MSK Flashcards
(124 cards)
1
Q
3x inflammatory categories of joint pain? Forms of autoimmune joint conditions? Forms of non-inflammatory joint pain?
A
Auto-immune, crystal arthritis, infection
Rheumatoid arthritis, spondylo-arthropathy (HLA-B27), connective tissue disease (vasculitis)
Degenerative e.g. osteoarthritis, non-degenerative fibromyalgia (sports medicine)
2
Q
What is inflammation? 4 pillars of inflammation? How might this present?
A
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
3
Q
Features of inflammatory joint pain? Degenerative joint pain?
A
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
4
Q
History for joint pain? Patterns of pain for bones, inflammatory, osteoarthritis, neuralgic, referred?
A
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
5
Q
Usual joint distribution for rheumatoid, osteo and psoriatic arthritis?
A
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
6
Q
Chronicity of joint symptoms? What are Bouchard’s and Heberden’s nodes? Raynaud’s phenomenon and disease?
A
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
7
Q
What is ESR? Rises in what? More inflammation when what happens? Why? Why false positives?
A
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
8
Q
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?
A
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
9
Q
Other rheumatological tests?
A
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
10
Q
What is HLA B27? Vast majority of B27 (+) do not get what? Why linked with disease?
A
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
11
Q
What features do spondyloarthropathies have in common?
A
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
12
Q
What is ankylosing spondylitis? What does it lead to? Pathophysiology?
A
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
13
Q
Typical presentation of ankylosing spondylitis?
A
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
14
Q
Associations with ankylosing spondylitis?
A
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
15
Q
Tests for ankylosing spondylitis?
A
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
16
Q
Schober’s test for ankylosing spondylitis? Management for AS?
A
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
17
Q
Psoriatic arthritis occurs in what % of people with psoriasis? Patterns?
A
40-60%
Symmetrical polyarthritis; DIP joints; asymmetrical large joint oligoarthritis, spinal, psoriatic arthritis mutilans (rare, 3%,) 60-70% = HLA B27 +ve
18
Q
Radiology of psoriatic arthritis? Tool used for diagnosis? Management?
A
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
19
Q
What is reactive arthritis? Used to be known as what? Typically causes what? Obvious diff diagnosis?
A
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
20
Q
Most common infections triggering reactive arthritis? Associations? S+S?
A
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
21
Q
Tests for reactive arthritis? Management?
A
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
22
Q
What is osteoporosis defined by? What are common/ more likely if trabecular or cortical bone is affected? Prevalence?
A
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
23
Q
Risk factors for osteoporosis? Age-independent RFs?
A
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
24
Q
Pathology and investigations for osteoporosis?
A
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
25
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
26
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
27
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
28
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
29
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
30
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)
31
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
32
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
33
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
34
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
35
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
36
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
37
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
38
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
39
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
40
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
41
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
42
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
43
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
44
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
45
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
46
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
47
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
48
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
49
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
50
What is normal but low in osteomalacia, excess what also? This is the reverse of what condition? What is the result if this process occurs and osteomalacia is the result if it occurs after what?
Normal= amount of bone, mineral content= low, excess= uncalcified osteoid and cartilage
Osteoporosis- mineralisation= unchanged, but overall bone loss
Rickets, after fusion of epiphyses
51
What is SLE (systemic lupus erythematous)? Leads to autoimmune disease due to deficiency of what? Increased prevalence in who, can be triggered by what?
Generation of autoantibodies (ANA) vs self-antigens--> B cell secretion--> tissue damage via immune complex formation and deposition and complement activation
C1q, C2 and C4--> impaired clearance of apoptotic cells and immune complexes--> tissue damage
Increased in black/ Asian women and those w/ HLA B8, DR2 or DR3 +ve, by EBV
52
S+S and immunology of SLE?
Malaise, fatigue, myalgia, fever, lymphadenopathy, weight loss, alopecia, nail fold infarcts, oral ulcers, non-infective endocarditis, Raynaud's phenomenon, migraine, stroke, retinal exudates, erythema in butterfly distribution on cheeks of face and across bridge of nose
ANA +ve> 95%m high anti-double stranded DNA (dsDNA) titre +ve in 60%, ENA may be +ve in 20-30%, RF +ve in 40%, antiphospholipid antibodies may also be +ve
53
Tests for SLE? Management?
