Comprehensive Flashcards for Osteoarthritis, Rheumatoid Arthritis, Osteoporosis, Gout, Pain Pathways & Assessment, Opioids & Cannabis (Lecture Notes Review)

A comprehensive set of practice questions spanning OA, RA, OP, gout, pain pathways & assessment, opioids, and medicinal cannabis based on the provided lecture notes.

What is osteoarthritis (OA)?

A chronic, slow-progressive, degenerative joint disease characterized by breakdown of articular cartilage, leading to pain, stiffness, reduced range of motion, and functional impairment.

Which joints are most commonly affected by OA?

Knees, hips, hands, and spine.

How does OA epidemiology differ by sex before and after age 50?

Before age 50, OA is more common in males; after age 50 (post-menopause), it is more common in females.

What is the leading modifiable risk factor for knee OA and why?

Obesity; excess weight increases joint loading and promotes systemic inflammation.

Describe a typical OA clinical presentation.

Pain that is deep, aching, worsens with activity and improves with rest; stiffness (gelling phenomenon) after inactivity; limited joint motion; instability in weight-bearing joints; asymmetrical joint involvement.

Which hand deformities are characteristic of OA?

Heberden nodes (DIP) and Bouchard nodes (PIP); square appearance at the first carpometacarpal joint (thumb base).

What imaging findings are typical in OA?

Joint space narrowing, osteophytes, subchondral sclerosis, subchondral cysts, and bone deformity.

Do radiographic OA changes always reflect symptom severity?

No; radiographic changes do not always match symptom severity.

What are the goals of OA treatment?

Enable pain coping, maintain/optimise physical function and activities of daily living, minimise disability, and maximise health-related quality of life.

Name a topical NSAID option for OA.

Volataren (diclofenac), Nurofen (ibuprofen), Feldene Gel (piroxicam).

What is capsaicin used for in OA and its dosing?

Topical capsaicin (0.025%) applied to the painful area 3–4 times daily (TID-QID); common ADR is a burning sensation.

Compare NSAIDs with paracetamol for OA pain relief.

NSAIDs are generally more effective for pain and function in OA due to inflammation; paracetamol is safer for some patients but less effective for inflammatory pain.

What are GI risk factors for NSAID-induced GI toxicity?

Older age (>65), sepsis, heart failure, cirrhosis, volume depletion; history of peptic ulcer/GI bleeding/H. pylori; concurrent anticoagulants/antiplatelets/SSRIs/corticosteroids; alcohol use.

How can NSAID GI toxicity risk be reduced?

Use the lowest effective dose for the shortest duration, use topical NSAIDs when possible, consider PPIs or H2 blockers, COX-2 selective NSAIDs in high GI risk patients, and monitor closely.

Which NSAID has the lowest CV risk but higher GI risk?

Naproxen.

Which OA treatment involves intra-articular corticosteroid injections and what is a longest-acting corticosteroid option?

Intra-articular corticosteroids; Triamcinolone acetonide is among the longest-acting options (provides longer duration of action, e.g., up to weeks).

What are contraindications to intra-articular corticosteroid injections?

Local or systemic infection, prosthetic joint in the target site, unstable fracture involving the joint, uncontrolled diabetes, ongoing anticoagulation, and certain systemic conditions.

What is intra-articular hyaluronan and its mechanism?

Hyaluronan acts as a lubricant when injected into a joint, reducing friction and pain by mimicking synovial fluid; may reduce joint pressure and inflammation.

Name other intra-articular treatments used in OA besides steroids and hyaluronan.

Platelet-rich plasma (PRP), adipocyte (fat cell) injections, and stem cell therapies (experimental/current evidence limited).

What class of drug is duloxetine in OA management and when is it indicated?

Duloxetine is a serotonin–norepinephrine reuptake inhibitor (SNRI); used as an adjunct when paracetamol/NSAID alone are insufficient or in patients with widespread pain or depression. Dose typically starts low and may rise to 60–120 mg/day.

