MSK Flashcards
Brief pathology of osteoarthritis
Degenerative progressive destruction of cartilage from repeated mechanical forces
Disruption of chondrocytes prevents rebuilding
Usually in synovial joints
Why is obesity considered a pro-inflammatory state?
Bc it releases IL1, TNF and adipokines
RF of osteoarthritis
Older age
High intensity labour
Joint hypermobility
Diabetes
F > M
Obesity
COL2A1 collagen type 2 gene plays a role
Why is age a risk factor for OA?
Cumulative effect of traumatic insult and ↓ of neuromuscular function
Main pathological features of OA
Loss of cartilage
Disordered bone repair
Key Presentation - OA
Painful joints, stiffness < 30 mins in morning
Worse throughout the day
Occurs at PIP (Bouchard) and DIP (Heberden)
What effects do oestrogen have on bone turnover?
And hence, what is a RF for MSK diseases e.g. osteoporosis, OA?
Oestrogen has restraining effect on bone turnover
∴ EARLY MENOPAUSE results in ↓ trab. Th, strength and bone connections
List 4 other signs/symptoms of OA
Joint pain on movement
Tenderness
Crepitus
Asymmetrical joint involvement
Ix Osteoarthritis
XRAY - LOSS
Loss of joint space
Osteophytes
Subchondral sclerosis (more white on XR)
Subchondral cysts
DDx OA
RA
Gout
Psoriatic arthritis
Tx OA
1. Px education & lifestyle changes
(weight loss if obese, physiotherapy, occupational therapy)
2. Analgesic ladder
a). Paracetamol, topical NSAIDs, topical capsaicin
b). Oral NSAIDs (+ PPI)
c). Opiates e.g. codeine, morphine
also, intra-articular steroid injections - hyaluronic acid
If extreme, joint replacement
(avoid steroids before surgery bc immunosuppressive)
What type of hypersensitivity reaction is RA?
Type III
RF RA
Female! (premenopausal women 3x more affected than men)
HLA-DR4 and HLA-DRB1 (more susceptible, associated w/ ↑ severity)
FHx
Stress
Infection
Smoking
What are the diagnostic criteria for RA?
Need 4/7 to be diagnostic
Rheumatoid nodules
Rh factor POS
Radiographic changes (XR LESS)
Arthritis of hand joints
Morning stiffness > 30 mins
Symmetrical
State and describe hand deformities found w/ RA
Ulnar deviation
Boutonniere deformity - PIP flexion, DIP hyperextension
Swan neck deformity - PIP hyperextension, DIP flexion
State 10 other signs/symptoms of RA
Digital infarcts along nail bed
Anaemia - normochromic/cytic
Palpable lymph nodes
Bursitis
Tenosynovitis
Warm, red, tender joints
Joint pain worse in mornings/cold
Loss of function
Popliteal cyst
Rheumatoid nodules at pressure points
Sicca
Carpal tunnel syndrome
Fatigue and malaise
Symmetrical
DIPs are usually spared!
Ix RA
FBC/Bloods
Rh factor POS (sensitive)
Anti-CCP POS (specific, not routine)
↑ ESR, ↑ CRP, ↑ Platelets
XR - LESS
Loss of joint space
bone Erosions
Soft tissue swelling
Soft bones (osteopenia)
Genetic testing
State some extra-pulmonary manifestations of RA
Caplan’s syndrome (esp in coal miners)
Felty’s syndrome
Anaemia of chronic disease
Lymphadenopathy
2° Sjogren’s syndrome
Amyloidosis
DDx RA
Psoriatic arthritis
OA
Symmetrical seronegative spondyloarthropathies
Tx RA
MDT treatment!
- NSAIDs (+PPI)
Steroids initially, for flare ups to settle - DMARDs e.g. methotrexate, leflunomide, sulfasalazine hydroxychloroquine (mildest DMARD ∴ preferential if disease isn’t too severe)
a) one of above
b) 2 of above
c) Methotrexate + TNF inhibitor
d) Methotrexate + biologic e.g. Rituximab
Remember :
OA less convincing response to NSAIDs than RA
RA - worse w rest, better w movement. OA is opposite
RA - symmetrical, OA - not
At what age, is the peak bone mass?
29 years
State 1° causes of osteoporosis
Post-menopause
Age
bc oestrogen protects bone!
