Misc

Question 1

Acetaminophen

Answer 1

MOA: Reversibly inhibits cyclooxygenase, mostly in CNS. Inactivated peripherally.

Clinical use: Antipyretic, analgesic, but not anti-inflammatory. Used instead of aspirin to avoid Reye syndrome
in children with viral infection

Adverse effects: Overdose produces hepatic necrosis; acetaminophen metabolite (NAPQI) depletes glutathione and
forms toxic tissue byproducts in liver. N-acetylcysteine is antidote—regenerates glutathione

Question 2

Aspirin

Answer 2

MOA: NSAID that irreversibly inhibits cyclooxygenase (both COX-1 and COX-2) by covalent acetylation
–> ↓ synthesis of TXA2 and prostaglandins. ↑ bleeding time. No effect on PT, PTT. Effect lasts
until new platelets are produced

Clinical use: Low dose (< 300 mg/day): ↓platelet aggregation. Intermediate dose (300–2400 mg/day): antipyretic
and analgesic. High dose (2400–4000 mg/day): anti-inflammatory

Adverse effects: Gastric ulceration, tinnitus (CN VII), allergic reactions (especially in patients with asthma or nasal
polyps). Chronic use can lead to acute kidney injury, interstitial nephritis, GI bleeding. Risk of
Reye syndrome in children treated with aspirin for viral infection. Toxic doses cause respiratory
alkalosis early, but transitions to mixed metabolic acidosis-respiratory alkalosis.

Question 3

Celecoxib

Answer 3

MOA: Reversibly and selectively inhibits the cyclooxygenase (COX) isoform 2 (“Selecoxib”), which is
found in inflammatory cells and vascular endothelium and mediates inflammation and pain;
spares COX-1, which helps maintain gastric mucosa. Thus, does not have the corrosive effects
of other NSAIDs on the GI lining. Spares platelet function as TXA2 production is dependent on
COX-1.

Clinical use: Rheumatoid arthritis, osteoarthritis

Adverse effects: ↑ risk of thrombosis, sulfa allergy.

Question 4

Ibuprofen, naproxen, indomethacin, ketorolac, diclofenac, meloxicam, piroxicam.

Answer 4

Nonsteroidal anti-inflammatory drugs

MOA: Reversibly inhibit cyclooxygenase (both COX-1 and COX-2). Block prostaglandin synthesis.

Clinical use: Antipyretic, analgesic, anti-inflammatory. Indomethacin is used to close a PDA

Adverse effects: Interstitial nephritis, gastric ulcer (prostaglandins protect gastric mucosa), renal ischemia
(prostaglandins vasodilate afferent arteriole), aplastic anemia.

Question 5

Leflunomid

Answer 5

MOA: Reversibly inhibits dihydroorotate dehydrogenase, preventing pyrimidine synthesis. Suppresses
T-cell proliferation.

Clinical use: Rheumatoid arthritis, psoriatic arthritis.

Adverse effects: Diarrhea, hypertension, hepatotoxicity, teratogenicity.

Question 6

Alendronate, ibandronate, risedronate, zoledronate.

Answer 6

Bisphosphonates

MOA: Pyrophosphate analogs; bind hydroxyapatite in bone, inhibiting osteoclast activity.

Clinical use: Osteoporosis, hypercalcemia, Paget disease of bone, metastatic bone disease, osteogenesis
imperfecta.

Adverse effects: Esophagitis (if taken orally, patients are advised to take with water and remain upright for 30
minutes), osteonecrosis of jaw, atypical femoral stress fractures.

Question 7

Teriparatide

Answer 7

MOA: Recombinant PTH analog. ↑ osteoblastic activity when administered in pulsatile fashion.

Clinical use: Osteoporosis. Causes ↑ bone growth compared to antiresorptive therapies (eg, bisphosphonates).

Adverse effects: ↑ risk of osteosarcoma (avoid use in patients with Paget disease of the bone or unexplained
elevation of alkaline phosphatase). Avoid in patients who have had prior cancers or radiation
therapy. Transient hypercalcemia.

Question 8

Etanercept

Answer 8

TNF-α inhibitor

MOA: fusion protein (decoy receptor
for TNF-α + IgG1 Fc),
produced by recombinant
DNA.
Etanercept intercepts TNF.

Clinical use: Rheumatoid arthritis, psoriasis,
ankylosing spondylitis

Adverse effects: Predisposition to infection,
including reactivation of
latent TB, since TNF is
important in granuloma
formation and stabilization.
Can also lead to drug-induced
lupus.

Question 9

Infliximab,
adalimumab,
certolizumab,
golimumab

Answer 9

TNF-α inhibitor

MOA: Anti-TNF-α monoclonal
antibody.

Clinical use: Inflammatory bowel disease,
rheumatoid arthritis,
ankylosing spondylitis,
psoriasis

Adverse effects: Predisposition to infection,
including reactivation of
latent TB, since TNF is
important in granuloma
formation and stabilization.
Can also lead to drug-induced
lupus.