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VETM 443 Pharmacology > NSAID/Cannabis Pharmacology > Flashcards

NSAID/Cannabis Pharmacology Flashcards

(60 cards)

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1
Q

How are inflammatory mediators created

A
  1. cell lipid bilayer through phospholipase to arachidonic acid

Lipoxygenase will metabolize arachidonic acid to leukotrienes/lipoxin
- increased vascular permeability
- leukocyte adhesion, activation, chemotaxis

COX1 and 2 will metabolize arachidonic acid to prostanoids
- prostaglandin: PG D2 and E2 = vasodilation, fever, pain
- prostacyclin = vasodilation, reduced clotting
- thromboxane = vasodilation, increased clotting

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2
Q

What levels does steroids and NSAIDs act on in the inflammatory mediator production cycle

A

steroids inhibit phospholipase
- which normally converts cell lipid bilayer to arachidonic acids

NSAIDs inhibit COX1 and/or COX2

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3
Q

Compare the functions of COX1 and 2

A

COX 1
- homeostatic functions, meaning it is constitutively active
- makes thromboxane and prostaglandins

COX2
- active during inflammation from macrophages and inflammatory cells
- prostaglandin and prostacyclin

both can impact each other

NSAIDs are typically non-specific

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4
Q

Compare the effects of COX
1 and 2 on gastric mucosa, kidney, platelet, vascular endothelium

A

gastric mucosa
- cox 1 = increase mucus and perfusion
- cox 2 = post damage ulcer healing function

kidneys - both types act to maintain perfusion

platelet
- cox 1 = increase thromboxane and increase clotting
- cox 2 = increase prostacyclin which reduces clotting

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5
Q

What are 3 main characteristics of prostanoids and how does COX receptors influence?

A

local effect via paracrine or autocrine signalling

short half life

their effect depends on the type of prostanoid, receptor, location

COX1 - typically associated with prostanoids associated with
- GI mucosal integrity
- platelet function
- vascular function
- homeostasis

COX2 - typically associated with prostanoids
- fever
- pain
- inflamm

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6
Q

What are 6 applications for NSAID use

A

anti-inflammation

anti-pyretic

septic shock

antithrombotic

anti-cancer

analgesic

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7
Q

How do NSAIDS cause anti-inflammatory effect

A

prostaglandins cause positive feedback due to vasodilation and an increase in inflammatory cytokines

NSAID will act to reduce prostaglandin synthesis

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8
Q

How do NSAIDS cause the analgesic effect

A

peripherally it will remove prostaglandins that will sensitize nociceptors

centrally it will affect COX 1 and 2 in the spinal cord
- normally when COX2 is upregulated it releases PG E2 resulting in a reduced depolarization threshold = wind up/ hyperalgesia/sensitization

NSAIDS can act synergistically with opioids

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9
Q

How do NSAIDS have an anti-pyretic effect

A

increased PG E2 results in a hypothalamus set point change

Reduced PGE2 will lower/normalize that set point

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10
Q

What is septic shock? What are the phases?

A

bacterial/LPS/endotoxin causes active inflammation
- mediators cause immunosuppression/vasodilation/increased vascular permeability/reduced perfusion/fever/reduced inotropy/metabolic disorder/thrombosis

all can cause hypotension and multiorgan failure

  1. non-progressive shock - perfusion is maintained to vital organs
  2. progressive shock - poor perfusion/metabolite abnormalities/lactic acidosis
  3. irreversible
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11
Q

How does NSAID impact septic shock?

A

NSAIDs don’t bind the endotoxin but may improve septic shock
- may not be worth the reduced perfusion NSAIDs can cause

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12
Q

What is commonly used to treat septic shock in cows

A

flunixin

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13
Q

What is the anti-thrombotic mechanism of NSAIDS

A

COX2 selective and non-selective NSAIDs can have an impact on COX1 receptors

COX 1 receptors increase thromboxane = increased platelet aggregation/activation

aspirin selectively and irreversibly inhibit COX1

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14
Q

What is the mechanism of action of anti-cancer use of NSAID

A

Tumors can sometimes upregulate COX2
- usually TCC/SCC/melanoma

NSAID restores apoptosis and reduced angiogenesis

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15
Q

Which NSAID are commonly used to treat TCC in dogs

A

firocoxib

meloxicam

deracoxib

they are COX2 selective

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16
Q

Which NSAID are commonly used to treat SCC in horses

A

piroxicam

non-selective

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17
Q

What are the pharmacokinetic features of NSAIDS

A

they are highly protein bound
- varied volume of distribution, consider drug interactions

good PO absorption - lipophilic weak acids

liver metabolism

varied half life
- species and individual variation
ex. aspirin in cows = 32min/cat = 22-45h

