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RHEUMATOLOGY AND MSK Flashcards

1
Q

what are the clinical features of frozen shoulder?

A
  • Shoulder stiffness
  • Decreased active and passive range of movement
  • Positive coracoid pain test: pain elicited by direct pressure on the coracoid
  • Positive shoulder shrug test: inability to abduct the arm to 90o in the plan of the body and hold the position
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2
Q

how is frozen shoulder managed?

A
  • analgesia
  • physiotherapy
  • intra-articular steroids
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3
Q

what is frozen shoulder?

A
  • chronic fibrosing condition
  • insidious and progressive severe restriction of both active and passive shoulder range of motion
  • absence of a known intrinsic disorder of the shoulder.
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4
Q

what are the clinical features of complex regional pain syndrome?

A
  • Chronic pain
  • Limb pain with radiation
  • Allodynia and hyperalgesia
  • A feeling that the affected limb or digit does not belong
  • Oedema
  • Trophic skin and nail changes
  • Erythema or bluish appearance
  • Local sweating changes or sweating asymmetry
  • Muscle weakness
  • Tremors
  • Dystonic posturing
  • Contractures
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5
Q

what criteria is used to diagnose complex regional pain syndrome?

A

-Budapest diagnostic criteria

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6
Q

how is complex regional pain syndrome managed?

A
  • Offer desensitisation therapy
  • Offer physiotherapy and occupational therapy
  • Offer a low dose TCA, gabapentin or pregabalin for neuropathic pain
  • Offer topical local anaesthetic patches with lidocaine
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7
Q

what are the clinical features of granulomatosis with polyangiitis?

A
  • Otorrhoea.
  • Rhinorrhoea.
  • Epistaxis.
  • Sinus pain.
  • Oral and nasal mucosal ulceration.
  • Nasal septal perforation.
  • Saddle nose deformity.
  • Cough.
  • Haemoptysis.
  • Pleuritic chest pain.
  • Oliguria.
  • Microscopic haematuria.
  • Proteinuria.
  • Red cell casts in urine.
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8
Q

which autoantibodies are positive in GPA?

A
  • cANCA

- pANCA

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9
Q

What is seen on renal biopsy in GPA?

A
  • Necrotising microvascular glomerulonephritis
  • Absent immune deposits
  • Glomerular crescents.
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10
Q

how is GPA managed?

A
  • non-organ threatening disease, offer methotrexate or mycophenolate mofetil with a glucocorticoid
  • organ or life threatening disease, offer cyclophosphamide or rituximab with a glucocorticoid
  • rapidly progressive renal failure or pulmonary haemorrhage, consider plasma exchange
  • Upon remission with these therapies, offer azathioprine, methotrexate or rituximab and continue to taper glucocorticoids
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11
Q

what are the risk factors for primary raynauds?

A
  • Female gender
  • Positive family history
  • Smoking
  • Migraine
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12
Q

what are the risk factors for seccondary raynauds?

A
  • CTD
  • Use of vibratory equipment
  • Haematological conditions including cryoglobulinaemia, polycythaemia, protein C deficiency, protein S deficiency, and antithrombin III deficiency.
  • Endocrine disorders such as hypothyroidism, phaeochromocytoma, and carcinoid syndrome.
  • Drugs, including beta-blockers, ergot derivatives, methylphenidate.
  • Exposure to occupational chemicals such as vinyl chloride.
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13
Q

what are the clinical features of Raynaud’s?

A
  • Clearly demarcated pallor of the digits, followed by at least one colour change (e.g. cyanosis or erythema).
  • Colour changes that start at the tip of the finger then spread downwards to more digits.
  • Associated symptoms such as numbness, and paraesthesia on rewarming.
  • Other extremities may be affected such as the tip of the nose, ear lobes, tongue, or nipples.
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14
Q

what changes are suggestive of secondary Raynaud’s?

A
  • Digital ulcers, gangrene, or ischaemia of one or more digits.
  • Onset over age of 30 years.
  • Episodes are intense, painful, or asymmetrical.
  • History or clinical features of a connective tissue disorders such as sclerodactyly or pitting scars on the fingertips
  • Positive anti-nuclear antibody tests.
  • Abnormal nail-fold capillaries.
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15
Q

how is Raynaud’s managed?

A
  • lifestyle measures
  • prophylactic nifedipine or amlodipine
  • sympathectomy or prostacyclin infusion
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16
Q

what are the clinical features of sarcoidosis?

A
  • Non-Productive cough.
  • Dyspnoea that worsens with disease progression.
  • Wheezing.
  • Lymphadenopathy.
  • Photophobia.
  • Red painful eye (anterior uveitis).
  • Blurred vision.
  • Erythema nodosum.
  • Chest wall pain.
  • Fatigue.
  • Weight loss.
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17
Q

what is seen on CXR in sarcoidosis?

A
  • Bilateral hilar lymphadenopathy
  • Pulmonary infiltrates
  • Fibrosis.
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18
Q

what are the serum features of sarcoidosis?

A
  • raised urea and creatinine

- hypercalcaemia

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19
Q

how is sarcoidosis managed?

A

-Offer oral (prednisolone) or inhaled (budesonide) corticosteroids

  • For advancing disease:
  • –Add a cytotoxic agent (methotrexate or azathioprine)
  • –Administer supplemental oxygen
  • For acute respiratory failure:
  • –Offer an IV corticosteroid or an oral corticosteroid (prednisolone) if able to tolerate oral intake.
  • –Administer ventilatory support and oxygen for patients with oxygen saturation < 88%
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20
Q

what are the clinical features of GCA?

A
  • New onset localised headache that is usually unilateral, in the temporal area.
  • Scalp tenderness.
  • Systemic features such as fatigue, anorexia, weight loss and depression.
  • Features of polymyalgia rheumatica
  • Intermittent jaw claudication, causing pain in the jaw muscles while eating.
  • Visual disturbances in one or both eye such as partial or complete loss of vision, described as a feeling of shade covering one eye.
  • Mononeuropathy or polyneuropathy of both arms or legs.
  • Absent superficial temporal artery pulse.
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21
Q

how is GCA diagnosed?

A
  • raised ESR
  • temporal artery biopsy which is the definitive diagnosis: Granulomatous inflammation; Multinucleated giant cells. This should be performed within 7 days of commencing steroid therapy
  • FDG-PET scan: increased uptake in large vessels
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22
Q

how is GCA managed?