State 2° causes of osteoporosis
SHATTERED
Steroid use
Hyperthyroidism/hyperparathyroidism
Alcohol/Smoking
Thin (low BMI < 22)
Testosterone low
Early menopause
Renal or liver failure
Erosive / inflammatory bone disease
Dietary calcium low
Key presentation of osteoporosis
Fractures!
Esp if happens when/where it shouldn’t happen
Ix Osteoporosis
DEXA Scan BMD measurement
T score (esp at hip)
(then compared against gender-matched YA average)
> -1 normal
Between -1 and -2.5 = Osteopenia
<-2.5 = Osteoporosis
ALSO : FRAX score - 10 year probability of major fracture
When ↓ seru Ca2+,
Parathyroid gland secretes PTH
∴ ↑ bone resorbtion and Ca2+ released into blood stream
When ↑ serum Ca2+,
Parathyroid gland produces calcitonin,
inhibits PTH secretions,
↑ bone formation and Ca2+ absorbed from bloodstream
What happens to trabecular architecture with age?
↓ Trab Th
↓ Connections between horizontal trabeculae
∴ ↓ Trab strength (∴ ↑ risk of fractures)
Why are horizontal trabeculae so important?
Makes bones a LOT stronger
Eular-Buckling theory
During bone turnover due to oestrogen deficiency, what type of bone is mostly lost?
Cancellous bone
What occurs if there’s too much mineralisation in bones?
Become stiff and shatter
What occurs if there’s too little mineralisation in bones?
Bones aren’t strong and break
What occurs if there’s too little mineralisation in bones?
Bones aren’t strong and break
What do bloods show in osteoporosis?
Ca2+, phosphate, alkaline phosphate are all normal
Tx Osteoporosis
Lifestyle changes - Avoid falls!!
Quit smoking, ↓ alcohol, healthy weight
Adcal D3 (Vit D + Calcium)
-
Oral bisphosphonate (↓ osteoclastic activity)
e.g. alendronate (10mg daily), risendronate (5mg daily) - Denosumab or Strontium ranelate or Teriparatide
ALSO : consider Hormone Replacement Therapy in young post-menopausal women
What does ESR stand for?
Erythrocyte Sedimentation Rate
Define ESR
Measure of how quickly erythrocytes will fall to bottom of tube
What does ESR measure?
Fibrinogen values
Rise w/ inflammation bc erythrocytes stick together and ∴ fall faster
How does ESR rise and fall?
Rises and falls SLOWLY (days to weeks)
What causes ESR to rise falsely? (False positives)
Female
Age
Obesity
SE Asian
Hypercholestrolaemia
High Immunoglobulin (myeloma)
Full form of CRP
C-Reactive Protein
Define CRP
Acute phase protein, released in inflammation
Where is CRP produced?
In liver in response to IL-6
How does CRP rise and fall?
QUICKLY - high at 6 hours, peaks at 48 hours
∴ if patient has infection in 24 hours, ESR won’t have risen but CRP will have
SPINEACHE go
Sausage digit (dactylitis)
Psoriasis
Inflammatory back pain
NSAID good response
Enthesitis (heel)
Arthritis
Crohn’s / Colitis / ↑CRP (but CRP can be normal)
HLA B27
Eye (uveitis)
What joint do Spondyloarthropathies typically affect?
Spinal and sacroiliac joints
Spondyloarthropathies are _____
seronegative (no RhF)
HLA-B27 encoded by
Major histocompatibility complex on chromosome 6
Why does HLA-B27 cause disease?
Causes autoimmune disease by molecular mimicry
Infection occurs and infection agents have peptides v similar to HLA-B27
∴ immune system launches attack on HLA-B27
Epidemiology of Ankylosing Spondylitis
*More common and severe in Males
*Presents in late teens/20s
↓ Incidence in African and Japenese people
Native NA ↑ incidence
Ix Ankylosing Spondylitis
Bloods -
HLA-B27 positive
↑ CRP, ↑ ESR
Normocytic anaemia
XR
MRI
Schober’s test!
Why can you perform an MRI for ankylosing spondylitis?
Bc before bamboo spine, bone marrow oedema occurs first - showed by MRI
What XR signs are there in Ankylosing spondylitis?