Non-pharmacological OA options.

Weight-bearing and aerobic exercises; weight loss; heat/cold therapy; walking aids; joint protection strategies; education; cognitive-behavioral therapy; physical and occupational therapy.

What are five patient education points for OA?

OA progression is usually slow/minimal; symptoms can fluctuate; symptoms do not always correlate with radiographs; modifiable risk factors exist; set realistic goals and expectations.

What is OA prognosis prognosis in terms of joints affected (spine, knees, hips)?

Spine, knees and hips are associated with poorer prognosis in OA.

What complementary medicines may be used in OA and their general evidence level?

Fish oil (omega-3) and glucosamine sulfate; evidence is low to moderate and mainly as adjuncts, not disease-modifying.

Explain PRN vs ATC dosing in OA pain management.

PRN: as-needed dosing for intermittent pain to reduce exposure; ATC: regular dosing to maintain steady analgesia and prevent pain spikes.

What is the mechanism of action and onset for methotrexate (MTX) in RA (not OA)?

MTX is a csDMARD that suppresses inflammation and immune responses by inhibiting dihydrofolate reductase; onset typically 1–2 months with weekly dosing and folic acid supplementation.

RA definition.

Rheumatoid Arthritis is a chronic systemic autoimmune disease with persistent synovial inflammation leading to progressive joint destruction, deformity, disability, and possible extra-articular manifestations.

RA gender predominance and age pattern.

RA affects about 1% of the population with a female predominance; female predominance is less pronounced in older adults.

Key genetic factor in RA pathogenesis.

Genetic predisposition including HLA-DR4 (and sometimes HLA-DR1); individuals with HLA-DR4 have higher risk (about 3.5x).

Common environmental factors linked to RA.

Smoking, chronic lung disease, infections, obesity, low vitamin D.

What is pannus in RA?

Inflamed, proliferative synovial tissue that invades cartilage and bone, driving joint destruction.

RA clinical features: morning stiffness duration and symmetry.

Morning stiffness lasting >1 hour; symmetric joint involvement, especially hands and feet; joint swelling, warmth, tenderness, reduced ROM.

RA hand deformities to know.

Ulnar deviation; Swan neck deformity (PIP hyperextension with DIP flexion); Boutonnière deformity (PIP flexion with DIP hyperextension); Z-thumb deformity.

RA extra-articular involvement examples.

Rheumatoid nodules; vasculitis; pulmonary effusion and fibrosis; ocular conditions including Sjogren syndrome; Felty syndrome (splenomegaly with neutropenia and thrombocytopenia).

RA serologic markers.

Rheumatoid factor (RF) and anti-CCP (ACPA); elevated CRP and ESR; synovial fluid leukocytosis.

RA diagnostic criteria snapshot.

Arthritis in ≥5 joints with morning stiffness >1 hour for >6 weeks; symmetric joint involvement; RF or CCP positive; elevated CRP/ESR; radiographic erosions.

RA treatment-to-target concept.

Set a specific goal (remission or low disease activity) and adjust therapy regularly to reach it; reduce inflammation and prevent damage.

First-line DMARDs in RA and why.

Conventional synthetic DMARDs (csDMARDs) with methotrexate as first line; slows disease progression and is often combined with NSAIDs or corticosteroids for symptom control.

MTX dosing and folic acid use in RA.

MTX dose: 10–25 mg orally/SC weekly; folic acid 5–10 mg weekly (on a different day from MTX) to reduce toxicity; onset 1–2 months.

MTX contraindications.

Pregnancy/breastfeeding; chronic hepatic disease; significant renal impairment (CrCl <10 mL/min); active infections; significant bone marrow suppression.

MTX adverse effects.

GI upset, mucositis, photosensitivity; hepatotoxicity; bone marrow suppression; rare pulmonary fibrosis.

Leflunomide mechanism and onset.

Inhibits dihydroorotate dehydrogenase, reducing pyrimidine synthesis and activated T lymphocyte proliferation; onset ~1 month.

