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SP1 Pharmacology > Lecture 26 4/30/24 > Flashcards

Lecture 26 4/30/24 Flashcards

1
Q

What are the characteristics of acute inflammatory pain?

A

-soft tissue trauma or inflammation
-adaptive role in facilitating tissue repair
-hyperalgesia of injured area and surrounding tissue

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2
Q

What are the characteristics of chronic inflammatory pain?

A

-duration greater than 3-6 months
-offers no useful function or survival advantage
-affects quality of life and function

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3
Q

What are the steps of inflammatory response to tissue injury?

A

-release of inflammatory mediators
-vasodilation of local blood vessels
-granulocyte and monocyte migration
-swelling of tissue

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4
Q

Which inflammatory mediators are involved in inflammatory pain?

A

-histamine
-prostaglandins
-leukotrienes
-complement proteins (C3a/C5a/C5b67)
-IL-1, IL-6, TNF-alpha
-bradykinin
-fibrin/fibrinopeptides

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5
Q

How do steroids function?

A

by blocking PLA2

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6
Q

How do firocoxib and carprofen function?

A

by blocking COX-2

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7
Q

How do aspirin, flunixin, phenylbutazone, and meloxicam function?

A

by blocking both COX-1 and COX-2

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8
Q

How does ketoprofen function?

A

by blocking COX-1, COX-2, and 5-Lox

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9
Q

Why it important to know whether a drug impact COX-1 versus COX-2?

A

-COX-2 must be targeted to eliminate pain
-blocking COX-1 can impact the protective effects of prostaglandins

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10
Q

Where in the body is constitutive/non-inducible COX-2 found?

A

-kidneys
-GI tract
-lung

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11
Q

What is COX-2 involved in besides pain sensation?

A

-gene expression
-neoplasia
-bone modeling

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12
Q

Which type of NSAID is safer on the GI tract?

A

COX-2 selective NSAIDs

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13
Q

What are the pharmacokinetics of NSAIDs?

A

-well absorbed orally
-irritating if given IM or SQ
-lipophilic and low VD
-very high plasma protein binding
-enhanced penetration in inflammatory exudate
-mostly eliminated by liver
-may have extensive enterohepatic recycling

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14
Q

How do NSAIDs interact with furosemide?

A

-NSAIDs suppress early preload reducing effect
-can increase kidney toxicity

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15
Q

How do NSAIDs interact with ACE inhibitors?

A

-NSAIDS suppress some of the vasodilating effect
-can increase kidney toxicity

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16
Q

How do NSAIDs interact with fluoroquinolones?

A

may decrease seizure threshold

17
Q

How do NSAIDs interact with aminoglycosides?

A

may increase renal toxicity

18
Q

How do NSAIDs interact with antacids?

A

antacids can interfere with NSAID oral absorption

19
Q

Why is it not recommended to mix steroids and NSAIDs?

A

leads to an additive effect for COX suppression based on PLA2 suppression upstream

20
Q

What are the adverse effects associated with NSAIDs?

A

-GI ulcers
-kidney toxicity

21
Q

What mediates the adverse effects seen with NSAIDs?

A

inhibition of protective prostaglandins

22
Q

Why are cats more sensitive to NSAID toxicity?

A

lack of glucuronidation pathway

23
Q

What are the characteristics of GI toxicity associated with NSAIDs?

A

-most common dose-limiting factor
-caused by protective prostaglandin suppression
-gastrointestinal adaptation typically occurs after a week of therapy
-must prevent toxicity in long-term use

24
Q

What are the characteristics of renal toxicity associated with NSAIDs?

A

-due to reduced renal blood flow
-leads to decrease in glomerular filtration
-major concern in perioperative period, during hypotensive and hypovolemic conditions, in animals with congestive heart failure, and in animals with chronic renal disease

25
Q

What are the characteristics of NSAID hematological and liver toxicity?

A

-can cause idiosyncratic hepatotoxicity
-should be avoided in animals with bleeding disorders
-should be avoided during surgery if hemorrhage is a potential concern

26
Q

Why are NSAIDs often used preoperatively?

A

to reduce nociceptive windup

27
Q

Which aspects of the nerve conduction pathway can NSAIDs impact?

A

-transduction
-modulation
-perception

28
Q

What are the therapeutic uses of NSAIDs?

A

-acute trauma/surgery
-colic pain in horses
-pain from cancer
-osteoarthritis pain
-antithrombotic action
-cancer treatment

29
Q

What are the general principles of NSAID use?

A

-use the lowest NSAID dose and frequency to achieve desired outcome
-watch for renal, hepatic, and coagulation disorders
-apply cytoprotective measures
-use preemptively when possible

30
Q

What are the characteristics of aspirin?

A

-unspecific COX inhibitor
-oral bioavailability
-causes local GI irritation
-metabolized by liver via glucoronide conjugation
-considerable species differences in reabsorption

31
Q

What are the uses of aspirin?

A

-analgesic
-anti-inflammatory
-antiplatelet

32
Q

What are the adverse effects associated with aspirin?

A

-GI irritation and ulcer formation
-decreased clotting
-cartilage damage in arthritic dogs possible

33
Q

How should NSAID adverse effects be managed?

A

-IV fluids
-gastroprotectant therapy
-monitoring of coagulation parameters
-use of washout period when switching NSAIDs

34
Q

Why are cats at greater risk for NSAID adverse effects?

A

-deficiencies in metabolism
-decline in renal function with age

35
Q

When using NSAIDs in cats, what must be considered?

A

-give with food when possible
-adjust dose to smallest amount possible
-short term use only

36
Q

Which NSAIDs are approved for short term use in cats?

A

-meloxicam
-robenicoxib

37
Q

Why can NSAIDs be dosed less frequently in camelids?

A

better oral absorption in camelids compared to other ruminants

38
Q

What are the characteristics of grapiprant?

A

-not technically an NSAID
-PGE2-receptor antagonist
-blocks EP4 receptor, which mediates sensation of sensory neurons
-adverse effects are similar to other NSAIDs, but likely less toxic

SP1 Pharmacology (27 decks)

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