MSK Flashcards
3x inflammatory categories of joint pain? Forms of autoimmune joint conditions? Forms of non-inflammatory joint pain?
Auto-immune, crystal arthritis, infection
Rheumatoid arthritis, spondylo-arthropathy (HLA-B27), connective tissue disease (vasculitis)
Degenerative e.g. osteoarthritis, non-degenerative fibromyalgia (sports medicine)
What is inflammation? 4 pillars of inflammation? How might this present?
Reaction of microcirculation, movement of fluid and WBCs into extra-vascular tissues, pro-inflammatory cytokines
Red(rubor,) painful (dolor,) hot (calor), swollen (tumour)
Hot, painful, red, swollen joint, stiffness, poor mobility/ function, deformity
Features of inflammatory joint pain? Degenerative joint pain?
Pain eases with use, stiffness, significant >60 mins, early morning/ at rest (evening), swelling, synovial +/- bony, pt demographics e.g. young, psoriasis, family history, joint distribution e.g. hands and feet, responds to NSAIDs
Pain increases with use clicks/ clunks
Stiffness, not prolonged <30 minutes, morning/ evening, swelling, none, bony, not clinically inflamed, pt demographics e.g. older, prior occupation/ sport, joint distribution e.g. 1st CMCJ, DIPJ, knees
Less convincing response to NSAIDs
History for joint pain? Patterns of pain for bones, inflammatory, osteoarthritis, neuralgic, referred?
Where, nature, stiffness, swelling, history of symptoms, how has this affected function
Pain at rest and night= tumour, infection, fracture Pain and stiffness in joints in the morning, at rest and with use
Pain on use at end of day
Pain and paraesthesia in dermatomal distribution, worsened by specific activity= root/ peripheral nerve compression
Pain unaffected by local movement
Usual joint distribution for rheumatoid, osteo and psoriatic arthritis?
Rheumatoid= PIP and MCP joints of hands, wrists and MTP joints of feet, shoulders, elbows, knees and ankles Osteo= weight-bearing joints i.e. knees, hips, cervical and lumbosacral spine and feet, DIP, PIP and CMC joints Psoriatic= distal joints in fingers/ toes, lower back, wrists, knees or ankles
Chronicity of joint symptoms? What are Bouchard’s and Heberden’s nodes? Raynaud’s phenomenon and disease?
Rheumatoid= builds up, gout- days episodic, chronic phase= years, reactive= gradual decrease, palindromic rheumatoid= peaks over years
Calcium at the joints, bony swelling at DIP joints
Peripheral digital ischaemia, pale= ischaemic, blue= deoxygenated, red= reactive hyperaemia
What is ESR? Rises in what? More inflammation when what happens? Why? Why false positives?
Erythrocyte sedimentation rate, with inflammation/ infection
Quicker RBCs drop= more inflammation, more coated in proteins, increased fibrinogen, fall faster
Age, female, obesity, racial difference, hypercholesterolaemia, high IGs, SLE
What is CRP? Produced by liver in response to what? Other blood tests for rheumatological conditions? In RA look for what? Look for what in SLE?
Acute phase protein- pentameric peptide
1L-6
Rises and falls rapidly- high @6 hours, peak 48 hours , binds to damaged cells and activates complement and increases phagocytosis by macrophages
FBC- Hb for anaemia, WCC- leucopenia in SLE, U&E for renal involvement, LFTs for hepatotoxic drugs
Rheumatoid factor and cyclic citrullinated peptide (CCP)
ANA which binds to antigens within the cell nucleus and double stranded DNA- dsDNA
Other rheumatological tests?
Urine tests- urine dipstick- blood and protein, protein estimation (protein/ creatinine ratio,) microscopy (for red cells and casts)
Synovial fluid- microscopy for inflam cells, crystals in gout, gram stain and culture if sepsis?
