NEET PG Musculoskeletal & Anti-Inflammatory Pharmacology Glossary 2026: NSAIDs, DMARDs, Anti-Gout Drugs and Muscle Relaxants

You are staring at your musculoskeletal pharmacology notes, probably thinking "how do I memorize all these drug mechanisms before NEET PG 2026?" NSAIDs blend into each other. DMARD names look like alphabet soup. Anti-gout drugs feel random. And muscle relaxants? You cant even pronounce half of them.

Here's what's different about this glossary — it's the final piece in the NEET PG pharmacology series. While other resources dump information, this gives you the exact mechanism mnemonics, side effect patterns, and MCQ angles that show up repeatedly in NEET PG and INICET 2026. Every drug here has appeared in the last 3 years of Indian PG entrance exams.

The musculoskeletal system touches everything — orthopedics, rheumatology, internal medicine, emergency medicine. Miss these pharmacology concepts and you lose points across multiple subjects. But master these 47 high-yield drugs with their mechanisms and you've locked down 15-20 marks minimum.

This isnt another textbook chapter. It's your final revision weapon.

Drug Classification Overview

Musculoskeletal pharmacology divides into four major categories:

1. NSAIDs (Non-Steroidal Anti-Inflammatory Drugs) - First-line for inflammation and pain
2. DMARDs (Disease-Modifying Anti-Rheumatic Drugs) - Conventional and biological agents for autoimmune conditions
3. Anti-Gout Drugs - Acute and chronic gout management
4. Muscle Relaxants - Central and peripheral acting agents

Each category has distinct mechanisms, but overlap exists. NSAIDs treat acute gout. Some DMARDs are repurposed cancer drugs. Muscle relaxants work at different sites of the motor pathway. Understanding these connections helps you tackle combination questions that NEET PG loves to ask.

NSAIDs: Non-Steroidal Anti-Inflammatory Drugs

Mechanism of Action

NSAIDs work by inhibiting cyclooxygenase (COX) enzymes, blocking prostaglandin synthesis. Two COX isoforms exist:

• COX-1: Constitutive enzyme, protective prostaglandins in GI tract, kidneys, platelets

• COX-2: Inducible enzyme, inflammatory prostaglandins at injury sites

Mnemonic: "COX-1 Protects, COX-2 Inflames"

Non-Selective COX Inhibitors

#### Aspirin (Acetylsalicylic Acid)

• Mechanism: Irreversible COX-1 and COX-2 inhibition via acetylation

• Clinical Uses: Analgesic (325-650mg), anti-inflammatory (3-6g/day), antiplatelet (75-100mg)

• Pharmacokinetics: Zero-order kinetics at high doses, 80% protein bound

• Adverse Effects: GI bleeding, Reye syndrome (children), salicylism, hyperuricemia

• MCQ Mnemonic: "ASPIRIN = A-cetylation Stops Prostaglandin In Reversible INhibition (it's actually irreversible!)"

#### Ibuprofen

• Mechanism: Reversible COX-1/COX-2 inhibition, slight COX-1 selectivity

• Dose: 400-800mg TID, maximum 3200mg/day

• Advantages: Better GI tolerance than aspirin, available OTC

• Adverse Effects: Less GI toxicity, fluid retention, hypertension

• Drug Interactions: Reduces antihypertensive effect of ACE inhibitors

#### Diclofenac

• Mechanism: Potent COX inhibition, excellent tissue penetration

• Routes: Oral, topical, intramuscular, IV

• Clinical Uses: Rheumatoid arthritis, osteoarthritis, acute pain

• Adverse Effects: Higher cardiovascular risk, hepatotoxicity

• MCQ Focus: Often asked about topical formulations and liver monitoring

#### Indomethacin

• Mechanism: Potent COX inhibition + additional CNS effects

• Unique Uses: Patent ductus arteriosus closure (neonates), Bartter syndrome

• Adverse Effects: Severe CNS toxicity (headache, dizziness, confusion)

• MCQ Mnemonic: "INDO-methacin = IN-Ductus closure + DO-n't use long-term (CNS toxicity)"

After reviewing NSAID mechanisms, Oncourse's adaptive question bank automatically surfaces targeted MCQs on COX selectivity and drug interactions, helping you identify which specific concepts need more focus.

Selective COX-2 Inhibitors

#### Celecoxib

• Mechanism: Selective COX-2 inhibition, COX-1 sparing

• Advantages: Reduced GI ulceration and bleeding

• Cardiovascular Risk: Increased thrombotic events (VIGOR trial)

• Contraindications: Sulfonamide allergy, recent MI, stroke

• MCQ Focus: Questions often contrast GI vs CV risk profiles

#### Etoricoxib

• Mechanism: Highly selective COX-2 inhibitor

• Half-life: 22 hours (once daily dosing)

• Clinical Uses: Osteoarthritis, rheumatoid arthritis, acute gout

• Adverse Effects: Hypertension, edema, cardiovascular events

NSAID Adverse Effects & Contraindications

High-Yield Contraindications:

• Active GI bleeding or peptic ulcer disease

• Severe renal or hepatic impairment

• Heart failure or recent MI (especially COX-2 selective)

• Third trimester pregnancy (premature ductus closure)

• Aspirin allergy (cross-reactivity risk)

Practice targeted NSAIDs mechanism MCQs to reinforce these concepts.

