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Pharmacology Exam 3 > NSAIDs > Flashcards

NSAIDs Flashcards

1
Q

NSAIDs

A
  • Non-Steroidal Anti-Inflammatory Drugs
  • decrease pain, fever, inflammation
  • inhibit production of prostaglandins from arachidonic acid by the cyclooxygenase (COX) enzymes
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2
Q

COX-1

A
  • constitutive prostaglandins
  • housekeeping
  • protective effect on gastric mucosa
  • platelet function
  • renal blood flow
  • some inducible inflammatory role
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3
Q

COX-2

A
  • inducible prostaglandins
  • pain
  • inflammation
  • fever
  • some constitutive “housekeeping” role
    • kidney, brain, uterus
    • healing gastric ulcers
    • species differences
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4
Q

non-selective NSAIDs

A
  • block both COX-1 and COX-2
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5
Q

selective NSAIDs

A
  • only block COX-2
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6
Q

COX-1: COX-2 ratios

A
  • [IC50] of each isoform
  • ratio > 1 = preference for COX-2 (selective)
  • carprofen 1.75, meloxicam 12.27
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7
Q

contraindications for NSAIDs

A

due to COX-1 effects

  • renal disease (low BP->first organ affected is kidney)
  • liver disease
  • GI disease
  • mast cell tumor
  • risk of bleeding or low BP in sx
  • on corticosteroids
  • Cushingoid
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8
Q

renal blood flow and NSAIDs

A
  • PGs maintain RBF during periods of hypotension (COX-1 > COX-2)
  • important during general anesthesia and sx
  • pre-operative use of NSAIDs (selective)
    • IV fluid support
    • BP monitoring and support
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9
Q

NSAIDs and platelet function

A
  • COX-1 –> PGG & PGH –> thromboxane
  • thromboxane allows platelets to aggregate
  • COX-1 inhibition causes decreased thromboxane synthesis in the platelet
  • most NSAIDs inhibit COX by competitive inhibition when drug is removed
  • effect on platelet function is 48-72 hours
  • selective (COX-2) inhibition- little effect
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10
Q

aspirin and platelet function

A
  • aspirin acetylates COX-1 enzyme irreversibly
  • platelets are unable to synthesize more COX (no nucleus)
  • effect lasts the life of platelets (10 days)
  • no sx for 7-10 days!
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11
Q

perioperative use of NSAIDs

A
  • nonselective NSAIDs-not recommended
  • COX-2 selective NSAIDs
    • rimadyl and meloxicam (injectable)
    • no documented effects on renal function or platelet function
    • pre-operatively for preemptive analgesia
    • administer 30-60 minutes prior to recovery (time to take out PGs)
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12
Q

gastric mucosal protection

A
  • increase mucus secretion
  • increase bicarbonate secretion
  • increase epithelial cell renewal
  • increase mucosal BF
  • decrease acid secretion
  • prostaglandins, nitric oxice, autonomic nervous system
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13
Q

gastric mucosal protection and NSAIDs

A
  • block COX-1 and subsequently prostaglandins and PGE
    • PGE: most important in protecting gastric mucosa
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14
Q

mechanisms of NSAID-induced gastritis

A
  • inhibition of COX
  • decreased production of PGE
  • concurrent administration of misoprostol (synthetic PGE) decreases severity of NSAID gastropathy with non-selective NSAIDs
  • decrease in gastric mucosal BF
    • increase in neutrophil adherence to vascular endothelium
    • leukotrienes cause chemotaxis for neutrophils and other inflammatory cells, vasoconstriction and increased vascular permeabilityd
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15
Q

NSAID elimination

A
  • metabolized by liver
  • glucuronidation or oxidative enzymes
    • glucuronidation most common
    • depends on NSAID
  • metabolites exreted in bile or urine
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16
Q

corticosteroids

A
  • do not inhibit prostaglandin synthesis
  • therefore they:
    • are not analgesics
    • do not inhibit platelet function
    • do cause GI dysfunction, but by a different mechanism than NSAIDs
17
Q

corticosteroids and gastric mucosal protection

A

block:

  • increased mucus secretion
  • increased bicarbonate secretion
  • increased epithelial cell renewal
  • increased mucosal BF
  • decreased acid secretion
18
Q