Sacroiliitis
Enthesitis
Dagger sign
Syndesmophytes
BAMBOO SPINE
Ankylosing Spondylitis, diagnose if :
Age at onset < 45 years
At least 3 months back pain
XR/MRI shows sacroiliitis + at least 1 SPINEACHE feature
State some other signs/symptoms of Ankylosing Spondylitis
Worse with rest
Slow onset morning stiffness > 30 mins
Fatigue
Buttock/thigh pain - sacroiliac joints
Rashes/skin changes
Describe Schober’s test
Make a point at L5
Put a finger 10cm above and 5cm below
Px bends forwards
If distance between 2 fingers is < 20 cm, supports a diagnosis of Ankylosing Spondylitis
Rf for Ankylosing Spondylitis
HLA-B27!
Environment : Klebsiella, Salmonella, Shigella
Differences between Ankylosing Spondylitis and RA
RA affects smaller joints and is usually symmetrical
AS affects spine and is asymmetrical
Is HLA-B27 diagnostic for ankylosing spondylitis?
NO!
Red flags for back pain
TUNA FISH
Trauma, TB
Unexplained weight loss & night sweats
Neurological deficits, bowel/bladder incontinence
Aage <20 and > 55
Fever
IVDU
Steroid use or immunosuppressed
History of cancer, early morning stiffness
What is Scleroderma?
Multi-system disease w/ involvement of skin. Vascular damage (fibrosis) of small arteries, arterioles and capillaries.
Epidemiology of Scleroderma
Female!
30 - 50 years
Rare in children
RF Scleroderma
Exposure to vinyl chloride, silica dust, rapeseed oil, trichloroethylene
Drugs - bleomycin
Genetics
Types of Scleroderma
- Diffuse - CREST + organ problem
- Limited - just CREST
What are the FIRST symptoms usually in Scleroderma?
Raynaud’s
Sclerodactyly
Ix Scleroderma
Bloods - norm anaemia
RhF+
For limited : Anti-centromere antibodies
For diffuse : Anti-topoisomerase-1 (anti SCL-70) antibodies & anti-RNA polymerase III
CXR - exclude other causes
Hand XR - see calcium deposits
Barium swallow - confirm oesophageal dysmotility
What systemic effects can Scleroderma have?
GI - heartburn, dysphagia, malabsorption, pseudo-obstruction
Renal - AKI, CKD, acute hypertensive crisis
Lung - fibrosis, pul HTN
Heart - arrhythmias
Tx Scleroderma
No cure. Immunosuppressants used to slow progression - cyclophosphamide
MDT - physio
Treat symptoms
Raynaud’s : vasodilators - nifedipine
Analgesia
PPI for reflex
Pul HTN - sildenafil
etc
Prognosis Scleroderma
~ 12 years after diagnosis (avg)
However, if limited, could have normal lifespan
Complications of Sjorgren’s
B-Cell lymphoma !!!!!!
A patient comes in with a red, hot, swollen joint. What do you do?
ASPIRATE IT ALWAYS !!!!!!!!!!!!!!
COULD BE SEPTIC ARTHRITIS
Causes of Septic arthritis
S. Aureus
Neisseria gonorrhoea - sexually active, young
Staph. Epidermis - prosthetic joint
E.coli / Klebsiella - immunocomp
H. influenzae - infants, but rare bc immunisation now
RF Septic Arthritis
> 80 years, infants (always suspect in ANY joint problem in children)
Pre-existing joint disease
DM
Prosthetic joints
Immunosuppress
Penetrating trauma
Key presentation Septic Arthritis
*Knee, hip, shoulder
Acute, painful, red, hot, swollen joint
SEPTIC UNTIL PROVEN OTHERWISE
Other signs/symptoms of septic arthritis
Fever
Impaired range of motion
Refusing to bear weight
Monoarthritis
Ix Septic Arthritis
ALWAYS ASPIRATE FIRST -> GS !!
FBC - ↑ WBC, neutrophilia
Blood cultures
Polarised light microscopy - exclude gout/pseudogout
What would you see in the aspirate of a patient with Septic Arthritis?
Turgid fluid - non-transparent
Leukocytes
Send for gram-stain
Normal = yellow, clear, thin
Why is Septic Arthritis a medical emergency?
Can destroy joint in under 24 hours !!!!!!!!
Tx Septic Arthritis
Stop immunosuppressive drugs (e.g. methotrexate) and anti-TNF for as long as on Abx
ANTIBIOTICS !
Empirical e.g. flucloxacillin
then pathogen-directed, 3-6 weeks
(IF on steroids, double dose. If not, then don’t give steroids)
What Abx against S. Aureus?
