MSK Flashcards
Characteristics of pain in degenerative joint disease?
Pain increases with use, clinks and cluncks
Characteristics of pain in inflammatory joint disease?
Pain eases with use
When do you get stiffness in inflammatory joint disease?
Greater than 60 mins in the morning and when at rest
When do you get stiffness in degenerative joint disease?
LEss than 30 mins, not prolonged in the morning
What is the swelling like in inflammatory joint disease?
Synovial swelling can be bony, usually hot and red
What is the swelling like in degenerative bone disease?
Swelling, not synovial, bony. clinically not inflammed
What population is more typical of inflammatory bone disease?
Young, psoriasis, family history
What population is more typical of degenerative bone disease?
Older, prior occupation/sport
Where does inflammaotory joint disease affect?
Hands and feet
Where does degenrative joint disease afffect?
1st CMCJ, DIPJ, knees
How does degenerative joint disease respond to NSAID’s
Not convincingly
How does inflammatory joint disease respond to NSAIDs?
Responds well
What is the definition of osteoarthritis?
Long term chronic degenerative bone disease. Loss of cartilage in joints resulting in bones rubbing together. Creating stiffness pain and impaired movement
What are the risk factors for OA?
High intensity labour, older age, high BMI
How do patients with OA present?
Painful joints which are stiff for 30mins or less in the morning. pain worse throughout the day
What are heberdens nodes?
A bony swelling in the distal interphalangeal joint
What is a bouchard node?
A bony swelling in the proximal interphalangeal joint.
What is the acronym for remebering signs on x-ray for OA?
LOSS
What does LOSS stand for?
L - loss of joint space
O - Osteophytes
S - Sclerosis
S - Subchondral cycsts
How do you manage OA?
Analgesia and joint replacaement
What are the complications of OA?
Destruction of the joint and loss of function
What is rheumatoid arthritis?
Autoimmune destruction of the synovium causing damage to bone cartilage, tendons and ligaments.
Which joints are typically affected in RA?
Small symmetrical joints of the hands, wrists and feet.
Risk factors for RA?
Young, female, family history, other autoimmune disease
Symptoms of RA?
Painful, swollen, stiff joints for more than an hour in the morning.
Better with movement
Signs of RA?
Swan neck thumb, ulnar deviation and boutonniere deformity.
What is a boutonniere deformity?
Where the middle joint of the finger will not straighten due to damage to the tendons in the finger.
What blood tests would you do for RA?
Anti CCP, rheumatoid factor, raised ESR/CRP
What is AntiCCP?
An antibody usually present in patients with RA
What is the acronym for X-ray signs in RA?
LESS
What does LESS stand for?
L - Lost joint space
E - Erosion
S - Soft tissue swelling
S - Soft bones
How would you treat RA?
NSAIDs, Steroids, Methotrexate, Rituximab
What are DMARDs?
They alter the disease process by stopping or slowing the inflammatory process, reducing pain.
What is rituximab?
Targets anti-TNF which causes inflammation, therefore reducing levels of inflam. Works quicker than DMARDs
What are the complications of RA?
Cervical spinal cord compression, weakness and loss of sensation.
Lung involvement, interstitial lung disease and fibrosis.
What is gout?
Overproduction and under excretion of uric acid causing build up in joints.
What are the risk factors for gout?
Middle age, overweight, male, high purine diet, increased cell turnover.
What type of crystals are formed in gout?
Mono-sodium urate crystals
What foods are rich in purines?
Red meat, liver and seafood
What foods can also cause gout?
High fructose (sweets), high saturated fat
What are the first-line investigations for gout?
Polarised light microscopy of the synovial fluid
What does microscopy show in gout?
Negatively birefringent urate crystals
What blood tests would you do for gout?
Serum urate, levels may be raised but could also be normal.
What are the differential diagnoses for gout?
Septic arthritis with any acute monoarthropathy
What pain releif can you give for gout?
High dose NSAIDS or colchicine if NSAIDs are CI.
What should you prescribe if greater than 1 attack of gout per year?
Allopurinol
How to prevent gout?
Lose weight, change diet, reduce alcohol consumption.
Which joints are most commonly affected in gout?
1st metatarsal (big toe), distal interphalangeal joints.
What is pseudogout?
Deposition of calcium pyrophosphate crystals in the joint surface
Which joints does pseudogout affect?
KNEE, wrist, shoulder, elbows,
Presentation of pseudogout>?