Imaging- plain X-rays, USS, MRI, PET, isotope bone scanning
What is HLA B27? Vast majority of B27 (+) do not get what? Why linked with disease?
Class I surface antigen- all except RBCs, encoded by MHC on chromosome APC
Ankylosing spondylitis or any related diseases
Infectious agents has peptides similar–> auto-immune response, mis-folding theory, HLA B27 heavy chain homodimer hypothesis
What features do spondyloarthropathies have in common?
1) Seronegativity- rheumatoid factor -ve 2) HLA B27 association 3) Axial arthritis- pathology in spine and sacroiliac joints–> inflam back pain 4) Asymmetrical large-joint oligoarthritis or monoarthritis 5) Ethesitis- inflam of site of insertion of tendon/ ligament–> bone 6) Dactylitis- inflam of digit 7) Extra-articular manifestations e.g. iritis, oral ulcers
SPINEACHE- sausage digits, psoriasis, inflam back pain, NSAID good response, enthesitis (heel,) arthritis, chrones/ elevated CRP, HLA B27 EYE- uveitis
What is ankylosing spondylitis? What does it lead to? Pathophysiology?
Chronic inflam disease of spine and sacroiliac joints, unknown aetiology
Inflam of axial skeleton- new bone–> bamboo spine, inflam in sacro-iliac joint, syndesmophytes will grow- whole spine may become fused
Inflam of bone–> excessive repair phase, causes overstimulation and formation of syndesmophytes, anti-TNF drugs takes time to help
Typical presentation of ankylosing spondylitis?
Young adult male in late teens/ 20s, symptoms over more than 3 months, lower back pain and stiffness and sacroiliac pain in buttock region, takes at least 30 mins for pain to improve in morning, symptoms can have flares, vertebral fractures= key complication
Associations with ankylosing spondylitis?
Systemic- like weight loss, fatigue, chest related to costovertebral and costosternal joints, enthesitis- plantar fascilitis, achilles tendonitis, dactylitis, anaemia, anterior uveitis, aortitis, heart block, restrictive lung disease, pulmonary fibrosis, IBD
Tests for ankylosing spondylitis?
Clinical supported by imaging- MRI= most sensitive and better at detecting early disease
Sacroillitis= earliest X-ray feature- look for irregularitis, erosions or sclerosis affecting lower half of sacroiliac joints
Vertebral syndesmophytes= characteristic
Increased CRP/ESR, 88%= HLA B27 +ve
Schober’s test for ankylosing spondylitis? Management for AS?
Find L5 vertebrae, mark point 10cm above and 5cm below, ask pt to bend forward as much as poss, measure distance between points
If distance= <20cm, indicates restriction in lumbar movement, helps support diagnosis
NSAIDs- consider switching if not adequate improvement after 2-4 weeks
Steroids- for flares, oral, IM or joint injections
Anti-TNF- infliximab, adalimumab or certolizumba pegol
Secukinumab= MAb against IL-17, if NSAIDs and anti-TNF= inadequate
Physio, exercise, avoid smoking, bisphosphonates, tx of complications, surgery for deformities
Psoriatic arthritis occurs in what % of people with psoriasis? Patterns?
40-60%
Symmetrical polyarthritis; DIP joints; asymmetrical large joint oligoarthritis, spinal, psoriatic arthritis mutilans (rare, 3%,) 60-70% = HLA B27 +ve
Radiology of psoriatic arthritis? Tool used for diagnosis? Management?
Erosive changes, ‘pencil-in-cup’ deformity in severe cases, nail changes in 80%, synovitis, acneiform rashes and palmo-plantar pustulosis
PEST tool
NSAIDs, DMARDs, anti-TNF agents, IL12/23 blockers
What is reactive arthritis? Used to be known as what? Typically causes what? Obvious diff diagnosis?
Synovitis occurs in the joints
Reiter syndrome
Acute monoarthritis- affecting single joint in lower limb presenting with a warm, swollen and painful joint
Septic arthritis / gout
Most common infections triggering reactive arthritis? Associations? S+S?