1) Anti-dsDNA antibody titres 2) Complement: reduced C3, C4 3) High ESR, also BP, urine for casts or protein, FBC, U&E, LFTs, CRP, skin or renal biopsies may be diagnostic
General= high-factor sunblock, hydroxychloroquine, unless CI, reduces disease activity and improves survival
Maintain= NSAIDs and hyodroxychloroquine for joint and skin symptoms, azathioprine, methotrexate, belimumab- for auto-AB +ve disease where disease activity= high
Mild flares= hydroxychloroquine/ low-dose steroids
Moderate= DMARDs or mycophenolate
Severe= high-dose steroids, mycophenolate, rituximab
54
Management of lupus nephritis and prognosis?
More intensive immunosuppression with steroids and cyclophosphamide or mycophenolate, BP control= vital, renal replacement therapy may be needed
80% survive 15 years, increased long-term risk of CVD and osteoporosis
55
APPL syndrome often occurs as what? Antibodies? Causes what (CLOTS?) Dx and Tx?
As a primary disease
Anticardiolipin and lupus anticoagulant, anti-Beta glycoprotein 1
Coagulation defect, Livedo reticularis, Obstetric (recurrent miscarriage), Thrombocytopenia
Thrombotic tendencies affects cerebral, renal and other vessels
Persistent antiphospholipid antibodies with clinical features
Anticoagulation; seek advice in pregnancy- warfarin, LMWH for pregnancy plus aspirin to prevent complications
56
What is Sjogrens syndrome? 2 types? Associated with what antibodies? Epidemiology?Test to diagnose?
Chronic inflammatory AI disorder, destruction of epithelail exocrine glands- lacrimal and salivary glands especially
Anti-RO and anti-La antibodies
More common in females, associated with HLA- B8/ DR3, onset= 40-50s
Primary= occurs in isolation, absence of RA/ any AI diseases
Secondary= related to SLE/ RA
Schirmer test- inserting folded piece of filter paper under lower eyelid with stip hanging out over eyelid, left in for 5 minutes and distance along strip hanging becomes moist= measured, should be 15mm, <10mm= significant
57
Pathophysiology and presentation of Sjogrens syndrome?
Lymphocytic infiltration and fibrosis of exocrine glands, especially lacrimal and salivary glands
Dry eyes, dry mouth, salivary and parotid gland enlargement, skin and vagina dryness, many= only dryness and fatigue
58
Other tests for Sjogrens and tx?
Rose-Bengal staining may show keratitis, anti-RO and anti-La antibodies may be present, ANA= usually +ve, RA= +ve in 38%, may be hypergammaglobulinaemia, biopsy= focal lymphocytic aggregation
Hypromellose (artifical tears,) frequent drinks, sugar-free pastilles/ gums, NSAIDs and hydrochloroquine= arthralgia, immunosuppressants in severe systemic disease, artifical saliva and vaginal lubricants
59
Most pts with scleroderma have what? What is systemic sclerosis? 2 main types of systemic sclerosis?
Systemic sclerosis
Multisystem disease with involvement of skin and Raynaud's phenomenon, distinct from localised scleroderma such as morphea, does not involve internal organ disease
Limited cutaneous and diffuse cutaneous
60
Epidemiology of systemic sclerosis? Risk factors pathophysiology?
Highest case- specific mortality of any autoimmune rheumatic diseases, occurs worldwide, more common in females, peak= between 30-50 y/o, rare in children
Exposure to vinyl chloride, silica dust, adulterated rapeseed oil, drugs such as bleomycin, genetic
Increased fibroblast activity--> abnormal growth of connective tissue--> inflammation--> auto-antibody production--> vascular damage and fibrosis- in skin, GI tract and other internal organs
61
Presentation of limited cutaneous systemic sclerosis (CREST syndrome)? What antibody most associated with this? Tx?
Calcinosis- deposits in soft tissue, Raynauds, OEsophageal and gut dysmotility, Sclerodactyly- swollen tight digits, Telangiectasia- spider veins
Anti-centromere antibodies
Keep warm, stop smoking, avoid cold triggers for Raynaud's, physio for healthy joints, occy health, regular emollients, Nifedipine for Raynaud's--> SI= oedema, flushing, headache and palpitations
62
Diffuse cutaneous sytemic sclerosis includes what features? What antibodies? Control, tests and prognosis?
CREST syndrome plus many internal organs--> CI issues= HTN and CAD, lung= pulm HTN and pulm fibrosis, kidney problems- glomerulonephritis and scleroderma renal crisis- severe HTN+ renal failure
Antitopoisomerase-1 in 40% and anti-RNA polymerase in 20%
Poor prognosis, control BP meticulously, perform annual ECHO and spirometry
63
Txs for systemic sclerosis?