A
  • Start immediate glucocorticoid therapy (prednisolone 40-60 mg) to be tapered off over 12-18 months if possible.
  • Start methylprednisolone pulse therapy (500mg-1g IV for 3 days) followed by conventional glucocorticoid therapy in patients with visual or neurological symptoms, or 60-100mg orally for 3 days if IV therapy is not possible
  • Consider MTX therapy (up to 25mg weekly) in those patients at high risk of glucocorticoid toxicity or who relapse
  • Offer tocilizumab in addition to a tapered course of glucocorticoids if there is relapsing or refractory disease, or in people at high risk of glucocorticoid toxicity.
  • Offer calcium carbonate and vitamin D (ergocalciferol) for osteoporosis prevention.
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23
Q

what are the clinical features of Takayasu’s arteritis?

A
  • Upper or lower limb claudication.
  • Absent pulses.
  • Unequal blood pressure.
  • Vascular bruits (such as subclavian or carotid bruits).
  • Low grade fever.
  • History of TIA.
  • Myalgia.
  • Arthralgia.
  • Weight loss.
  • Fatigue.
  • Dizziness on upper limb exertion.
  • Hypertension.
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24
Q

what are the diagnostic criteria for Takayasu’s arteritis?

A
  • Onset of disease = 40 years
  • Claudication of an extremity
  • Reduced brachial artery pulsation
  • Difference in systolic blood pressure >10 mmHg between the arms
  • Aortic or subclavian artery bruit
  • Angiographic abnormality
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25
Q

how does takayasu’s arteritis appear on CT angiography and doppler USS?

A

-segmental narrowing or occlusion of vessels

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26
Q

How is takayasu’s arteritis managed?

A
  • Offer prednisolone 1mg/kg/day orally
  • Offer aspirin 75 mg daily
  • Offer methotrexate and folic acid, azathioprine, mycophenolate mofetil or cyclophosphamide in patients with release during glucocorticoid tapering.
  • Offer infliximab if initial immunosuppression fails
  • Offer surgery or endovascular intervention for significant limb claudication or severe ischaemic organ dysfunction.
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27
Q

what are the clinical features of Buerger’s disease?

A
  • Current smoking history.
  • Paraesthesia.
  • Rest pain.
  • Cold sensation
  • Cyanosis.
  • Plantar claudication
  • Absent pulses.
  • Gangrene of the distal phalanges.
  • Positive Allan test whereby both radial and ulnar arteries are occluded resulting in ischaemia.
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28
Q

what is seen on arterial duplex scanning/CT angiography in thromboangiitis oliterans?

A
  • Non-atherosclerotic occluded vessels

- Corkscrew shaped collateral vessels (Martorell’s sign).

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29
Q

how is thromboangiitis oliterans managed?

A
  • Urgent smoking cessation
  • Offer nifedipine for critical ischaemia.
  • Offer intravenous antibiotic therapy (metronidazole and benzylpenicillin sodium) for infection or wet gangrene.
  • Offer tramadol for pain relief.
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30
Q

what are the clinical features of a popliteal cyst?

A
  • Popliteal bulge
  • Knee pain
  • Leg swelling
  • Calf tenderness
  • A sudden pop with increased pain, redness and warmth may indicate dissection or rupture of the cyst
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31
Q

what are the risk factors for developing a popliteal cyst?

A
  • Knee joint trauma
  • Underlying knee joint arthritis
  • Underlying knee joint infection
  • Increasing age
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32
Q

how is a popliteal cyst managed?

A
  • If asymptomatic, no treatment is required
  • Consider simple analgesia and physiotherapy for pain management
  • Perform cyst aspiration and intra-cystic corticosteroid injection
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33
Q

what are the clinical features of cryoglobulinaemia?

A
  • Arthralgia
  • Weakness
  • Purpura and leukocytoclastic vasculitis
  • Peripheral neuropathy
  • Lower extremity vascular purpura
  • Hypertension due to renal involvement
  • Hyperviscosity syndrome: diplopia, ataxia, headache, confusion and retinal haemorrhage/thrombosis
  • Acrocyanosis and Raynaud’s phenomenon
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34
Q

how is cryoglobulinaemia diagnosed?

A

-fasting qualitative serum cryoglobulins: present

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35
Q

how is cryoglobulinaemia managed?

A
  • Manage the underlying condition: antivirals for HCV
  • Offer immunosuppression with prednisolone, cyclophosphamide or azathioprine
  • Rituximab can be used if these treatments fail
  • Plasmapheresis should be used when patients have a life or organ threatening cryoglobulinaemia
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36
Q

what are the clinical features of muscle cramps?

A
  • Nocturnal onset
  • Gatrocnemius, with or without, foot involvement
  • Duration <10 minutes
  • Unilateral
  • Precipitation by trivial movements and forceful contractions
  • Visible or palpable muscle knotting
  • Good response to passive or active stretching
  • Normal physical examination
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37
Q

how are muscle cramps managed?

A
  • To alleviate an attack, advise stretching and massaging the affected muscle
  • To reduce the frequency of attacks, stretch the affected muscles 3 times a day
  • A trial of quinine 200-300mg at bedtime for 4 weeks
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38
Q

what are the clinical features of ankylosing spondylitis?

A
  • Episodic pain in one or both buttocks and low back pain and stiffness, typically worse in the morning and relieved by exercise.
  • Retention of the lumbar lordosis during spinal flexion
  • Paraspinal muscle wasting
  • Uveitis/iritis
  • Costochondritis
  • Peripheral joint involvement is asymmetrical and affects a few, predominantly large joints.
  • Fatigue
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39
Q

what criteria are used to diagnose ankylosing spondylitis?

A

-Modified New York

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40
Q

how does grade 1 ankylosing spondylitis appear on x-ray?

A

-some blurring of joint margins

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41
Q

how does grade 2 ankylosing spondylitis appear on x-ray?

A

-minimal sclerosis with some erosion

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42
Q

how does grade 3 ankylosing spondylitis appear on x-ray?

A

-definite sclerosis on both sides of the joint and severe erosions with widening of the joint space with or without ankylosis

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43
Q

how does grade 4 ankylosing spondylitis appear on x-ray?

A

-complete ankylosis (fixation of the joint)

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44
Q

what are the ASAS/OMIR criteria for MRI?

A
  • Active inflammatory lesions such as bone marrow oedema, synovitis, enthesitis and capsulitis
  • BMO/osteitis is essential for diagnosis of active sacroiliitis
  • Structural damage lesions such as sclerosis, erosions, fat deposition and ankylosis
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45
Q

how is ankylosing spondylitis managed?

A
  • NSAIDs
  • Adalimumab, certolizumab pegol, etanercept, golimumab and infliximab are recommended, as options for treating severe active ankylosing spondylitis in adults whose disease has responded inadequately to, or who cannot tolerate, NSAIDs.
  • Secukinumab is recommended as an option for treating active ankylosing spondylitis in adults whose disease has responded inadequately to conventional therapy (NSAIDs or TNF alpha inhibitors).
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46
Q

what are the clinical features of OA?

