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5th Year Revision > Y3 - Rheum > Flashcards

Y3 - Rheum Flashcards

1
Q

What is dermatomyositis and polymyositis?

A

Idiopathic muscle diseases characterised by inflammation of striated msucle, causing proximal muscle weakness.

ie. trouble squatting, climbing stairs

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2
Q

How does D and P present?

A
  • 40-50 years old
  • painless
  • insidious onset of Symmetrical proximal muscle weakness (shoulder and pelvic girdle muscle wasting)
  • Characteristic rash
    • photosensitive so on exposed areas like scalp, face, neck
    • linear plaques on dorsal hands (Gottrons papules)
    • Dilated nail fold capillaries
    • dry cracked palms and fingers (Mechanics hands)
    • Periorbital oedema
    • Violet rash (heliotrope rash) on eyelids
    • Erythema over hips (Holster sign)
    • Erythema over neck and shoulders (shawl or V sign)
    • Later on Upper oesophagus striated muscle can be affected = dysphagia, aspiration pneumonia
  • Later on Diaphragmatic involvement = resp failure
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3
Q

What are the diagnostic criteria of Dermatomyositis and Polymyositis

A
  • symmetrical proximal muscel weakness
  • raised serum muscle enzyme levels
  • typical “myositis triad” changes on EMG
  • Needle Muscle Biopsy evidence of myositis (fibre necrosis + regenration in association with an inflammatory cell infiltrate with lymphocytes around the blood vessels/muscle fibres)
  • Typical Rash
  • PM if >=3 of the first 4 of above
  • DM if rash + >=2 of first 3 of above
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4
Q

How would you Investigate D and P

A
  • ESR and CRP raised
  • Raised ALT (from muscle) with other LFTS normal
  • 80% are antinuclear antibody positive
  • Anti-Jo1 and Anti-Mi2
  • get an extended muscle auto-antibody panel
  • MRI shows abnormally inflamed muscle
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5
Q

How would you manage D and P?

A
  • High dose corticosteroids = Prednisolone for a month then taper once myositis is less clinically active
  • Repeat EMG/MRI/Biopsy to monitor
  • Long term control via methotrexate/ Azathioprine/ Ciclosporin once steroid has been reduced
  • Rituximab can be used in autoantibody +ve cases
  • IVIG also useful
  • Dermatomyositis = sun protection, hydrochloroquine for rash
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6
Q

What is fibromyalgia?

A

a disorder of central pain processing, resulting in chronic widespread pain in all 4 quarants (both sides and above and below the waist).

Allodynia (heightened and painful response to innocuous stimuli) is also present

Can be induced by sleep depriation = causes hyper-actiation in response to noxious stimulation

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7
Q

How would fibromyalgia present?

A
  • female 9:1 male
  • joint/muscle stiffness
  • profound fatigue
  • unrefreshed sleep
  • numbness
  • tension headaches
  • irritable bowel/bladder syndrome
  • depression and anxiety
  • poor concentration, memory “fibrofog” forgetfulness

On examination

  • no physical MSK or neuro abnormalities
  • may have “tender points” on palpation of muscles
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8
Q

How would you manage fibromyalgia?

A
  • reassure that it is not arthritis ie the pain is not damaging to the joints
  • explanation of symptoms!
  • Low dose amitryptiline or pregabalin
  • Opiates not reccomended
  • Cognitive behavioural therapy
  • Supervised aerobic exercise regimen over 3 months
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9
Q

What is Giant Cell Arteritis?

A

A chronic (inflammatory granulomatos arteritis) vasculitis of large/medium sized vessels that occurs in association with PMR in individuals over 50.

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10
Q

How does GCA present?

A
  • unilateral boring temporal headache
  • tongue or jaw claudication
  • visual changes like AION
  • scalp tenderness esp over temporal artery
  • PMR
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11
Q

How would you diagnose GCA?

A
  • raised esr, crp, PV
  • new onset localised headache
  • tenderness or decreased pulsation of temporal artery
  • new visual symptoms
  • temporal artery US = halo sign
  • temporal artery biospy = necrotising arteritis
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12
Q

How would you manage GCA?