Hydroxychloroquine use in RA and potential side effect.

csDMARD; dose 200–400 mg daily; onset slow (2–6 months); main concern is retinopathy with long-term use.

Sulfasalazine in RA: mechanism, dose, onset, key side effects.

Anti-inflammatory effects; dose up to 3 g/day; onset 1–3 months; side effects include GI upset, reversible oligospermia, hepatic toxicity, hypersensitivity (G6PD deficiency risk).

Azathioprine in RA: TPMT testing importance.

Azathioprine is a prodrug; TPMT testing is done before treatment because low TPMT activity leads to toxic metabolite accumulation and marrow suppression.

Biologic DMARDs (bDMARDs) classes and examples.

Targeted therapies (e.g., TNF-α inhibitors like etanercept, adalimumab; abatacept; rituximab; tocilizumab; anakinra).

Tofacitinib, baricitinib, upadacitinib in RA.

tsDMARDs; JAK inhibitors targeting intracellular pathways to reduce inflammation.

Corticosteroids in RA: role and dosing.

Glucocorticoids provide rapid symptom relief and act as bridge therapy until DMARDs take effect; typical short-term dosing is low-to-moderate (e.g., 5–15 mg daily).

Pregnancy considerations for RA meds (safe vs teratogenic).

Safe options include sulfasalazine (with folic acid), hydroxychloroquine, and certain corticosteroids; teratogenic agents include methotrexate, leflunomide; plan preconception with rheumatologist.

What is the gold standard imaging for central osteoporosis assessment?

Central DXA (cDXA) of hip and lumbar spine; gold standard for osteoporosis diagnosis and monitoring.

DXA score terms: T-score vs Z-score.

T-score compares to young healthy adults; Z-score compares to age-, sex-, and ethnicity-matched controls. T-score ≤ -2.5 defines osteoporosis; between -1 and -2.5 defines osteopenia.

FRAX vs Garvan tools.

FRAX estimates 10-year hip/any fracture risk based on 11 factors; Garvan includes falls history and fracture risk with a 4-question approach.

OP risk factors: non-modifiable vs modifiable.

Non-modifiable: female sex, aging, low body weight, prior fragility fracture; Modifiable: smoking, alcohol, glucocorticoids, low calcium, low vitamin D, sedentary lifestyle.

Primary vs secondary osteoporosis.

Primary: postmenopausal and age-related due to hormonal changes; Secondary: osteoporosis due to underlying disease, medications, or other factors.

Bisphosphonates: mechanism and common options.

Inhibit osteoclast-mediated bone resorption; examples include alendronate, risedronate (oral, weekly), and zoledronic acid (IV, yearly).

Bisphosphonates: dosing considerations and contraindications.

Oral forms must be taken on an empty stomach with water, remain upright 30–60 minutes; contraindicated in hypocalcemia, esophageal disorders, pregnancy; adjust for renal function.

Denosumab mechanism and dosing.

Human monoclonal antibody against RANKL; inhibits osteoclast formation and activity; 60 mg subcutaneously every 6 months; lifelong treatment if continued.

Raloxifene mechanism and key contraindication.

SERMs with estrogen-agonist effects on bone; antagonist on breast/endometrium reducing breast cancer risk; contraindicated in high risk of VTE.

Teriparatide (PTH 1-34) use and duration.

Anabolic agent increasing bone formation; 20 mcg daily subcutaneously for up to 24 months; high cost and limited duration.

Romosozumab mechanism and sequencing with bisphosphonates.

Sclerostin inhibitor that increases bone formation and reduces resorption; after stopping, switch to bisphosphonate or denosumab to maintain gains.

Estrogen-containing therapy in OP: risks and indications.

HRT can be used for prevention/treatment of postmenopausal osteoporosis in selected women; risks include VTE, stroke, breast/endometrial cancer; use lowest effective dose for shortest duration.

Calcium: key functions and supplement options.