DMARDs: Disease-Modifying Anti-Rheumatic Drugs

DMARDs slow or halt rheumatoid arthritis progression by targeting specific immune pathways. They divide into conventional synthetic (csDMARDs), targeted synthetic (tsDMARDs), and biological (bDMARDs).

Conventional DMARDs

#### Methotrexate (MTX)

• Mechanism: Dihydrofolate reductase inhibition → impaired DNA synthesis in rapidly dividing cells

• Dosing: 7.5-25mg weekly (NEVER daily for RA)

• Route: Oral or subcutaneous injection

• Monitoring: CBC, liver function, pulmonary function

• Adverse Effects: Hepatotoxicity, pulmonary fibrosis, mucositis, teratogenicity

• Antidote: Leucovorin (folinic acid) rescue

• MCQ Mnemonic: "MTX = Must Take X-tra folate (leucovorin) to avoid toxicity"

#### Sulfasalazine

• Mechanism: Anti-inflammatory via inhibition of NF-κB, possibly 5-ASA metabolite

• Metabolism: Colonic bacteria cleave to sulfapyridine + 5-aminosalicylic acid

• Clinical Uses: Rheumatoid arthritis, ankylosing spondylitis, IBD

• Adverse Effects: GI upset, oligospermia, hemolysis (G6PD deficiency)

• Monitoring: CBC (reversible oligospermia in males)

#### Hydroxychloroquine

• Mechanism: Antimalarial with immunomodulatory effects, lysosomal pH alteration

• Dosing: 200-400mg daily, weight-based dosing (<6.5mg/kg/day)

• Unique Advantage: Lowest toxicity among DMARDs

• Adverse Effects: Retinal toxicity (rare but irreversible), QT prolongation

• Monitoring: Annual ophthalmologic examination after 5 years

• MCQ Focus: Questions emphasize retinal screening protocols

#### Leflunomide

• Mechanism: Dihydroorotate dehydrogenase inhibition → pyrimidine synthesis blockade

• Active Metabolite: A771726 (extremely long half-life: 2 weeks)

• Loading Dose: 100mg daily × 3 days, then 10-20mg daily

• Adverse Effects: Hepatotoxicity, teratogenicity, peripheral neuropathy

• Washout: Cholestyramine for rapid elimination (pregnancy planning)

• MCQ Mnemonic: "LEF-lunomide = LEF-t pyrimidines behind (blocks synthesis)"

Oncourse's spaced repetition flashcards reinforce DMARD mechanisms at scientifically optimal intervals, ensuring these complex pathways stick before your exam.

Biological DMARDs

#### TNF-α Inhibitors

Infliximab (Chimeric Monoclonal Antibody)

• Mechanism: TNF-α neutralization, prevents inflammatory cascade

• Route: IV infusion at weeks 0, 2, 6, then every 8 weeks

• Clinical Uses: RA, IBD, psoriasis, ankylosing spondylitis

• Adverse Effects: Infection risk, lymphoma, lupus-like syndrome

• Contraindications: Active TB, hepatitis B reactivation risk

Adalimumab (Fully Human Monoclonal)

• Route: Subcutaneous injection every 2 weeks

• Advantage: Lower immunogenicity than chimeric antibodies

• Pre-treatment Screening: TB, hepatitis B, CBC, LFTs

Etanercept (Fusion Protein)

• Mechanism: Soluble TNF receptor that binds and neutralizes TNF-α

• Route: Subcutaneous twice weekly or weekly

• Unique Feature: Also binds lymphotoxin-α

MCQ Mnemonic for TNF Inhibitors: "TNF = Tumor Necrosis Factor → Terrible iNfection Fear"

#### IL-6 Receptor Antagonist

Tocilizumab

• Mechanism: IL-6 receptor blockade → reduced acute phase reactants

• Route: IV monthly or subcutaneous weekly

• Monitoring: CRP may be unreliable (blocks IL-6 pathway)

• Adverse Effects: Elevated transaminases, neutropenia, GI perforation

#### B-Cell Depletion

Rituximab

• Mechanism: Anti-CD20 monoclonal antibody → B-cell depletion

• Dosing: Two IV infusions separated by 2 weeks

• Duration: B-cell depletion lasts 6-9 months

• Pre-medication: Methylprednisolone, antihistamines (infusion reactions)

Targeted Synthetic DMARDs (JAK Inhibitors)

#### Tofacitinib

• Mechanism: JAK1/JAK3 inhibition → blocks cytokine signaling

• Route: Oral (major advantage over biologics)

• Adverse Effects: Increased infection risk, thromboembolism, elevated cholesterol

• Monitoring: CBC, lipid profile, liver function

Explore comprehensive DMARD pharmacology lessons for detailed mechanism coverage.