Currently no cure, immunosuppressive regimens, IV cyclophosphamide, monitor BP and renal function, early detection of pulm HTN, regular ACE-i or ARBs decrease risk of renal crisis
64
What is polymyositis? Where skin is involved? Epidemiology? Risk factors and aetiology?
Rare muscle disorder of unknown aetiology, inflammation and necrosis of skeletal muscle fibres, dermatofibrosis
Rare-adults and children, more common in females
Viruses implicated= Coxsackle, rubella and influenza, HLA-B8/DR3 higher risk
65
Presentation of polymyositis and dermatomyositis?
Symmetrical progressive muscle weakness and wasting- affecting proximal muscles of shoulder and pelvic girdle, difficulty squatting, going upstairs, rising from chair, raising hands above their head, pharyngeal and laryngeal and resp muscles--> dysphagia, dysphonia and resp failure
Skin changes; heliotrope- purple of eyelids, nailfold erythema, Gottron's papules: roughened red papules over the knuckles, elbows and knees
Extra-muscular= fever, arthralgia, Raynaud's, interstitial lung fibrosis and myocardial involvement, malignancy= 30%
66
Tests for polymyositis and dermatomyositis?
Muscle biopsy- fibre necrosis and inflam cell infiltrates- CONFIRMS, muscle enzymes- creatine kinase, ESR not usually raised
DM= ANA positive, RF= positive 50%, MSAs- myositis-specific antibodies, electromyography, MRI- inflamed muscles
67
Tx for polymyositis and dermatomyositis?
ORAL PREDNISOLONE until 1 month after inactive, tapered down slowly, immunosuppressives and cytotoxics in resistant cases, hydroxychloroquine/ topical tacrolimus for skin disease
68
Mixed connective tissue disease combines features of what? What is Marfan's syndrome? Ehler Danlos syndrome?
Systemic sclerosis, SLE and polymyositis
CT disorder with decrease in EC microfibril formation and poor elastic fibres- 1/4 with no family history
CT disorder caused by defect in structure, production or processing of collagen or proteins that interact w/ collagen
69
Modifiable risk factors for MSK health? Life course approach?
Vit D/ calcium- dietary/ supplements, weight management- calories, physical inactivity- balance, strength, mobility, injury prevention
Maternal health- smoking, diet, vit D
Child health- physical activity, diet
Adult health- injury prev, workplace
Healthy ageing- weight loss, dietary protein, Ca2+, vit D, strength and balance
70
Things to think about in screening?
The condition- freq/ severity, epidem, incidence, prev, history- understood
The test- simple, safe, precise, validated, suitable cut off, test from collect--> delivery acceptable, agreed policy on further diagnostic investigation with +ve patients and choices available
Intervention- effective at pre-symp--> effective outcomes, agreed on who should be offered interventions
Pros outweight cons, opportunity cost- economically balanced to expenditure
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What is hip dysplasia screened for? Uncertainty about screening for osteoporosis?
Part of physical exam of newborn and 6-8 week old babies
Early detection, diagnosis confirm and cons management can reduce need for surgery and better outcomes
US screening not for all babies unless part of research project, could--> overdiagnose
Accuracy, effect of Tx and changes in lifestyle on some fracture types, effects of those identified being at fracture risk, research= fractures not reduced
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Presentation of septic arthritis? What is affected in >50% cases? Organisms common?
Pain, swelling, redness, hotness, systemically unwell, increased ESR/CRP
Knee
S.aureus, gram -ve bacilli, streptococci, neisseria gonorrhoea, anaerobes, mycobacteria and fungi
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Risk factors for septic arthritis? Investigations? Tx?
Pre-existing joint disease, DM, chronic renal failure, recent surgery, prosthetic joints, IV drug abuse, ulcers, local skin breaks, immunosuppression
Urgent joint aspiration for SF microscopy, diff diag= crystal arthropathies, blood cultures for AB guidance, immunosuppression or infection?
Stop IS drugs temporarily, start empirical IV ABs after aspiration, IV flucloxacillin, vancomycin, cefotaxime if gonococcal/ gram -ve, rest/ splint/ crutches/ refer to physio
ABs--> oral and CRP declined= discharged
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What is gonococcal arthritis? What is osteomyelitis? Why is incidence increasing? 80% acute is in who with what? Can be usefully sub-classified on the basis of what?