Essential for bone/teeth, muscle contraction, coagulation; supplements include calcium carbonate (40% elemental Ca, first-line) and calcium citrate (21%) with fewer GI interactions; avoid taking with PPIs when using carbonate.

Vitamin D role in bone health.

Essential for calcium absorption; cholecalciferol (D3) or ergocalciferol (D2) convert to 25(OH)D then to active 1,25(OH)2D (calcitriol); deficiency treated with loading and maintenance dosing.

Vitamin D deficiency symptoms and deficiency risks.

Rickets (children), osteomalacia (adults), increased fracture risk, muscle weakness; risk factors include limited sun exposure and malabsorption.

Gout: definition and hyperuricemia.

Gout is a crystal-induced arthritis due to monosodium urate crystals in joints/tissues; hyperuricemia is elevated serum uric acid without necessarily gout symptoms.

Gout epidemiology in Australia and sex distribution.

Gout affects about 1.7% of Australians; higher prevalence in Aboriginal Torres Strait communities; more common in males and in older individuals; incidence increasing worldwide.

Gout pathophysiology: uric acid production and excretion.

Uric acid derived from dietary purines and endogenous breakdown of nucleic acids; about 2/3 excreted by kidney, 1/3 by gut; imbalances lead to hyperuricemia.

Key enzymes involved in gout pathophysiology.

PRPP synthetase (upregulated in gout) and HGPRTase (deficiency increases uric acid production).

Lesch-Nyhan syndrome.

X-linked disorder due to HGPRT deficiency causing excessive uric acid, developmental issues, dystonia, self-injurious behavior.

Gout clinical phenotypes: podagra, interval gout, tophaceous, atypical, nephropathy.

Podagra: acute monoarthritis of the first MTP (great toe); interval gout: asymptomatic; tophaceous gout: urate deposits in soft tissue; atypical gout: polyarthritis; gouty nephropathy: urate crystals in kidney.

Acute gout attacks: common trigger/time of day.

Typically nocturnal due to fluid shifts in joints and urate crystal precipitation during sleep.

Gout diagnosis gold standard.

Joint aspiration showing monosodium urate crystals; serum urate levels can be elevated but are not diagnostic alone.

First-line treatment for acute gout attacks.

NSAIDs (e.g., indomethacin 25–50 mg 2–4 times daily; max 200 mg/day), or intra-articular corticosteroids; colchicine can be used with caution.

Colchicine mechanism and dosing for acute gout.

Inhibits microtubule polymerization, reducing leukocyte migration; typical regimen: 1 mg now then 0.5 mg in 1 hour (total 1.5 mg) within 24 hours; avoid >2–3 days due to toxicity.

Colchicine interactions and toxicity considerations.

CYP3A4 and P-glycoprotein pathways; grapefruit juice inhibits CYP3A4 increasing colchicine levels; dose adjustments needed in renal/hepatic impairment.

Allopurinol mechanism, starting dose and max.

Xanthine oxidase inhibitor reducing uric acid production; starting dose 50 mg daily, titrate to target SUA with max 900 mg/day; HLA-B*58:01 risk (common in Asian descent) for hypersensitivity.

Preventing urate-lowering therapy flare when starting allopurinol.

Co-administer colchicine 0.5–0.6 mg daily for 6 months or NSAIDs short-term to prevent flare.

Febuxostat: when used and cautions.

Non-purine xanthine oxidase inhibitor; alternative to allopurinol; potential increased risk of cardiovascular events; adjust dose in liver impairment.

Uricosurics: mechanism and cautions.

Increase uric acid excretion by inhibiting proximal tubule reabsorption; ensure good hydration to prevent nephrolithiasis; benzobromarone not approved in Australia.

Acute gout nephrolithiasis rate and urine pH influence.

Nephrolithiasis occurs in about 15% of gout patients; uric acid stones form in acidic urine (pH <5.5) and dissolve in neutral/alkaline urine.