Anti-Gout Drugs

Gout management has two phases: acute attack treatment and chronic uric acid lowering. Different drugs target different points in the uric acid pathway.

Acute Gout Treatment

#### Colchicine

• Mechanism: Microtubule polymerization inhibition → neutrophil dysfunction

• Dosing: 1.2mg at first sign, then 0.6mg 1 hour later (max 1.8mg/24h)

• Pharmacokinetics: Hepatic metabolism, renal elimination

• Adverse Effects: Diarrhea (dose-limiting), myopathy, bone marrow suppression

• Drug Interactions: CYP3A4 inhibitors increase toxicity

• MCQ Mnemonic: "COL-chicine = COL-lapses microtubules → COL-on problems (diarrhea)"

#### NSAIDs for Acute Gout

• First Choice: Indomethacin 50mg TID × 3-5 days

• Alternatives: Ibuprofen, diclofenac, naproxen

• Contraindications: Renal disease, heart failure, GI bleeding

#### Corticosteroids

• Indications: NSAIDs and colchicine contraindicated/ineffective

• Routes: Oral prednisolone, intra-articular injection, IV methylprednisolone

• Dosing: Prednisolone 30-40mg daily × 5-7 days

Chronic Uric Acid Lowering Therapy

#### Allopurinol

• Mechanism: Xanthine oxidase inhibition → reduces uric acid production

• Dosing: Start 100mg daily, titrate to serum urate <6mg/dL

• Pharmacokinetics: Active metabolite oxypurinol (longer half-life)

• Adverse Effects: Severe cutaneous reactions (HLA-B*5801 association)

• Drug Interactions: Increases toxicity of azathioprine, 6-MP

• MCQ Focus: Often asked about azathioprine interaction mechanism

#### Febuxostat

• Mechanism: Selective xanthine oxidase inhibition (non-purine analog)

• Advantages: Can use in mild-moderate renal impairment

• Dosing: 40-80mg daily, more potent than allopurinol

• Adverse Effects: Cardiovascular events (FDA warning)

#### Probenecid

• Mechanism: Uric acid reabsorption inhibition in proximal tubule

• Indication: Underexcretion of uric acid (normal production)

• Contraindications: CKD (GFR <50), history of kidney stones

• Drug Interactions: Reduces penicillin excretion

• MCQ Mnemonic: "PRO-benecid = PRO-motes uric acid elimination"

#### Rasburicase

• Mechanism: Recombinant urate oxidase → converts uric acid to allantoin

• Indication: Tumor lysis syndrome prevention

• Contraindications: G6PD deficiency (hemolysis risk)

• Route: IV infusion in oncology settings

Practice anti-gout drug MCQs to master these high-yield mechanisms.

Gout Drug Selection Algorithm

Muscle Relaxants

Muscle relaxants work at different levels of motor control. Central agents modify CNS pathways, while peripheral agents target the neuromuscular junction or muscle fibers directly.

Centrally Acting Muscle Relaxants

#### Baclofen

• Mechanism: GABA-B receptor agonist in spinal cord

• Clinical Uses: Spasticity (cerebral palsy, spinal cord injury), trigeminal neuralgia

• Route: Oral or intrathecal pump

• Pharmacokinetics: Crosses blood-brain barrier poorly (hence intrathecal route)

• Adverse Effects: Sedation, weakness, withdrawal seizures (abrupt discontinuation)

• MCQ Mnemonic: "BAC-lofen = BAC-k pain via GABA-B receptors"

#### Tizanidine

• Mechanism: α2-adrenergic agonist → reduced presynaptic excitation

• Clinical Uses: Muscle spasticity, tension headaches

• Pharmacokinetics: Short half-life (2.5 hours), hepatic metabolism

• Adverse Effects: Hypotension, sedation, hepatotoxicity

• Monitoring: Liver function tests (risk of hepatotoxicity)

#### Cyclobenzaprine

• Mechanism: CNS depression, structurally similar to tricyclic antidepressants

• Clinical Uses: Acute muscle spasm, fibromyalgia

• Pharmacokinetics: Long half-life (18 hours), extensive first-pass metabolism

• Adverse Effects: Anticholinergic effects (dry mouth, urinary retention)

• Contraindications: Recent MAO inhibitor use, hyperthyroidism

Performance analytics through Oncourse help identify which muscle relaxant mechanisms you're missing most frequently, enabling targeted revision in your final weeks.