Occurs w/disseminated gonococcal infection
Inflammation of bone, or BM due to infection
Due to prevalence of predisposing conditions (DM, PVD)
Kids, teens and adults get contiguous osteomyelitis- often associated w/ trauma
Causative organism, route, duration, anatomic location of the infection and it also depends on if there is suppuration (pus) or sclerosis (increased bone density)
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Host factors for osteomyelitis? Pathogenesis? Haematogenous OM in who? RFs for bacteraemia?
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Behavioural factors (risk of trauma), pre-existing bone/ joint issue, vascular supply, immune deficiency
Microorganisms infect bone through blood, from local areas of infection/ penetrating trauma including joint replacement or internal fixation of fractures/ secondary periapical periondonitis in teeth
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Haematogenous OM occurs in adults>50 y/o- vertebra, clavicle/ pelvis>> long bones or in kids or in IV drug users
Central lines, dialysis, sickle cell disease, catheterisation, UTI
Microbial surface components--> matrix molecules--> e.g. s.aureus binds host proteins and can survive intracellularly in cultures and macrophages
Microbiology= usually s.aureus, coagulase neg staph or aerobic gram -ve bacilli, salmonella= common in SCD and pseudomonas aeruginosa, serratia marcescens= common in IV drug users
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Area usually affected when infection is contracted through bloodstream in OM?
Metaphysis of the bone- leukocytes enter infected area--> release enzymes that lyse bone attempting to engulf organisms, pus--> bone's blood vessels, penetrates midshaft, goes to either end forming vascular loop in metaphysis-->impairing their flow, endothelial BM= absent, predisposing transition of bacteria from blood--> this site, capillaries here lack/ have inactive phagocytic lining cells, allow growth of microorganisms
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In children the metaphysis of bone is what? With age what happens to metaphysial blood flow? Lumbar vertebral veins communicate with those of pelvis by what? Retrograde flow from where may be a source of bacteria to these vertebrae?
Metabolically active with large flow of blood predisposing vasculature to infection
It slows but vertebrae become more vascular- bacterial seeing of vertebral endplate= more likely
Valveless anastamoses
Urethral, bladder and prostatic infections
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Acute changes in OM on histology? Chronic changes? Inflammatory exudate in marrow leads to increased what?
Inflammatory cells, oedema, vascular congestion, small vessel thrombosis
Necrotic bone, new bone formation, neutrophil exudates, lymphocytes and histiocytes
Intramedullary pressure, with extension of exudate into bone cortex rupture through periosteum, interruption of periosteal blood supply causing necrosis, leaves pieces of separated dead bone= 'sequestra'
New bone forms here 'involucrum'
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S+S of osteomyelitis?
Symptoms: onset-several days, dull pain at site of OM, may be aggravated by movement
Signs- systemic: fever, rigori, sweats, malaise, local: acute OM- tenderness, warmth, erythema and swelling
Chronic OM- tenderness, warmth, erythema and swelling, draining sinus tract, deep/ large ulcers fail to heal despite several weeks tx, non-healing fractures
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Vertebral OM in what vertebrae? Can cause what via posterior extension? Anterior/ lateral extension can lead to what? Can present as what?
Lumbar> thoracic> cervical
Epidural and subdural abscesses/ even mengitis
Paravertebral, retropharyngeal, mediastinal, subphrenic, retroperitoneal or psoas abscesses
Septic arthritis--> infection through cortex--> pus into joint- knee, hip and shoulder, more common in infants due to patent transphyseal blood vessels and immature growth plate
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Diagnosis of OM?
Acute= high WCC, chronic can have normal WCC, raised ESR/ CRP
Plain radiographs- chronic= cortical erosion, periosteal reaction, mixed lucency, sclerosis, sequestra and soft tissue swelling
MRI= BM oedema from 3-5 days, delineates cortical, BM and soft tissue inflammation, CT, nuclear bone scan if metal work makes CT/ MRI impossible
Bone biopsy- for MB and histology
Positive blood cultures- remove need for invasive diagnostic testing
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Diff diagnosis and tx of OM?
Soft tissue infection, Charcot joint, avascular necrosis of bone, gout, fractures, bursitis, malignancy
Surgical- debridement, hardware placement/ removal, AM therapy- tailored to culture and sensitivity findings, pending culture, broad spectrum empiric therapy, bone penetration of drug
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Features of TB OM?
