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Pharm Test 1 > antiinflamm 1 > Flashcards

antiinflamm 1 Flashcards

1
Q

non-pharmalogical therapeutic options for inflammation

A

Non-Pharmacological
* Rest
* Heat / Cold
* Weight reduction
* Surgery

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2
Q

pharmalogical therapeutic options for inflammation

A
  1. Non-steroidal anti-inflammatory drugs (NSAIDs)
  2. Glucocorticoids
  3. misc others
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3
Q

what is the mechanism of action of aspirin?

A

inhibition of prostaglandin synthesis

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4
Q

main benefits of NSAIDs

A

NSAIDs are a family of chemically dissimilar drugs that produce three main benefits:
* Anti-inflammatory effects
* Antipyretic effects
* Analgesic effects

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5
Q

prostoglandins are in this categoy

A

eicosanoids

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6
Q

normal physiological roles of Eicosanoids (mainly prostaglandins)

A

Prostaglandins (PGs) are required for normal homeostasis in all tissues

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7
Q

how are prostoglandins synthesized? What enzymes help with this?

A

They are synthesized from arachidonic acid by cyclo- oxygenase (COX) enzymes
There are two main COX enzymes, COX1 & COX2

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8
Q

what is COX1? what does it do?

A

COX1 is a normal housekeeping enzyme present at low levels in most tissues
-helps synthesize prostoglandins which help maintain tissue blood flow
-helps synthesize thromboxane in platelets > promotion of platelet aggregation
-helps synthsize prostacyclin > inhibition of platelet aggregation, vasodilation

-PGE2 and PGI2 also involved in gastric mucosa protection

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9
Q

what does thromboxane do and how is it made?

A

Synthesized by COX1 in platelets
Promotion of platelet aggregation

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10
Q

what does prostacyclin do and what enzymes are important for making it?

A

Inhibition of platelet aggregation
Vasodilation
Other protective functions
-COX1 and 2

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11
Q

why is COX2 important? how do levels compare to COX1, generally?

A

COX2 is normally present at much lower levels than COX1 in most tissues, but is important for homeostasis in a few tissues (e.g., renal medulla, gastric mucosa)
Involved in healing of gastric ulcers

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12
Q

roles of eicosanoids (mainly prostaglandins) in inflammation? what is the importance of the COX enzymes?

A

-COX2 is up-regulated in response to plasma membrane damage or inflammatory mediator release
-COX2 induction is a local response that occurs at the site of cell damage or mediator release
> marked vasodilation occurs, promoting inflammation:
* Redness
* Swelling
* Heat
* Pain
* Loss of function

> COX2 stimulates production of various PGs and prostacyclin
Increased blood flow at site of injury or mediator release

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13
Q

Mechanism of action of NSAIDs and general effects

A

NSAIDs inhibit ( -) cyclooxygenase enzymes
Most NSAIDs inhibit both COX1 & COX2
 Reduces synthesis of PGs, including those that promote vasodilation
 Reduces blood flow to site
 Reduces sensitization of nociceptors
 Alleviates inflammation

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14
Q

mechanism of adverse effects of NSAIDs in gastric mucosa

A

The normal protective effects of PGs in the stomach are inhibited, resulting in:
* Decreased blood flow, bicarb secretion, & mucus secretion
* Increased acid secretion
> gastric bleeding +/- ulceration (the most common adverse effect associated with NSAIDs)

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15
Q

what are the important gastric effects of PGE2 & PGI2?

A

↓ acid secretion by gastric parietal cells, ↑ bicarb & mucus secretion, ↑ vasodilation

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16
Q

Mechanism of adverse effects of NSAIDs on platelets

A

Only COX1 is present in platelets
NSAIDs inhibit the conversion of AA to thromboxane in platelets
> result is a slightly increased general tendency to bleed

17
Q

Mechanism of adverse effects of NSAIDs on the kidney

A

COX enzymes produce PGs that maintain adequate blood flow to many tissues, including the renal medulla
-Excessive COX inhibition can lead to
renal medullary hypoxia & papillary necrosis

18
Q

what are coxibs? what is a problem that can get worse with coxid administration and why?

