglobinemia: oxidative injury to erythrocytes with consequent anemia and Heinz body formation
41
Q

How is acetaminophen (paracetamol) metabolised?

A

conjugation with glucuronide and sulfate by transferase enzymes

42
Q

Why is acetaminophen (paracetamol) contraindicated in cats?

A
  • cats have deficient glucuronidation but acteaminophen relies on conjugation with glucuronide and sulfate by transferase enzymes
43
Q

Name 6 clinical signs of methaemoglobinemia and its relecance in acetaminophen (paracetamol) administration?

A
  1. cyanosis
  2. facial edema
  3. prolapse of con­junctival membranes
  4. brown blood
  5. brown urine
  6. tachypnea + dyspnea
44
Q

Discuss the mechanisms of action of metamizole/dipyrone?

A
  • COX­3 inhibition
  • activation of opioid and cannabinoid systems
45
Q

Name 3 properties of metamizole/dipyrone?

A
  • analgesic
  • antipyretic effects
  • only weak antiinflammatory
46
Q

What is the recommended metamizole/dipyrone dose for post-operative pain?

A

25–35 mg/kg IV q8hr

47
Q

Discuss the impact of metamizole/dipyrone on coagulation?

A
  • Caution in patients with coagu­lopathies
  • metamizole/dipyrone alone or with meloxicam resulted in decreased platelet aggregation in healthy dogs (did not affect thromboelastometry or BMBT)
48
Q

Name 2 side effects of metamizole/dipyrone in cats with IM/IV administration?

A
  1. salivation
  2. vomiting
49
Q

How long should the wash-out period be between corticosteroids + NSAIDs according to clinical experience?

A
  • at least 48–72 hours (anecdotally)
50
Q

Discuss the role of corticosteroids in pain management?

A

little scientific evidence to support their use in pain management

51
Q

Name 7 adverse effects of corticosteroids?

A
  1. PU/PD
  2. Polyphagia
  3. GI disorders + ulceration
  4. iatrogenic hyperadrenocorticism
  5. muscle atrophy
  6. increased risk of infection
  7. poor wound healing

Adverse effects are more easily induced after corticoste­roids than NSAIDs.

52
Q

Name 2 non-selective NSAIDs?

A
  1. ketoprofen
  2. flunixin
  3. phenylbutazone
  4. +/- etodoloac (preferential for COX2 in some studies)
53
Q

What is the eliminiation half-life of aspirin?

A

dog: 7.5hr
cat: 37.5hr (up to 45hr)

54
Q

What is the eliminiation half-life of carprofen?

A

dog: 11-14hr
cats: 21hr (up to 49hr)

55
Q

What is the eliminiation half-life of deracoxib?

A

dog: 3hr
cat: 8hr

56
Q

What is the eliminiation half-life of cimicoxib?

A

dog: 3-8hr
cat: ?

57
Q

What is the eliminiation half-life of firocoxib?

A

dog: 6hr
cat: 12hr

58
Q

What is the eliminiation half-life of meloxicam?

A

dog: 24hr (up to 36hr)
cat: 15-26hr

59
Q

What is the eliminiation half-life of ibuprofen?

A

dog: 5hr
cat: not given

60
Q

What is the eliminiation half-life of naproxen?

A

dog: 74hr
cat: not given

61
Q

What is the protein binding capacity of NSAIDs?

62
Q

Name 2 pharmacokinetic properties of NSAIDs?

A

weak acids
highly lipophilic at tissue pH
LogP > 2 (lipid/water partition coefficients)

63
Q

What is the volume of distribution of NSAIDs?

A
  • varies considerably among the NSAIDs
64
Q

What is the VoD of firocoxib in dogs?

A

Dogs: ~4.6L/kg

65
Q

What is the VoD of meloxicam in dogs/cats?

A

Dogs: ~0.32 +/– 20% L/kg
Cats: 0.245 L/kg (VD/F)

66
Q

What is the VoD of carprofen in dogs/cats?

A

Dogs: 0.14 +/– 0.02L/kg
Cats: 0.14 +/– 0.05L/kg

67
Q

What is the VoD of robenacoxib in dogs/cats?

A

Dogs: 84% non‐fed; 62% fed
Cats: 49% non‐fed, 10% fed

68
Q

Name 5 selective COX2-inhibitors?

A
  1. Deracoxib
  2. Robenacoxib
  3. Cimicoxib
  4. Mevacoxib
  5. Firocoxib (most highly seletive of all)
69
Q

Name 2 preferential COX2-inhibitors?

A
  1. carprofen
  2. meloxicam

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