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Clinical Anesthesia > NSAIDS > Flashcards

NSAIDS Flashcards

1
Q

Describe the benefits of using an NSAID for peri-operative analgesia

A
  • Decrease peripheral inflammation
  • Anti-pyretic
  • Anti-coagulant
  • Anti-endotoxemic
  • Anti-neoplastic
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2
Q

Describe the process of tissue injury

A

Results from their effects when a cell’s phospholipid membrane is damaged (tissue injury

  • Phospholipase forms arachidonic acid from exposed lipids at the injury site, which interacts with cyclooxygenase (COX) and lipoxygenase (LOX) to form a variety of eicosanoids, leukotrienes, and prostaglandins
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3
Q

What are the roles of prostacyclins, prostaglandins, and leukotrienes?

A
  • Prostacyclins: homeostatic functions as well as being a vital component of the inflamm process that can incite pain
  • Leukotrienes: recruit inflammatory cells
  • Prostaglandins (PGE2 and PGI2): enhance nociception by sensitizing peripheral nociceptive terminals to other inflamm mediators; also involved in spinal nociception and central hyperalgesia
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4
Q

NSAIDs work on what part of the tissue inflammatory process?

A

They decrease the activity of the COX enzymes, resulting in a decrease in prostaglandins (PG), prostacyclin (PGI2), and thromboxane (TXA2) production

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5
Q

Describe COX-1

A
  • Constitutive enzyme
  • produces PGs and TXA2 that are imperative for normal homeostatic functions
    • ​PGE2 and PGI2: regulate blood flow to GI tract and kidneys and regulate renal water and electrolyte balance; also maintain GI mucosal integrity/secretions
    • TXA2: platelet aggregation and normal platelet function
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6
Q

Describe COX-2

A
  • Inducible enzyme (except in brain and kidneys - constitutive)
  • Plays important role in healing gastric ulcers and regulating renal blood flow during conditions of reduced blood flow
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7
Q

Why are COX-2-selective NSAIDs no longer the best choice for reducing inflammation without major side effects?

A

Because it was discovered that both are constantly expressed in different tissues and each enzyme is important for different homeostatic functions

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8
Q

Which NSAIDs are considered to have the highest inhibitory ratio (ie. More COX2 selective)?

A

The -coxib class of NSAIDS (e.g. firocoxib, deracoxib, robenacoxib)

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9
Q

Carprofen and meloxicam are considered what type of NSAIDs?

A

COX-2 preferential (lesser inhitibitory ratio than the coxibs)

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10
Q

T or F: No matter how selective an NSAID is for COX-2, none of the currently marketed NSAIDs has a complete absence of COX-1 suppression

A

True

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11
Q

Describe some of the pharmacokinetic properties of NSAIDs

A
  • Weak acids - allows decent absorption w/ oral ingestion
    • ​feeding may increase/inhibit/delay absorption of NSAIDs (ie. Robenacoxib)
  • Highly protein bound and lipid soluble
  • Extensive hepatic metabolism and urine excretion
    • exception: some NSAIDs undergo extensive entero-hepatic recirculation (toxicity risk)
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12
Q

Why might the plasma concentration of an NSAID be low or non-existent even though the NSAID is still exhibiting its COX-inhibiting analgesic effect?

A

Because NSAIDs tend to concentrate in inflamed tissues where they exert their action while also extensively binding to plasma proteins, decreasing the amount of free drug available in plasma

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13
Q

Describe the GI effects of NSAIDs

A
  • Most frequently cited reason to d/c NSAIDs
  • range from mild gastritis, anorexia, V/D, to gastric ulceration and bleeding (rare)
  • increased risk: concurrent steroid admin, _>_2 NSAIDs at one time, concurrent GI dz
  • COX-1 AND COX-2 selective can be devastating to GI tract
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14
Q

What is an example of a drug that can be used to treat GI injury from NSAID use?

A

Misoprostol - it’s a prostaglandin E analog that directly inhibits gastric acid secretion from parietal cells while providing similar protective effects of PGs on the lining of the GI tract

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15
Q

Describe the effects of NSAIDs on the kidneys

A
  • Kidneys depend on COX 1 and 2 for PG synthesis
  • NSAIDs are NOT inherently nephrotoxic—> renal injury occurs as a result of inhibiting renal PG synthesis
  • risk factors: pre-existing renal dz, dehydration, hypovolemia, shock, co-admin of steroids, general anesthesia
  • C/S: azotemia, decr urine production, salt retention, peripheral edema
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16
Q

T or F: NSAIDs can never be used in cats with CKD

A
  • FALSE; studies show that low dose meloxicam is safe to use in euvolemic cats with stable CKD
17
Q

Describe the effects of NSAIDs on the liver

A
  • Liver toxicity can be either intrinsic or idiosyncratic
    • ​typically reversible
  • the liver is primarily responsible for metabolizing most NSAIDs
  • there is NO evidence that prescribing NSAIDs to a dog with pre-existing liver dz increases the chances of developing hepatic injury
  • should recheck liver enzymes 7-90d following initiation of NSAID therapy
18
Q

Describe the effects of NSAIDs on coagulation

A
  • COX-1 inhibition will halt synthesis of thromboxane, thereby decreasing platelet function
  • Non-selective NSAIDs (aspirin or ketoprofen) may increase the chance of perioperative bleeding, however, studies have shown it is safe to use ketoprofen in healthy dogs (no change in BMBT)
  • Coxib type NSAIDs do not affect platelet function
19
Q

Why are cats much more susceptible to acetaminophen toxicity?

A

Because they lack the ability of hepatic glucuronidation to break it down, so it’s converted to sulfanation, which breaks acetaminophen down into toxic compounds, resulting in hepatic necrosis, Heinz body anemia, methemoglobinemia, and facial edema EVEN at clinically relevant doses

20
Q

NSAID use should be reserved for use in what kind of patients?

A

Those that are euvolemic and hydrated with no evidence of gastric or renal disease, are not on steroids, do not have platelet disorders, and are older than 6 weeks old (decr hepatic metabolism capabilities and PGs are important for organ maturation)

21
Q

What is the generally accepted washout period between switching NSAIDs?

A

7 days

22
Q

Describe acetaminophen

A
  • It is a COX-3 inhibitor
  • NOT FDA approved in animals
  • MOA is centralized in the brain and does NOT cause peripheral inhibition of PGs
    • thus may be an optimal choice in dogs w/ GI ulceration or CKD
  • oral form has limited bioavailability in dogs
23
Q

Describe Grapiprant (Galliprant)

A
  • Approved for treating OA in dogs
  • EP4 receptor inhibitor - PG receptor expressed in dog joints
  • very wide margin of safety - no effects up to 15x labeled dose!
  • Primary SE: mild GI upset
24
Q

What is the MOA of corticosteroids as anti-inlammatories?

A
  • Inhibit phospholipase A2, which prevents membrane phospholipids from entering the arachidonic acid cascade

Clinical Anesthesia (15 decks)

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