Gout pharmacologic options for chronic management.

Colchicine; allopurinol; febuxostat; probenecid; benzbromarone (uricosurics) with titration to target SUA.

Gout diet and lifestyle advice.

Balanced diet, adequate fluids, limit purine-rich foods if possible; maintain healthy weight; avoid alcohol and high-fructose beverages; exercise.

Pain physiology: transduction, conduction, transmission.

Transduction: nociceptor activation by mechanical, thermal, chemical stimuli; Conduction: action potentials along A-delta and C fibers; Transmission: signals travel to spinal cord and brain via nociceptive pathways.

Types of nociceptors and fibre types.

A-delta (fast, sharp pain) and C fibers (slow, dull pain); ABeta fibers sense non-noxious stimuli.

Pain modulation mechanisms.

Descending pathways with endogenous opioids, norepinephrine, and serotonin can dampen pain; central sensitization can amplify pain signals.

What is DN4 used for?

DN4 assessment tool used to identify neuropathic pain.

What is the WHO Analgesic Ladder concept?

A staged approach to pain management—start with non-opioids, add weak opioids and adjuvants for mild–moderate pain, escalate to strong opioids for severe pain; include adjuvants and non-pharmacologic strategies.

Opioids: basic MOA.

Activate opioid receptors to inhibit nociceptive transmission via decreased calcium influx, increased potassium efflux, and inhibition of adenylyl cyclase, reducing neurotransmitter release.

Opioid receptor types and their distribution.

Mu (MOR), delta (DOR), kappa (KOR), and ORL-1; MOR is primarily responsible for analgesia and many side effects; receptors are widely distributed in CNS and peripheral tissues.

What is opioid tolerance and what are its main mechanisms?

Tolerance is the need for higher doses to achieve the same effect; mechanisms include receptor downregulation/desensitization, intracellular signaling adaptations, and NMDA receptor involvement.

What is opioid dependence and withdrawal symptoms?

Dependence is physiological adaptation; withdrawal can include agitation, hyperalgesia, autonomic symptoms (sweating, mydriasis), GI symptoms, and flu-like symptoms when opioids are stopped.

Naloxone and methylnaltrexone use.

Naloxone reverses opioid-induced respiratory depression; methylnaltrexone is a peripherally acting antagonist used for opioid-induced constipation without reversing analgesia.

Opioid conversion safety principle.

When switching opioids, use a 25–50% lower dose than the calculated equi-analgesic starting dose due to incomplete cross-tolerance; titrate based on response.

What are common opioid adverse effects?

Nausea, vomiting, constipation, sedation, respiratory depression, pruritus from histamine release (some opioids), urinary retention, myosis.

Cannabinoids: main active components and receptor targets.

THC (psychoactive) and CBD (non-intoxicating); THС acts mainly on CB1 (brain) and CB2 (immune system); CBD modulates inflammation and has a different receptor profile (5-HT1A, etc.).

Endocannabinoid system components.

Endocannabinoids (anandamide, 2-AG), cannabinoid receptors (CB1, CB2), and enzymes for synthesis/metabolism.

THC vs CBD pharmacodynamics in pain management.

THC provides analgesia, euphoria, appetite stimulation; CBD provides anti-inflammatory, neuroprotective, and anxiolytic effects with less psychoactivity; combinations (ratios) influence efficacy and tolerability.

Cann medicinal product forms used in Australia.

Nabiximols (whole plant extract), nabilone, dronabinol (synthetic THC); several products on ARTG with varying CBD/THC content.

General safety considerations for medicinal cannabis.

Not first-line; assess risks/benefits; consider mental health history; potential for contraindications in pregnancy, psychosis, cardiovascular disease; monitor for drug interactions via CYP450 pathways.

Cannabis pharmacokinetics: inhaled vs oral forms.

Inhaled: rapid absorption, effects within minutes, 2–4 hours duration; oral: slower onset (30–90 min) with 8–24 hour duration; bioavailability lower for oral forms.