Gastroenteritis/ STI, chlamydia, gonorrhoea–> gonococcal septic arthritis
Bilateral conjunctivitis, anterior uveitis, circinate balantis- dermatitis of head of penis
Iritis, keratoderma blenorrhagica- brown, raised plaques on soles and palms, circinate balantis, mouth ulcers, enthesitis
Tests for reactive arthritis? Management?
ESR and CRP increase, culture stool if diarrhoea, infectious serology, sexual health review, X-ray may show enthesitis with periosteal reaction, 60-85%= HLA B27 +ve, aspiration to exclude infecetion/ crystals
No specific cure, splint affected joints acutely; treat with NSAIDs or local steroid injections, consider sulfasalazine or methotrexate if symptoms >6 months, treating original infection may make little difference to arthritis, antibiotics
What is osteoporosis defined by? What are common/ more likely if trabecular or cortical bone is affected? Prevalence?
Systemic skeletal disease- low bone mass and micro-architectural deterioration of bone tissue–> increase in bone fragility and susceptibility to fracture
May be 1 or 2ndary–> another condition/ drugs
Trabecular= crush fractures of vertebrae, cortical bone= long bone fractures more likely (femoral neck)
More in females, women lose trabeculae with age, men= stable numbers, fracture risk is less
Risk factors for osteoporosis? Age-independent RFs?
Parental history, alcohol>4 units daily, inflammatory cytokines increase bone resorption, BMI<22, prolonged immobility and untreated menopause
SHATTERED:
Steroid use of prednisolone, endocrine disease- Hyperthyroidism and hyperparathyroidism, Cushing’s syndrome, hypercalciuria, Alcohol and tobacco use increase, Thin/ immobile, Testosterone decrease, Early menopause, Renal/ liver failure, Erosive/ inflammatory bone disease, Dietary Ca2+ decrease/ malabsorption; diabetes mellitus 1
Pathology and investigations for osteoporosis?
Decrease in trabecular thickening–> decrease in connection between horizontal trabeculae–> decrease trabecular strength and increased susceptibility to fracture
DEXA(low sensitivity/ specificity, often with hindsight after fracture,) low radiation and measure important fracture sites, T score= no. of standard deviations, each 1 decrease of SD in bone mineral density–> 2.6x increase in risk of hip fracture
T score meanings? Bloods? Management considerations?
> 0, BMD better than reference, 0 to -1= BMD in top 84%, -1 to -2.5= osteopenia, -2.5 or worse= osteoporosis
Ca2+, PO43- and alk phos normal
Specific investigations for secondary if suggestive history
Loss of BMD may not be entirely irreversible, age, number of RFs and BMD guide guide pharmacological approach e.g. FRAX tool- 10 yr risk of osteoporotic fracture in untreated patients, DEXA not necessary if age>75 years, lifestyle measures should apply to all
Lifestyle measures for osteoporosis? E.gs of anti-resorptive pharmacological measures for osteoporosis? Anabolic measures?
Quit smoking and reduce alcohol consumption, weight-bearing exercise may increase BMD, balance to reduce fall risk, Ca2+ and vit-D rich diet, home-based fall-prevention programme w/ visual assessment and a home visit
Decrease osteoclast activity and bone turnover e.g. bisphosphonates, HRT, Denosumab
Increase osteoclast activity and bone formation e.g. Teriparatide
1st line bisphosphonate for osteoporosis? Why good? If intolerant give what? How should patients take these pills? SEs?
