Summary BNF Chapter 10 Notes - Musculoskeletal

RHEUMATOID ARTHRITIS (RA)

QUICK PATHOPHYSIOLOGY RECAP:
- RA = Chronic autoimmune polyarthritis which is SYMMETRICAL
- Like many other autoimmune disorders (e.g. asthma, IBDs), RA causes FLARE UPS

SYMPTOMS (Joint Pain & Stiffness)
- Morning stiffness of affected joints > 1 hour RA typically affects small,
- Swelling of affected joints during the day interphalangeal joints of hands & feet
- Joint pain at NIGHT  awakening – but can affect larger joints too

Like tremor in Parkinson’s, pain is worse at rest but improves with activity

COMPLICATIONS OF RA: (if left untreated)
- Joint deformities: chronic inflammation  bone & cartilage erosion  joint
misalignment  deformities
- Extra-articular inflammation: inflammation can occur at other organs e.g. mucosa,
heart, lungs (this can be FATAL)
- Carpal tunnel syndrome: inflamed carpal tunnel  compression of median nerve

DIAGNOSTIC MARKERS OF RA (from blood tests):
- C-reactive protein (CRP) – INCREASED in RA CRP & ESR are non-
o CRP is involved in activating the complement system specific biomarkers of
- Erythrocyte Sedimentation Rate (ESR) – INCREASED in RA INFLAMMATION

RA TREATMENT
OVERVIEW:
- Like IBDs, RA-treatment aims to INDUCE & MAINTAIN REMISSION (prevent relapse)
- As soon as Dx is confirmed – START DMARD treatment (even if symptoms are mild)

TREATMENT REGIMEN:
1- Start with conventional DMARD (MTX, SSZ, Leflunomide) w/ or w/out a STEROID
o DMARDs take 2-3 MONTHS before they start working – steroids work
instantly – so creates a bridge until DMARDs kick in
o DMARDs can be used chronically, but steroids CANNOT  complications:
 Osteoporosis
 Adrenal insufficiency
 Psychiatric reactions
2- If still no remission – combine TWO conventional DMARDs
3- If still no remission – combine ONE conventional DMARD w/ ONE biological DMARD

NSAIDs can be used for short courses to relieve pain – but be cautious of INTERACTIONS:
- NSAIDs & Steroids = both inhibit COX  increase GI bleeding risk
- NSAIDs & MTX = NSAIDs  renal impairment  MTX toxicity (so monitor MTX-level)

NSAIDs do NOT have notable interactions with other DMARDs (only MTX)

, Although it’s a DMARD,
HCQ can worsen PSORIASIS
– cautionary use

HYDROXYCHLOROQUINE (HCQ)
MOA:
- Similar to calcineurin inhibitors  inhibits synthesis/activity of IL-2  less T & B-cell
activation  immunosuppression (NOT as strong as other DMARDs)

INDICATIONS: Normally used where other conventional DMARDs have failed in RA

SIDE EFFECTS:
1- RETINOPATHY: can present as blurred vision, change in iris colour – damage can be
IRREVERSIBLE (so regular eye checks are important)
- HCQ-induced retinopathy is uncommon – but incidence increased by RISK FACTORS:
o Using HCQ > 5 years (greater cumulative exposure)
o Having renal and/or hepatic impairment (less clearance of drug)
2- Other ADRs of immunosuppressants: infection risk, anaemia, GI effects


GOUT
PATHOPHYSIOLOGY RECAP:
- GOUT = chronic monoarthritic disorder characterised by HYPERURICAEMIA
- Uric acid (UA) levels are naturally very high in many of us due to purine metabolism
- Many people w/ hyperuricaemia are ASYMPTOMATIC (not considered to have gout)
- When UA precipitates out of ECF  sharp UA crystals  accumulate in joints & SC
tissue  arthritis (inflamed joints)

CAUSES:
- Increased consumption of purines (metabolised to UA)
o Shellfish, Red Meat, Organ Meats (e.g. Liver) & Alcohol (source of purines)
- Reduced clearance of UA
o Renal impairment reduces excretion of UA
- Side effects of drugs:
o Diuretics: have hypovolemic effect  increases risk of UA precipitation
o Cytotoxics: risk of TLS  release of purines into ECF  metabolised to UA

SYMPTOMS
- Inflammation in the 1st metatarsal phalangeal (MTP) joint – AKA the big toe joint
- Gouty tophi: UA build-up in SC tissue  painful nodules – often affects ears/fingers
- Kidney stones: late COMPLICATION of gout (if left untreated)

Like RA, gout causes flare ups – these are EXTREMELY PAINFUL – so reducing
hyperuricaemia is essential in maintaining remission

Gout Vs Rheumatoid Arthritis (RA)
Gout Rheumatoid Arthritis
- Cause: Hyperuricaemia - Cause: Autoimmune attack
- Often monoarticular - Often polyarticular
- Often asymmetrical joint involvement - Often symmetrical joint involvement
- Complications: Tophi, kidney stones - Complications: deformities, endocarditis,
- Treatment: carpal tunnel syndrome
- Remission: XOi - Treatment:
- Flares: NSAIDs (NOT aspirin), steroids, - Remission: DMARDs
colchicine - Flares: NSAIDs, steroids