A
  • high dose PO prednisolone for atleast 2 weeks before tapering!!!
  • if visual symptoms = IV methylprednisolone for 3 days then prednisolone
  • low dose aspirin to reduce thrombotic risk
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13
Q

What is gout? What are some risk factors?

A
  • Inflammatory arthritis related to hyperuricaemia (urate>6.8)
  • Affects 1st metatarsophalangeal joint
  • Also causes deposits of monosdium urate crystals in joints/soft tissues
    • Tophi (eg on extensor elbow surfaces)
    • Urate nephropathy
    • Uric acid nephrolithiasis

Risk factors

  • high purine = meats/seafood
  • high alcohol = beer (high purine)
  • obesity
  • renal disease
  • HTN
  • Meds = thiazide diuretics, etc
  • Smoking
  • DM
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14
Q

How would you investigate gout?

A
  • Foot Xray = Martels sign adjacent to tophaceous deposits
  • aspirate joint fluid + examine under polarising light microscope = MSU crystals
  • US of joints = double contour sign
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15
Q

How would you manage Gout?

A
  • Nsaid + colchicine + corticosteroid
  • urate lowering therapy like allopurinol or febuxostat (xantine oxidase inhibitors)

General

  • reduce purine rich foods (seafood, red meat, fructose)
  • Increase vit c and dairy
  • reduce alcohol and beer
  • smoking cessation
  • increase hydration
  • regular exercise and optimal weight maintenance
  • Fenofibrate for dyslipidaemia
  • Losartan for HTN
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16
Q

What is pseudogout?

A

caused by calcium pyrophosphate crystals occuring in older women with OA.

affects knees and wrists and will show as chondrocalcinosis on Xray

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17
Q

What is hypermobility spectrum disorder?

A

A pain syndrome in people where their joints move beyond normal limits.

Typically due to connective tissue disease like marfans, Ehlers Danlos type 2, osteogenesis imperfecta, bone shape, hypotonia, etc.

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18
Q

How would HSD present?

A
  • joint pain worse after activity
  • soft tissue rheumatism eg epicondylitis
  • abnormal skin = papyraceous scars, hyperextensible, thin, striae
  • marfanoid habitus
  • arachnodactyly
  • drooping eyelids, myopia
  • hernias and uterine/rectal prolapses
  • recurrent subluxations or dislocations
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19
Q

How would you manage HSD?

A
  • Use the Beighton Score
  • strengthening exercises to reduce subluxation
  • splinting and surgical interventions potentially
  • Paracetamol
  • Specialist input
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20
Q

Osteoarthritis is covered in Surgery-Ortho.

How would you manage it?

A
  • Physio and strengthening exercises
  • Weight loss and walking sticks to reduce loading of hip/knee joints
    • also laterally wedged insoles for medial compartment OA
  • regular paracetamol 1st line
    • NSAIDs short term + PPI
  • Topical Nsaids and topical capsaicin can be useful
  • intraarticular corticosteroid injections also useful
  • Surgery eg replacement arthroplasty
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21
Q

What is osteoporosis?

A

Low bone mass and deterioration of bone tissue resulting in compromised bone strength and increased risk of fracture.

Increased bone breakdown by osteoclasts.

Decreased bone formation by osteoblasts.

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22
Q

What are some modifiable and non-modifiable risk factors of osteoporosis?

A

Non modifiable

  • old age
  • female
  • caucasian/south asians
  • fhx
  • hx of trauma fracture

Modifiable

  • low bmi <21
  • premature menopause <45 years old (low oestrogen)
  • calcium/vit d deficiency
  • inadequate physical activity
  • cigarette smoking
  • excessive alcohol
  • iatrogenic = corticosteroids, aromatase inhibitors
  • Secondary = Coeliac disease, hyperPTH, eating disorders, hyperthyroidism, multiple myeloma
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23
Q

How would you investigate osteoporosis?

