MSK Flashcards
What is Osteoarthritis?
Loss of articular cartilage
Wear & tear of joints
MC type of arthritis
RF OA
Elderly
After 55 years, females (menopause increases risk)
Previous joint trauma
Genetics
Obesity
RA
Gout
Obesity - low-grade inflam state, not mechanical RF
Joint hypermobility
Occupation! - manual labour (small joints of hands), farming (hips), football (knees)
OSTEOPOROSIS = ↓OA RISK !
Signs / Symptoms OA
Typical Px : Elderly patient w/ hip or knee pain (weight-bearing joints) or carpometacarpal joint (base of thumb)
Asymmetrical!
LESS THAN 30 mins morning stiffness
↓Pain with rest
Pain at end of day
↑Pain with activity
Crepitus
Bony swellings - DIP (Heberden’s) and PIP (Bouchard’s)
Effusion
Synovitis
Functional impairment
Tenderness
Deformities
DDx OA
RA
Gout
Pseudogout
Causes OA
Most - 1º (idiopathic)
2º - caused by other diseases e.g. obesity, haemochromatosis,
??
Ix OA
XR - LOSS
Loss of joint space
Osteophytes
Subchondral sclerosis
Subchondral cysts
CRP might be elevated
Rheum factor + ANA = NEG
MRI - shows early articular cartilage injury and subchondral BM changes
Aspiration of synovial fluid - if painful effusion, shows viscous fluid w few leucocytes
Main pathological features of OA
Loss of cartilage
Disordered bone repair
Tx OA
Conservative :
Px ed
Exercise
↓weight
Physio
Footwear
Occupational therapy
Walking aid
Medical
> Topical - NSAIDs, Capsaicin
> Oral - NSAIDs (caution!) w/ PPI if long term, paracetamol
Opioids - if above hasnt worked
not rlly gonna offer unless rllyyy bad and nothing else works ->
Intra-articular steroid injections (only short term relief - 2-10 weeks) - hyaluronic acid
Surgery
Remove osetophytes
Joint replacement - if VERY severe
Arthroscopy - ONLY if loose bodies (lasts only 10-15 years)
What is a loose body?
When small pieces of articular cartilage break off and “floats” in synovial fluid
Causes joints to lock
What are some indications of a loose body?
Uncontrollable pain (esp at night)
Significant limitations
What is Rheumatoid Arthritis?
A chronic, autoimmune, inflammatory symmetrical polyarthritis
RF RA
Female BEFORE menopause (After menopause, incidence is equal between M and F)
Family history
Smoking!!
Autoimmune conditions
Stress
Infection
Signs / Symptoms RA
Joint pain worse in mornings/with cold
Morning stiffness > 30 mins
Loss of function
Fatigue + malaise
Pain decreases with use
Warm, red, tender joints
Joints : SYMMETRICAL!
Small = MCP + PIP (not DIP usually)
Large (as disease progresses) = wrists, elbows, shoulders, knees, ankles
HAND DEFORMITIES : usually at IP joints
1. Ulnar deviation
2. Swan neck (or Z thumb)
3. Boutonniere deformity
Rheumatoid nodules at pressure points - elbow
Carpal tunnel syndrome
Popliteal cyst
What happens in a swan neck deformity?
PIP hyperextension
DIP flexion
What happens in a Boutonniere deformity?