A
  • Pain
  • Stiffness on a morning lasting <30 minutes
  • Functional difficulties: knee locking or giving way
  • Bony deformities: Bouchard’s nodes (PIPJ), Heberden’s nodes (DIPJ) and squaring of the base of the thumb (CMCJ)
  • Limited range of motion and an antalgic gait
  • Tenderness
  • Crepitus
  • Effusion
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47
Q

how is OA diagnosed?

A

-Diagnose osteoarthritis clinically without investigations if a person: is 45 or over and
has activity-related joint pain and has either no morning joint-related stiffness or morning stiffness that lasts no longer than 30 minutes.

-Perform an x-ray of the affected joints: osteophytes (new bone formation); joint space narrowing; subchondral sclerosis; subchondral cysts

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48
Q

how is OA managed?

A
  • appropriate footwear
  • exercise
  • alternative pain relief
  • topical NSAIDs and oral paracetamol
  • intra-articular corticosteroid
  • joint surgery
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49
Q

what are the clinical features of sJIA?

A
  • Symmetrical and polyarticular arthritis
  • Severe myalgia and abdominal pain for the duration of quotidian fevers with the presence of evanescent erythematous rash
  • serositis
  • Dermographism between fevers
  • Leucocytosis with neutrophilia, high inflammatory markers and thombocytosis
  • Macrophage activation syndrome
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50
Q

what are the clinical features of oligoarticular JIA?

A
  • Arthritis affecting 1-4 joints during the first 6 months of disease. There are two subcategories:
  • Persistent oligoarthritis: affecting no more than 4 joints throughout the disease course
  • Extended oligoarthritis: affecting a total of more than 4 joints after the first 6 months
  • asymmetric in the lower limbs
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51
Q

what are the clinical features of RF positive polyarthritis?

A
  • Arthritis affecting 5 or more joints during the first 6 months of disease.
  • Rheumatoid factor (RF) is positive
  • symmetrical
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52
Q

what are the clinical features of RF negative polyarthritis?

A
  • Arthritis affecting 5 or more joints during the first 6 months of disease.
  • Rheumatoid factor (RF) is negative
  • Heterogenous disease group, with ANA positive and chronic anterior uveitis
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53
Q

what are the clinical features of psoriatic JIA?

A
  • Arthritis and psoriasis
  • Dactylitis
  • Nail pitting or onycholysis
  • Psoriasis in a first degree relative
  • small joint polyarthritis in younger patient
  • oligoarticular in older patients
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54
Q

what are the clinical features of ERA JIA?

A
  • Arthritis and enthesitis
  • The presence of or a history of sacroiliac joint tenderness and/or inflammatory lumbosacral pain
  • HLA-B27 antigen
  • Acute symptomatic anterior uveitis
  • History of ankylosing spondylitis, enthesitis related arthritis, sacroiliitis with inflammatory bowel disease, Reiter’s syndrome or acute anterior uveitis in a first degree relative
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55
Q

how is JIA managed?

A
  • NSAIDs
  • intra-articular corticosteroids
  • DMARDs: MTX, SSZ and LEF
  • Abatacept, adalimumab, etanercept or tocilizumab
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56
Q

what are the complications associated with JIA?

A
  • uveitis
  • MAS
  • joint erosion
  • disease flare
  • osteopenia
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57
Q

what are the clinical features of reactive arthritis?

A
  • Asymmetrical oligoarthritis is most typical, but polyarticular and monoarticular variants occur
  • Axial arthritis: non-specific low back pain or buttock pain and stiffness, particularly during times of inactivity
  • Fever, fatigue and weight loss
  • Enthesitis
  • Oral ulcers
  • Keratoderma blennorhagicum
  • Circinate balanitis
  • Conjunctivitis
  • Anterior uveitis
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58
Q

how is reactive arthritis managed?

A
  • NSAIDs
  • Prednisolone
  • intra-articular corticosteroids
  • SFZ, MTX and AZA are indicated where disabling symptoms persist for 3 or more months or there is erosive joint damage
  • short course Abx for causative organism
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59
Q

what are the clinical features of RA?

A
  • Active, symmetrical arthritis lasting >6 weeks
  • Joint pain and swelling
  • Morning stiffness lasting >1 hour
  • Swan neck deformity: DIP hyperflexion with PIP hyperextension
  • Boutonniere’s deformity: PIP flexion with DIP hyperextension
  • Ulnar deviation
  • Rheumatoid nodules
  • Fatigue
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60
Q

what is palindromic RA?

A

-monoarticular attacks lasting 24-48 hours

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61
Q

what is transient RA?

A
  • self-limiting
  • last less than 12 months and leaving no permanent joint damage
  • Usually seronegative for RF and ACCP
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62
Q

what is remitting RA?

A

-a period of several years during which the arthritis is active, but then remits leaving minimal damage

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63
Q

what is chronic persistent RA?

A
  • Relapsing and remitting course over many years

- Seropositive patients tend to develop greater joint damage

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64
Q

what is rapidly progressive RA?

A
  • The disease progresses remorselessly over a few years and leads rapidly to joint damage and disability
  • it is usually seropositive
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65
Q

what is seronegative RA?

A
  • initially affects the wrists more often than the fingers and has a less symmetrical joint involvement
  • Negative for RF and ACCP
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66
Q

what are the x-ray features of RA?

A
  • soft tissue swelling
  • juxta-articular osteoporosis
  • joint space narrowing
  • subchondral cyst formation
  • subluxation of joints
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67
Q

how is RA managed?

A
  • symptom control with NSAIDs
  • short term glucocorticoids for disease flares
  • MTX, LEF, SZS or HCQ alone or in combination
  • for severe disease, offer biologic therapy (high intensity DMARD therapy and DAS28 5.1)
  • offer rituximab if there is inadequate response
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68
Q

what are the risk factors for septic arthritis?

A
  • Pre-existing joint disease
  • Joint prostheses
  • Intravenous drug misuse
  • Immunosuppressive medication
  • HIV infection
  • Alcohol use disorder
  • Diabetes
  • Previous intra-articular corticosteroid injection
  • Recent joint surgery
  • The presence of other infections including skin infections and cutaneous ulcers
  • Exposure to ticks (may indicate arthritis associated with Lyme disease).
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69
Q

what are the clinical features of septic arthritis?

A
  • Hot, swollen, painful joint
  • Restricted movement
  • Joint is often held in a position that maximises the joint space fully: fully extended knee; hip abducted, flexed and externally rotated
  • Limitation of active and passive movement, with reluctance to move or allow movement
  • Fever
  • Large, single joint affected
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70
Q

how is septic arthritis diagnosed?

A

-joint aspiration: bacteria in cloudy culture fluid

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71
Q

how is septic arthritis managed?