A
  • DEXA bone scan of lumbar spine and hip is gold standard
  • T score of -2.5 or less is diagnostic
    • Normal is greater or equal to -1
    • Osteopenia is -1 to -2.5
  • Xray showing rib or vertebral compression fractures without trauma hx should prompt evaluation for osteoporosis
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24
Q

How would you manage osteoporosis?

and osteopenia

A

Osteopenia

  • weight bearing exercises
  • vitamin D3 supplements (800-2000IU/day)
  • Limiting alcohol
  • smoking cesssation
  • dietary advice for calcium

Osteoporosis

  • vit d + calcium supplements
  • oral bisphosphonates
    • 2nd line = denosumab or teriparatide
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25
Q

What is polymyalgia Rheumatica?

A

a pain and stiffness syndrome of the shoulder, hip girdles and neck.

Characterised by proximal morning stiffness/pain

26
Q

How would PMR present?

A
  • around 70 year olds
  • new onset proximal limb pain and stiffness (neck, shoulders, hips)
    • difficulty rising from chair or combing hair
  • night time pain
  • systemic symptoms eg. fatigue, weight loss, low grade fever
  • depression
  • GCA?

o/e

  • decreased range of movement of shoulders, neck, hips
  • muscle strength is normal but may be tender
27
Q

How would you investigate PMR?

A
  • raised ESR, CRP, PV
  • temporal artery biopsy if GCA symptoms
  • ALP may be raised and GGT too
  • mild normochromic normocytic anaemia
28
Q

How would you manage PMR?

A
  • start prednisolone due to clinical suspicion and the dramatic response within 5 days will be diagnostic.
    • 15mg prednisolone daily dose then taper down gradually
    • supplement with calcium + vitamin D + bisphosphonates
  • Methotrexate can be steroid sparing in relapsing patients
  • If no response to steroids, think infection, cancer, RA, etc.
29
Q

What is Raynauds phenomenon

A

A painful idiopathic condition due to vasospasm of the digital arteries.
Can also be precipitated by stress, cold (relieved by heat)

Characterised by colour changes in response to a cold stimulus:

White = inadequate blood flow

Blue = venous stasis

Red = rewarming hyperaemia (typically also with numbness, burning sensation and paina s fingers warm up)

30
Q

What things/diseases are associated with Raynauds phenomenom?

A

Diseases

  • scleroderma
  • SLE
  • Sjogrens syndrome
  • dermatomyositis and polymyositis

Physical causes

  • heavy vibrating tools
  • cervical rib
  • sticky blood ie cryoglobulinaemia

Drugs eg. beta blockers

31
Q

How would you manage raynauds phenoenon?

A
  • keep warm (gloves etc) and avoid smoking!!!
  • CCB 1st line
    • phosphodiesterase-5-inhibitors and prostacyclins are 2nd line
32
Q

What is CREST syndrome?

A
  • Calcinosis
  • Raynauds
  • Oesophageal Dysmotility
  • Sclerodactyly
  • Telangiectasia
33
Q

What is Rheumatoid Arthritis?

A
  • An Autoimmune disease with Rheumatoid Factor and Anti-Citrullinated Cyclic Peptide
  • T and B cells produce RF and Anti-CCP
  • stimulated macrophages and fibroblasts release TNFa
  • inflammatory cascade leads to synoviocyte proliferation = boggy joint swelling
34
Q

How does RA present?

A
  • female 3:1
  • 30-50 years old
  • progressive, peripheral, symmetrical polyarthritis
  • usually MCPs, PIPs, MTPs, spares DIPs (OA has herbeden)
  • >6 weeks hx of morning stiffness lasting over 30mins
  • Fatigue and malaise

o/e

  • soft tissue swelling and tenderness
  • swan neck PIP deformity (fixed hyperextension)
  • Boutonniere PIP deformity (fixed flexion)
  • Rheumatoid nodules at elbow
  • carpal tunnel?

Extra-articular manifestations

  • ECs = carpal tunnel, higher cardiac risk, cord compression
  • 3As = anaemia, amyloidosis, arteritis
  • 3Ps = pericarditis, pleural disease, pulmonary disease
  • 3Ss = sjogrens, scleritis, splenic enlargement (+ neutropenia = feltys syndrome)
35
Q

How would you investigate RA?

