MSK & Rheum - Collated from sources such as Passmed, Zero to Finals, AMBOSS, BMJ best practice PDF

Title MSK & Rheum - Collated from sources such as Passmed, Zero to Finals, AMBOSS, BMJ best practice
Course Medicine
Institution Cardiff University
Pages 36
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Summary

Collated from sources such as Passmed, Zero to Finals, AMBOSS, BMJ best practice...


Description

ARTHRITIS    

>6 wk hx = chronic inflammatory arthritis 1 joint involved = monoarthritic 2-4 joints = Oligoarthritis 5 joints involved = polyarthritis

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DDx for joint problems If there’s systemic signs, bilateral, anti-CCP & RhF +’ve  RA If there’s no inflammatory markers, it’s asymmetrical and they’re old  OA Asymmetrical, DIP involved, sausage fingers, hx of psoriasis  PA Acute pain, big toe, uric acid ^  Gout >50, shoulder and hip pain, systemic sx, inflammatory markers  PMR Dry eyes, dry mouth, anti-Ro1, anti-LA, (70% ANA)  Sjogren’s Hx of bleeding probs, multiple miscarriages  APLS Oro-genital ulcers, monoarticular arthritis  Behcet’s

OA      

Seen in 60+ yrs with a gradual onset - months/yrs Px’s with pain on movement Unilateral/Asymmetrical Knees, hips, hands Morning stiffness Men Smokers HLA-DR4, HLA-DR1 Infections can trigger it Px with painful stiff joints of hands and feet + systemic sx e.g. fatigue, weight loss Symmetrical Morning stiffness >30 mins Severe disease can cause Episcleritis and atlanto-axial subluxation o Neck involvement with RA  NEUROLOGICAL EMERGENCY - can cause nerve impingement O/E: Ulnar deviation, Swan-neck, Boutonniere, painless nodules below the elbow DOESN’T INVOLVE DIP JOINT ^ risk of heart disease and Ca o CVD is what kills pt’s

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1:10 have lung complications 2x as likely to get depression RARE: Felty’s syndrome = RA + Splenomegaly + Neutropoenia

Investigations  Anti-CCP in 80% if pt’s  RhF +’ve in 70% o Not specific, also +’ve in Hep C, SLE, Endocarditis, AIDS, Sjogren’s, Neoplasm  30% are ANA +’ve, associated with a worse prognosis  Signs of inflammation e.g. ^ CRP, ^ ESR  USS can show subclinical inflammation - in early arthritis clinics a same-day USS is used (not diagnostic)  XR hands and feet - if showing signs, it’s already advanced: ABCDE’S  Abnormal alignment  Bones - periarticular OP  Cartilage - symmetrical joint space loss  Deformities  Erosions  Soft tissue swelling  Refer urgently to rheumatology if:  Small joints of hands and feet are affected  >1 joint affected  There’s been a delay of 3 months between sx onset and px  NORMAL INVESTIGATIONS DON’T RULE OUT RA & SHOULDN’T STOP REFERRAL DAS-28 Assesses disease severity using computer tool looking at how many joints are involved (BUT doesn’t include the feet)  3.5-5.1  Dual therapy  >5.1  Immediate triple therapy (threshold for biologics)  Aiming for 5.1)

Septic Arthritis  Systemically unwell  Risk factors - recent joint replacement, DM, immunocompromised e.g. malignancy  Hot, painful, swollen joint  usually KNEE  Kocher criteria for Dx (don’t need all): o Fever >38.5 o Non-weight bearing o ^ ESR o ^ WCC  Most commonly caused by Staph aureus (also causes the worst sx) o ~20% is Strep - pneumonia or viridians o If young and sexually active - Neisseria gonorrhoea o Elderly, frail, immunocompromised - E coli (or other gram -‘ve) Mx  Urgent orthopaedic review  Emergency joint aspiration/needle decompression and culture - Need to send off before starting Abx, but don’t need to wait for results o Only CI = metallic joint replacement (get ortho surgeons)  IV Abx for 2 weeks, oral for 4 weeks o Flucloxacillin normally o If elderly + gram -‘ve cover e.g. 3rd generation cephalosporin - Cefuroxime o If gonorrhoea is suspected - Ceftriaxone  May need arthroscopic lavage  Mobilise early once well as joints stiffen quickly