Hot swollen tender joint, usually knees
Signs of pseudogout?
Recent injury to the joint in the history.
What investigations for pseudogout?
Joint aspirate and polarised light.
What crystals show under polarised light in pseudogout?
Rhomboid positive birefringent crystals
Management of pseudogout?
NSAIDS or colchicine
Complications of pseudogout>
Damage to the joint and loss of function over time
Risk factors for pseudogout?
Old age, Diabetes, osteoarthritis, joint trauma/injury, hyperparathyroidism and haemochromatosis, excess iron or calcium.
What is Ankylosing spondylitis?
An inflammatory condition that mainly affects the spine leading to stiffness and pain.
Which gene do most patients with AS have?
HLA-B27
Risk factors for AS?
Males:females 3:1, late teens/twenties
Which are the key joints affected in AS?
Sacroiliac joints, joints of the vertebral column
What is the pathophysiology of AS?
Inflammation caused pain and stiffness, fibrosis and scarring which progresses to bone formation and fusion of the spine.
What are the key presentations of AS?
Lower back pain and stiffness with sacroiliac pain that extends to the buttock.
Pain worse with rest, Improves with movement, worse at night and in the morning,
What X-ray changes might you see with AS?
Bamboo spine, very straight spine with fused vertebrae.
What investigations would you do for AS?
Inflammatory markers CRP and ESR, Genetic testing for B27, X-ray, MRI if X-ray doesn’t show anything;.
What is Schober’s test?
Tests the restriction in the lumbar spine
How do you perform schober’s test?
Find L5 on patient, draw a mark 10cm above, draw a mark 5cm below.
Ask patient to bend, measure the distance between the 2 marks.
Less than 20cm shows lumbar spine restriction
What other conditions are assciated with AS?
Inflammatory bowel disease, such as crohns.
How would you manage AS?
NSAID’s to control pain
Steroids during flares, anti - TNF drugs, monoclonal antibody against IL17
What is osteoporosis?
Reabsorption of bone out competes the building of bone leading to reduced bone mass and brittle bones
What are the primary causes of OP?
Menopause and aging, oestrogen protects the bone.
What is an acronym for the secondary causes of OP?
SHATTERED
What does shattered stand for?
S - Steroid use H - Hyperthyroidism A - Alcohol/smoking T - Thin/low BMI T - Low testosterone E - Early menopause R - Renal or liver failure E - Erosive/ inflammatory bone disease D - Dietery calcium low, malabsorption.
What are the presentations of OP?
Usually asymptomatic until a fracture, usually a hip fracture.
What investigations can you do for osteoporosis?
DEXA - mineral bone density scan.
Less than -2.5 is osteoporosis
What is the risk score used to predict fracture risk?
FRAX
What is the management of OP?
Lifestyle changes less alcohol, regular weight bearing exercise, vitD supplements and calcium rich diet.
Bisphosphates, alendronic acid
What advice should you give when taking bisphosphonates?
Take on an empty stomach first thing in the morning 30 mins before food. Stay upright for 30mins after taking it to prevent ulceration.
What is psoriatic arthritis?
T-cell mediated attack of the joints in people with psoriasis
What are the symptoms of psoriatic arthritis?
Joint pain, swelling and stiffness. Red and warm joints
What are the patterns of PA?
Oligoarthritis, asymmetrical., Affects distal interphalengeal joints
What investigations would you do in psoriatic arthritis?
Bloods - HLAB27, raised WBC and ESR/CRP. RF negative. X-ray
What x-ray changes would you see with psoriatic arthritis?
Pencil in cup erosive changes
What is the treatment for psoriatic arthritis?
Physio, NSAIDS and DMARDs
What is reactive arthritis?
Joint inflammation following a GI/GU infection.
When might you develop reactive arthritis?
If you’ve had an STI such as chlamydia or gonorrhea
If you’ve had glandular fever or food poisoning.
Joint symptoms of reactive arthritis?
Inflammatory monoarthritis, most commonly affecting knees, hips, feet, toes and ankles
What other symptoms of reactive arthritis?
Can’t see - conjuctivitis/uveitis
Can’t pee - Urethritis
Can’t climb a tree - oligoarthritis/polyarthritis
What investigations would you do in reactive arthritis?
Raised ESR/CRP, stool culture, STI screen, X-ray evidence of enthesitis.
How to treat reactive arthritis?
Treat cause of infection with antibiotics, NSAIDS +/- steroid joint injections.