Flucloxacillin
Erythromycin
Doxycycline
Tetracycline
Causes of Osteomyelitis
Staph. Aureus
Salmonella - if sickle cell anaemia
Staph - coagulase neg (epsa)
H. influenzae
How does bacteria reach the joints to cause septic arthritis?
Direct inoculation or via haematogenous spread
Key presentation of OM
Dull pain at site of OM
Onset - several
Non-specific tenderness and pain
Reluctance to weight bear
Name some systemic symptoms of OM
Fever
Rigors
Sweat
Malaise
Ix OM
FBC - ↑ ESR, ↑ CRP, ↑ WBC, but can be normal in chronic
XR - can see periosteal reaction, low sensitivity/specificity for OM i.e. cannot exclude
GS : Bone biopsy (but must be done thru not infected tissue)
MRI - best imagine to establish diagnosis
must be done after XR
Blood cultures
Tx OM
Antibiotics - tailored to culture
If vascular disease, less reliable Abx penetration ∴ longer duration
Surgery if severe
DDx OM
Charcot joint! - damage due to sensory nerves affected by DM
Gout
Fracture
Ix Psuedogout
Joint aspirate and polarised light - rhomboid crystals, positively birefringent, no bacterial growth
GS : XR - Chondrocalcinosis
Hidden sites for psoriasis
Behind ear/inside ear
Scalp
Pitting in nails/ onokylisis
Umbilicus
Penile
Natal cleft
State the types of Psoriatic Arthritis
5 patterns of disease
- Asymmetrical oligoarthritis
- Symmetrical seronegative polyarthritis
- Spondylitis
- Distal interphalangeal arthritis
- Arthritis mutilans
Describe symmetrical polyarthritis
Females
Hands, wrists, ankles and DIP joints
MCP less common (∴ unlike RA but otherwise v similar)
Describe asymmetrical oligoarthritis
Mainly fingers, toes and feet
Only a few joints
Describe spondylitic psoriatic arthritis
Males
Back stiffness, sacroiliitis, alanto-axial joint involvement.
Can also affect - spine, achilles tendone, plantar fascia
Key presentation of Psoriatic Arthritis
Plaques of psoriases - in hidden areas
Onycholysis
Dactylitis
Enthesitis
Ix Psoriatic Arthritis
Bloods - HLA-B27, ↑ ESR
NEG RhF and NEG anti-CCP
GS : XRAY
Erosion in DIP, periarticular new bone formation
Oateolysis
Pencil-in-cup deformity
Tx Psoriatic Arthritis
Similar to RA -
NSAIDs
DMARDs - methotrexate, sulfasalazine, leflunomide
TNF-i or monoclonal antibodies - etanercept, infliximab, adalimumab
Steroid injection
Physio
Complications of Psoriatic Arthritis
Arthritis mutilans
Most severe form
Occurs in phalanxes
Osteolysis of bones around joint - causes progressive shortening
Skin folds as digit shortens - telescopic finger
Ix Anti-phospholipid Syndrome
Anti-cardiolipin antibody test
Anti-B2-glycoprotein test
Lupus anticoagulant test
^ All 3 are needed to diagnose
Positive test on at least 2 ocassions 12 weeks apart
What does the anti-cardiolipin antibody test test for?
IgG or IgM antibodies that bind to cardiolipin (neg charged phospholipid)
What does the lupus anticoagulant test detect?
Changes in ability of blood to clot
Tx Anti-Phospholipid Syndrome
Manage risk factors e.g. smoking
Long term warfarin (LMWH if trying to conceive)
Prophylaxis e.g. for stroke - aspirin or clopidogrel
Anti-Phospholipid Syndrome causes
CLOTs
Coagulation defect
Livedo reticularis
Obstetric issues
Thrombocytopenia
Key presentation of Anti-Phospholipid Syndrome
Thrombosis !!!!!!!!!
e.g.
Arteries - stroke, MI, TIA
Veins - Budd-chiari syndrome, DVT, PE
Miscarriage !!
Cause of Anti-Phospholipid Syndrome
HLA-DR7 mutation + Environmental trigger
e.g. infection (malaria), drugs (CV drugs - propranolol, anti-psychotic - phenytoin)
How soon after an infection do clinical signs of reactive arthritis occur?
1-4 weeks
What is small vessel vasculitis called?
