Advanced Pharm Exam 1 Flashcards
(177 cards)
Aspirin- drug class?
NSAID: COX inhibitor (1st generation- inhibits COX-1 (stronger) & COX-2)
Aspirin- MOA?
Nonselective COX inhibitor, rapid binding/inhibition:
COX-1 inhibition leads to irreversible modification of platelets (last the life of platelet ~8days, until turnover), leading to decreased platelet aggregation and decreasing risk of stroke and MI.
COX-2 inhibition inhibits prostaglandin production, which decreases inflammation pathway including, decreasing pain and fever.
Aspirin induces ATLs, anti-inflammatory compounds.
Aspirin- adverse effects?
Gastro- GI distress, heartburn nausea, GI bleed, perforation, GI ulceration (with long-term use)
Renal- Renal impairment
Reyes Syndrome- in children: encephalopathy and fatty liver degeneration
Aspirin- indications
RA, OA (when other non-pharm routes and topical NSAIDs don’t work) - esp. when in multiple joints or hip joint
Aspirin- excretion?
Kidneys
What are the corticosteroid prototype drugs?
Prednisone, hydrocortisone, cortisone, methylprednisolone
Corticosteroids- indications?
RA, OA, asthma, Crohn’s disease, UC, IB
Used for inflammatory/immunologic disorders
Used as adjunctive for short term admin., during acute or exacerbation
Ibuprofen- indications?
RA and OA, pain relief, dysmenorrhea
Aspirin- max dose
3900mg PO
Ibuprofen- max dose?
3200mg/day PO over 3-4 doses
400mg every 4-6hours PRN
Ibuprofen- adverse effects?
Cardiovascular risk- thrombotic events, MI, stroke
GI risk- bleeding, ulceration, perforation (stomach/intestines)- GI risks higher for elderly
Corticosteroids- adverse effects
hypothalamic-pituitary-adrenal axis suppression: adrenal insufficiency
osteoporosis: from decreased osteoblasts decreasing bone formation and increased osteoclasts increasing bone resorption and decreased intestinal calcium leading to hypocalcemia leading to increased PTH leading to removal of calcium from the bone into blood
short term: hyperglycemia, BP changes, edema, GI bleed, poor wound healing, increased risk of infection, hypokalemia/hyperkalemia
Corticosteroids- MOA
Decrease prostaglandin & decrease leukotrienes -> decreased pro-inflammatory metabolites -> decreased inflammation
interrupted inflammatory process -> [decreased mediator synthesis -> decreased swelling, redness, pain, warmth AND decreased phagocytes -> decreased lysosomal enzymes -> decreased tissue injury -> decreased inflammation AND decreased lymphocyte proliferation -> decreased immune inflammatory response]
Ibuprofen- MOA?
Nonselective COX inhibition:
Cox-1 reversible inhibition (weaker than Aspirin) -> decreased platelet aggregation (not as long as Aspirin) -> decreases thrombotic events
Cox-2 inhibition -> decreases prostaglandin precursors -> decreased inflammatory response -> pain, fever, inflammation
Naproxen- drug class?
NSAID: 1st gen.- nonselective COX inhibitor
What are the NSAID prototype drugs?
Aspirin, Ibuprofen, Naproxen, Celecoxib, Indomethacin, Ketorolac
Indomethacin- drug class?
NSAID
Indomethacin- indications?
RA, OA, gout, closure of neonatal patent ductus arteriosus
Indomethacin- MOA?
COX inhibition -> decreased prostaglandin -> vasoconstriction (for patent ductus arteriosus) AND decreased inflammation AND decreased pain
Indomethacin- max dose?
150mg / day
Indomethacin- adverse effects?
Increased risk for CNS side effects: severe frontal headache, dizziness, vertigo, light-headed, confusion
Celecoxib- contraindications?
Patients with heart disease or recent CABG surgery
Celecoxib- drug class?
NSAID- 2nd gen. selective COX-2 inhibitor
Celecoxib- indications?
RA, OA, ankylosing spondylitis, migraine, pain, dysmenorrhea