What are advantages and disadvantages to this type of drug, and when do we want to use it?

A

Some drugs are highly selective for COX2 (called ‘coxibs’), but pre-existing gastric epithelium lesions can become exacerbated by coxib administration, since products of COX2 are involved in healing of ulcers
The take-home message is that NSAIDs that selectively target COX2 produce fewer adverse GI events as long as GI lesions are not present initially
Coxibs also cause less bleeding, since platelet aggregation is not inhibited

19
Q

shared pharmacokinetic properties of NSAIDs

A
  • Weak acids
  • Highly protein bound
  • Hepatic metabolism (Phase 2 conjugation)
  • Variable elimination
20
Q

shared adverse effects of NSAIDs

A
  • GI ulceration*
  • Inhibition of platelet aggregation > bleeding*
  • Inhibition of uterine motility
  • Inhibition of PG-mediated renal perfusion
  • Renal papillary necrosis in dehydrated animals (a problem with many NSAIDs)
21
Q

Shared contraindications for NSAIDs

A

“As with all non-steroidal anti-inflammatory drugs (NSAIDs), administration of this drug is advised against in the following circumstances:
* Animals with gastro-intestinal ulcers, renal disease, hepatic disorders, hypoproteinemia, dehydration, or cardiac disease;
* A known hypersensitivity to the drug;
* Concurrent use of other NSAIDs or corticosteroids.”

22
Q

shared clinical uses of NSAIDs

A

For the relief of musculoskeletal & inflammatory pain, including post-operative pain

23
Q

what does aspirin do? what specied is it approved for? what is tis mechanism and what are its effects?

A

Aspirin (acetylsalicylic acid; ASA) The only NSAID that blocks COX enzymes irreversibly

Approved for use in cattle & horses

In vitro it is a non-selective inhibitor of COX 1 & 2, but in vivo it acts mainly to inhibit COX 1

Anti-inflammatory, antipyretic, analgesic
* Effective for musculoskeletal / cutaneous pain, but poor for visceral pain
* T1⁄2: horse and cow ~1 h, pig 6 h (much longer in dogs [10 h] and cats [38 h]), but irreversible binding to COX enzymes produces prolonged effects in many species, even with low doses
* Narrow therapeutic margin
* Metabolized to salicylic acid (active form)
* Only available in oral formulations

24
Q

adverse effects and contraindications of aspirin

A

Adverse effects:
* *Bleeding; inhibits platelet function
-bovine platelets not affected
* Dose-dependent *gastric ulceration (subclinical at low doses)

  • Renal damage in dehydrated animals
  • Avoid in cats (deficient in glucuronide conjugation)

Contraindications:
* Cats (though it has been used)
* Animals with bleeding disorders
* Animals prone to GI ulcers
(e.g., those receiving glucocorticoids)

25
Q

what is phenylbutazone? what is it used for and what is its mechanism?

A

The most popular NSAID for horses
Non-selective inhibitor of COX 1 & 2
Anti-inflammatory, antipyretic, analgesic
* For musculoskeletal & inflammatory pain

  • Duration of action in horses: 24 h
  • Narrow therapeutic margin
  • Oral and IV formulations
26
Q

adverse effects of phenylbutazone and contraindications

A

Adverse effects:
* *GI ulceration common; more likely
with high dosages or prolonged use

  • Renal papillary necrosis in dehydrated animals
  • IM injection causes tissue necrosis

Contraindications:
* Animals with bleeding disorders
* Animals prone to GI ulcers
(e.g., those receiving glucocorticoids)

27
Q

what is carprofen? what is it used for and what is the mechanism? what isa. possible ADR?

