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

NSAIDS (Non-Steroidal Anti-Inflammatory Drugs) Flashcards

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
Q

NSAID Elimination - extra note

A

Due to differences in metabolism and elimination, terminal half-lives vary greatly between species, breeds, individuals

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26
Q

NSAIDS chart on pharmacokinetics

A

Do not extrapolate dose rates & intervals from one species to another

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27
Q

NSAID - Therapeutic effects

A

Anti-inflammatory - Analgesic - Antipyretic (anti-fever) - Antithrombotic (anti-clots) - Antiendotoxic (? LPS, maybe)

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28
Q

NSAID Anti-inflammatory effects

A

Acute vs. chronic inflammation - Not as potent as corticosteroids, but DON’T delay epidermal wound healing

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29
Q

What anti-inflammatory effect do NSAIDS have on eicosanoids

A

Eicosanoid synthesis inhibition

30
Q

Eicosanoids

A

Thromboxane, prostacycline, PGs

31
Q

NSAIDS analgesic effect

A

PG synthesis inhibition in absense & presence of inflammation - Peripheral & central sites of action

32
Q

NSAIDS vs. steroids

A

-Steroids delay epidermal wound healing, NSAIDS don;t - Steroids inhibit PG synthesis but not direct analgesics like NSAIDS

33
Q

NSAID peripheral site of action

A

PGs sensitize neurons to bradykinin pain-producing effects. This is blocked

34
Q

NSAID Central site of action

A

PG’s induce pain @ spinal cord level, descending mechanisms (opioidergic, adrenergic). NSAIDS block this

35
Q

NSAIDS antipyretic effect

A

Reduce fever (not hyperthermia or normal body temp)

36
Q

What is the mechanism/sequence of NSAID antipyretic effect?

A

Endotoxin –> IL1 –> hypothalmic epithelium –> PGE2 –> EP3 receptors –> Temp set-point increased –> Fever

37
Q

NSAID Antithrombotic effect

A

Inhibition of TXA2 production in platelets

38
Q

Mechanism of NSAID antithrombotic effect

A

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
Q

NSAID Antiendotoxic effect

A

Endotoxins produce some effects through PG production (not good evidence to support NSAID use for this, maybe if given prophylactically)

40
Q

NSAIDS clinical uses

A

Osteoarthritis - Soft tissue inflammation - Analgesia - Antithrombosis - Endotoxemic syndrome (?) - Cancer (?)

41
Q

NSAID in osteoarthritis (DJD)

A

Reduce inflammation & pain - Chondroprotective vs. Chondrotoxic - Titrate dose to a minimum - Take as necessary not continuously - Tablets with food - use antiulcer drug!

42
Q

NSAIDS - Chondroprotective vs. chondrotoxic

A

PGs are involved in chondrocyte-mediated degredation of cartilage matrix - High concentrations suppress cartilage matrix synthesis

43
Q

NSAIDS - Situations for anti-inflammatory use

A

Inhibit acute response - Shipping fever - Calf pneumonia - Musculoskeletal conditions - Postoperative

44
Q

Which NSAID drugs are used to treat inflammation?

A

Phenylbutazone - Flunixin - Ketoprofen - tolfenamic acid - carprofen - meloxicam

45
Q

NSAID Analgesia treatments

A

Perioperatively - Preemptive analgesia - Trauma - Musculoskeletal conditions - Equine colic

46
Q

Which NSAIDS are used perioperatively?

A

Deracoxib & Firecoxib

47
Q

Which NSAIDS are used for preemptive analgesia

A

Carprofen & meloxicam (beware hypotension)

48
Q

Which NSAIDS are used for musculoskeletal conditions?

A

Carprofen - Meloxicam - Phenylbutazone

49
Q

Which NSAIDS are used for equine colic?

A

Flunixin, ketoprofen, carprofen, dipyrone

50
Q

When would you use NSAIDS for antithrombosis?

A

Aortic thromboembolism - Heartworm Disease - Laminitis - Navicular disease - Disseminated intravascular coagulation

51
Q

Which drug is best for antithrombosis?

A

Acetylsalicylic acid

52
Q

Which endotoxemic syndromes would you use NSAID treatment?

A

E. coli mastitis - Equine colic - Colitis X syndrome - Metritis - Mastitis-metritis-agalactia syndrome - Septic peritonitis

53
Q

Which NSAIDS would be used for endotoxemic syndromes?

A

Flunixin - Phenylbutazone - Carprofen - Keoprofen - Dipyrone - Meloxicam

54
Q

When are NSAIDS used for cancer?

A

COX-2 up-regulation - Growth factors & angiogenesis - Bladder transitional cell carcinoma - Mammary adenocarcinoma - Transmissible venereal tumor

55
Q

NSAIDS used in cancer treatment?

A

Piroxicam & coxibs

56
Q

NSAID Adverse effects

A

GI irritation/ulcer - Kidney damage - Liver damage - Increased bleeding time - Methemoglobinemia - Agranulocytosis

57
Q

NSAID - GI irritation/ulceration

A

Oral ulcers - Gastroduodenal - Right dorsal colitis - Abomasal

58
Q

NSAID Kidney damage

A

Hypotension - Hypovolemia - Renal insufficiency - Urinary tract obstruction - Papillary necrosis

59
Q

NSAID Liver damage - specific druge

A

Carprofen (USA vs UK) -Acetaminophen (Acetylcysteine, Silymarin, Vit C, Cimetidine)

60
Q

Which NSAID causes increased bleeding time?

A

Acetylsalicylic acid

61
Q

Which NSAID causes methemoglobinemia?

A

Acetaminophen

62
Q

Which NSAID causes agranulocytosis

A

Phenylbutazone & dipyrone

63
Q

NSAID drug interaction with glucocorticoids

A

Increased chance of GI irritation/ulceration

64
Q

NSAID drug interaction with warfarin, anesthetics, other NSAIDS

A

Drug displacement from plasma proteins

65
Q

NSAID drug interaction with furosemide

A

Decreased renal excretion and diuretic effect

66
Q

NSAID drug interaction with digoxin

A

Decreased digoxin excretion (longer half life, effects of digoxin last longer)

67
Q

NSAID drug interaction with ACE inhibitors, aminoglycosides, polymixin

A

Kidney damage & toxicity

68
Q

NSAID contraindications

A

Glucocorticoid therapy - Anticoagulant therapy or poisoning - Severe renal disease - Severe hypotension

69
Q

NSAID Precautions

A

Mild renal disease - Hepatic disease - Hypoproteinemia - Late pregnancy - Gastrointestinal ulceration - Dehydration

70
Q

NSAID the future

A

Non-acidic drugs - COX-2 selective inhibitors - nitro-NSAIDS - PG receptor antagonists

RUSVM Pharmacology I (19 decks)

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