Peripherally Acting Muscle Relaxants

#### Dantrolene

• Mechanism: Blocks ryanodine receptors → prevents calcium release from sarcoplasmic reticulum

• Unique Indication: Malignant hyperthermia treatment and prevention

• Other Uses: Spasticity (cerebral palsy, multiple sclerosis)

• Route: Oral for spasticity, IV for malignant hyperthermia

• Adverse Effects: Hepatotoxicity (major concern), muscle weakness

• MCQ Focus: Always think malignant hyperthermia when you see dantrolene

• MCQ Mnemonic: "DAN-trolene = DAN-gerous hyperthermia rescue"

Neuromuscular Junction Blockers (Brief Review)

While not traditional muscle relaxants, these appear in musculoskeletal pharmacology sections:

#### Succinylcholine

• Mechanism: Depolarizing NMJ blocker (ACh receptor agonist)

• Clinical Use: Rapid sequence intubation

• Adverse Effects: Malignant hyperthermia, hyperkalemia

• Reversal: None (wait for metabolism)

#### Rocuronium

• Mechanism: Non-depolarizing NMJ blocker (ACh receptor competitive antagonist)

• Advantages: Rapid onset, predictable duration

• Reversal: Sugammadex (specific reversal agent)

Review comprehensive pharmacology concepts to connect these mechanisms with clinical applications.

High-Yield Drug Interactions & Contraindications

Major Drug Interactions

Pregnancy & Lactation Considerations

Contraindicated in Pregnancy:

• Methotrexate (Category X - teratogenic)

• Leflunomide (Category X - requires washout)

• NSAIDs in third trimester (ductus arteriosus closure)

• Mycophenolate (Category D - teratogenic)

Relatively Safe Options:

• Sulfasalazine (Category B - folate supplementation)

• Hydroxychloroquine (Category C - continue if needed)

• Prednisolone (Category B - crosses placenta minimally)

• Low-dose aspirin (Category B up to 32 weeks)

MCQ Strategy & High-Yield Topics

Most Frequently Tested Concepts

1. NSAID mechanisms and selectivity - Distinguish COX-1 vs COX-2 effects
2. Methotrexate monitoring - Know leucovorin rescue and contraindications
3. Allopurinol interactions - Especially with azathioprine and 6-MP
4. Malignant hyperthermia - Dantrolene mechanism and indication
5. TNF inhibitor screening - TB and hepatitis B reactivation risks
6. Colchicine toxicity - Diarrhea and drug interactions
7. Pregnancy categories - Which DMARDs are safe/contraindicated

Question Pattern Recognition

NEET PG loves to test:

• Mechanism of action with clinical correlation

• Adverse effect patterns and monitoring requirements

• Drug interactions with clinical significance

• Contraindications in specific populations

• Dosing schedules and administration routes

INICET frequently asks:

• First-line therapy selection for specific conditions

• Monitoring requirements for high-risk drugs

• Alternative agents when first choice is contraindicated

• Combination therapy rationales

Study these patterns with targeted pharmacology flashcards that use spaced repetition to lock in these concepts.

Frequently Asked Questions

Which NSAIDs are safest for patients with cardiovascular disease?

Non-selective NSAIDs like ibuprofen carry less CV risk than COX-2 selective agents. However, naproxen has the best cardiovascular safety profile among NSAIDs. Consider topical preparations to minimize systemic exposure.

How long should DMARDs be continued in rheumatoid arthritis?

DMARDs are typically lifelong therapy. Methotrexate remains first-line, often combined with biologics in severe disease. Stopping DMARDs usually leads to disease flare within months.

Can allopurinol be started during an acute gout attack?

No, starting allopurinol during acute gout can worsen the attack. Wait until inflammation resolves, then start with colchicine prophylaxis for 3-6 months while titrating allopurinol to target uric acid levels.

What is the antidote for methotrexate toxicity?

Leucovorin (folinic acid) rescue. Give within 24-48 hours of MTX overdose. Dose depends on MTX levels - higher MTX levels require higher leucovorin doses and longer duration.

Which muscle relaxant is used for malignant hyperthermia?

Dantrolene is the specific treatment for malignant hyperthermia. It blocks calcium release from sarcoplasmic reticulum, preventing the hypermetabolic crisis. IV administration is critical - have it readily available in ORs.

Are biologics safe during pregnancy?

Most biologics are Category B or C. TNF inhibitors like adalimumab and infliximab can be continued through pregnancy if disease activity is high. Rituximab should be avoided due to B-cell depletion in the fetus.

This comprehensive glossary gives you the mechanism clarity and MCQ strategy needed to excel in musculoskeletal pharmacology. The key is connecting drug mechanisms to clinical applications - exactly what NEET PG and INICET test most heavily.

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