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RUSVM Pharmacology I > NSAIDS (Non-Steroidal Anti-Inflammatory Drugs) > Flashcards

NSAIDS (Non-Steroidal Anti-Inflammatory Drugs) Flashcards

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1
Q

NSAIDS - definition

A

Non-steroidal drugs that prevent inflammation by **inhibiting COX enzymes**

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2
Q

NSAIDS- Mechanism of action

A

*picture* Inhibit prostaglandin synthesis

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3
Q

NSAIDS - Chemical classification - 2 groups

A

Carboxylic acids & Enolic acids

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4
Q

NSAIDS - name the carboxylic acids

A

Salicylates - Indoleacetic acids - Propionic acids - Antranillic acids

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5
Q

Salicylate NSAID

A

Acetylsalicylic acid

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6
Q

Endoleacetic acid NSAID

A

Etodolac

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7
Q

Propionic acid NSAIDS

A

Carprofen & Ketoprofen

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8
Q

Antranillic acid NSAIDS

A

Flunixin & tolfenami acid

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9
Q

NSAIDS - Enolic acids

A

Oxicams & Pyrazolones

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10
Q

Oxicam NSAID

A

Meloxicam

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11
Q

Pyrazolone NSAIDS

A

Phenylbutazone & dipyrone

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12
Q

NSAID classification by COX inhibition

A

COX-1 selective - Nonspecific COX - COX-2 preferential - COX-2 selective

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13
Q

COX-1 selective inhibitors

A

Acetylsalicylic acid

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14
Q

Nonspecific COX inhibitors

A

Flunixin, ketoprofen, phenylbutazone (PBZ)

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15
Q

COX-2 perferential inhibitors

A

Deracoxib, carprofen, meloxicam

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16
Q

COX-2 selective inhibitors

A

Firocoxib, robenacoxib

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17
Q

NSAIDS Absorption

A

PO or IM good

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18
Q

Which NSAIDS bind to feed?

A

PBZ, flunixin, meclofenamic acid

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19
Q

NSAIDS Distribution

A

Affected by inflammation - 95-99% plasma protein bound - Penetrate CNS but not into milk

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20
Q

NSAIDS Discuss distribution/movement in blood stream

A

Low volumes of distribution (0.1-0.3 L/kg) - Plasma protein extravasation - Drug displacement

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21
Q

NSAID Metabolism

A

Interspecies, interbreed, with-in breed differences - Phase I & II liver enzyme systems - Active metabolites

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22
Q

NSAIDS Beagle metabolism oddness

A

Beagle dogs expressing CYP2D15 metabolize celecoxib 3x faster than those not expressing it

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23
Q

NSAID Active metabolites

A

Acetylsalicylic acid–> salicylic acid // Phenylbutazone–>oxyphenbutazone

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24
Q

NSAID Elimination

A

Mainly urine (drug & metabolites) - Biliary excretion (enterohepatic recirculation -naproxen)