PIP flexion
DIP hyperextension
Extra-Articular symptoms RA
Soft tissue :
Nodules! - usually at pressure points
Bursitis
Tenosynovitis
Muscle wasting
Haematological
Palpable lymph nodes
Splenomegaly
Anaemia
Felty’s triad (rare)
Eyes
Sicca
Sjogren’s
Episcleritis
Scleritis
Neuro
Mild sensory neuropathy (peripheral - legs>arms)
Cord compression
Myelopathy
Skin
Vasculitis
Lungs
Pleural effusion
Rheum nodules
Diffuse fibrosing alveolitis
Diagnostic criteria RA
Needs 4/7 of following
- Morning stiffness > 30 mins
- Arthritis of 3 or more joints
- Arthritis of hand joints
- Symmetrical
- Rheumatoid nodules
- Rheumatoid factor pos
- Radiographic changes - LESS
DDx RA
SLE
Psoriatic arthritis
Symmetrical seronegative spondyloarthropathies
Ix RA
XR - LESS
Loss of joint space
Erosions (peri-articular)
Soft tissue swelling
Soft bones (osteopenia)
Bloods
> Rheum factor = POS in 70% patients (but not specific)
> Anti-CCP = POS, vvv specific but not routinely done (If pos = worse prognosis)
> FBC - ↑ platelets, ↑ ESR, ↑ CRP, normochromic normocytic anaemia
MRI/US - erosions at joint margins and bones
If effusion present, then aspiration of joint = CLoudy bc ↑↑WBC
Tx RA
Upon diagnosis : 1st Line :
DMARDs - Methotrexate, Leflunomide
+
5-asa - Sulfasalazine
2nd Line:
Biologic - TNF-inhibitor
–
Symptom control - NSAID
–
If acute exacerbations, steroids (IM methyprednisolone)
MDT management - Rheum, OT, physio, GP
What is Osteoporosis?
Low bone mass
∴ bone fragility + ↑ fracture risk
What is osteopenia?
Precursor to osteoporosis
T score between -1 and -2.5
What is Osteomalacia?
Poor bone mineralisation
bc lack of calcium (adult form of rickets)
∴ soft bones
Causes Osteoporosis
1º - post-menopause & age
2º - ↑bone turnover, SHATTERED
Steroid use (prednisolone)
Hyperthyroidism/Hyperparathyroidism
Alcohol/smoking
Thin (low BMI)
Testosterone low
Early menopause
Renal or liver failure
Erosive/inflammatory bone disease e.g. RA, myeloma
Dietary calcium low
Why does early menopause/post-menopause cause Osteoporosis?
Oestrogen protects bones
RF Osteoporosis
Think : Patient, Disease, Medication
Also think : SHATTERED
Patient
Old age
Female
FHx
↓BMI
Alcohol & smoking
Diet - ↓Ca2+ (lactose intolerant)
Athletes
Disease
Joint disease (RA, SLE)
Hyperthyroidism, Hyperparathyroidism
↑Cortisol - Cushing’s
↓Oestrogen/Testosterone
Renal disease (↓Vit D)
Previous fractures
Anorexia
Medication
Corticosteroids
Hormonal
Pathophysiology Osteoporosis
Essentially : ↑Resorption by osteoclasts, ↓formation by osteoblasts
W/ age, trab architecture changes :
↓Trab thickness
↓Connections in horizontal trab
∴ ↓Trab strength and ↑ fracture risk
–
Oestrogen def causes remodelling imbalance
What is osteoporosis characterised by?
- ↑↑Bone turnover
- Mostly cancellous bone loss
- Microarchitectual disruption
∴ NET LOSS OF BONE
Why is horizontal trabeclae very important?
Eular-Buckling theory
What is Eular-Buckling theory?
Baso,
In a column, less likely to bend or snap if there are fixed points
don’t quote me on this but basically what it means i think
Signs / Symptoms Osteoporosis
ASYMPTOMATIC UNTIL FRACTURE
Hip - neck of femur (if elderly falls on side/back)
Wrist - Distal radius, Colle’s/Smith’s fracture (fall on outstretched arm)
Verterbra - shorter/stooping, sudden onset on pain in spine - often radiates to front
Fragility fractures
Ix Osteoporosis
DEXA BMD (Dual energy XR & absorptiometry bone mineral density) - T-score
< - 2.5 + fracture = severe OP
< -2.5 = OP
between -1 and -2.5 = osteopenia
> -1 = Normal
–
XR
FRAX - fracture risk assessment (age, sex BMI, prev. fractures, steroids)
FBC - normal Calcium phosphate and alklaine phosphate
Tx Osteoporosis
1st line - ORAL BISPHOSPHONATES
1- alendronate daily
2 - diff oral bis e.g. risendronate
3 - If CI to bis, then strontium ranelate (↓ fracture rate)
Denosumab - monoclonal Ab, inhibits RANK which would otherwise activate osteoclasts
–
HRT - in menopausal women
Raloxifene - SERM (selective oestrogen receptor modulator), similar to HRT
–
Testosterone for men
How should you tell patients to take bisphophonates?