A
  • Offer IV flucloxacillin, or clindamycin if penicillin allergic
  • If MRSA is suspected, give vancomycin or teicoplanin
  • If gonococcal arthritis or gram-negative infection is suspected, cefotaxime or ceftriaxone is recommended
  • Aspirate the joint to dryness as often as is needed
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72
Q

what are the clinical features of MSK lower back pain?

A
  • Low back pain with no radiation
  • Absence of any red-flag features
  • No neurological symptoms
  • Dull, gnawing, tearing, burning or electric pain associated with muscle spasm
  • Lack of pain on flexion or relief on extension
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73
Q

how is MSK lower back pain managed?

A
  • analgesia
  • benzodiazepine for muscle spasm
  • exercise therapy
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74
Q

what are the clinical features of transient synovitis?

A
  • Sudden onset of pain in the hip following viral infection
  • Limp
  • No pain at rest, but the hip is typically held abducted and externally rotated
  • Decreased range of movement, particularly internal rotation (positive log roll)
  • The pain may be referred to the knee.
  • The child is afebrile or has a mild fever and does not appear ill.
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75
Q

how is transient synovitis managed?

A
  • Rest and NSAIDs

- traction may be needed

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76
Q

what are the clinical features of limited cutaneous systemic sclerosis?

A
  • Raynaud’s phenomenon developing upto 15 years before
  • Skin involvement limited to the hands, feet, face and forearms
  • Flexion deformities of the fingers
  • Beak like nose
  • Microstomia
  • Painful digital ulcers
  • Well demarcated telangiectasia
  • Dilated nail fold capillaries
  • Digital ischaemia
  • Pulmonary hypertension and interstitial disease
  • Bright, shiny skin of hands and feet
  • Prayer sign, claw hand deformities, carpal tunnel syndrome and calcinosis
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77
Q

what are the clinical features of diffuse cutaneous systemic sclerosis?

A
  • Oedematous in onset with skin sclerosis and concomitant Raynaud’s phenomenon
  • Diffuse swelling and stiffness of the fingers is rapidly followed by extensive skin thickening which can involve most of the body
  • Atrophic skin with loss of hair
  • Lethargy, anorexia and weight loss
  • GORD and dysphagia
  • Anal incontinence
  • Malabsorption due to dilatation and atony of the small bowel
  • Renal involvement: active hypertensive renal crisis
  • Pulmonary fibrosis and hypertension
  • Myocardial fibrosis leading to arrhythmias and conduction defects
  • Pericarditis
  • Can occur without skin involvement (SSc sine Scleroderma)
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78
Q

which antibodies are present in systemic sclerosis?

A
  • ANA
  • anti-Scl70 or anti-topoisomerase 1 or anti RNA polymerase positive in DcSSc.
  • Anti-centromere, speckeld or nucleolar antibodies occur in LcSSc
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79
Q

how is raynauds in SSC managed?

A
  • CCB or ARB
  • SSRIs, alpha-blockers and statin therapy can also be considered
  • Phosphodiesterase type 5 inhibitors are increasingly used
  • IV prostanoid (Iloprost) and digital sympathectomy
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80
Q

how are digital ulcers in SSC managed?

A
  • Optimise oral vasodilator therapy and analgesia
  • Sildenafil
  • In severe, active digital ulceration, patients should receive IV prostanoid
  • In patients with recurrent, refractory digital ulcers, a phosphodiesterase type 5 inhibitor or IV prostanoid and an endothelin receptor antagonist should be considered
  • Digital sympathectomy with or without botox should be considered for severe and/or refractory cases
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81
Q

how is lung fibrosis in SSC managed?

A

-IV cyclophosphamide

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82
Q

how is GI disease in SSC managed?

A
  • PPI and H2 receptor antagonists
  • Prokinetic dopamine antagonists
  • Parenteral nutrition for patients with severe weight loss refractory to enteral supplementation
  • Intermittent broad-spectrum antibiotics (ciprofloxacin) are recommended for intestinal overgrowth
  • Loperamide or laxatives used for symptomatic management of diarrhoea or constipation
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83
Q

how is systolic HF in SSC managed?

A
  • Consider immunosuppression with or without a pacemaker
  • Consider an implantable cardioverter defibrillator
  • ACE-I and carvedilol
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84
Q

how is diastolic HF in SSC managed?

A

-Diuretics, including spironolactone and furosemide

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85
Q

what is morphea?

A

-Irregular discoloured and thickened patches of skin than can occur on the arms, legs or body

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86
Q

what is linear scleroderma?

A

-Areas of skin involvement spread out along lines, with streaks of involved skin that appears most often on the hand or foot

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87
Q

what is linear scleroderma en coup de sabre?

A

-Linear scleroderma on the head and face, including formation a deep furrow along the scalp with tight, hard skin extending onto the forehead

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88
Q

how is juvenile scleroderma managed?

A
  • For mild morphea, topical treatment with calcipotriene cream is often sufficient
  • Linear scleroderma responds well to methotrexate
  • Severe cases of Parry Romberg Syndrome may require referral to a craniofacial surgeon
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89
Q

what are the clinical features of Behcets syndrome?

A
  • Oral ulcers on the moist mucosal surfaces of the mouth
  • Painful genital ulcers
  • Uveitis
  • Acne
  • Erythema nodosum on the lower extremities
  • Superficial thrombophlebitis
  • Hypopyon: precipitation of inflammatory cells in the anterior chamber
  • Stroke
  • Memory loss
  • Headache, confusion and fever as a result of meningeal involvement
  • Haemoptysis, cough, SOB or chest pain with pulmonary involvement
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90
Q

How is behcet’s syndrome diagnosed?

A

-Perform a pathergy test: induration with or without the formation of a pustule within 48 hours

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91
Q

how is mucocutaneous behcets managed?

A
  • Initial therapy: Oral colchicine 500mcg BD, Topical steroid mouthwash or spray or Topical NSAID mouthwash and antibiotics
  • Step-up therapy: Azathioprine 2.5mg/kg, Tacrolimus up to 4mg twice a day or Corticosteroid
  • If the step-up therapy is ineffective, offer infliximab 5mg/kg for 4 doses and then switch to adalimumab 40mg every other week or etanercept 50mg once a week
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92
Q

how is eye disease in Behcet’s managed?

A
  • Initial acute therapy:
  • –Topical, intraocular steroids
  • –1000mg IV methylprednisolone 3 times a year or oral prednisolone 1mg/kg/day
  • Maintenance therapy includes oral steroid, azathioprine 2mg/kg/day or ciclosporin 2.5-5mg/kg/day
  • If there is a flare, or this treatment is ineffective, offer infliximab 5mg/kg for 4 doses and then switch to adalimumab 40mg every other week or etanercept 50mg once a week
  • If this is ineffective, offer interferon alpha 30mcg once a week for 6 months or rituximab, one cycle of 2 infusions (1000mg/infusion)
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93
Q

how is major organ disease managed in Behcet’s?