A

Approved for use in dogs
-Somewhat selective for COX 2, therefore fewer GI adverse effects compared to other NSAIDs (incl. meloxicam)
-Anti-inflammatory, antipyretic, analgesic
* May be a centrally mediated mechanism responsible
for its marked analgesic effects
* Narrow therapeutic margin
* Rare but serious Type B ADR: idiosyncratic acute hepatotoxicity in <1 in 2,000 dogs; can be fatal
> monitor hepatic function before & during therapy

Used mainly to manage musculoskeletal pain associated with arthritis, trauma, & surgery

GI ulcers & perforation are uncommon
Vomiting, anorexia, and diarrhea are the most common adverse effects
Avoid in cats

28
Q

what is ketoprofen? What is its mechanism of action and what does it do?

A

Approved for use in most species
Inhibits COX enzymes non-selectively, and to some extent LOX enzymes > inhibits leukotriene & bradykinin production in addition to inhibiting PG synthesis

Anti-inflammatory, antipyretic, analgesic

29
Q

what is flunixin? what is it used for and what does it do? possible issue?

A

Approved for use in horses & cattle
-Inhibits COX enzymes non-selectively, also inhibits some leukocyte functions
-Anti-inflammatory, antipyretic, analgesic
- High dosages or prolonged use cause GI ulceration

30
Q

what is meloxicam? what is it used for? what is the mechanism?

A

Anti-inflammatory, analgesic, antipyretic
* For alleviation of musculoskeletal pain
(e.g., osteoarthritis, surgical pain) & inflammation in dogs, cats, pigs, & cattle
* Inhibits both COX1 & COX2 (COX2 more so)
-relatively safe!

31
Q

deracoxib approved for what? what does it have little effect on?

A

Approved for dogs only
-Approved for osteoarthritis, post-op pain
-Little effect on platelets/bleeding because platelet COX1 not inhibited significantly

32
Q

most common adverse effect with non-selective NSAIDs - how can we alleviate?

A

The most common adverse effect with non-selective NSAIDs is GI ulceration & bleeding, which is greatly reduced with coxibs if the patient has no pre-existing gastric lesions (COX2 PGs are involved in healing of GI lesions)

33
Q

what type of drug is firocoxib? whats its use? contraindications?

A

Firocoxib (Previcox®)
“Indications: …for the control of pain and inflammation associated with osteoarthritis and for the control of post-operative pain and inflammation associated with soft-tissue and orthopedic surgery in dogs”

Do not administer Previcox® or any NSAID if gastro-intestinal ulceration or bleeding is suspected. Do not administer concurrently with corticosteroids or other non-steroidal anti-inflammatory drugs. Do not administer to dehydrated animals.

34
Q

what type of drug is firocoxib? whats its use? contraindications?

A

“…indicated for the relief of pain and inflammation associated with osteoarthritis in dogs”
“…for the relief of acute pain and inflammation associated with cat bites and scratches with and without abscesses and musculoskeletal injuries such as sprains and strains in cats
“…in the control of postoperative pain and inflammation associated with onychectomy, ovariohysterectomy and castration in cats”
“Contra-indications: …cats with gastrointestinal ulcers; …cats that are dehydrated, …cats with impaired cardiac, renal or hepatic function, or coagulation abnormalities; …concurrent use of other NSAIDs or corticosteroids;”

35
Q

coxib risk in humans and why? animals too?

A

In humans, long-term coxib use is associated with increased MI risk
Coxibs block only COX2, and therefore inhibit PGI2 synthesis while leaving TXA2 synthesis intact
This tips the balance in favour of aggregation > overall increased risk of intravascular coagulation and therefore stroke & myocardial infarction
This is a concern with chronic use

> > This problem is best-documented in humans; not known whether coxibs increase risk of MI or stroke in veterinary species

36
Q

what is the mechanism of action of acetaminophen? what does it do and what should it be used for?

A

Inhibits PG synthesis centrally (in CNS) > antipyretic, analgesic

Little peripheral activity so poor anti-inflammatory effect & no effect on blood clotting

> not considered an NSAID

> Think of it as a veterinary toxicant

Pharm Test 1 (15 decks)

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