A
  • RF and anti-CCP
  • FBC = normocytic anaemia
  • CRP, ESR, PV elevation
  • Xray changes later on = LESS
    • Loss of Joint space
    • Erosions (periarticular)
    • Soft tissue swelling
    • Subluxation
  • US and MRI in early disease
36
Q

How would you manage RA?

A
  • 1st line is DMARDs monotherapy = oral Methotrexate (can cause interstitial lung fibrosis, nausea, etc)
    • with short term bridging with glucocorticoids
  • 2nd line Try combination of DMARDs (methotrexate, sulfasalazine, leflunomide)
  • 3rd line try biologics like Sarilumab + Methotrexate
    • if DAS28 is 5.1 (scoring system that counts joints affected)
  • 4th line is Rituximab + Methotrexate
  • NSAIDs + PPI for pain
  • Podiatry, Occupational therapy, Physio
  • can give corticosteroids acutely
    • co-prescribe vit d and bisphosphonates due to fracture risk
37
Q

What is Sjogrens syndrome?

A

Chronic autoimmune inflammatory disorder characterised by diminished lacrimal and salivary gland secretion

38
Q

How does Sjogrens present?

A

MADFRED

  • Myalgia
  • Arthralgia
  • Dry mouth
  • Fatigue
  • Raynauds phenomenom
  • Enlarged parotids
  • Dry eyes
  • commonly associated with coeliac, PBC, autoimmune thyroid disease
39
Q

How would you investigate Sjogrens?

A
  • anti Ro, anti La antibodies in 90%
    • pregnanc patients with antiRo are at risk of foetal loss, complete heart block fo foetus, and neonatal lupus syndrome in newborn as it crosses placenta.
  • RF in 40%
  • anti ds DNA
  • ANA antibodies in 75%
  • Schirmers test = assess lacrimal gland output over 5 mins
  • Salivary gland biopsy = focal lymphocytic infiltration of exocrine glands eg salivary/lacrimal/bartholins etc.
    *
40
Q

How would you manage Sjogrens?

A
  • artifical tears
  • artificial saliva, sugar free gum/pastilles
  • skin emollients, vaginal lubricants
  • immunosuppressants and steroids rarely
41
Q

What are spondyloarthropathies?

A

A group of conditions that affect the spine and peripheral joints.

Associated with HLA-B27.

These are Ankylosing Spondylitis, Enteropathic Arthritis, Psoriatic arthritis, Reactive arthritis

42
Q

What is Ank Spon and how does it present

A
  • young men/teens present with bilateral buttock pain, chest wall and thoracic pain
    • worse in the morning, relieved by exercise
    • retention of lumbar lordosis in spinal flexion
  • O/E
    • loss of lumbar lordosis
    • exaggerated thoracic kyphosis
    • Schobers test
    • Reduced chest expansion = PIF
43
Q

How would you investigate/manage Ank Spon?

A
  • High CRP and ESR
  • MRI spine and Sacroiliac joints
  • Xray shows bamboo spine (calcification of intervertebral ligaments and fusion fo facet joints and syndesmophytes)

Manage

  • Nsaids
  • Physio (preventative exercises can stop syndesmophytes forming)
  • TNFa inhibitors (golimumab, adalimumab, etanercept etc), IL17 inhibitors can also be used if NSAIDs not enough to reduce inflammatory symptoms
44
Q

What is psoriatic arthritis and how does it present?

A
  • oligoarthritis
  • dactylitis or “sausage” digit
  • dystrophic nails on affected digit
  • deformities like arthritis mutilans “telescopic fingers”
45
Q

How would you investigate and manage psoriatic arthritis?

A
  • CRP raised
  • MRI shows central joitn erosions
  • Xray shows “pencil in cup” appearance

Management

  • Nsaids 1st line (similar to ank spon)
    • good for pain but can worsen skin
    • Hydroxychloroquine for skin
  • 2nd line = DMARDs (methotrexate), TNF Inhibitors (adalimumab), IL17 inhibitors, etc
  • Local synovitis can try intra-articular corticosteroid injections
46
Q

What are the extra-articular manifestations of Ank Spon?