A
  • Initial therapy: IV steroid or azathioprine 2.5mg/kg/day
  • Step up therapy: Cyclophosphamide IV pulses of 10mg/kg at increasing intervals, every 2 weeks for 12 weeks
  • Biologic therapy: offer infliximab 5mg/kg for 4 doses and then switch to adalimumab 40mg every other week or etanercept 50mg once a week
  • If ineffective, offer rituximab, one cycle of 2 infusions (1000mg/infusion)
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94
Q

what are the clinical features of bursitis?

A
  • Pain and tenderness at the site of a bursa
  • Decreased active range of movement
  • Swelling
  • Low grade temperature, erythema and warmth in septic bursitis
  • Painful arc on shoulder abduction if subacromial
  • Lateral hip pain if trochanteric
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95
Q

how is bursitis managed?

A
  • Advise conservative measures such as rest, ice, reduced activity, compression bandaging and simple analgesia
  • Consider aspiration if the effusion is large and a corticosteroid injection into the bursa
  • If septic bursitis is suspected, aspirate the bursa and give flucloxacillin or clarithromycin if penicillin allergic. Erythromycin is preferred in pregnancy
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96
Q

what is pseudo gout?

A

-Calcium pyrophosphate deposition

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97
Q

what are the clinical features of pseudogout?

A
  • Painful and tender joints
  • Involvement of shoulders, wrists and MCPJ
  • Sudden worsening of OA
  • Red and swollen joints
  • Joint effusion and fluctuance
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98
Q

how is pseudo gout diagnosed using arthrocentesis?

A

-intracellular or extracellular positively birefringent rhomboid shaped crystals under polarised light

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99
Q

what are the x-ray features of pseudo gout?

A
  • linear, stippled radio-opaque deposits in the fibro-cartilage or hyaline articular cartilage of joints
  • calcified tendons
  • subchondral cysts
  • progressive rapid joint degeneration or bony collapse
  • predominant involvement of the patellofemoral joint in the knee
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100
Q

how is an acute presentation of pseudogout managed?

A
  • Advise conservative measures with cool packs and rest, with simple analgesia such as paracetamol and NSAIDs
  • Offer joint aspiration with intra-articular corticosteroid injection
  • If intra-articular steroids are refused or ineffective, offer systemic prednisolone 10-20mg orally once daily or colchicine if steroids and NSAIDs are contraindicated
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101
Q

how is chronic pseudogout managed?

A
  • Offer oral NSAIDs with gastroprotection (PPI) or low dose colchicine if contraindicated
  • Offer low dose corticosteroid, methotrexate or hydroxychloroquine for prophylaxis of chronic disease
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102
Q

what are the clinical features of charge-strauss syndrome?

A
  • History of asthma and rhinitis.
  • Focal numbness or weakness (typically mononeuritis multiplex)
  • Nasal discharge of stuffiness.
  • Palpable purpura and petechiae, skin nodules, leukocytoclastic angiitis with palpable purpura, livedo reticularis, urticaria, necrotic bullae and digital ischaemia
  • Wheeze.
  • Haemoptysis
  • Shortness of breath or cough.
  • Abdominal pain, bleeding, bowel ischaemia and perforation, appendicitis and pancreatitis
  • Sensory or motor deficits.
  • Tachypnoea.
  • Low grade chronic constitutional symptoms
  • Heart failure, myocarditis and myocardial infarction
  • Glomerulonephritis, hypertension and CKD
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103
Q

which antibody is positive in churg-strauss syndrome?

A

-pANCA

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104
Q

how is churg-strauss syndrome managed?

A
  • non-organ threatening disease, offer methotrexate or mycophenolate mofetil with a glucocorticoid
  • organ or life threatening disease, offer cyclophosphamide or rituximab with a glucocorticoid
  • rapidly progressive renal failure or pulmonary haemorrhage, consider plasma exchange
  • Upon remission, offer azathioprine, methotrexate or rituximab and continue to taper glucocorticoids
105
Q

what are the clinical features of costochondritis?

A
  • Chest pain, worse on movement of the chest wall, especially with inspiration
  • Chest wall tenderness
  • Chest wall swelling (Tietze’s Syndrome)
106
Q

how is costochondritis managed?

A
  • Advise the use of NSAIDs with PPI gastroprotection

- If unresponsive, offer intra-articular corticosteroid injection

107
Q

what are the clinical features of TMJD?

A
  • Cyclical pain in myofascial pain and dysfunction, continuous pain in internal derangement
  • Joint clicking or crepitus
  • Abnormal mandibular movement
  • Masticatory muscle tenderness
108
Q

how is TMJD managed?

A
  • simple analgesia and conservative management
  • diazepam for acute severe pain
  • amitriptyline or gabapentin if chronic
  • refer for botox, intra-articular steroids or surgery
109
Q

what are the clinical features of scoliosis?

A
  • Postural asymmetry
  • Absent or minimal pain
  • Normal neurology
  • Paraspinal prominences on forward bending
  • Scoliometer measurement of >5o at paraspinal prominence
  • Symmetrical abdominal reflexes
  • Shoulder, waist line, thoracic wall and breast asymmetry
110
Q

how is scoliosis diagnosed?

A
  • Clinical diagnosis
  • standing PA and lateral x-rays of spine: coronal plane spinal curvature >10°; hypo- or hyperkyphosis of the thoracic spine
111
Q

how is scoliosis managed?

A
  • Advise regular exercise to build core strength
  • Perform observational monitoring x-rays
  • Offer spinal bracing
  • If there is evidence of associated complications, offer spinal arthrodesis
112
Q

what are the clinical features of ACL injury?

A
  • Audible pop
  • Rapid knee swelling
  • Unable to continue activity
  • Sensation of knee instability or buckling
  • Pain
  • Positive Lachman’s test
  • Positive pivot shift manoeuvre
113
Q

what is seen on MRI in ACL injury?

A
  • ACL fibres appear disrupted

- blurry on T1-weighted images with abnormal high signal on T2 weighted images

114
Q

how is ACL injury managed?

A
  • Offer protected weight bearing, rest, ice, compression, elevation and NSAIDs
  • Offer physiotherapy to allow return to normal activity
  • Offer surgical repair for highly active individuals
115
Q

what are the clinical features of osteosarcoma?

A
  • Worsening limb pain over weeks to months, more severe at rest and at night
  • Pain is described as deep, dull, boring and relentless
  • Mass or swelling that is usually firm, tender and warm to touch
  • Limp
  • Overlying skin ulceration
116
Q

what is seen on x-ray in osteosarcoma?

A
  • radiolucent lesion with areas of mottled radiodensity and ill-defined margins
  • neoplasm is usually located in the metaphysis of long bone
  • periosteal reaction in the form of Codman’s triangle or a sunburst appearance is common
  • sometimes soft tissue mass can be appreciated on conventional radiographs
117
Q

how is osteosarcoma managed?