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18
Q

List the adverse effects associated with NSAID administration? There are 2 main ones

A

mainly
- GI irritation/ulcers
- renotoxicity

hepatotoxicity
hemorrhage
blood dyscrasia/clotting inhibition
delay parturition
delay soft tissue healing
delayed fracture healing
specific drug warnings
- deracoxib (narrow therapeutic index)
- firocoxib (not for young)

no adverse cardiovascular effects

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19
Q

How does the mechanism of action of GI irritation/ulceration of NSAIDS

A

COX1 = GI protection

COX2 = ulcer healing

ulceration due to NSAIDs are acidic

NSAIDs also undergo enterohepatic recycling causing increased exposure in the duodenum

high plasma half life so if you are switching NSAIDs give 5-7d, if not = increase irritation

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20
Q

What are the clinical signs associated with GI ulcers in dogs and horses

A

dog
- vomiting
- melena
- reduced aappeetite

horses
- diarrhea
- colic
- reduced appetite

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21
Q

What is the mechanism of action of NSAIDS on renotoxicity

A

it is not a problem if the patient is healthy/hydrated

causes renal papillary crest necrosis and acute renal failure due to decreased PGE2

higher risk if used
- during anesthesia
- hypovolemia
- dehydrated

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22
Q

In what animals are NSAIDS contraindicated in? Why?

A

COX2 is needed for renal development

not for neonate or pregnant

shouldn’t use post-GI anastomosis sx

avoid in foals
- if you have to then use COX2 selective

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23
Q

How is COX1 vs COX 2 selectivity assessed

A

COX 1 / COX 2 ratio

drug concentration needed to inhibit 50% of COX1 / drug concentration needed to inhibit 50% COX2

