MSK/CT - Pharm Flashcards
Acetominophen MOA
REVERSIBLY inhibits COX, mostly in CNS
Inactivated peripherally
Acetominophen use
Antipyretic and analgesic, but NOT anti-inflammatory
use in kids with viral illnesses
Acetominophen toxicity
Zone III hepatic necrosis
NAPQI = toxic, depletes glutathione (regenerate with NAC = antidote)
Asprin MOA
IRREVERSIBLY inhibits COX-1 and COX-2 via acetylation.
Causes decrease in TXA2 (increase bleeding time via decreased platelet aggregation) and prostaglandins
Asprin use:
LD = anti-coagulant MD = antipyretic and analgesic HD = anti-inflammatory
Asprin toxicity:
- Tinitus
- Gastric ulcers
- Chronic = GI bleed, ARF, AIN
- Reyes in kids with viruses
- Early respiratory alkalosis, then mixed with metabolic acidosis
Celecoxib MOA
REVERSIBLY inhibit COX-2 - inflammatory cells and endothelium for pain and inflammation [NOT gastric mucosa or platelets]
Celecoxib Use
RA
OA
NO GI effects
Celecoxib toxicity
Thrombosis:
Block endothelium VD without blocking platelet aggregation –> pro-coagulant state
sulfa
NSAIDs
REVERSIBLY inhibit COX 1 and COX 2
NSAIDs specific use
Indomethacin closes PDA, acute gout attacks, treats DI,
NSAID toxicity
- interstitial nephritis
- gastric ulcers
- renal ischemia
Bisphosphonates:
Alendronate, other ___dronates
Bisphosphonate mechanism
PPi analog: bind hydroxyapatite in bone, and inhibit osteoclast activity
Bisphosphonates use
OP
Hypercalcemia (from malignancies)
Pagets
Bisphosphonates toxicity
- Erosive esophagitis
- Jaw osteonecrosis