Alendronate oral- cheap, effective, been used for ages, prevention in long-term steroid use also
Etidronate/ risedronate (oral)
With plenty of water while remaining upright for >30 minutes before eating/ or other drugs
Ibandronate/ Zoledronate (IV/ oral) also
Photosensitivity, GI upset, oesophageal ulcers- stop if dysphagia or abdo pain, rarely= jaw osteonecrosis, atypical femoral fracture, avoid in renal impairment/ CI in those w/ hypocalcaemia
Prescribe to smoking/ dental disease with care as can increase risk of jaw osteonecrosis
Reduced absorption if taken w/ calcium salts and antacids and iron salts
HRT can prevent osteoporosis in who, stop and may increase what? Increases what however? Denosumab is what and how does it work?
In post-menopausal women by reducing risk of fractures by 50%, can stop bone loss and may increase bond density by 10%, prevents hot flushes and other menopausal symptoms and reduces risk of colon cancer
Breast cancer, stroke, CV disease, venous thrombo-embolic disease and vaginal bleeding
MaB binds to RANK ligand,- RANK cannot bind to RANKL thus differentiation of osteclasts doesn’t occur, decreased resorption, given SC twice yearly, gives good fracture risk reduction, rebound increase of bone turnover when it is stopped
How does Teriparatide work? What other things may also be given for osteoporosis?
Useful in those who suffer further fractures despite tx with other agents, reduces risk of fractures by >50% and increases bone density by up to 20% and improves trabecular structure, potential increased risk of renal malignancy
Ca2+ and vit D if evidence of deficiency, target above 75nmol/L
Strontium ranelate helps decrease fracture rates, alternative in those intolerant of bisphosphonates
Raloxifene- selective oestrogen receptor modulator acts similarly to HRT, decreased breast cancer risk
Calcitonin- may reduce pain after a vertebral fracture
Testosterone- may help in hypogonadal men by promoting trabecular connectivity
What is vasculitis? It causes what or what? It can affect what and may be what or what?
Inflammation and necrosis of blood vessel walls w/ subsequent impaired blood flow—> vessel wall destruction and endothelial injury, causes destruction/ stenosis
Can affect the vessels of any organ and presentation depends on the organ that is involved, may be a primary condition/ secondary to other diseases (SLE, RA, hepatitis B&C, HIV)
Histology for vasculitis shows what? Characterised how? ANCA +ve and -ve vasculitis includes what?
Shows vessel wall infiltration w/ neutrophils, mononuclear cells +/- giant cells, fibrinoid necrosis and leukocytoclasis (destruction of WBC)
Size of blood vessel affected and whether ANCA +ve/-ve
Predilection for resp tract and kidneys, includes peri-nuclear ANCA associated microscopic polyangitis, glomerulonephritis and Churg-Strauss syndrome and cytoplasmic- ANCA associated granulomatosis w/ poly-angitis (GPA)
Henoch- Schonlein purpura, goodpasture’s syndrome and cryoglobulinaemia
What does large-vessel vasculitis affect and examples? Medium-vessel vasculitis? Small-vessel disease? ANCA-negative?
Aorta and major tributaries e.g. GCA, polymyalgia rheumatic, Takayasu’s arteritis
Medium and small-sized arteries and arterioles e.g. PAN, Kawasaki’s disease
ANCA-associated: microscopic polyangitis, granulomatosis with polyangitis
Essential cryoglobulinaemia, cutaneous leucocytoclastic vasculitis
Conditions associated with vasculitis? Infective and non-infective? Diff diagnosis and tests?
Infective- subacute infective endocarditis, non-infective= vasculitis with RA, SLE, scleroderma, polymyositis, dermatomyositis, good pasture syndrome and IBD
Sepsis–> subacute bacterial endocarditis, hepatitis, malignancy or cholesterol emboli
ESR/ CRP increase, ANCA may be +ve, increased creatinine if renal failure, urine= proteinuria, haematuria, casts on microscopy, angiography +/- biopsy may be diagnostic
What is GCA (large-vessel)? Common in who? Symptoms?