GOUT  

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Disorder of Purine metabolism HYPERURICAEMIA o Due to impaired renal excretion e.g. renal failure o HTN o Hyperparathyroidism o Down’s Syndrome o Sarcoidosis o Hypercholesteremia o Diseases of rapid cell turnover e.g. psoriasis, Ca with chemotherapy ^ risk o Diet high in sugar, fizzy drinks, red meat or shellfish Typically seen in middle aged men Oestrogen is protective so rare in premenopausal women

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Gouty arthritis = uric acid crystal deposition in joints - see nodules (‘Tophi’) similar to those in RA - but can be seen on the ears and Achilles tendon as well as the elbow and fingers like RA nodules Diuretics can cause gout Px with severe pain, swelling and erythema o Worse with alcohol In 50% the 1st MTP is affected - if this is, and it’s a typical hx, no need to investigate

Investigations  Clinical Dx  Joint microscopy and culture = negatively birefringent, needle-shaped urate crystals on polarised light microscopy  Serum uric acid >380 umol/L o In an acute Gout attack, Uric acid actually DECREASES - so normal Urate doesn’t exclude Dx  Joint XR is normal  Screen for CV risk factors and renal disease in everyone with Gout

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Mx: Acute attacks Self-limiting so eventually will recover 1st line = high dose NSAID’s + PPI for 1-2 days, or Colchicine PO o Colchicine is better for pt’s with peptic ulcers, renal impairment, very elderly (basically where NSAID’s aren’t great) o If CI consider Oral or IM Steroids o If it’s monoarticular gout + co-morbidity  intra-articular steroids Don’t stop preventative tx during acute attack

Mx: Prevention  Lifelong Urate Lowering Therapy  Allopurinol - lower starting dose and titration if there’s renal impairment o Started 2 wks AFTER an acute attack as it can ^ risk of gout flares  Febuxostat is 2nd line - check LFT’s 1st  Give Colchicine when starting or up-titrating ULT dose as prophylaxis against acute attacks, for 6 months o NSAID’s or Coxib are 2nd line to Colchicine for prophylaxis Pseudogout  Calcium pyrophosphate dihydrate crystal deposition  Usually in the knee, wrist, shoulder hip, spine  Px with fever, confusion, pain, swelling  Usually has a trigger e.g. o Trauma o Surgery o Hypomagnesaemia o Hyperparathyroidism o Haemochromatosis o Infection  Intermittent attacks of acute arthritis - less severe than gout Investigations  Synovial fluid analysis = rhomboid positively birefringent crystals  XR shows chondrocalcinosis - this is a major risk factor for developing pseudogout

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Mx NSAID’s or Colchicine Steroid injections

SPONDYLOARTHROPATHIES Psoriatic Arthritis  In ~30% of people with psoriasis  ~60% are HLA-B27 +’ve  Asymmetric  Distal distribution e.g. DIP, feet. Can affect sacroiliac joints and spine  Erosive change with bone proliferation  ‘Sausage fingers’ - (dactylitis) and nail changes  XR’s show erosive changes, ‘arthritis mutilans’, dislocation of joints o Pencil in cup appearance (can also be seen in Ssc, RA or reactive arthritis  Mx with DMARD’s and anti-TNF’s Reactive Arthritis  Usually younger pt’s  After infection BUT no evidence of ongoing infection e.g. normal ESR, no synovial fluid abnormalities o Chlamydia is a key cause (SARA) but ask about any previous infection  Triad of Reiter’s syndrome: Can’t see, can’t pee, can’t bend your knee 1) Arthritis 2) Urethritis 3) Conjunctivitis  Only tx if sx have been ongoing for >6 months - DMARD’s Ankylosing Spondylitis        

Usually young men 3 months o Better with exercise o NOT relieved by rest o Worse in the morning for >30 mins o Wakes them up at night  Limited lumbar spine ROM  Limited chest expansion

 Bilateral sacroiliitis  grade 2 or (sacroiliitis is usually symmetrical and bilateral)  Unilateral sacroiliitis grade 3 or 4

Investigations  XR o Romanus lesions (shiny corner sign) o Vertebral body squaring o Bamboo spine  MRI if XR is -‘ve  HLA-B27 test if they have 3 of the Dx criteria Mx Exercise therapy Drug tx: 1. NSAID’s 2. Corticosteroid injection 3. DMARDs or anti-TNF therapy (after failing with 2 different NSAID’s)  Is there’s spinal hyperkyphosis or severe hip involvement - surgery  OP assessment every 2 years o DXA for the spine may be ^^ due to syndesmophytes and calcification - do the hip for a more accurate picture  Mx cardiovascular risk factors e.g. HTN, obesity, smoking, lipid modification  