A

6As

  • Anterior Uveitis
  • Aortic Incompetence
  • AV Block
  • Apical Lung Fibrosis
  • Amyloidosis
  • igA nephropathy
47
Q

What is reactive arthritis and how does it present?

A
  • acute asymmetrical lower limb arthritis
  • occurs days-2 weeks post infection such as Salmonella/Shigella/Campylobacter OR Chlamydia trachomatis
  • Skin = circinate balanitis in uncircumcised males, keratoderma blennorrhagica (painless red raised plaques)
  • Nail Dystrophy
  • Eyes = conjunctivitis, uveitis
  • Enthesitis = plantar fasciitis, achilles tendon enthositis, dactylitis
48
Q

How would you investigate and manage reactive arthritis?

A
  • serology, microbiology
  • Inflammatory markers raised
  • joint aspiration (cloudy yellow fluid with neg culture, neg crystals, 20000wbc)

Management

  • Treat infection
  • NSAIDs
  • oral corticosteroids or injections for pain
  • Relapses = sulfasalazine or methotrexate
    • 2nd line = TNFa inhibitors
49
Q

What is Enteropathic Arthritis?

A
  • IBD patients who develop arthropathy
  • 2/3 develop peripheral arthritis
  • 1/3 develop axial disease

2 types of peripheral disease

  • Type 1 = oligoarticular, asymmetric, correlation with IBD flares
  • Type 2 = polyarticular, symmetrical, less correlation with IBD flares
50
Q

How would you manage enterophathic arthritis?

A
  • DMARDs (sulfasalazine) as NSAIDs can flare IBD.
  • TNF inhibitors like infliximab, adalimumab etc can treat both IBD and arthritis
51
Q

What is systemic lupus erythematous? Key signs and symptoms?

A

complex multisystem autoimmune disease

Signs and Symptoms = SOAP BRAIN

  • Serositis = pleurisy (bilateral) + pleural effusions, pericarditis
  • Oral ulcers
  • Arthritis (symmetrical small joint arthralgia like RA)
  • Photosensitivity (malar/butterfly/discoid rash)
  • Blood disorders = low wcc, lymphopenia, thrombocytopenia, haemolytic anaemia
  • Renal involvement = glomerulonephritis
  • Autoantibodies (ANA positive in 90%)
  • Immunologic tests eg. lwo complements
  • Neurologic disorders eg. seizures/psychosis
52
Q

How would you investigate SLE?

A
  • ESR and Plasma Viscosity raised
  • Anaemia and Leukopenia on FBC
  • Antinuclear Antibody positive
  • AntiRo, AntiLa, AntiSm
  • Anti dsDNA rise with disease activity
    • C3 and C4 fall with disease activity
  • Antiphospholipid antibodies increase risk of pregnancy loss and thrombosis
  • Urinalysis for renal disease (and u&es)
  • Skin biopsy
  • Renal biopsy
53
Q

What are some lupus skin signs

A
  • butterfly erythema
  • vasculitic lesions on fingertips and nail folds
  • urticaria
  • purpura
  • photosensitivity (especially antiRo)
  • Livedo reticularis
  • palmar and plantar rashes
  • alopecia
  • Raynauds
  • Discoid lupus = only skin involvement
54
Q

How would you manage SLE?

A
  • sun protection
  • healthy lifestyle to prevent cvs risk
  • hydrochloroquine = rash
  • NSAIDs = arthralgia, arthritis, fever, serositis
  • Mycophenolate Mofetil is used most (cyclophosphamide 2nd line but causes infertility so used in older sufferers)
    • also azathioprine, rituximab, etc.
  • Short course prednisolone for flares
  • High dose corticosteorids and immunosuppressants = renal/cns disease
  • cutaneous lupus = topical corticosteroids
55
Q

What is systemic sclerosis? (also known as scleroderma)

A

Increased fibroblast activity resulting in abnormal growth of connective tissue. This elads to vascular damage and fibrosis.