May be slower onset, systemic symptoms, epidemiology different from pyogenic OM, blood culture= less use, biopsy essential- prolonged culture, caseating granulomata, induced sputum may help, 12 month tx
84
What bacteria is much more of a significant problem in the upper limbs? Why so difficult?
Propioniobacteria, colonisers of human from above waist, shed by blinking eyes, more of a threat in upper limb prostheses and spines, common contaminants of MB cultures
Slow growing, contaminants take 7 days to grow, longer when--> clinical infection, often don't trigger blood culture systems
Very indolent organisms, may not raise inflam markers
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Incidence of bone and soft tissue tumours in genders? History for MSK tumours?
Bone= slightly higher in males, almost equal for soft tissue
Presenting complaint- mass, pain, loss of function?, history of complaint- duration, how issue came to attention
Past medical history and medication history, social history- current level of function
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Red flag symptoms for MSK tumours? What may help to provide a clue as to nature of disease? Examination? Investigations?
Rest pain, night pain, lump present- tender, enlarging, deep to fascia, loss of function, neurological symptoms, unwell/ weight loss
Age of the patient
Look, feel, move, assess function of joint/ limb, masses present- size, shape etc
Blood tests, plain X-rays, US, CT- better for bone quality as well as solid tumours, staging CT of chest, abdo, pelvis, MRI-reactive changes of soft tissue/ bone marrow, bone scan- for skeletal metastases
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What can plain X-rays look at for MSK tumours? Special signs x3?
See what the lesion is doing to the bone and vice-versa, definition, bone density, zone of transition, periosteum reaction, osteoblastoma vs osteosarcoma
Codmans triangle= osteosarcoma, Ewing's, GCT, osteomyelitis, metastasis
Sunburst appearance= osteosarcoma, Ewing's
Onion-skin appearance- Ewing's
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US good for what with MSK tumours? CT used for? MRI displays what?
Quick, cheap for assessing soft tissue masses, real time assessment, no radiation, differentiate between normal and abnormal, solid vs cystic
3D reconstruction of bony lesions, can help plan resection, also used for staging
Soft tissue involvement of bony mass, periosteum and endosteal reaction, skip lesions, soft tissue masses, heterogenous masses= more suspicious of malignancy
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3 phase bone scan? Other modalities x2?
Arterial- 1 minute- blood delivery
Blood pooling- 5 mins- capillary dilation
Delayed- 2-4 hours - uptake within bone
Gamma camera, technetium (Tc99-MDP)
PET-CT- positron emission with CT
Whole body MRI scan- improve identification of mets in STS
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Bone/ soft tissue sarcoma MDT people? Suspect this ensure do what before proceeding? How is biopsy done for MSK tumours?
Orthopaedic surgeon with expertise in oncology, oncologist, radiologist, histopathologist, MDT co-ordinator and nursing/ rehab staff, discuss with pt with MDT before invasive intervention
By operating surgeon/ consultant radiologist at specialist centre, longitudinal incision in line with planned incision for future surgical procedure, shortest route to tumour, access only one muscular compartment, ensure sample= representative, drain to be placed in line with incision, send sample---> microbiology and microbiology
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How is staging done for MSK tumours? Grading of malignant tumours done using what system?
X-ray: ensure whole bone is imaged, limb alignment views for lower limb, MRIL useful to assess for skip lesions, stage distally- CT chest/ abdo/ pelvis, bone scan, whole-body MRI scan
Enneking system- G0= benign, G1=low grade malignant, G2= high grade malignant
Grade 1= latent, Grade= active, progressive growth limited by natural barriers, Grade 3= aggressive
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Where are osteosarcomas prone to occur, parosteal osteosarcomas, chondrosarcomas, giant cell tumours, chordomas and adamantinomas? How would you describe an X-ray with a suspected tumour?
Knee, distal femur, pelvis, knee, sacrum and tibia
Describe radiographic view, anatomical location, epiphysis/ metaphysis, diaphysis, bone/ cartilage forming, bone destruction/ reaction, zone of transition
Benign lesions= sealed off from bone by sclerotic rim, aggressive lesions permeate through bone
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What is a sarcoma? Most common in who? Vast majority are what and most common are what? Types (affect type of tissue)?