VASCULITIS Polymyalgia rheumatica      

Giant cell vasculitis Usually seen in >50 y/o Rapid onset of sx - aching, morning stiffness in proximal limb muscles o NOT WEAKNESS May have mild polyarthralgia, lethargy, depression, low-grade fever, anorexia, night sweats Skip lesions Muscle bed arteries are most affected - shoulder and hip girdle pain

Investigations  ^ inflammatory markers  ESR >40 mm/hr  Creatinine Kinase and EMG are normal Mx

 Prednisolone 15 mg/OD o 15mg for 3 weeks o 12.5mg for next 3 weeks o 10mg for the next 6-10 wks o Decrease by 1mg every 3 weeks afterwards Temporal arteritis  Giant cell arteritis  3 = Dx: o 50 y/o o New onset, localised headache o Temporal artery tenderness or decreased pulsation o ESR 50mm/hr o Temporal artery biopsy +’ve  May also have scalp pain  Complicated GCA signs:  Jaw/tongue claudication  Visual disturbance - needs attention as it can cause irreversible sudden blindness

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Investigations Bloods: ESR, CRP ^, FBC - anaemia of chronic disease Temporal artery biopsy  skip lesions Aortic Angiography

Mx  Prednisolone 40-60 mg/OD until sx and investigations are normal o Complicated GCA = IV Methylprednisolone 500-1000mg for 3 days before starting PO Prednisolone 60mg  + Omeprazole + bisphosphonate + vit D (due to SE’s of long-term steroids)  150mg Aspirin - reduces rate of visual loss and CVA’s Polyarteritis nodosa      

Affects medium sized / small blood vessels Unknown cause 40-60 y/o Can affect nerves, joints, heart, kidneys, GI tract HBV is a major risk factor Px with: o General malaise o Fevers o Night sweats o Weight loss o Myalgia/arthralgia o Erythema nodosum o Mononeuritis multiplex o Abdo pain or Blood in stools if GI involved o SOB or chest pain if heart involved o HTN if Kidney involved

Investigations  ^ CRP, ESR  FBC: normochromic, normocytic anaemia, neutrophilia, ^ plt’s  Angiography and biopsy of affected tissues

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Mx PO Prednisolone + DMARD If it’s HBV related - Prednisolone + plasma exchange + lamivudine

Takayasu arteritis   



Rare 10mmHg (and difference between the arms/legs) o Subclavian or aortic bruit o Visual disturbances o Suspect in young people who have a stroke + ^CRP/ESR

Investigations  Contrast Angiography - skip lesions  Bloods: anaemia, ^ESR/CRP, antibody -‘ve

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Mx Steroids 1mg/kg (max 80mg) o Step-down approach - aim for 10mg/day by 6 months + Methotrexate or Azathioprine

Behcet’s disease   

Systemic vasculitis Mostly in Mediterranean people Diagnostic criteria:  Recurrent oral ulceration (3x in 1 yr) + 2 of the following: o Recurrent genital ulcers o Eye lesions e.g. uveitis, retinal vasculitis  CAN CAUSE BLINDNESS o Skin lesions o +’ve pathergy test  Arthritis occurs in 50% - usually monoarticular

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Mx Topical corticosteroids for oro-genital ulcers PO steroids if they’re severe + LA gel Colchicine or Thalidomide to control ulcers Azathioprine, ciclosporin, tacrolimus or IFN-a for ophthalmic problems

Buerger’s disease   

Aka Thromboangiitis obliterans Thrombotic occlusion of lower limb vessels (small and medium vessels) Typically, in young male smokers  Proximal pulses present, pedal pulses lost o Intermittent claudication o Ischaemic ulcers o Raynaud’s o Thrombophlebitis

Investigations  Angiogram - ‘corkscrew’ collateral vessels

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Mx QUIT SMOKING No cure - can give anticoagulants, vasodilators, NSAID’s