What is septic arthritis?
A hot, swollen, acutely painful joint. It can destroy a joint in 24 hours
Which joint is most commonly affected in septic arthritis?
The knee joint
What are the risk factors for septic arthritis?
Pre-existing joint disease, DM, immunosuppression, chronic renal failure, recent joint surgery, prosthetic joints, IV drug abuse, over 80
How is the infection spread to the joint in septic arthritis?
Pathogenic inoculation of microbes. it either occurs by direct inoculation or haematogenous spread.
Which organisms commonly cause septic arthritis?
Staph aureus, streptococci and neisseria gonococcus.
What are the symptoms of septic arthritis?
Fever, large joint, single joint, Symptoms out of proportion with the underlying disease.
What are the differential diagnoses for septic arthritis?
Gout and pseudo gout.
What investigations should be done in septic arthritis?
Urgent joint aspiration for synovial fluid microscopy and culture.
What is osteomyelitis?
An inflammatory condition caused by an infection of bone typically only involving 1 bone.
What is the most common organism causing osteomyelitis?
Staph aureus
What are the risk factors for osteomyelitis>
Penetrating injury, IV drug use, diabetes, HIV infection, recent surgery, distant or local infection, sickle cell, RA.
What are the symptoms of osteomyelitis?
Limp or reluctance to weight bear, non specific pain at site of infection, malaise and fatigue, fever
What investigations for osteomyelitis?
FBC: WBC may be raised in acute, ESR/CRP usually raised. Blood cultures may be positive indicating infective organism.
Management of osteomyelitis
If patient is unwell give flucloxacillin upon reaching hospital.
Blood cultures to give right antibiotic.
What is SLE?
Antibodies attack soft tissue causing inflammation and damage
What are the risk factors for SLE?
Young, black, women
What is the presentation of SLE?
Butterfly rash, weight loss, fever, fatigue, joint pain, mouth ulcers.
What investigations would you do in SLE?
ESR raised, CRP normal
ANA and aDsDNA antibodies present
How to manage SLE?
Ibuprofen, Cyclophosphamide (DMARD) hydroxychloroquine, prednisolone and methotrexate
What are the complications of SLE?
Cardiac, lung, and kidney involvement. Widespread inflammation causing damage.
What are the names of 3 primary bone tumours?
Osteosarcomas, fibromas and sarcomas
What are the 5 commonest cancers to metastasise to the bone?
Bronchus, Breast, Brostate, Byroid and Bidney (the 5 B’s)
What are the symptoms of a secondary bone tumour>
Pain at tumour location, malaise, pyrexia, aches, pains, hypercalaemia
What is fibromyalgia?
Non-specific muscular disorder with unknown cause, can cause pain all over the body.
What are the risk factors for fibromyalgia?
Women, poor socioeconomic status, 20-50 years old.
What are the symptoms of fibromyalgia?
Fatigue, brain fog, pain, morning stiffness, chronic pain that is widespread.
What are the investigations for fibromyalgia?
Do FBC, X-ray to rule out any other causes
How to diagnose fibromyalgia?
Patient must have had pain/ tenderness lasting longer than 3 months on both right and left sides of the body above and below the diaphragm and at 11 out of 18 tender points.
Non-pharmacological treatments for fibromyalgia?
Keep patient active, i.e. going back to work. Graded exercise programmes such as strength and aerobic training.
Relaxation, physio and CBT
Pharmacological treatments for fibromyalgia?
10-20mg amitriptyline, 150-300mg of pregabalin if this doesn’t work.
Complications of fibromyalgia
Affect quality of life, anxiety, depression, insomnia, opiate addiction.
What is osteomalacia?
Poor mineralisation of bone
Deficiency of which vitamin causes osteomalacia/rickets?
Vitamin D
How do rickets and osteomalacia differ?
Rickets occurs if this happens during bone growth and osteomalacia is after the epiphyses
What are the signs/symptoms of rickets?
Growth retardation, hypotonia, apathy in infants, knock knees and bowed legs.
What are the symptoms of osteomalacia?
Bone pain and tenderness, fractures, waddling gait, low phosphate, and vit D deficiency.
What would plasma tests show for osteomalacia>
Low calcium, low phosphate (not enough to mineralised the bone)high ALP, high pth, low 25 hydroxy vitamin D
Gold standard tests for osteomalacia?
Bone biopsy showing incomplete mineralisation
How to treat osteomalacia/rickets?