Rare tumour arising from mesenchymal origin, in elderly, also tumours of peripheral nerve sheath, usually affects the leg
Of cancellous bone, cartilage, fat, muscle, vascular or haemopoietic tissues
Carcinoma= from epithelial cells
Superficial sarcomas= skin
Osteosarcoma, chondrosarcoma, liposarcoma, TNM classification used, more than 50 histological subtypes
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How are low grade and intermediate/ high grade sarcomas treated? Deep sarcomas S+S? Dermatofibrosarcoma (DFSP)? Angiosarcoma? Kaposi's sarcoma? Ewing's sarcoma?
Surgically, sometimes radiation therapy/ chemotherapy= used
Combination of surgery, chemotherapy and/ or radiation therapy
Slowgrowing, enlarging, painless, pressure effects, weight loss, malaise and rigours
Usually on chest of men, difficult to remove
Face scalp, elderly, prone to local recurrence and distant metastases
From blood vessels, in people who have AIDs
Bone sarcoma often of pelvis/ femur- young males- surgery or multi-modality Tx
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Tests and Tx for sarcomas? Challenges?
Biopsy, PET, bone scan/ bone marrow, MRI, CT, bloods
History, examination, imaging- US, then MRI, angiography and CT chest, tend to spread to chest
Biopsy- diagnosis and grading, MDT
Recommendation for Tx in specialist centres, clinical trials national/ international collaborations, clinical trials national/ international collaborations, larger phase III clinical trials- general, all sarcomas, small phase II trials
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Side effects of radiotherapy? Chemotherapy side effects? (early/ late) Surgery types?
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Early= tiredness, skin inflammation, hair loss
Late= lymphoedema, joint stiffing, pathological fracture
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Anaemia, thrombocytopenia, neutropenia, mouth ulcers, thrush, constipation, neurotoxicity, hair loss, tiredness
Late= cardiotoxicity, nephrotoxicity, neurotoxicity, osteopenia, fertility, second malignancies
Wide, marginal, functional compartmentectomy, amputation
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How are fractures managed?
Reduction, immobilisation, rehabilitation
Analgesia, examination- neurovascular, pre and post immobilisation
Fracture--> haematoma= neutrophils, macrophages and platelets--> soft callus--> osteoblasts, woven bone--> remodelled
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What is RA characterised by? Epidemiology? Presentation?
Chronic systemic inflammatory disease, characterised by a symmetrical deforming peripheral polyarthritis
Young: 30-50 y/o, women= x3 more common, familial, HLA-DR4 association
Symmetrical swollen, painful and stiff small joints of hands and feet- worse in morning, larger joints may become involved, pain>30 mins, eases with use
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Physical examination/ signs of RA? Pattern of joint movement? Extra-articular manifestations?
Ulnar deviation, swan neck deformity, Z thumb, rheumatoid nodules, active synovitis- red, hot swollen joints
Symmetrical, most commonly: wrists and feet, rarely DIPJs
Nodules, carpal tunnel syndrome, anaemia, lungs, eyes, Felty's syndrome- Ra+ splenomegaly + neutropenia
Caplan's= pneumoconiosis+ RA--> intrapulm nodules
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Investigations for RA?
RA= +ve in 70% cases, high titres associated with severe disease, erosions and extra-articular disease
Anti-CCP= highly specific for RA with 70-80% sensitivity
Anaemia of chronic disease- increased platelets, high ESR and CRP
X-rays= LESS- soft tissue swelling, juxta-articular osteopenia and reduce joint space, later= bony erosions, subluxation or complete carpal destruction
US and MRI can identify synovitis more accurately
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Management of RA? Increased risk of what disease in RA?
2x DMARDs- one being methotrexate, analgesia, steroids- reduce symptoms and inflam- good for acute exacerbations
CV and cerebrovascular disease- atherosclerosis is accelerated
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Fracture types? Fracture complications?
Transverse, linear, oblique, nondisplaced, oblique- displaced, spiral, greenstick, comminuted/ multi-fragmentary
Damage to surrounding structures- vascular, nerve, soft tissue, organs
Contamination- infection
Compartment syndrome- in arm/ leg, damage to blood supply, pressure build-up in compartment, can compromise limb
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Early systemic complications in fractures? Late complications?
Fat embolus, shock, crush syndrome, pulmonary embolism, pneumonia, PE and pneumonia= usually after injury
Delayed union, mal union- usually fault from us e.g. wrist fractures- accept position in elderly, put in bad cast--> deformity
Avascular necrosis- cut off blood supply to bone, die, worn away leads to arthritis as bone becomes stiff, osteomyelitis
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2 types of neck of femur fractures? Types of extracapsular fractures? Presentation and management? Total hip replacement and hemi-arthroplasty involves what? What is DHS?