Cranial/ temporal arteritis–> granulomatous arteritis of aorta and larger vessels- extra-cranial branches of carotid arteries
Elderly >50 y/o, increased with age, x2 in women
Headache, temporal artery and scalp tenderness, jaw claudication, amaurosis fugax–> can lead to anterior ischaemic optic neuropathy, sudden blindness, typically in one eye, dyspnoa, morning stiffness and unequal or weak pulses, at risk of CVA
Diagnosis and tests for GCA? Management and prognosis?
3+ of age>50, new headache, temporal artery tenderness, palpable or decreased pulsation, ESR>50mm/h, abnormal artery biopsies showing necrotising arteritis w/ mononuclear infiltrate or granulomatous inflammation
ESR and CRP increase, platelets increased, alk phos increased, Hb decreased, temporal artery biopsy within 7 days starting steroids, skip lesions occur
Start prednisolone PO immediately, steroid sparing agents- azathioprine, methotrexate, biologics, prophylaxis of osteoporosis, DEXA scan
2-year course then complete remission, reduce pred once symptoms have resolved and decrease in ESR, consider risks and benefits of long-term steroid treatment, give PPI and bisphosphonate
Epidemiology and risk factors for polymyalgia rheumatica? Presentation?
Elderly, those over 50, more common in females
SLE, polymyositis
Sudden onset of severe pain and stiffness of shoulders and neck, hips, lumbar spine, limb girdle pattern, worse in morning, lasting from 30 minutes- several hours, mild polyarthritis of peripheral joints, 1/3= fatigue, fever, depression, weight loss
Diff diagnosis and diagnosis for polymyalgia rheumatica? Tx?
RA, spondyloarthropathies, SLE, polymyositis, osteoarthritis, malignancy, chronic pain syndrome e.g. fibromyalgia and depression
Clinical history- always over 50, both ESR and CRP raised, ANCA negative, alk phos raised, anaemia may be present, temporal artery biopsy, creatinine kinase= normal
Corticosteroids reduce symptoms within 24-48 hours e.g. oral predinisolone, diagnosis questioned if not improved, decrease dose slowly, give GI and bone protection e.g. lansoprazole, alendronate and Ca2+ and vit D
Epidemiology of polyarteritis nodosa (PAN)? Risk factors? Pathophysiology?
Usually middle-aged men, more common in males, associated with hep B
Male, hep B, RA, SLE, scleroderma
Necrotising vasculitis–> aneurysms and thrombosis in medium sized arteries–> infarction in affected organs, severe systemic symptoms
Presentation of polyarteritis nodosa(medium vasculitis)?
Fever, malaise, weight loss, myalgia, dramatic acute features follow= due to organ infarction
Neurological: mononeuritis multiplex due to arteritis of vasa nervorum= numbness, tingling, abnormal/lack of sensation and inability to move part of body
Abdominal: pain due to arterial involvement of abdominal viscera, GI haemorrhage due to mucosal ulceration
Renal: haematuria, proteinuria, HTN and acute/ chronic kidney disease occur
Cardiac: coronary arteritis–> MI and HF
Skin: subcut haemorrhage and gangrene occur, lung involvement= rare
Diff diagnosis and diagnosis of polyarteritis nodosa? Tx?
Fever from infection, Crohn’s, connective tissue disease, other vasculitis
Anaemia, WCC riased, ECR raised, ANCA negative, biopsy of kidney in particular for HTN and other damage- can be diagnostic
Angiography- micro-aneurysms in hepatic, intestinal or renal vessels
Control BP- ACEi e.g. ramipril, corticosteroids e.g. prednisolone in comb with immunosuppressive drugs e.g. azathioprine or cyclophosphamide, hep B with antiviral after initial tx with steroids
Symptoms, test and tx of microscopic polyangitis?
Renal failure, p-ANCA +ve, control BP thoroughly, most respond to corticosteroids and cyclophosphamide, hep B treated with an antiviral after initial tx with steroids
Granulomatosis with polyangitis (Wegener’s granulomatosis) affects what? Tests?