higher ratio = more COX2 specific

there is lots of species variation

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24
Q

What is the mechanism of action of the clotting inhibition of NSAIDs

A

it can inhibit thromboxane which reduces clotting

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25
What is the mechanism of action of the delayed soft tissue healing and fracture healing of NSAIDs
reducing inflammation can reduce healing COX2 has role in healing shouldn't use post-GI anastomosis sx - require fast healing
26
What NSAIDs are commonly used in dogs
carprofen deracoxib firocoxib meloxicam robenacoxib
27
What NSAIDs are commonly used in cats
meloxicam robenacoxib no on-label use labelled
28
What NSAIDs are commonly used in horses
flunixin meglumine - main firocoxib phenylbutazone
29
What NSAIDs are commonly used in cow
ketoprofen - main flunixin meloxicam aspirin
30
What 4 factors should you consider when giving NSAIDS
anti-inflam effects are more effective when given early age hydration species (cats are more susceptible)
31
Scenario: soft tissue sx in dogs and cats what NSAIDs should you give
dog - carprofen (works in 1h if SC) or meloxicam (if IV - immediate, SC = 2-6h) given pre-op cat - robenacoxib or meloxicam pre-op
32
Scenario: orthopedic sx in a dog or cat what NSAIDs should you give
dog - carprofen post op cat - robenacoxib or meloxicam + additional analgesics
33
Scenario: osteoarthritis/MSK pain in a dog or cat what NSAIDs should you give
dog - firocoxib (most effective) - meloxicam - carprofen cat - meloxicam - reduce dose if using long term - robenacoxib increases in adverse effects if used long term
34
Scenario: osteoarthritis/MSK pain in horses what NSAIDs should you give
phenylbutazone for MSK pain + flunixin for visceral pain = short term firocoxib = long term tx
35
Scenario: laminitis pain in horses what NSAIDs should you give
if endotoxic - aspirin may increase perfusion to foot acute - non-selective can prevent neuropathic pain chronic - transition from non-selective to COX2 selective
36
Scenario: GI pain/sx in horses what NSAIDs should you give
flunixin
37
In what animals is phenylbutazone not allowed
food animals if cows have coliform mastitis/lameness/dehorning/castration use meloxicam or flunixin meloxicam half life IV/PO - 17-26h flunixin half life IV = 4-7h
38
What is the mechanism of action of grapiprant?
PGE2 EP4 receptor antagonist
39
What is grapiprant commonly used for?
OA pain
40
What other considerations should you think about when giving grapiprant
not for pyrexia treatment - EP4 receptors not involved with pyrexia dont use with other NSAIDs there is no evidence in pregnant or lactating or animals under 9mo
41
How should you switch NSAIDs
give 1 week washout - may need an alternate tx in that time 10 half lives for drug clearance do not give 2 at same time - because highly protein bound = competitive for protein results in increased active drug in system (displace from protein) do not give with steroid
42
What is the mechanism of action of aspirin? What is the use for it?
acetylsalicylic acid irreversible COX 1 and 2 inhibitor with varied half life increased hemorrhage risk cat with FATE/HCM heartworm tx dog
43
What is ibuprofen used for
nothing GI/renotoxic
44
What is acetaminophen? What is its mechanism? How is its used?
not technically an NSAID central COX inhibitor - reduced pain/fever but not anti-inflam dogs - ok cats - toxic glucuronidation
45
What animals are naproxen used in? What animals is it not used in?
horse sometimes - but rare not dogs - highly enterohepatic recirculation = more adverse
46
What is piroxicam used for?
anticancer - TCC dog - SCC horse lots of adverse effects
47
What is gabapentin? What is its mechanism?
not an NSAID similar structure to GABA but doesn't act on a GABA receptor binds Ca channels and inhibit neurotransmitter release - antiepileptic
48
What is gabapentin used for mainly
pain treatment with an opioid - pre or post op chronic pain reduced FAS (cats esp.) limited evidence of analgesic effect
49
What receptors do cannabinoids act on
cannabinoid receptor 1 or 2 in CNS there are endogenous cannabinoids that act on them - anandamide - 2- archidonylglycerol
50
What are the 3 main cannabinoids
tetrahydrocannabinol THC cannabidiol cannabinol
51
What is the mechanism of action of THC
It is the main psychotropic element interact with endocannabinoid receptors - mainly CB1 in brain - also CB2 in immune cells (some brain) modulate dopamine signalling - excitation and inhibition
52
What are the proposed uses for THC
anti - epileptic - anxiety - emetic - diarrheal - neoplasia anorexia tx metabolism disorder tx bronchodilator reduce intraocular pressure for glaucoma
53
What are the pharmacokinetics of THC in humans
It has reduced bioavailability - it is water insoluble - inhale = 10-30% absorb - PO = 5-20% absorb lipophilic = can enter and stay in brain/fat - if eaten with lots of fat = slower release (increase AUC) metabolized by CYP450 and hepatic recirculation excretion in feces and urine half life can vary depending on frequency of use
54
What are the pharmacokinetics of THC in dogs
similar to humans but 1000x more CB1 and 2 receptors cause toxicity - high morbidity - low mortality
55
What is the mechanism of action of cannabidiol
It is the main non-psychotropic component It has reduced CB1 receptor affinity weak inverse agonist for CB2 weak CB1 and 2 agonism through anandamide metabolism and increased endogenous cannabanoid (like 2 archidonyl glycerol) there are many drug targets
56
What are the pharmacokinetics of cannabidiol
It is poorly bioavailable a half life of 5-13h cytochrome P450 metabolism it is very lipophilic few adverse effects associated - long term administration may be associated with ALP with no other liver signs
57
What are the proposed uses for cannabidiol
antiepileptic antianxiety analgesia anti-neoplasia
58
What is the mechanism for analgesia from cannabidiol
increased endogenous cannabanoid desensitize TRPV1 and TRPA1 channel activate serotonin receptor inhibit adenosine transporter - adenosine increased and reduced inflammation reduced cytokine signalling glycine receptor signalling
59
What are veterinarians in Canada allowed to do about cannabis
they can't prescribe provide education for clients (can advise) - ensure they know the risks Can manage cases and management if the owner has gotten iit on their own There are no animal product
60
What things must you consider if advising an owner giving cannabis
practice within the scope of clinical competence weight evidence with other options consider known risks obtain informed consent monitor and be available to treat adverse events aware of misuse and abuse of product

VETM 443 Pharmacology (23 decks)

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