A
  • Perform wide surgical resection and reconstruction
  • If disease is high grade at presentation, offer neoadjuvant and adjuvant chemotherapy with methotrexate, doxorubicin and cisplatin
  • Offer local radiotherapy if there is doubt over surgical clearance
  • Mifamurtide for the treatment of high-grade resectable non-metastatic osteosarcoma
118
Q

what are the risk factors for gout?

A
  • Male
  • Consumption of meat, seafood and alcohol
  • Use of diuretics
  • Use of ciclosporin, tacrolimus, pyrazinamide, aspirin
  • High cell turnover
119
Q

what are the clinical features of gout?

A
  • Rapid onset of severe pain
  • Morning joint stiffness
  • Mono or oligoarticular pattern
  • Swelling and joint effusion
  • Tophi over extensor surface joints
  • Erythema and warmth
120
Q

how is gout diagnosed on arthrocentesis?

A
  • WBC >2x109

- strongly negative birefringent needle shaped crystals under polarised light

121
Q

how is acute gout managed?

A
  • NSAIDs or coxibs
  • If NSAIDs are not tolerated or contraindicated, give colchicine 500micrograms BD-QDS or a corticosteroid
  • In patients with an acute illness and comorbidity, joint aspiration and intra-articular corticosteroid is the treatment of choice
122
Q

how is chronic gout managed?

A
  • allopurinol
  • febuxostat
  • sulfinpyrazone or probenecid or benzbromarone
123
Q

how is chronic tophaceous gout managed?

A
  • Urate lowering therapy
  • If initial ULT fails, pegloticase IV every 2 weeks
  • rasburicase
124
Q

what are the clinical features of dupuytren’s contracture?

A
  • A firm and thickened palmar nodule over the metacarpal head at the level of the distal palmar crease, proximal to the MCP joint
  • Palmar skin changes, with skin thickening, tethering, puckering or pitting
  • Pretendinous cords
  • MCP or PIP joint contracture
  • Patient unable to lay hand flat on table (Hueston table-top test)
125
Q

how is Dupuytren’s contracture managed?

A
  • none if no loss of function
  • surgical release of contracture
  • corticosteroid injection with painful nodules
126
Q

what are the clinical features of familial Mediterranean fever?

A
  • Periodic fever lasting 12 to 72 hours
  • Abdominal pain that precedes the fever and lasts longer
  • Altered bowel habit: usually constipation but may have diarrhoea
  • Acute monoarticular joint pain and swelling
  • Erysipelas-like skin lesions: tender, erythematous, raised and well demarcated, usually 10-15cm in diameter and found below the knee
  • Pleuritic chest pain
  • Acute myalgia
  • Hepatosplenomegaly
127
Q

how is familial Mediterranean fever managed?

A
  • For an acute attack, give paracetamol or NSAIDs and colchicine
  • When FMF is confirmed, treat with colchicine
  • If there is poor response to colchicine, offer treatment with anakinra, etanercept, tocilizumab, canakinumab or allogenic haematopoietic stem cell transplant
128
Q

what are the clinical features of Felty’s syndrome?

A
  • Splenomegaly
  • Joint deformities and rheumatoid nodules
  • RA
129
Q

what are the blood features of Felty’s syndrome?

A
  • neutropenia
  • anaemia
  • thrombocytopenia
  • raised CRP
  • elevated ALP and transaminases
  • positive RF, anti-CCP and ANA
130
Q

how is felty’s syndrome managed?

A
  • MTX, with SFZ or LEF added on
  • rituximab
  • G-CSF with severe neutropenia
  • splenectomy
131
Q

what are the clinical features of fibromyalgia?

A
  • Chronic pain
  • Diffuse tenderness on examination
  • Fatigue unrelieved by rest
  • Sleep and mood disturbance
  • Cognitive dysfunction
  • Headaches
  • Numbness and tingling sensations
  • Stiffness
132
Q

how is fibromyalgia managed?

A
  • offer simple analgesia
  • Offer amitriptyline, duloxetine or pregabalin/gabapentin
  • Offer a short course of diazepam for muscle spasms
  • A tailored exercise programme may be beneficial
  • Offer CBT, psychotherapy and relaxation techniques
133
Q

what are the clinical features of polyarteritis nodosum?

A
  • Fever.
  • Weight loss.
  • Myalgia and arthralgia.
  • Mononeuritis multiplex.
  • Paraesthesia.
  • Muscle tenderness.
  • Abdominal pain.
  • Skin manifestation such as livedo reticularis (a net-like cyanotic discolouration around pale skin).
  • Testicular pain
  • High diastolic pressure.
134
Q

how is polyarteritis nodosum managed?

A
  • corticosteroid therapy
  • If patients relapse despite steroid therapy, add cyclophosphamide
  • Azathioprine can also be used as maintenance therapy
  • Intravenous immunoglobulin (IV-Ig) and aspirin are effective in childhood PAN but, in resistant cases, either steroid or infliximab has a role
135
Q

what are the clinical features of iliotibial band syndrome?

A
  • Sharp or burning pain superior to the lateral joint line
  • Positive Noble’s test
  • Positive Ober’s test
  • Positive modified Thomas’ test
  • Reduced hip abductor strength
  • Genu varum
  • Hind foot and forefoot varum
  • Pes cavus
  • Prominent lateral femoral epicondyle, tight iliotibial tract and tensor fascia lata
  • Weak gluteus medius, maximus and tensor fascia lata
  • Tightness and weakeness in the quadriceps, iliotibial tract and lateral retinaculum
136
Q

how is iliotibial band syndrome managed?

A
  • Offer short course NSAIDs and rest
  • Refer to physiotherapy
  • If the pain is unresponsive to NSAIDs, offer a corticosteroid injection
137
Q

what are the clinical features of osgood schlatter disease?

A
  • Pain of the tibial tubercle, worsened by forceful extension of the knee
  • Localised tenderness
  • Activity limitation
  • Localised swelling or warmth
  • Prominence of the tibial tubercle
  • Pain at the tubercle with resisted knee extension
138
Q

how is osgood schlatter disease managed?

A
  • Offer paracetamol or NSAIDs with intermittent ice packs
  • activity modification
  • physiotherapy
139
Q

what are the clinical features of good pastures syndrome?

A
  • Shortness of breath.
  • Haemoptysis.
  • Cough.
  • Haematuria
  • Reduced urine output.
  • Oedema.
140
Q

which antibody is positive in good pastures syndrome?

A

-anti-GBM

141
Q

how is good pastures syndrome managed?

A
  • Offer oral prednisolone and cyclophosphamide.
  • Offer plasmapharesis until anti-GBM is undetectable.
  • Advise smoking cessation.
142
Q

how are the kidneys affected in goodpastures syndrome?

