Musculoskeletal Flashcards
(21 cards)
aspirin
MOA: irreversibly* inhibit COX1 + 2 by acetylation
- decrease synthesis of TXA2 and Prostaglandins
- increase bleeding time
- no effect on PT, PTT,
- NSAID
Use
- low dose: decrease platelet aggregation (baby aspirin for heart disease)
- intermediate dose: antipyretic and analgesic
- high dose: anti- inflammatory
Toxicity
- gastric ulcers
- tinnitus (CN 8)
- Chronic use: acute renal fail, interstitial nephritis, upper GI bleed
- Reye’s syndrome in kids with viral infection
- Respiratory alkalosis (Stimulate respiratory center)
- Anion gap metabolic acidosis
- Do not use in gout –> decrease uric acid clearance
Cox 1
Cox 2
COX1: platelets
- TXA2
- -> thrombosis
- always expressed
COX2: endothelium
- prostacyclin (PGI2)
- -> decrease thrombosis
- mediates inflammation and pain
- expressed in inflamed tissues only
Ibuprofen
NSAID MOA: reversible inhibition of COX 1+2 - Block prostaglandin synthesis Use - antipyretic - analgesic - anti-inflammatory Toxicity - interstitial nephritis - gastric ulcer (PG protect gastric mucosa) - renal ischemia (PG vasodilate afferent arteriole)
Naproxen
NSAID MOA: reversible inhibition of COX 1+2 - Block prostaglandin synthesis Use - antipyretic - analgesic - anti-inflammatory Toxicity - interstitial nephritis - gastric ulcer (PG protect gastric mucosa) - renal ischemia (PG vasodilate afferent arteriole)
Indomethacin
NSAID MOA: reversible inhibition of COX 1+2 - Block prostaglandin synthesis Use - antipyretic - analgesic - anti-inflammatory - close PDA Toxicity - interstitial nephritis - gastric ulcer (PG protect gastric mucosa) - renal ischemia (PG vasodilate afferent arteriole)
Ketorolac
NSAID MOA: reversible inhibition of COX 1+2 - Block prostaglandin synthesis Use - antipyretic - analgesic - anti-inflammatory Toxicity - interstitial nephritis - gastric ulcer (PG protect gastric mucosa) - renal ischemia (PG vasodilate afferent arteriole)
Diclogenac
NSAID MOA: reversible inhibition of COX 1+2 - Block prostaglandin synthesis Use - antipyretic - analgesic - anti-inflammatory Toxicity - interstitial nephritis - gastric ulcer (PG protect gastric mucosa) - renal ischemia (PG vasodilate afferent arteriole)
Celecoxib
COX-2 inhibitor MOA: reversible inhibition of COX2 - found in inflammatory and vascular endothelium - mediates inflammation and pain - spares mucosa b/c no COX1 effect - spares platelet function b/c TXA2 (platelet aggregator) depends on COX1 Use: - RA - Osteoarthritis -- in patients with gastric ulcers* toxicity - increased risk thrombosis* - sulfa allergy
Acetaminophen
MOA: reversible inhibition of cyclooxygenase
- mostly CNS
- inactivated peripherally
Use
- antipyretic
- analgesic
- not an anti-inflammatory
- use instead of aspirin to avoid Reye’s syndrome
Toxicity
- hepatic necrosis
- decreased sulfation and glucuronide conjugation in liver –> increased NAPQ1 metabolite depletes glutathione –> toxic tissue products in liver
- N-acetylcysteine is antidote – glutathione substitute that binds toxic metabolite + provides sulfahydryl group to enhance the non-toxic sulfation elimination of acetaminophene
Alendronate
- dronates
Bisphosphate MOA: pyrophosphate* analog - bind hydroxyapatite in bone - inhibit osteoclast activity Use: - osteoporosis - hypercalcemia - Paget disease of bone Toxicity: - corrosive esophagitis - osteonecrosis of jaw*
Allopurinol
MOA: inhibits xanthine oxidase
- decreased conversion of xanthine –> uric acid
Use:
- gout - give between attacks - decrease uric acid to prevent relapse
- lymphoma and leukemia to prevent tumor lysis syndrome
Toxicity
- steven johnson syndrome
- urate nephropathy
- increases concentrations of azathioprine and 6-MP
- Do not give salicylate
All but highest doses depress uric acid clearance
Febuxostat
MOA: inhibit xanthin oxidase
Use:
- chronic gout - decrease uric acid to prevent relapse
Probenecid
MAO: inhibit reabsorption of uric acid in PCT
- inhibits secretion of penicillin
Use:
- chronic gout - decrease uric acid to prevent relapse
Colchicine
MOA: bind and stabilize tubulin to inhibit polymerization
- impairs leukocyte chemotaxis and degranulation (primarily neutrophils)
Use:
- chronic gout
Toxicity
- GI side effects - diarrhea
Acute gout
- Goal is to control pain and inflammation
NSAID - naproxen, indomethacin
Glucocorticoids - oral or intraarticular
Etenercept
MOA: TNF decoy receptor - fusion protein: receptor for TNF- alpha + IgG1 Fc Use - RA - Psoriasis - Ankylosing spondylitis
Infliximab
MOA: TNF- alpha monoclonal antibody Use: - crohn's disease - RA - ankylosing spondylitis - psoriasis
Neostigmine
MOA: anticholinesterase - prevent ACh breakdown Use - Myasthenia gravis - Post-op neurogenic ileus + urinary retention - reverse neuromuscular junction blockade post op Toxicity (Treat = atropine + pralidoxime) -Diarrhea -Urination -Miosis -Bradycardia -Bronchospasm -Excitation of CNS + skeletal muscle -Lacrimation -Salivation -Sweating
Pyridostigmine
MOA: anticholinesterase - prevent ACh breakdown - stronger - longer 1/2 life Use: - Myasthenia gravis -- long acting Toxicity (Treat = atropine + pralidoxime) -Diarrhea -Urination -Miosis -Bradycardia -Bronchospasm -Excitation of CNS + skeletal muscle -Lacrimation -Salivation -Sweating
Edrophonium
MOA: anticholinesterase - prevent ACh breakdown - short 1/2 life Use: - diagnose Myasthenia gravis Toxicity (Treat = atropine + pralidoxime) -Diarrhea -Urination -Miosis -Bradycardia -Bronchospasm -Excitation of CNS + skeletal muscle -Lacrimation -Salivation -Sweating
Vemurafenib
- not phase specific
- MOA: small molecule inhibitor of forms of the B-Raf kinase with the V600E mutation
- Use:
- metastatic melanoma