Intracapsular, extracapsular
Intertrochanteric- above trochanter and subtrochanteric= below trochanter
Fall, groin pain, inability to weight bear, externally rotated and short, pain on axial loading
Straight leg raise- hurts= alarm bells
Analgesia, morphine, regional nerve block, try to operate if can
Replace head of femur, acetabulum= cup in and hemi-arthroplasty= less strenuous, shorter procedure, less damaging, don't long however
Hip not displaced, compression screw, plate on side of femur, screw= can take weight of joint
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Ankle fractures uses what classification? What is syndesmosis? Weber A, B and C meanings? Ottawa rules? Fracture dislocation can get what?
Weber- classification
Gap between tibia and fibula
A= below syndesmosis, B= at level, C= below level
Bone tenderness over lateral, medial malleolus and are they able to walk more than couple of steps
Can get fracture blister, skin wears away= open fracture- risk of infection, tension of ligaments- pressure on blood supply and nerves
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Tx for ankle sprains and open fractures? Compartment syndrome increases in what and pressure on what? Tx?
Analgesia, ICE, elevation, early mobilisation
Wet gauze, antibiotics, photos, splints, then into theatre
Increase in intra-compartmental syndrome, pressure on veins- collapse--> more blood into area
On nerves, then arteries- get 5 Ps- pain, pallor, perishingly cold paralysis and pulselessness
Take off cast, fasciotomy- 2x incisions either side, open up compartment, skin graft from thigh
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Presentation, investigations and tx for ACL injury? Red flags for cauda equina syndrome? Get rid of some what?
Swelling, pain, knee giving way
Positive Lachman's, anterior draw test, MRI
RICE, conservative- physio, surgical-tendon repair, artificial graft
Bilateral sciatica, severe/ progressive bilateral neurological deficit of legs- major motor weakness with knee extension, ankle eversion/ foot dorsiflexion, difficulty initiating micturition/ impaired sensation of urinary flow, untreated= irreversible, loss of sensation of rectal fullness, faecal incontinence, perianal, perineal or genital sensory loss, laxity of anal sphincter, given MRI
Ligamentum flavum
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Need to check what with shoulder dislocation? Acute/ chronic rotator cuff tears from how long? Management?
Neurovascular supply, sensation before and after relocating, anterior and posterior
3 months, partial/ full thickness tears
Conservative- analgesia, physio, corticosteroid, surgical= arthroscopic, open
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Gout typically presents with what? Most occurs at what joints? It can be what? Caused by deposition of what? Attacks may be precipitated by what things? Important diff diagnosis?
Acute monoarthropathy with severe joint inflammation, >50% at metatarsophalangeal joint of big toe, ankle, foot, small joints of hands, wrist, elbow or knee
Polyarticular
Monosodium urate crystals in and near joints
Trauma, surgery, starvation, infection or diuretics
Urate deposites--> tophi in pinna, tendons, joints and renal disease may occur
Septic arthritis
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Risk factors for gout? Diagnosis?
Male, obesity, high purine diet- meat and seafood, alcohol, diuretics, existing CV disease/ kidney disease, family history
Aspiration of joint fluid- no bacterial growth, needle shaped crystals, negative birefringent of polarised light, monosodium urate crystals
Joint X-ray- typically joint space maintained, lytic lesions in bone, punched out erosions, erosions can have sclerotic borders with overhandling edges
111
Tx of acute gout?
High-dose NSAID of if CI- use colchicine= effective but slower to work, NB in renal impairment, steroids- oral, IM or intra-articular, rest and elevate joint, ice packs and 'bed cages' can be effective
112
Prophylaxis of gout? Start if >1 attack in how long?
Allopurinol= xanthine oxidase inhibitor, reduces uric acid level
Lifestyle changes can reduce risk of developing gout
Lifestyle changes- losing weight, staying hydrated and minimising consumption of alcohol and purine-based food
12 months, tophi or renal stones
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Pseudogout caused by what crystals? Known as what? Typical presentation? Aspirated fluid and Xray show what?
Calcium pyrophosphate crystals
Chondrocalcinosis
Older adult with a hot, swollen, stiff, painful knee
Other- shoulders, wrists, hips
Can be chronic, affect multiple joints and can be asymptomatic and picked up on X-ray
No bacterial growth, calcium pyrophosphate crystals, rhomboid shaped crystals, positive birefringent of polarised light
Chondrocalcinosis- thin white line in middle of joint from calcium deposit= diagnostic
LOSS
114
Tx of pseudogout?