A

-Crescentic glomerulonephritis

143
Q

what are the clinical features of adult polymyositis?

A
  • General malaise, weight loss and fever
  • proximal muscle weakness
  • shoulder and pelvic girdle muscles become wasted but are not usually tender.
  • Movements such as squatting and climbing stairs become difficult.
  • As the disease progresses, involvement of pharyngeal, laryngeal and respiratory muscles can lead to dysphonia and respiratory failure.
144
Q

what are the clinical features of adult dermatomyositis?

A
  • Myalgia
  • Polyarthritis
  • Raynaud’s phenomenon
  • Rash affecting the eyelids, where heliotrope (purple) discoloration is accompanied by periorbital oedema
  • Gottron’s papules over the dorsal surface of the knuckles, wrists, elbows, knees and malleoli
  • Symmetrical violaceous erythematous macular rashes
  • Ulcerative vasculitis and calcinosis of the subcutaneous tissue
  • Muscle fibrosis
  • Joint contractures
145
Q

what are the clinical features of childhood dermatomyositis?

A
  • The typical rash of DM is usually accompanied by muscle weakness.
  • Muscle atrophy, subcutaneous calcification and contractures
  • Ulcerative skin vasculitis
  • recurrent abdominal pain due to vasculitis
146
Q

what is seen on EMG in poly/dermatomyositis?

A
  • abnormal spontaneous activity (fibrillation and positive sharp waves)
  • abnormal voluntary activity (low amplitude, short duration polyphasic motor potentials)
147
Q

which antibodies are present in dermatomyositis/polymyositis?

A
  • ANA
  • anti-Jo-1
  • anti-Mi-2
  • anti-SRP
  • Anti-PM-Scl positive
148
Q

how is polymyositis/dermatomyositis managed?

A
  • Prednisolone 0.5–1.0 mg/kg body weight continued until at least 1 month after myositis has become clinically and enzymatically inactive.
  • Pulsed IV methylprednisolone for the treatment of refractory inflammatory myositis
  • Early intervention with steroid-sparing agents such as methotrexate, azathioprine, ciclosporin and cyclophosphamide is common, especially where there is clinical relapse or rise in CK as the dose of steroids is reduced.
  • IVIG and plasmapheresis can be used in refractory cases
149
Q

what are the clinical features of lateral epicondylitis?

A
  • Tenderness over the common extensor tendon
  • Positive extensor carpi radialis brevis stretch (maximal passive wrist flexion with extended arm)
  • Pain during resisted wrist and digit extension
  • Elbow pain during or after flexion and extension
  • Exacerbation of pain with repetitive movement or occupational activity
  • Decreased grip strength
  • Pain in the lateral aspect of the elbow
150
Q

what are the clinical features of medial epicondylitis?

A
  • Pain at the medial aspect of the elbow
  • Tenderness approximately 5mm distal and lateral to the medial epicondyle
  • Increased pain with resisted forearm pronation or wrist flexion
  • Elbow pain during or after flexion and extension
  • Exacerbation of pain with repetitive movement or occupational activity
  • Decreased grip strength
151
Q

how is epicondylitis managed?

A
  • heat and ice
  • orthoses and rest
  • NSAIDs or paracetamol
  • physiotheraoy
  • surgery
  • extracorporeal shockwave therapy in refractory epicondylitis
152
Q

what are the clinical features of the acute febrile stage of Kawasaki’s disease?

A
  • Fever
  • irritability
  • cervical adenitis
  • conjunctivitis
  • rash
  • mucosal erythema
  • painful erythema of the hands and feet
  • arthralgia or arthritis
  • possible myocarditis, and pericarditis.
153
Q

what are the clinical features of the subacute stage of Kawasaki’s disease?

A
  • persistent irritability
  • poor appetite
  • conjunctival injection
  • desquamation of extremities
  • Cardiac abnormalities (coronary artery ectasia or aneurysms) may develop during this stage
154
Q

what are the diagnostic clinical features of Kawasaki’s disease?

A
  • fever >5 days and four other features of:
  • bilateral conjunctivital injection
  • red mucous membranes
  • cervical lymphadenopathy (cluster of grapes) with node diameter >1.5
  • diffuse, maculopapular erythematous rash
  • red and oedematous palms and soles or peeling of fingers and toes starting subungually
155
Q

how is Kawasaki’s disease managed?

A
  • IVIG in the first 10 days
  • Aspirin 80-100mg/kg
  • Infliximab, steroids, cyclophosphamide, ciclosporin, MTX or plasma exchange may be offered with persistent inflammation
156
Q

what are the constitutional features of SLE?

A
  • Fever
  • Weight loss
  • Lymphadenopathy
157
Q

what are the cutaneous features of SLE?

A
  • Alopecia
  • Oral/nasal ulcers
  • Photosensitivity
  • Malar rash
  • Discoid rash
  • Raynaud’s phenomenon
158
Q

what are the MSK features of SLE?

A
  • Arthritis/arthralgia

- Myalgia/myositis

159
Q

what are the cardiorespiratory features of SLE?

A
  • Pericarditis
  • Pleurisy
  • Pneumonitis
  • Myocarditis
  • Endocarditis
160
Q

what are the neurological features of SLE?

A
  • Seizures
  • Psychosis
  • Chorea
  • Transverse myelitis
161
Q

what are the renal features of SLE?

A
  • Proteinuria
  • Nephrotic Syndrome
  • End stage renal disease
162
Q

what are the haematological features of SLE?

A
  • Haemolytic anaemia
  • Leucopenia
  • Lymphopenia
  • Thrombocytopenia
  • Thrombosis
163
Q

which antibodies are present in SLE?

A
  • ANA
  • anti-dsDNA
  • anti-Sm
164
Q

how is the severity of SLE assessed?

A
  • BILAG 2004

- SELENA-SLEDAI

165
Q

How is mild SLE (BILAGC/SLEDAI<6)

A
  • Topical or oral prednisolone or IM or IA methylprednisolone
  • Hydroxychloroquine and/or methotrexate
  • NSAIDs for days to few weeks only
  • For maintenance, offer prednisolone <7.5mg/day, and hydroxychloroquine 200mg/day and/or methotrexate 10mg/week
166
Q

How is moderate SLE (BILAG 2 or more B/SLEDAI 6-12)

A
  • Offer prednisolone or 1-3 doses of IV methylprednisolone, or IM methylprednisolone
  • Offer azathioprine or methotrexate or mycophenolate mofetil or ciclosporin and hydroxychloroquine
  • For maintenance, offer prednisolone and azathioprine, or methotrexate or mycophenolate mofetil or ciclosporin and hydroxychloroquine
  • For refractory cases, consider belimumab or rituximab
167
Q

how is severe SLE (BILAG 1 or more A/SLEDAI >12)

A
  • Offer prednisolone or 1-3 doses of IV methylprednisolone or prednisolone
  • offer azathioprine or mycophenolate mofetil or cyclophosphamide IV or ciclosporin and hydroxychloroquine
  • For maintenance, offer prednisolone and mycophenolate mofetil or azathioprine or ciclosporin and hydroxychloroquine
  • Offer belimumab or rituximab in refractory cases
  • IVIG and plasmapheresis may be considered in patients with refractory cytopaenias, TTP, rapidly deteriorating acute confusional state and the catastrophic variant of APS
168
Q

what are the features of type 1 osteogenesis imperfecta?