w LOTS of water and sitting upright for > 30 mins
Wait at least 30 mins before eating
Mechanism of Bisphosphonates for Osteoporosis
Inhibits bone resorption by inhibiting enzyme Farnesyl Pyrophosphate synthase by removing ruffled border
∴ ↓osteoclast activity
Prevention Osteoporosis
Adcal D3 - VitD & Ca2+
Ca2+ rich diet
HRT - for postmenopausal women
Corticosteroids - consider prophylactic bis
Regular weight bearing exercise
Stop smoking and alcohol
DEXA scans
S/E Bisphosphonates
Osteonecrosis of jaw
GI distress
↓ Ca2+
Renal toxicity
Oesophageal ulcers
What is Systemic Lupis Erythematosus?
Inflammatory, multisystem, autoimmune condition
What is SLE assoc w?
Raynaud’s
Anti-Phospholipid syndrome
Typical Patient of SLE
Female
20 - 40 years old
More common in Afro-Caribbean and Asian population
RF SLE
Pre-menopausal women
Afro-Caribbean/Asian
Genetics - HLA: DR2, DR3, C4, A, Null Allele
Drugs - Hydralazine, Isoniazide, procainamide, penillamine !
UV light
Smoking
EBV
What type of hypersensitivity reaction is SLE?
TYPE 3
Pathophysiology of SLE
Autoantibodies are produced by B cells
These target autoantigens
∴ form IMMUNE COMPLEXES (T3) at a variety of sites
∴ complement system activated
∴ neutrophil influx
∴ INFLAMMATION
Signs / Symptoms SLE
Remitting and relapsing
V non-specific symptoms : Malaise, fatigue, myalgia, rash, weight loss, skin problems, fever
Correctable ulnar deviation
Haematologically :
Anaemia
Thrombocytopenia
Neutropenia
Lymphopenia
Raynaud’s
Ix SLE
MUST HAVE 4/11 OF FOLLOWING FOR DIAGNOSIS !!!!!!!!
MD SOAP BRAIN
Malar rush - butterfly rash on face
Discoid rash
Serositis - pleuritis, pericarditis
Oral ulcers
Arthritis (non-erosive - similar to RA)
Photosensitivity - rashes on sun exposed areas
Blood disorder - ALL LOW
Renal disease - proteinuria
Anti-nuclear antibody POSITIVE
Immunological disorder - anti ds-DNA
Neuro disorder - seizures, myasthenia gravis etc
∴ INVESTIGATIONS WILL INCLUDE :
> Anti-nuclear antibody test (sens but not spec)
> Double stranded DNA antibody (spec but not sens)
> Other Abs - RF, anti-cardiolipin, Anti-RO, Lupus antibodies
↑ ESR (CRP might be normal)
↓C3 + C4
MRI/CT brain
POP QUIZ!
Patient comes in with multi-systemic disorder, ↑ ESR but normal CRP
What do you think of?
SYSTEMIC LUPUS ERYTHEMATOSUS
Tx SLE
Avoid triggers - UV protections
Lifestyle - stop smoking, weight loss
Topical - suncream etc
–
If ACUTE - IV Cyclophosphamide + high dose prednisolone
If NOT severe - Anti-malarial e.g. hydroxychloroquine and/or steroids e.g. prednisolone
IF severe - Immunouppressives e.g. Cyclophosphamide, methotrexate, ciclosporin, azathioprine
NSAIDs
Anti-coagulants
Plasmapheresis
Monitoring SLE
Kidney function should be monitored!