Causes nose bleeds, crusty secretions, hearing loss, sinusitis, perforated nasal septum, cough wheeze and haemoptysis in lungs, CXR may show consolidation, glomerulonephritis
c-ANCA directed against PR3= most specific and raised in majority in patients, some express p-ANCA specific for MPO, increased ESR/ CRP, urinalysis for haematuria/ proteinuria, renal biopsy, CXR= nodules, CT= alveolar haemorrhage
Tx of granulomatosis w/polyangitis?
Severe= high dose corticosteroids and cyclophosphamide/ rituximab to induce remission
Severe renal disease= plasma exchange in addition, non-end organ threatening= moderate dose steroids and methotrexate/ azathioprine as maintenance, co-trimoxazole as prophylaxis against pneumocystis and staph colonisation
What is osteoarthritis? Risk factors? Diff diagnosis?
Commonest joint condition, non-inflam disorder of movable joints characterised by deterioration/ failure of articular cartilage and formation of new bone of joint surfaces and margins–> protease/ cytokine release–> inflammation–> joint damage(knee, hip, DIPJ, spine)
Usually primary, but may be secondary to joint disease/ other conditions
Genetic predisposition, trauma, deformities, occupation, obesity, increased bone density
Signs and symptoms of osteoarthritis?
Localised (usually knee/ hip): pain on movement and crepitus, worse at end of day, background pain at rest; joint gelling- stiffness after rest up to 30 minutes; joint instability
Generalised= commonly affected joints= DIPJ, thumb carpo-metacarpal joints and knees, may be joint tenderness, derangement and bony swelling w/ Heberden’s nodes at DIP, Bouchard’s nodes at PIP- may be intermittent (effusion) or continuous (capsular thickening), decreased range of movement and mild synovitis
RA, gout, osteonecrosis, neuropathic joint
Tests for osteoarthritis? X-ray signs? CT? Isotope bone scan? CRP?
Xray= Loss of joint space, Osteophytes, Subarticular sclerosis, Subchondral cysts
CT- joints that aren’t visible on X-ray- foot, ankle, hand, spine
Isotope bone scan- hot due to increased vascularity and new bone formation
CRP may be raised
Pathophysiology of osteoarthritis?
Progressive destruction and loss of articular cartilage with an accompanying periarticular bone response
Balance between production and degradation= lost, focal erosion of cartilage and chondrocytes die, failure of EC matrix synthesis, surface= fibrillated and fissured
Cartilage ulceration–> underlying bone increased stress, micro-fractures and cysts
Bone–> abnormal sclerotic subchondral bone and overgrowths at joint margins which become calcified = osteophytes
Non-medical tx of osteoarthritis? Pharm? Surgical?
Exercise- improve local muscle strength mobility of weight bearing joints, lose weight, local heat/ ice packs, bracing devices, joint supports, insoles, footwear, acupuncture, physio, occupational therapy
Paracetamol before NSAIDs, weak opioids if necessary e.g. DIHYDROCODEINE, intra-articular corticosteroid injections= short-term, systemic one not used, do no administer if going to be replaced
Arthroscopy- assess damage and remove loose bodies, arthroplasty- knee/ hip replacement, uncontrolled pain- at night particularly, limitation of function
Prosthetic joint= 10-15 years lifespan, need replacement
Osteotomy- cut bone to change shape/ length
Fusion- usually of ankle and foot to prevent painful grinding–> loss of mobility
What are examples of connective tissue diseases? 2x inherited syndromes? Features of these?
SLE, systemic sclerosis, Sjogren’s syndrome, dermatomyositis/ polymyositis, overlap syndromes
Marfan’s and Ehler-Danlos syndromes
Inflammation–> scarring in affected organs
Can–> organ failure
Early systemic involvement may not give rise to any symptoms
Any system can be affected: skin, kidneys, joints, lungs, blood cells and NS= common
Auto-antibodies often present
Inflammation can be treated with immunosuppressive drugs, damage= irreversible