AUTOIMMUNE CONNECTIVE TISSUE DISEASES SLE     



       o o o o o o o o o o o

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Autoimmune Females > males (10:1) - oestrogens can exacerbate HLA-DR2 and DR3 are associated Infectious triggers incl EBV, CMV, Hep-C Non-infectious triggers incl smoking, exposure to silica, solvents, pesticides or UV light (UVA > UVB photosensitivity is key), hyperprolactinaemia o Alcohol may be protective? Drug induced: HIP PMS Hydralazine Isoniazid Phenytoin Procainamide Methyldopa or Minocycline Sulphonamide Px: SOAP BRAIN MD Serositis Oral ulcers Arthritis Photosensitivity Blood disorders Renal involvement ANA +’ve Immunologic (anti-dsDNA, anti-Smith) Neurologic sx Malar rash Discoid rash o MSK  polyarthralgia with morning stiffness, OA or Fibromyalgia can co-exist, spontaneous tendon rupture o Mucocutaneous  butterfly rash (SPARES NASO-LABIAL FOLDS), discoid rash, photosensitivity, alopecia, ulcers o Renal  Nephritic syndrome (60% - usually diffuse proliferative), Nephrotic syndrome (10-15%) o Neuro  cognitive dysfunction, mood disorders, headaches, seizures o Haematological  anaemia (70%), lymphopenia and thrombocytopenia, lymphadenopathy, functional hyposplenism, DVT/PE o GI  oral ulcers, hepatosplenomegaly, IBS-like sx, oesophageal dysmotility o Pulmonary  pleurisy, pleural effusion, recurrent pneumonia, PE (if there’s APL antibodies), ILD o Cardiac  pericarditis (most common), accelerated atherosclerosis Also associated with Sjogren’s syndrome, hypothyroidism, OP, Vit D deficiency, infections, Raynaud’s, APLS ^ risk of malignancy Anything with scarring alopecia  think Lupus

Investigations  ANA +’ve (95%) by ELISA  Anti-dsDNA

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Anti-Smith RhF +’ve (20%) Anti-cardiolipin Anti-Ro (40%) & Anti-La (15% o Also seen in Sjogren’s  U1RNP (30%) o Also seen in Raynaud’s  Anti-histone antibodies = drug-induced Lupus  Consider Imaging e.g. CXR, HRCT, MRI if there’s neurological signs, DXA (for all PMP women) Mx Prednisolone - 30mg or 40mg if obese Minimise long-term use of steroids - topical preparations wherever possible Hydroxychloroquine to reduce flares (and clotting events) Mild  antimalarials (for rash), topical steroids/NSAID’s when needed Moderate  Azathioprine, methotrexate, ciclosporin If it’s just cutaneous  topical steroids over lesions. If resistant - topical tacrolimus or systemic dapsone or thalidomide  If it’s cerebral  IV cyclophosphamide + prednisolone

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Anti-phospholipid syndrome (APLS)   

Affects 25% of SLE pt’s (Secondary APLS) Can be triggered by infections e.g. HCV, VZV, CMV, 5th disease, HIV, gonorrhoea Px: CLOTs o Coagulation defects - strokes, DVT’s, PE’s, HTN, RAS o Livedo reticularis o Obstetric problems e.g. recurrent miscarriages (risk = 20%) o Thrombocytopenia  Clots or miscarriages >10 wks & +’ve Antibodies on 2 occasions = Dx  Catastrophic APLS = life-threatening form where 3 organ systems are involved - trauma can precipitate it

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Investigations Check Lupus anticoagulant & anti-phospholipid antibodies  2 screening tests Anti-cardiolipin IgG/M (if these are +’ve can diagnose even without the Lupus anticoagulant) Anti B2-glycoprotein IgG/M ^aPTT, normal PT Mx Mx vascular risk factors e.g. smoking cessation, weight loss, exercise, BP, lipid control Aspirin Anticoagulate e.g. Warfarin If clots occur - LMWH + long-term Warfarin o Prednisolone o IVIG o Rituximab Hydroxychloroquine can decrease thrombotic events

Dermatomyositis  Muscle inflammation + cutaneous sx o Symmetrical, proximal muscle weakness o Muscle biopsy showing signs of inflammation o ^ serum muscle enzymes (LDH, AST, ALT)

EMG evidence of myositis Cutaneous features e.g. Gottron’s papules, heliotrope rash (eyes), ‘shawl like’ distribution of an erythematous rash o Systemic features e.g. fever, weight loss, anorexia, fatigue o Can have calcific deposits in joints Female > Male More common in North American’s Can be associated with underlying CT disease or malignancy (paraneoplastic disorder - need to screen for Ca) Associated with dysphagia (50%), Cardiac (50%) - pericarditis, arrhythmia, ILD (30%), Arthritis (25%), Raynaud’s ^ risk of Ca Polymyositis - variant where there’s no skin manifestations o o