COX-1 and COX/LOX inhibitors

A
  • COX/LOX mechanism addresses some of the GI side effects of COX inhibition but does not address renal blood flow or platelet function
  • COX/LOX inhibitors are non-selective
  • effects of COX-1 inhibition are not known
  • use with caution for perioperative use or with renal disease
19
Q

cats and NSAIDs

A
  • reduced glucuronidation of drugs in cats
    • prolonged elimination half-lives
    • many NSAIDs
    • some NSAIDs (meloxicam) are cleared by oxidative enzymes in cats
  • more sensitive to renal effects of NSAIDs
    • species differences
    • COX-2 may have a more constitutive role in kidney in cats
20
Q

acetaminophen and cats

A
  • contraindicated
  • decreased glucuronidation -> metabolism by alternate pathways
  • toxic metabolite
    • N-acetyl-p-benzoquinone
    • methemoglobinemia
    • Heinz body anemia
  • detoxified by glutathione
    • antedote = acetylcysteine
    • glutathione precursor
21
Q

aspirin

A
  • relief of mild to moderate pain associated with musculoskeletal inflammation or osteoarthritis
  • rapidly absorbed in stomach/SI after oral admin
  • high first pass effect in liver to yield salicylic acid (main metabolite)
  • aspirin mainly inhibits COX-1, salicylic acid has more balanced COX-1/2 activity
  • widely distributed in tissues and fluids and crosses placental barrier
  • salicylate highly protein bound
  • metabolism and elimination via hepatic conjugation w/ glucoronic acid, followed by renal excretion
  • adverse effects: mucosal erosion and ulceration in dogs, vomiting and melena at ghigher doses
  • aspirin OD -> salicylate poisoning: severe acid/base abnormalities, hemorrhages, seizures, coma, death
22
Q

ketoprofen

A
  • acute pain (up to 5 days) in dogs and cats
  • horses: pain and inflammation with osteoarthritis or visceral pain (colic)
  • potent inhbitor of COX and bradykinin, may inhibit some lipooxygenase pathways
  • rapidly absorbed after oral administration
  • half life of 2-3 hrs in cats and dogs
  • metabolized in liver to inactive metabolites that are eliminated by renal excretion
  • adverse effects: GI upset and similar NSAID effects
23
Q

flunixin meglumine

A
  • non-selective COX inhibitor
  • treatment of visceral pain (equine colic)
  • may have anti-endotoxic activity
  • rapidly absorbed following PO or IM administration
  • elimination half- life is short (2-3 hrs)
  • primarily renal excretion
  • adverse effects: GI ulceration and erosion
  • has been used to treat mastitis and pulmonary emphysema in cattle (not approved)
24
Q

phenylbutazone

A
  • primarily COX-1?
  • tx of laminitis in horses
  • plasma half-life is 5-6 hr in horses/dogs and >30 hrs in cattle
  • absorbs to hay when given PO, may reduce GI absorption and bioavailability
  • metabolized by liver to active and inactive metabolites
  • excreted in urine
  • low therapeutic index
  • adverse effects: GI effects and depression, ulcers
25
Q

carprofen

A
  • manage pain and inflammation associated with osteoarthritis and acute pain associated with soft-tissue and orthopedic sx in dogs
  • half-life is ~ 8 hrs, highly protein bound
  • elimination via hepatic biotransformation, excretion of metabolites in feces and urine
  • greater selectivity for COX-2 but considered weak COX inhibitor
  • adverse effects: GI signs (V, D, GI ulceration), idiosyncratic hepatopathies
26
Q

meloxicam

A
  • potent inhibitor of prostaglandin synthesis
  • tx of acute and chronic inflammation associated with musculoskeletal dz, mgmt of postoperative pain
  • COX-2 selective
  • highly protein bound
  • long half life
  • safer for GI than non-selective
27
Q

deracoxib

A
  • control of postoperative pain and inflammation associated with orthopedic sx for up to 7 days
  • control of pain and inflammation associated with osteoarthritis
  • inhibits COX-2 mediated PGE-2 production
  • elimination half-life is 3 hrs in dogs
28
Q

firocoxib

A
  • control pain and inflammation associated with osteoarthritis
  • control of postop pain and inflammation associated with soft-tissue and orthopedic sx in dogs
  • rapidly absorbed after PO administration
  • eliminated by hepatic metabolism and fecal excretion
  • more selective for COX-2
  • highly protein bound
  • greater GI safety
29
Q

piroxicam

A
  • selective COX-2 inhibitor
  • extensive enterohepatic recycling in dogs resulting in prolonged plasma half-life
  • GI ulceration and bleeding, renal papillary necrosis in dogs
30
Q

robenacoxib

A
  • COX-2 inhibitor
  • osteopedic post-op pain, osteoarthritis
  • use for no more than 3 days
  • liver metabolism
31
Q

tepoxalin

A
  • non-selective COX and LOX inhibitor
  • rapidly absorbed
  • short plasma half-life, but has active metabolite
  • highly protein bound
  • adverse effects: GI

Pharmacology Exam 3 (9 decks)

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