Two different types = limited SSc and diffuse SSc

56
Q

How do limited and diffuse SSc present?

A

Limited SSc

  • CREST syndrome!
  • Calcinosis Cutis
  • Raynauds
  • Oesophgeal dysmotility
  • Sclerodactyly
  • Telangiectasia
  • many years of Raynauds, then scleroderma (skin thickening)
  • usually develops pulmonary arterial hypertension after 10 years of symptoms

Diffuse SSc

  • less common, higher mortality risk
  • sudden onset skin involvment = proximal to elbows and knees
57
Q

How would you investigate and manage systemic sclerosis?

A
  • inflammatory markers normal
  • Xray hands = calcinosis
  • CXR, High Res CT, etc = pulmonary disease
  • ECG and ECHO = PA HTN, HF, myocarditis, arrhythmias
  • Barium swallow for oesophageal dysmotility
  • Antibodies
    • ANA +ve
    • anti-centromere antibody in Limited SSC
    • Scl-70 topisomerase and antiRNA polymerase III in Diffuse SSc

Management

  • psychological support
  • CCB etc for Raynauds
  • Methotrexate or Mycophenolate Mofetil for skin thickening
  • ACE I for HTN crises and renal failure
  • short course prednisolone for flares (no cure htough)
  • PPI for GI symptoms like reflux
58
Q

What is vasculitis?

A

inflammatory blood vesse, disorders.

Symptoms are due to damage to blood vessel walls resulting in thrombosis, ischaemia, Bleeding, aneurysms.

Ie. purpura, joint/muscle pain, peripheral neuropathy, renal impairment, GI problems, anterior uveitis, scleritis, htn

59
Q

What are some small, medium and large vessel vasculitis?

A

Small

  • microscopic polyangiitis
  • Granulomatosis with polyangiitis (Wegeners)
    • cANCA +ve with PR3 antibodies
  • Eosinophilic granulomatosis with polyangiitis (Churg-Strauss)
  • IgA vasculitis (Henoch Schonlein Purpura)

Medium

  • Polyarteriitis nodosa
  • Kawasaki disease

Large

  • Takayasu arteritis
  • Giant Cell Arteritis
60
Q

How would you investigate/manage vasculitis? generally

A
  • CSR, ESR raised
  • AntiNeutrophil Cytoplasmic Antibodies (ANCA) is the blood test for vasculitis
    • there is p-anca = microscopic polyangiitis, Churg-Strauss syndrome
    • and c-anca = Wegeners granulomatosis

​Management

  • Rule out infection, stop offending drug
  • 1st line = corticosteroids
  • 2nd line = cytotoxic meds, immunomodulators, biologic agents (cyclophosphamide, methotrexate, azathioprine, etc)
61
Q

How would these conditions generally present?

Henoch Schonlein Purpura

Eosinophilic Granulomatosis with Polyangiitis

Microscopic polyangiitis

Granulomatosis with polyangiitis

Polyarteritis Nodosa

Kawasaki Disease

Takayasu’s arteritis

A

HSP (an iga vasculitis that is triggered by urti like tonsillitis or gastroenteritis)

= purpura, joint pain, abdo pain, renal involvement (iga nephritis)

EG with P

= severe asthma in late teens, high eosinophils

Microscopic polyangiitis

= renal failure, lungs (sob, haemotypsis)

Wegeners

= epistaxis and crusty nasal/ear secretions, saddle shaped nose (perf nasasl septum), wheeze and haemoptysis, rapidly progressing glomerulonephritis

Polyarteritis Nodosa

= associated with hep b, hep c, hiv

= causes renal impairment, strokes, MI, livedo reticularis (purple lace like rash)

Kawasaki disease

= strawberry tongue, cervical lymphadenopathy, 5 day high fever, erythematous rash, bilateral conjunctivitis, erythema/desquamation of palms and soles

= complications are coronary artery aneurysms

Takayasu’s arteritis

= <40 years old non specific symptoms or specific symptoms like arm claudication or syncope

5th Year Revision (14 decks)

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