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Investigations  ^ LDH, AST and ALT  ^ CK (50x norm in some cases)  ^ myoglobin in serum and urine in 70-80% of active disease cases  ANA (80%)  Anti-tRNA  Anti-Jo1 & Anti-SRP (associated with a worse prognosis)  Anti-SRP  Anti-Mi2-antibodies  CXR to rule out malignancy  Muscle biopsy & histology is Dx  EMG distinguishes myopathic from neuropathic weakness

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Mx Conservative  PT, sun cream (as photosensitive rash) Medical  GC’s to establish disease control o Prednisolone 1mg/kg/day with max 80mg - continue high-dose for 6 weeks o If severe pulse IV methylprednisolone 1g/day for 3 days o Using GC’s can cause steroid-induced myopathy and bone weakness (check Vit D and give Bisphosphonate cover) Azathioprine 50mg/day - increased to 150-200mg max o Screen for TPMT activity 1st o Azathioprine > Methotrexate (MTX) if there’s ILD, alcoholism, Liver disease o But MTX works faster and only has to be taken once weekly (15-25mg/week with 5mg Folic acid on a different day)

Raynaud’s 

Peripheral digital ischaemia due to paroxysmal vasospasm - fingers/toes ache and change colour  Brought on by cold or emotion  U1RNP associated  Pale = ischaemia  Blue = deoxygenation  Red = reactive hyperaemia (painful)  If it’s idiopathic = Raynaud’s disease  If there’s an underlying cause = Raynaud’s phenomenon e.g. o CT disorders like systemic sclerosis, SLE, RA, polymyositis or dermatomyositis o Occupational causes from using vibrating tools (common in young men) o Obstructive causes e.g. thoracic outlet obstruction, Buerger’s disease, atheroma, cervical rib o Blood related causes e.g. PCV, thrombocytosis o Drugs e.g. B-blockers o Hypothyroidism

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Mx Keep warm Stop smoking Nifedipine 5-20mg/8h PO IV prostacyclin’s PDE5 inhibitors PPI cover Evening primrose oil

Systemic sclerosis (SSc)             

Autoimmune connective tissue disease See Scleroderma (thickening of skin which is shiny), internal organ fibrosis and microvascular abnormalities Females > Males Peak age 20-50 years 50% of pt’s have painful finger ulcers - can be infected (usually with Staph aureus) Pulmonary HTN is often seen sub clinically Abdomen involved = systemic disease, just hands/feet = limited sclerosis (CREST) CREST syndrome  Calcinosis Raynaud’s phenomenon Esophageal dysmotility - most pt’s have reflux disease Sclerodactyly Telangiectasia

Investigations  Bloods: FBC, U&E - check for renal failure  Antibodies: o ANA (90% are ANA +ve) o Anti-centromere antibodies (70%) - associated with pulmonary HTN o Anti-SCL-70 - associated with lung fibrosis o Anti-RNA polymerase - associated with scleroderma and renal crisis  Respiratory exam and lung function tests to asses for fibrosis  Barium swallow to check for oesophageal dysmotility - may need a SALT assessment to check for safe swallow if they complain of dysphagia Mx     

IV Cyclophosphamide for organ involvement or progressive skin disease If there’s a renal crisis tx with ACEi’s acutely, RRT is needed long term Monitor BP and renal function Annual Echo’s and Spirometry Severe disease has a 50% mortality due to lung fibrosis and pulmonary HTN

Sjogren’s syndrome    

Dysfunction of salivary and lacrimal glands ^ lymphoma malignancy risk Can be 1o (on its own) or 2o (alongside another CT disorder) Dry eyes o >3 months o Feeling like sand or gravel is in eye o Using tear substitutes >3x/day o +’ve Schirmer’s test or Rose Bengal score

 Dry mouth o >3 months o Recurrent swollen salivary glands o Drinking lots of fluids in order to swallow food o Can do salivary sialography of scintigraphy  Also associated with ILD, dyspareunia (from decreased vaginal secretions), dry hair/skin, oesophagitis, malabsorption, arthritis o 25% have ^ Amylase o 30% have inflammatory arthritis  Systemic sx incl fatigue, fever, night sweats

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Investigations Anti-Ro and Ant...


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