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25
NSAID Elimination - extra note
Due to differences in metabolism and elimination, terminal half-lives vary greatly between species, breeds, individuals
26
NSAIDS chart on pharmacokinetics
Do not extrapolate dose rates & intervals from one species to another
27
NSAID - Therapeutic effects
Anti-inflammatory - Analgesic - Antipyretic (anti-fever) - Antithrombotic (anti-clots) - Antiendotoxic (? LPS, maybe)
28
NSAID Anti-inflammatory effects
Acute vs. chronic inflammation - Not as potent as corticosteroids, but DON'T delay epidermal wound healing
29
What anti-inflammatory effect do NSAIDS have on eicosanoids
Eicosanoid synthesis inhibition
30
Eicosanoids
Thromboxane, prostacycline, PGs
31
NSAIDS analgesic effect
PG synthesis inhibition in absense & presence of inflammation - Peripheral & central sites of action
32
NSAIDS vs. steroids
-Steroids delay epidermal wound healing, NSAIDS don;t - Steroids inhibit PG synthesis but not direct analgesics like NSAIDS
33
NSAID peripheral site of action
PGs sensitize neurons to bradykinin pain-producing effects. This is blocked
34
NSAID Central site of action
PG's induce pain @ spinal cord level, descending mechanisms (opioidergic, adrenergic). NSAIDS block this
35
NSAIDS antipyretic effect
Reduce fever (not hyperthermia or normal body temp)
36
What is the mechanism/sequence of NSAID antipyretic effect?
Endotoxin --\> IL1 --\> hypothalmic epithelium --\> PGE2 --\> EP3 receptors --\> Temp set-point increased --\> Fever
37
NSAID Antithrombotic effect
Inhibition of TXA2 production in platelets
38
Mechanism of NSAID antithrombotic effect
Preferential, irreversible inhibition of COX in platelets (TXA2--\> aggregating agent) over that of endothelial cells (PGI2--\> anti-aggregating agent) Increase in blood clotting time (slowed)
39
NSAID Antiendotoxic effect
Endotoxins produce some effects through PG production (not good evidence to support NSAID use for this, maybe if given prophylactically)
40
NSAIDS clinical uses
Osteoarthritis - Soft tissue inflammation - Analgesia - Antithrombosis - Endotoxemic syndrome (?) - Cancer (?)
41
NSAID in osteoarthritis (DJD)
Reduce inflammation & pain - Chondroprotective vs. Chondrotoxic - Titrate dose to a minimum - Take as necessary not continuously - Tablets with food - use antiulcer drug!
42
NSAIDS - Chondroprotective vs. chondrotoxic
PGs are involved in chondrocyte-mediated degredation of cartilage matrix - High concentrations suppress cartilage matrix synthesis
43
NSAIDS - Situations for anti-inflammatory use
Inhibit acute response - Shipping fever - Calf pneumonia - Musculoskeletal conditions - Postoperative
44
Which NSAID drugs are used to treat inflammation?
Phenylbutazone - Flunixin - Ketoprofen - tolfenamic acid - carprofen - meloxicam
45
NSAID Analgesia treatments
Perioperatively - Preemptive analgesia - Trauma - Musculoskeletal conditions - Equine colic
46
Which NSAIDS are used perioperatively?
Deracoxib & Firecoxib
47
Which NSAIDS are used for preemptive analgesia
Carprofen & meloxicam (beware hypotension)
48
Which NSAIDS are used for musculoskeletal conditions?
Carprofen - Meloxicam - Phenylbutazone
49
Which NSAIDS are used for equine colic?
Flunixin, ketoprofen, carprofen, dipyrone
50
When would you use NSAIDS for antithrombosis?
Aortic thromboembolism - Heartworm Disease - Laminitis - Navicular disease - Disseminated intravascular coagulation
51
Which drug is best for antithrombosis?
Acetylsalicylic acid
52
Which endotoxemic syndromes would you use NSAID treatment?
E. coli mastitis - Equine colic - Colitis X syndrome - Metritis - Mastitis-metritis-agalactia syndrome - Septic peritonitis
53
Which NSAIDS would be used for endotoxemic syndromes?
Flunixin - Phenylbutazone - Carprofen - Keoprofen - Dipyrone - Meloxicam
54
When are NSAIDS used for cancer?
COX-2 up-regulation - Growth factors & angiogenesis - Bladder transitional cell carcinoma - Mammary adenocarcinoma - Transmissible venereal tumor
55
NSAIDS used in cancer treatment?
Piroxicam & coxibs
56
NSAID Adverse effects
GI irritation/ulcer - Kidney damage - Liver damage - Increased bleeding time - Methemoglobinemia - Agranulocytosis
57
NSAID - GI irritation/ulceration
Oral ulcers - Gastroduodenal - Right dorsal colitis - Abomasal
58
NSAID Kidney damage
Hypotension - Hypovolemia - Renal insufficiency - Urinary tract obstruction - Papillary necrosis
59
NSAID Liver damage - specific druge
Carprofen (USA vs UK) -Acetaminophen (Acetylcysteine, Silymarin, Vit C, Cimetidine)
60
Which NSAID causes increased bleeding time?
Acetylsalicylic acid
61
Which NSAID causes methemoglobinemia?
Acetaminophen
62
Which NSAID causes agranulocytosis
Phenylbutazone & dipyrone
63
NSAID drug interaction with glucocorticoids
Increased chance of GI irritation/ulceration
64
NSAID drug interaction with warfarin, anesthetics, other NSAIDS
Drug displacement from plasma proteins
65
NSAID drug interaction with furosemide
Decreased renal excretion and diuretic effect
66
NSAID drug interaction with digoxin
Decreased digoxin excretion (longer half life, effects of digoxin last longer)
67
NSAID drug interaction with ACE inhibitors, aminoglycosides, polymixin
Kidney damage & toxicity
68
NSAID contraindications
Glucocorticoid therapy - Anticoagulant therapy or poisoning - Severe renal disease - Severe hypotension
69
NSAID Precautions
Mild renal disease - Hepatic disease - Hypoproteinemia - Late pregnancy - Gastrointestinal ulceration - Dehydration
70
NSAID the future
Non-acidic drugs - COX-2 selective inhibitors - nitro-NSAIDS - PG receptor antagonists

RUSVM Pharmacology I (19 decks)

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