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Pharmacology - VAP844 > Nonsteroidal Anti-Inflammatory Drugs (NSAIDs) > Flashcards

Nonsteroidal Anti-Inflammatory Drugs (NSAIDs) Flashcards

1
Q

Nonsteroidal Anti-Inflammatory Drugs

A

diverse group of drugs which inhibit to some extent the Cyclooxygenase enzymes

Large chemical diversity exists among the NSAIDs, not all the same

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2
Q

NSAID Mechanism of Action

A
  • Inhibition of Cycloxygenase (COX)
    • Cox-1
    • Cox-2
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3
Q

Prastaglandins

A
  • Local regulation of organ and tissue function
    • local control of vasculature of blood flow
    • Local control of GI environment
    • Local control of platelets
    • Local control of Renin release
  • Exception:
    • Endotoxemia resulting in systemic release of prostaglandin and systemic effects
      • Lipopolysaccharides (LPS) release from gram negative bacteria
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4
Q

Prostaglandins:

Cox-1

A
  • “Constitutive” enzyme
  • Local regulation in most cases
    • PGE
      • vasodilation
      • sensitization of nociceptors
      • Enhance inflammation
      • Fever
      • Gastroprotection
        • mucous secretion, bicarbonate secretion, increased blood flow, inhibition of acid secretion
      • Increase renal blood flow through vasodilation
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5
Q

Prostaglandins:

Cox-1

PGF2a

A

Necessary for parturition in most animals

Lutalyse used to scencronize cattle

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6
Q

Prostaglandins:

Cox-1

TBX

A

Thromboxane

Platelet aggregation, vasoconstriction

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7
Q

Prostaglandins:

Cox-2

A
  • “Inducible” enzyme
    • local regulation in most cases
    • PGE:
      • vasodilation, sensitization of nociceptors, inflammation, fever, maintain patency of ductus areteriosis, ovulation
      • Release of renin
    • PGI:
      • Prostacyclin: antagonist to Thromboxane
      • Produced in blood vessel walls resulting in vasodilation and inhibition of platelet aggregation
      • Sensitizes nociceptors
      • Gastroprotective similar to PGE
    • PGE and PGI:
      • Renal effects also include tubular effects
        • Increase renal blood flow (Dogs, +/- cats and horses)
        • Tubular release:
          • increased sodium excretion
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8
Q

Prostaglandins:

Cox-2

“Inducible” Enzyme

A
  • Up-regulated in some types of inflammation
  • Up-regulated in some types of pain
  • Up-regulated in gastric healing
  • Up-regulated in renal vasculature during renal hyptension
  • Cox-2 expressed in neoplastic tissue
    • Angiogenesis? Inflammation?
  • Constitutively expressed:
    • GI tract - gastroprotective
    • Renal - maintain renal blood flow and tubular functions
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9
Q

Lipoxygenase (LOX)

A
  • Catalyzes formation of Leukotrienes
  • Effects:
    • Vasocontristion (Antagonistic to PGs)
      • Decreases blood flow
    • Increase Gastric Acid Secretion
    • Pro-Inflammatory
      • Activation, recruitment, migration, and adhesion of inflammatory cells
      • Increased cytokine production (TNF-a, IL-1B)
    • Bronchoconstriction
    • Does nonselective COX inhibition increase leukotriense by shifting the AA pathway?
      • yes
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10
Q

Aspirin Triggered Lipoxin (ATL)

A
  • Potent anti-inflammatory action
  • Stimulate gastroprotective effects
  • Modulate T-cells and Macrophages
  • Aspirin induces Lipoxin formation by Cox-2
  • Product to Acetylated Cox-2, therefore Cox-2 inhibitors prevent formation and beneficial effects
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11
Q

Nociceptive Stimulation

A

Cox-2 is the primary driver for the pain pathway

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12
Q

Non-selective COX inhibitor

A

Effect Cox-1 and Cox-2 the same

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13
Q

Cox-2 Selective Inhibitor

A

Effects Cox-2 with no effect on Cox-1

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14
Q

Cox-2 Preferential Inhibitor

A

Cox-2 is mostly effected, but there are small effects on Cox-1

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15
Q

GI Tract Adverse Effects (AE) from NSAIDs

A
  • Vomiting, Diarrhea
  • Gastritis, enteritis, GIT ulceration, death
  • Right Dorsal Colitis in Horses
  • Direct irritation of GIT
  • Inhibition of both Cox-1 and Cox-2 produce greatest GIT adverse effects
    • Cox-2 selective and preferential NSAIDs have less GIT adverse effects compated to nonselective inhibitors
      • Except when there are underlying GI lesions
  • Are GI adverse effects to in part to increases LT formation?
    • Nonselective Cox and Lox inhibitor have low GIT adverse effects despite lack of Cox-2 selectivity
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16
Q

GIT Adcerse Effects from NSAIDs:

Cox-1

A

Mediates GIT homeostasis

17
Q

GIT adverse effects from NSAIDs:

Cox-2

A

Also mediates GIT homeostasis

Needed for GIT healing

Lipoxin = gastroprotective

18
Q

GIT Adverse Effects from NSAIDs:

Minimizing GI adverse effects

A
  • Appropriate patent selection
    • Avoid administration with corticosteroids and other NSAIDs
    • Avoid in animals with underlying GI issues
    • Avoid in animals with known sensitivity
  • Gastroprotective therapies
    • misoprostol (Synthetic Prostaglandin E)
    • Acid suppression
      • Proton Pump inhibitors
      • Histamine H2 antagonist
    • Sucralfate
19
Q

Renal Adverse Effects form NSAIDs

A
  • PGE is a local mediator renal blood flow
    • Cox-1 mediates blood flow “in healthy kidneys” in some species (not dogs)
    • In dogs, Cox-2 is constitutive in renal vasculature
    • Cox-2 up-regulated due to renal ischemia/hypotension
  • Renin release mediated in part by Cox-2
    • increase Cox-2 maintains renal blood flow
    • Increase Lox decreases renal blood flow
20
Q

Renal Adverse Effects form NSAIDs:

Increased by:

A
  • Hypotension
  • Pre-existing renal disease
  • Concurrent use of nephrotoxic drugs
  • Congestive heart failure
  • Sodium Depletion
    • Cox-2 upregulated in macular densa
    • Macula densa:
      • Renin-angiotensin-aldosterone (reabsorb sodium/water from urine), maintain blood pressure
21
Q

Hepatotoxicity

A
  • Idiosyncratic
    • can occur with any NSAId
    • No breed predispostions identified
    • Typically occurs whithin 21 days
    • Not dose-dependent
    • Often reversible with discontinuation of NSAID and supportive therapy
      • severe cases can be fatal
    • Unknown if reactions will occur with other NSAIDs
  • Dose dependent toxicity
    • overdose
    • Caution clients about flavored formulations
22
Q

Coagulation Inhibition

A

Primarily due to thromboxane inhibition

Cox-1 inhibition

Low dose aspirin irreversibly binds to thromboxane synthetase :anti-platelet effects”

23
Q

Hypercoagulable State

A

Cox-2 selective inhibitors

Inhibition of PGI

Less of a problem in most animals

24
Q

Myelosuppression

A

Rare, but serious

Associated primarily with:

Phenylbutazone - aplastic anemia

Dipyrone - Agranulocytosis

25
Q

Special Considerations:

Gastrointestinal Surgery/Disease

A
  • Enterotomy, gastrotomy, GDV
    • Cox-1
      • Gastroprotective
    • Cox-2
      • Upregulated in healing GIT
26
Q

Special Considerations:

Anesthesia

A
  • Short Anesthesia, <20 mins, less risk
  • Hypotension:
    • renal blood flow increased by COx-2 mediated vasodilation in dogs and all species
  • Fluids should be administered during anesthesia to animals on NSAIDs
27
Q

Special Considerations:

Shock/ Trauma

A
  • Increased adverse effects of NSAIDs
    • GIT:
      • blood flow already decreased due to shock
    • Renal blood flow:
      • Cox-2 dependant
    • NSAID analgesia limited to mild-moderate pain
  • Primary treatment of Pain/Shock
    • crystalloids
    • Colloids
    • Opioids
27
Q

Special Considerations:

Shock/ Trauma

A
  • Increased adverse effects of NSAIDs
    • GIT:
      • blood flow already decreased due to shock
    • Renal blood flow:
      • Cox-2 dependant
    • NSAID analgesia limited to mild-moderate pain
  • Primary treatment of Pain/Shock
    • crystalloids
    • Colloids
    • Opioids
28
Q

Indications

A

Analgesic

Antipyretic

Ameliorate the effects of endotoxins

Antiplatelets

Anti-inflammatory

29
Q

NSAID Efficacy

A
  • Is very good for mild to moderate pain
  • No NSAID has demonstrated a consistent increased efficacy compared to another NSAID
  • However an individual patient may respond better to a specific NSAID
  • Chronic and neuropathic pain may less responsive to NSAIDs
30
Q

Client Instructions: Dog

A
  • Recheck if:
    • Vomiting / diarrhea/ anorexia
    • Lethargy / depression
    • Yellow eyes / gums
31
Q

Client Instructions: Horses

A
  • Rechecke if:
    • poor performance
    • colic
    • diarrhea
    • decreased appetite
    • Weight loss
    • Bruxism (Teeth grinding)
32
Q

Concurrent Drug Use:
Adverse Effects

A
  • Corticosteriods (GIT)
  • Amphotericin (Renal)
  • Cisplatin (Renal)
  • Aminoglycosides (Renal)
  • Diuretics (Furosemide, Renal)
  • Serotonin Reuptake Inhibitors (GI, Bleeding)
33
Q

Concurrent Drug Use:

Decreased Efficacy

A
  • ACE inhibitors (Enalapril)
  • Diurectics (Furosemide)

Pharmacology - VAP844 (14 decks)

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