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NSAIDs, colchicine, joint aspiration, steroid injections, oral steroids
Joint washout (arthrocentesis)= option in severe cases
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115
Red flags for sinister causes of back pain?
Aged <20yrs or >55yrs old, acute onset in elderly, constant/ progressive pain, nocturnal pain, worse pain on being supine, fever, night sweats, weight loss, history of malignancy, abdominal mass, thoracic back pain, morning stiffness, bilateral/ alternating leg pain, neurological disturbance, sphincter disturbance, current/ recent infection, immunosuppression, e.g. steroids/ HIV, leg claudication
116
Examination of back pain?
With pt standing, gauge extent and smoothness of lumbar forward/ lateral flexion and extension
Test for sacroiliitis- palpate posteriorly down spinal length
Neurological: test lower limb sensation, power and deep tendon and plantar reflexes, digital rectal examination
Nerve root pain- worsened by coughing/ bending forward, straight leg test- L4-5, S1, Lasegue's sign= raising leg with knee extended= pain below knee, increases on foot dorsiflexion= irritation to sciatic nerve, femoral stretch test= pain in front of hip on lifting hip into extension pt lying face downwards
Signs generalied disease e.g. malignancy
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Causes of back pain: 15-30, 30-50 and >50 y/o?
Prolapsed disc, trauma, fractures, AS, spondylolisthesis, pregnancy
Degenerative spinal disease, prolapsed disc, malignancy
Degenerative, osteoporotic vertebral collapse, Paget's, malignancy, myeloma
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Investigations and tx of back pain?
FBC, ESR and CRP- myeloma, infection, tumour
U&E, ALP (Paget's), serum/ urine electrophoresis, PSA
MRI-imaging of choice, can detect disc prolapse, cord compression, cancer, infection or inflammation
Neurosurgical ref if deficit, diagnosis under review, education and self-management= non-specific back pain, normal activities, regular NSAIDs, codeine, low-dose amitriptyline/ duloxetine, psychosocial isues- chronic pain and disability
119
Risk factors for fibromyalgia? Associations? Features?
Female sex, middle age, low household income, divorced, low educational status
Other somatic syndromes- chronic fatigue syndrome, IBS, chronic headaches syndromes
Diagnosis depends on pain that is chronic> 3 months and widespread, profound fatigue= unrefreshing sleep and significant fatigue and pain with small increases in physical exertion, morning stiffness, paraesthesiae, headaches, poor conc, low mood, sleep disturbance
120
Investigations and Mx for fibromyalgia? Pharmacotherapy?
Diagnosis= clinical, over-diagnosis can consolidate illness behaviour, exclude other causes of pain and/or fatigue
MDT with engagement from pt, reman as active as they feel able, new symptoms reviewed, graded exercise programmes, aerobic and strength-based training, pacing of activity, relaxation, rehab, physio, CBT
Low-dose amitriptyline- relieve pain and improve sleep, pregablin- if ineffective, duloxetine/ SSRI with anxiety/ depression, steroids/ NSAIDs NOT- no inflammation
121
What does Paget's disease of the bone refer to? What does this lead to? Presentation?
Excessive bone turnover, due to osteoclasts and osteoblasts--> sclerosis (patchy areas of high density,) and low density (lysis)--> enlarged and misshapen bones with structural problems increase risk of pathological fractures, affects axial skeleton particularly
Bone pain, deformity, fractures, hearing loss if ear bones
122
Investigations for Paget's disease?
Bone enalargement and deformity, 'osteoporosis circumscripta'- well defined osteolytic lesions appear less dense than normal bone, 'cotton wool appearance' of skull, 'V-shaped defects' in long bones= V shaped osteolytic bone lesions within healthy bone
Raised alk phos, normal Ca2+ and phosphate
123
Management and 2 key complications of Paget's disease?
Bisphosphonates
NSAIDs for bone pain, Ca2+ and vit D supps, surgery= rare
Monitoring= checking ALP and reviewing symptoms, tx should normalise ALP and eliminate symptoms
Osteosarcoma and spinal stenosis- spinal canal narrows--> neurological symptoms, MRI diagnosed and spinal cord compression
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Most common places for tumours to spread to bone?
5 Bs: bronchus, breast, prostate, thyroid and kidney