Granulomatosis with Polyangiitis
aka Wegener’s Granulomatosis
RF Psuedogout
Females > 70years
Hyperthyroidism
Hyperparathyroidism
XS iron or calcium
RF Gout
Middle-age
Overweight
High purine diet (red meat, seafood)
Alcohol
Diuretics
FHx
Renal disease/existing CVD
RF RA
Middle age
Female! (3x more common)
FHx
Other autoimmune diseases
RF OA
High intensity labour
Older age
Obesity
Trauma
Female
FHx
What vessels does Giant Cell Arteritis affect?
Aorta and/or its major branches (carotid and vertebral arteries)
Often temporal artery!
RF Giant Cell Arteritis
> 50 years
Northern European
Females! (2-3x more common)
Hx of polymyalgia rheumatica
(RA, SLE, scleroderma)
Key presentation of Giant Cell Arteritis
Headache! new onset, unilateral over temporal area
Scalp tenderness (hurts to brush hair)
Other signs/symptoms of Giant Cell Arteritis
Jaw claudication
Visual disturbances! - blurred vision, diplopia, amaurosis fugax, blindness
On palpitation, temporal arteries tender and thickened
Pulse may be diminished
What type of vessels does Takayasu’s arteritis affect?
Large
What type of vasculitis affects medium-sized vessels?
Polyarteritis nodosa (PAN)
What type of vasculitis affects small vessels?
Granulomatosis with polyangiitis
Ix Giant Cell Arteritis
Bloods - ↑ ESR +/- ↑ CRP (v sensitive)
ANCA neg
ESR > 50 mm/hour
Ultrasound - Halo sign of temporal and axillary artery
GS : TEMPORAL ARTERY BIOPSY
shows giant cells, granulomatous inflammation
Tx Giant Cell Arteritis
High dose prednisolone (40-60mg) then gradual reduction
Long-term (12-18 months) ∴ give GI and bone protection -> Lansoprazole, alendronate, Ca2+, Vit D
if visual change - emergency! IV methylprednisolone
What locations does Polyarteritis Nodosa occur?
Medium muscular arteries, esp at branch points
Skin, GI tracts, kidneys, heart
NOT veins
RF Polyarteritis Nodosa
Associated with Hep B! (and Hep C, HIV)
More common in LICs
DDx Giant Cell Arteritis
Migraine
Tension headache
Trigeminal neuralgia
Polyarteritis nodosa
Presentation of Polyarteritis Nodosa
Cutaneous/subcutaneous nodules
Unilateral orchitis
Peripheral neuropathy - mononeuritis
Abdo pain
Livedo reticularis
HTN
Ix Polyarteritis Nodosa
Bloods - ↑ ESR +/- ↑ CRP
HBsAG
ANCA neg
Biopsy - transmural fibrinoid necrosis
Tx PAN
If Hep B neg - corticosteroids + immunosuppressant (cyclophosphamide)
If Hep B pos - corticosteroids, then antivirals, plasma exchange
Control BP - ACEi
Complications PAN
GI perforation & haemorrhages
Arthritis
Renal infarcts
Strokes
MI
Age of presentation of Granulomatosis with Polyangiitis
Late teenage years - early adulthood
Key presentation of Granulomatosis with Polyangiitis
Saddle shaped nose
Epistaxis (nosebleed)
Crusty nasal/ear secretions - hearing loss
Sinusitis
Cough, wheeze, haemoptysis
DDx Granulomatosis with Polyangiitis
Pneumonia (esp bc cough, wheeze, haemoptysis)
Ix Granulomatosis with Polyangiitis
Bloods - ↑ Eosinophils
c-ANCA !!!!!!!!!!
Histology - granulomas
Tx Granulomatosis with Polyangiitis
Corticosteroids
Cyclophosphamide
Complications of Granulomatosis with Polyangiitis
Glomerulonephritis
Describe Churg-Strauss
P-ANCA
No nasopharyngeal involvement
No granuloma
Small vessels?
check
Paget’s disease
Raised ALP
Ix Sjogren’s
Anti-Ro and Anti-La antibodies
Schirmer’s test
Tx Sjogren’s
Artificial tears, artificial saliva, vaginal lubricants
Hydroxychloroquine used to halt progression
What is Sjogren’s?
Autoimmune condition that affects exocrine glands
Difference between primary and secondary Sjogren’s
1º - condition occurs in isolation
2º - related to SLE or RA
RF Sjogren’s
FHx (first degree relative = 7x higher risk)
Female
> 39 years
