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29 Cards in this Set

  • Front
  • Back
Lipoxygenase
Converts arachidonic acid to leukotrienes
LTB4
Neutrophil chemotactic agent
LTC4, LTD4, LTE4
Bronchoconstriction

Vasoconstriction
Contraction of smooth muscle
Increased vascular permeability
PGI2
Prostacyclin

Inhibits aggregation of platelets
Decreases uterine tone
Vasodilates

"Platelet Gathering Inhibitor"
Phospholipase A2
Converts membrane lipids to arachidonic acid
COX-1, COX-2
Convert arachidonic acid to TxA2, prostacyclin (PGI2) and prostaglandin (PGE2)
PGE2
Prostaglandin

Increases: pain, temp, uterine tone
Vasodilates
TxA2
Platelet aggregation
Vasoconstriction
Zileuton
Lipoxygenase inhibitor. Prevents formation of Leukotrienes.
Montelukast/Zafirlukast
Leukotriene receptor inhibitor
COX-1 acts mainly on
gastric mucosa
COX-2 acts mainly on
inflammatory cells
Corticosteroid: mechanism for anti-inflammatory action
Inhibit Phospholipase A2
Inhibit protein synthesis required for COX-1, COX-2 production
NSAIDs
Acetaminophen
Aspirin

MOA
Inhibit COX-1, COX-2 formation of prostaglandins (PGE2)
Aspirin

1. MOA

2. Use and dosage

3. Toxicity
1. Irreversibly and covalently binds COX, decreasing synthesis of both PGE2 and TxA2

2. Low dose: anti-platelet
Intermediate dose: anti-pyretic and analgesic
High-dose: anti-inflammatory

3. Gastric upset. Renal failure, interstitial nephritis, upper GI bleed.
Reye's syndrome in kids after viral illness.
Reye's syndrome
Fatty liver and extreme encephalopathy, among other symptoms.

Caused by aspirin use in children post viral illness.
NSAIDs

1. MOA
2. Use
3. Toxicity
Ibuprofen, naproxen, indomethacin, ketorolac

1. Reversibly inhibits COX-1, COX-2, blocking PGE2 synthesis.

2. Anti-pyretic, analgesic, anti-inflammatory

3. Renal damage, aplastic anemia, GI distress, ulcers
COX-2 inhibitors

1. aka ____
2. MOA
3. Use
4. Toxicity
1. Celecoxib

2. Reversibly inhibits COX-2, found on inflammatory cells, vascular endothelium, mediating inflammation and pain.
Helps maintain gastric mucosa, no corrosive effects.

3. RA and OA

4. Increased risk of thrombosis.
Sulfa drug allergy.

Less toxicity to GI mucosa
Acetamenophen

1. MOA
2. Use
3. Toxicity
1. Reversibly inhibits COX in CNS. Inactivated peripherally.

2. Anti-pyretic, analgesic. NO ANTI-INFLAMMATORY properties. Used instead of aspirin in kids to avoid Reye's syndrome.

3. Hepatic necrosis after overdose.
Bisphosphonates

1. MOA
2. Use
3. Toxicity
1. Inhibit osteoclastic activity.

2. Malignancy-associated hypercalcemia, Paget Disease of the bone, post-menopausal osteoporosis.

3. Corrosive esophagitis, nausea, diarrhea
What is used to Tx:

Acute gout?
Chronic gout?
1. Colchicine

2. Probenecid and/or Allopurinol
Colchicine

1. MOA
2. Use
3. Toxicity
1. Stabilizes tubulin to inhibit polymerization, impairing leukocyte chemotaxis and degranulation.

2. Acute gout

3. GI toxicity
Probenecid

1. MOA
2. Use
3. Toxicity
1. Inhibit reabsorption of uric acid in PCT

2. Chronic Gout

3. inhibits secretion of penicillin
Allopurinol

1. MOA
2. Use
3. Toxicity
1. Inhibits Xanthine Oxidase, preventing conversion of xanthine to uric acid.

2. Chronic gout, lymphoma and leukemia to prevent tumor-lysis associated urate nephropathy.

3. Increases concentrations of azothioprine and 6-MP (metabolized by XO)
What drug should not be given in a patient with gout?
Salicylates and certain diuretics.

Salicylates decrease uric acid clearance.
TNF-a inhibitors (3)
Etanercept
Infliximab
Adalimumab
Etanercept

1. MOA
2. Use
1. TNF-a receptor decoy --> inhibits TNF-a

2. RA, psoriasis, ankylosing spondylitis
Infliximab

1. MOA
2. Use
3. Toxicity
1. anti-TNF-a Ab

2. Chron's, RA, ankylosing spondylitis

3. Predisposes to infxns (i.e. reactivation of latent TB)
Adalimumab

1. MOA
2. Use
1. anti-TNF-a Ab

2. RA, psoriasis, ankylosing spondylitis