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PLAB Pharmacology > Musculoskeletal, Skin, and Connective Tissue Pharmacology > Flashcards

Musculoskeletal, Skin, and Connective Tissue Pharmacology Flashcards

1
Q

acetaminophen–mechanism

A
  • reversibly inhibits cyclooxgenase
    • mostly in CNS
  • inactivated peripherally
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2
Q

acetaminophen–use

A
  • antipyretic
  • analgesic
  • NOT anti-inflammatory
  • used instead of aspirin to avoid Reye syndrome in children with a viral infection
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3
Q

acetaminophen–toxicity

A
  • overdose produces hepatic necrosis
    • acetaminophen metabolic (NAPQI) depletes glutathione and forms toxic tissue byproducts in liver
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4
Q

acetaminophen–antidote

A
  • N-acetylcysteine
    • regenerates glutathione
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5
Q

aspirin–mechanism

A
  • NSAID that irreversibly inhibits cyclooxygenase (COX-1 and COX-2) by covalent acetylation –> dec synthesis of TXA2 and prostaglandins
    • inc bleeding time
    • no effect on PT, PTT
    • effect lasts until new platelets are produced
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6
Q

aspirin–use

A
  • low dose (<300 mg/day): dec platelet aggregation
  • intermediate dose (300-2400 mg/day): antipyretic and analgesic
  • high dose (2400-4000 mg/day): anti-inflammatory
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7
Q

aspirin–toxicity

A
  • gastric ulceration
  • tinnitus (CN VIII)
  • chronic use can lead to:
    • acute renal failure
    • interstitial nephritis
    • GI bleeding
  • causes respiratory alkalosis early, but transitions to mixed metabolic acidosis respiratory alkalosis
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8
Q

what are children at risk for if have a viral infection that is treated with aspirin?

A

Reye syndrome

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9
Q

celecoxib–mechanism

A
  • reversibly inhibits specifically the cyclooxogenase (COX) isoform 2 which is found in inflammatory cells and vascular endothelium and mediates inflammation and pain
    • spares COX 1
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10
Q

what are the benefits of using celecoxib over other NSAIDs?

A
  • spares COX-1 which helps maintain gastric mucosa
    • so does not have the corrosive effects of other NSAIDs on the GI lining
  • spares platelet function as TXA2 production is dependent on COX-1
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11
Q

celecoxib–use

A
  • rheumatoid arthritis
  • osteoarthritis
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12
Q

celecoxib–toxicity

A
  • inc risk of thrombosis
  • sulfa allergy
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13
Q

name the NSAIDs

A
  • ibuprofen
  • naproxen
  • indomethacin
  • ketorolac
  • diclofenac
  • meloxican
  • piroxican
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14
Q

NSAIDs–mechanism

A
  • reversibly inhibit cyclooxygenase (both COX 1 and 2)
  • blocks prostaglandin synthesis
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15
Q

NSAIDs–use

A
  • antipyretic
  • analgesic
  • anti-inflammatory
  • indomethacin is used to close a patent ductus arteriosis
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16
Q

NSAIDs–toxicity

A
  • interstitial nephritis
  • gastric ulcer–prostaglandins protect gastric mucosa
  • renal ischemia–prostaglandins vasodilate afferent arteriole
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17
Q

leflunomide–mechanism

A
  • reversibly inhibits dihydroorotate dehydrogenase, preventing pyrimidine synthesis
  • suppresses T cell proliferation
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18
Q

leflunomide–use

A
  • rheumatoid arthritis
  • psoriatic arthritis
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19
Q

leflunomide–toxicity

A
  • diarrhea
  • HTN
  • hepatotoxicity
  • teratogenicity
20
Q

name the bisphosphonates

A
  • alendronate
  • ibandronate
  • risedronate
  • zoledronate
21
Q

bisphosphonates–mechanism

A
  • pyrophosphate analogs
  • bind hydroxyapatite in bone
    • inhibits osteoclast activity
22
Q

bisphosphonates–use

A
  • osteoporosis
  • hypercalcemia
  • Paget dz of the bone
  • metastatic bone dz
  • osteogenesis imperfecta
23
Q

bisphosphonates–toxicity

A
  • esophagitis
    • if taken orally, patients are advised to take with water and remain upright for 30 minutes
  • osteonecrosis of jaw
  • atypical stress fractures
24
Q

teriparatide–mechanism

A
  • recombinant PTH analog given subcutaneously daily
  • inc osteoblastic activity
25
Q

teriparatide–use

A
  • osteoporosis
    • causes inc bone growth compared to antiresorptive therapies
      • ie. bisphosphonates
26
Q

teriparatide–toxicity

A
  • transient hypercalcemia
27
Q

name the chronic gout drugs (preventive)

A
  • allopurinol
  • febuxostat
  • pegloticase
  • probenecid
28
Q

name the acute gout drugs

A
  • NSAIDs
  • glucocorticoids
  • colchicine
29
Q

allopurinol–mechanism

A
  • competitive inhibitor of xanthine oxidase
    • decrease conversion of hypoxanthine and xanthine to urate
  • increase concentrations of azathioprine and 6 MP
    • both normally metabolized by xanthine oxidase
30
Q

other uses for allopurinol besides gout

A
  • used in lymphoma and leukemia to prevent tumor lysis–associated urate nephropathy
31
Q

febuxostat–mechanism

A
  • inhibits xanthine oxidase
32
Q

pegloticase–mechanism

A
  • recombinant uricase that catalyzes metabolism of uric acid to allantoin ( a more water soluble product )
33
Q

probenecid–mechanism

A
  • inhibits reabsorption of uric acid in the proximal convoluted tubule
    • also inhibits secretion of penicillin
    • can precipitate uric acid calculi
34
Q

name the NSAIDs used for gout

A
  • naproxen
  • indomethacin
35
Q

what type of NSAID should not be used for acute gout and why?

A
  • salicylates
    • all but the highest doses depress uric acid clearance
    • even high doses (5-6 g/day) have only minor uricosuric acitvity
36
Q

glucocorticoids–mechanism for use in acute gout

A
  • oral
  • intra-articular
  • parenteral
37
Q

colchicine–mechanism

A
  • binds and stabilizes tubulin to inhibit microtubule polymerization
    • impairs neutrophil chemotaxis and degranulation
38
Q

colchicine–use

A

acute and prophylactic use for gout

39
Q

colchicine–toxicity

A

GI side effects

40
Q

name 2 TNF alpha inhibitors

A
  • etanercept
  • infliximab, adalimumab
41
Q

what do TNF alpha inhibitors predispose a patient to and why?

A
  • all TNF alpha inhibitors predispose to infection, including reactivation of latent TB
    • b/c TNF is important in granuloma formation and stabilization
42
Q

etanercept–mechanism

A
  • fusion protein–receptor for TNF alpha + IgG1 Fc
    • produced by recombinant DNA
      • “Etanercept is a TNF decoy receptor”
43
Q

etanercept–use

A
  • rheumatoid arthritis
  • psoriasis
  • ankylosing spodylitis
44
Q

infliximab, adalimumab–mechanism

A
  • anti TNF alpha monoclonal antibody
45
Q

infliximab, adalimumab–use

A
  • inflammatory bowel disease
  • rheumatoid arthritis
  • ankylosing spondylitis
  • psoriasis
46
Q

rasburicase–mechanism

A
  • recombinant uricase that catalyzes metabolism of uric acid to allantoin
47
Q

rasburicase–use

A
  • prevention and treatment of tumor lysis syndrome

PLAB Pharmacology (17 decks)

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