Give vitamin D supplements, give calcium D3 forte if dietary insufficient, IM calcitriol if due to malabsorption.
What is vasculitis?
Inflammation of the wall surrounding the blood vessels.
How is vasculitis catorgarised?
By the size of the vessel
Which blood vessels does GCA affect?
The aorta and its major branches (carotid and verteral arteries) temporal artery often involved
What are the risk factors for GCA>
Over 50 years, northern european descent, females more common, history of polymyalgia rheumatica
What are the presentations of GCA?
New onset headache particularly over temporal area, scalp tenderness (hurts to brush hair), jaw claudication, visual disturbances such as amaurosis fugax.
What investigations for GCA?
Raised ESR and CRP, Halo sign on temporal and axillary artery, temporal artery biopsy/
Whats the gold standard for GCA diagnosis?
Temporal artery biopsy showing giant cells.
Whats the management of GCA?
High dose prednisalone ASAP
40-60mg
What are the complications of GCA?
Blindness, irreversible neuropathy.
What is Takayasu’s arteritis?
A large cell arteritis
Which vessels does Takayasus most commonly affect?
Aorta and its branches, also affect the pulmonary arteries.
What people are typically affected by takayasu’s arteritis?
below 40, female and Asian populations
What is the presentation of takayasu’s arteritis
Pulseless disease, arm claudication, syncope
What are the investigations for Takyasu’s
Angiography, granulomatous inflammation on histology, elevated ESR and CRP
How to manage takayasu’s?
Steroids
What is polyarteritis nodosa?
A medium artery vasculitis
Which parts of the body does polyarteritis nodosa most commonly affect?
Nerve/ skin involvement
Features of polyarteritis nodosa
Peripheral neuropathy, subcut nodules, abdo pain, unilateral orchitis.
What disease is commonly associated with polyarteritis nodosa?
Hep B
How to manage polyarteritis nodosa?
Corticosteroids and antivirals if associated with hep B.
What is Kawasaki disease ?
A medium cell arteritis associated with mucocutaneous lymph nodes
What ages does kawasaki disease most commoinly affesct?
Children under 5
What are the symptoms of Kawasaki disease?
Fever for greater than 5 days, nonpurulent bilateral conjunctivitis, strawberry tongue, erythema, and desquamation of palms and soles.
What is the treatment for kawasaki disease?
Aspirin and IV immunoglobulins
What is pagets disease of the bone?
Abnormal osteoclast activity causes excessive bone resorption followed by haphazard bone growth
What are the developing sy,ptoms of pagets?
Bone growth can impinge on nerves and cause pain, overgrowth of the cranial and facial bones, hearing loss and vision loss from impingement on those nerves.
What would blood tests for pagets disease show?
Elevated alkaline phosphatase, normal calcium, phosphate ad PTH.
What do X-rays for pagets show?
Lytic lesions, thickened bone cortices.
How to manage pagets?
analgesia and bisphosphonates
What is marfans syndrome?
A connective tissue disorder affecting the fibrillin gene resulting in connective tissue issues
What is the presentation of marfans?
Tall, long limbs and fingers, hypermobility, high arch palate
What is the ghent criteria for diagnosing marfans?
It takes into accoint, enlarged aorta, lens dislocation, and at least 4 skeletal problems in the diagnosis.
Management of marfans?
Avoid intense exercise and caffeine, beta blockers or ARBS
yearly echo and review by opthamologists.
Complications of marfans?
Mitral/aortic valve prolapse
aortic aneurysms, lens dislocation, pneumothorax, gord, scoliosis.
What is pectus excavatum?
An indented breast bone
What is pectus carniatum?
Protruding breast bone
What is ehlers danlos syndrome?
A group of connective tissue disorders caused by faulty collagen.
What is the presentation of ehlers danlos?
joint hypermobility, easily stretched skin, easy brising, chronic joint pain, re-occuring dislocations
Treatment for ehlers danlos
Physio, OT, psycological support
What is antiphospholipid syndrome?
An immune condition with antiphospholipid antibodies causing the blood to become prone to clotting and is in a hypercoaguable state.
What are the risk factors for antiphospholipid?
Diabtests, HTN, obesity, female, Autoimmune disease, smoking, oestrogen therapy for menopause
Presentation of antiphospholipid?
Thrombosis, recurrent miscarragees, thrombocytopaenia
Management of antiphospholipid
Long term warfairn, preganant women on LMWH.