What is Gout?
Inflammatory arthritis assoc w/ hyperuricaemia
Negatively bifringent needle-shaped monosodium urate crystals
Typical patient of Gout
Men > 40 years !
Chinese, Polynesian, Filipino IF westernised diet (not in native county!)
Causes Gout
1. Under-excretion of Uric Acid
Hyperuricaemia
Alcohol
Obesity
DM (insulin resistance = ↑insulin)
HTN
Hypothyroidism, Hyperparathyroidism
Drugs - low dose aspirin, diuretics, lead poisoning, ethambutol, pyrazinamide, cyclosporine, tacrolimus
Renal - defect in URAT1 transported in kidney, seen in kidney disease
2. XS purines TOO MUCH RED MEAT, ORGAN MEAT, SHELLFISH, ANCHOVIES, ALCOHOL
Also : Metabolic syndrome - hyperlipidaemia
Lesch-Nyhan syndrome
3. ↑Production of uric acid
Chemo/Radiotherapy
Surgery - cell death
Carcinoma
Psoriasis
Myeloproliferative diseases - polycythaemia vera
Causes of Gouty attack
Anything that causes sudden alteration in uric acid conc
Aggressive intro/Sudden stop of hypo-uricaemic therapy
Alcohol/Shellfish binges
Sepsis, MI, acute severe illness
Trauma, surgery, dehydration
RF Gout
↑ Alcohol
Purine rich foods - shellfish, organ meat etc
High fructose intake - sugar
FHx
Age
Obesity
DM
IHD
HTN
Pathophysiology Gout
Purine from diet
Gets converted -> Hypoxanthine -> Xanthine
Then, Xanthine -> Uric acid
Catalysed by xanthine oxidase
Excreted in kidneys
–
If ↑↑Uric acid, XS is converted to monosodium urate crystals and deposited in tissues - TOPHI
Monosodium urate crystals can cause inflammation - ∴ more pain
Tends to form in peripheral joints (big toe) bc temperature is cooler and/or if previous trauma in joint
Signs / Symptoms Gout
Sudden onset of agonising pain, swelling and tenderness and redness - “toe on fire”
Pain precipitated by excess food, alcohol, dehydration, diuretic therapy
Recurrent episodes
Red, shiny, warm, PAINFUL joint w white deposits (tophi) on skin
Skin over joint has peeled off
DDx Gout
Septic Arthritis
Tophaceous gout
Ix Gout
JOINT ASPIRATION!! - to rule out septic arthritis, ALWAYS RULE OUT A RED, HOT JOINT
X-Ray ! - punched out erosions near joint
GS!! Polarised light microscopy - neg bifringent needle shaped monosodium crystals
Bloods - raised serum urate (can be normal)
POP QUIZ
A patient comes in with a hot, red joint. What do you do?
ASPIRATE ASPIRATE ASPIRATE!!!
ALWAYS RULE OUT A RED, HOT JOINT
to rule out septic arthritis
Tx Gout
Lifestyle - kcal restriction, modify diet, weight loss, ↓alcohol
DAIRY - protective! & cherries, vitamin C
–
1st line - NSAIDs e.g. ibuprofen
2nd line - Colchicine (If NSAIDs CI)
Prophylaxis - Xanthine oxidase inhibitors e.g. Allopurinol ! (rapidly reduces serum urate levels)
DO NOT use Allopurinol during acute attack!! Wait 3 weeks after attack to give
& ALSO give Colchicine for 6 months OR NSAID for 6 weeks otherwise will induce a gouty flare
Febuxostat if Allopurinol CI
What is Pseudogout?
Deposition of calcium pyrophosphate crystals in joints
Usually larger joints!
Knee > Wrist > Shoulder > Ankle > Elbow