A
  • Fractures
  • Wormian bones in the skull, and the vault may overhang the base causing basilar compression
  • Rapid teeth erosion
  • Blue sclerae
  • Corneal arcus
  • Aortic regurgitation and mitral valve prolapse
  • Joint hypermobility, with flat feet, hyper-extensible large joints and dislocations
  • Hearing loss
169
Q

what are the features of type 2 osteogenesis imperfecta?

A
  • lethal
  • multiple fractures (frequently occurring in utero)

-short limbs due to faulty conversion of normal mineralised cartilage to defective bone matrix.

170
Q

what are the features of type 3 osteogenesis imperfecta?

A
  • Born with fractures and the skull well ossified
  • Progressive deformity of skull, long bones, spine, chest and pelvis
  • The face appears triangular with a large vault, prominent eyes and a small jaw
  • Sclera is blue in infancy but normal in childhood
  • Patients rarely walk and have very short stature
171
Q

what are the features of type 4 osteogenesis imperfecta?

A
  • Fractures at birth
  • Bowing of legs or recurrent fractures on walking
  • Normal colour sclera
  • Reduced stature
  • Hyperplastic callus appearing as swollen, painful vascular swellings over long bones
172
Q

what are the features of type 5 osteogenesis imperfecta?

A
  • moderately deforming

- patients exhibit moderate-to-severe bone fragility of long bones and vertebral bodies

173
Q

what are the features of type 6 osteogenesis imperfecta?

A
  • accumulation of osteoid due to a mineralisation defect, in the absence of a disturbance of mineral metabolism
  • sclerae are white or faintly blue and DI is uniformly absent.
  • All patients have vertebral compression fractures.
174
Q

what are the features of type 7 osteogenesis imperfecta?

A
  • fractures at birth
  • bluish sclerae
  • early deformity of the lower extremities
  • coxa vara
  • osteopenia
  • Rhizomelia (proximal limb shortening)
175
Q

how is osteogenesis imperfecta managed?

A
  • Multidisciplinary care including physiotherapy, rehabilitation, bracing and surgical interventions.
  • bisphosphonates: IV pamidronate
176
Q

what are the clinical features of osetochondritis dissecans?

A
  • Pain exacerbated by activity
  • Location of pain is the anteromedial aspect of the knee with knee flexed to 90 degrees, the lateral aspect of the elbow, or the posteromedial aspect of the dorsiflexed ankle, or the anterolateral aspect of plantar-flexed ankle
  • Effusion
  • Locking and catching of joint
  • Absence of history of trauma
177
Q

what is seen on x-rays of osteochondritis dissecans?

A
  • knee x-ray: osteochondral lesion; free intra-articular loose bodies; malalignment; arthrosis
  • lower limb extremity film: malalignment with weight bearing line passing through involved compartment
178
Q

how is osetochondritis dissecans managed?

A
  • paracetamol and NSAIDs
  • physiotherapy
  • surgery
179
Q

what are the clinical features of mixed CTD?

A
  • Digital pallor and pain
  • Arthritis or arthralgia
  • Swollen hands
  • Sclerodactyly
  • Dilated nail fold capillaries
  • Dyspnoea/cough
  • GORD and heartburn
  • Myalgias or myositis
  • Haematuria
  • Lymphadenopathy
  • Alopecia
  • Skin rashes: malar rash, discoid lesions, acrosclerosis with telangiectasias and calcinosis
  • Proximal muscle weakness
  • Trigeminal neuralgia
  • Headaches
  • Neuropsychiatric disease
  • Peripheral neuropathy
  • Fever
180
Q

which antibody is required for a diagnosis of mixed CTD?

A

-Anti-U1 ribonucleoprotein

181
Q

how is mixed connective tissue disease managed?

A
  • NSAIDs to treat the pain and inflammation.
  • hydroxychloroquine.
  • in more severe cases systemic corticosteroids are used.
  • Adjuvant therapy with steroid-sparing agents such as cyclophosphamide and ciclosporin
  • Calcium-channel blocking agents such as nifedipine for Raynaud’s.
  • Oesophageal dysfunction: PPI
  • Prostaglandins for secondary pulmonary hypertension.
  • phosphodiesterase inhibitors such as sildenafil for raynauds and SPH
  • Endothelin receptor antagonists such as bosentan for pulmonary hypertension
182
Q

what are the clinical features of Paget’s disease of bone?

A
  • Asymptomatic
  • Long bone or back pain
  • Pathological fractures
  • Bony deformities: frontal bossing, prognathism, bone bowing
  • Increased local temperature
  • Hearing loss (skull involvement)
183
Q

how are the bone profile bloods affected in Paget’s disease?

A
  • elevated ALP

- Normal calcium, phosphorus and PTH

184
Q

how is Paget’s disease managed?

A
  • NSAIDs and paracetamol

- bisphosphonates, calcium and vitamin D

185
Q

what are the causes of osteomalacia?

A
  • Vitamin D deficiency
  • CKD: renal osteodystrophy
  • Hypophosphataemia
  • Type 2 renal tubular acidosis
  • Bisphosphonates, aluminium containing phosphate binders, prolonged TPN or dietary fluoride
  • Inborn errors of metabolism
  • Cystic fibrosis
186
Q

what are the clinical features of osteomalacia?

A
  • Fractures
  • Diffuse bone pain and tenderness
  • Proximal muscle weakness
187
Q

what are the clinical features of rickets?

A
  • Growth retardation
  • Hypotonia
  • Knock knees and bowed legs
  • Widened epiphyses at the wrists
  • Hypocalcaemic tetany
188
Q

how does the bone profile appear in osteomalacia?

A
  • normal or low calcium
  • low vitamin D
  • low serum phosphate
  • High PTH
  • High ALP
189
Q

how is osteomalacia managed?

A
  • Offer calcium and vitamin D replacement with colecalciferol or ergocalciferol in malabsorption syndromes
  • In patients with x-linked hypophosphateaemic rickets, type 1 and 2 vitamin D dependent rickets, oncogenic osteomalacia and Fanconi’s syndrome, offer calcium, Vitamin D and phosphate
190
Q

what are the clinical features of osteoporosis?

A
  • Back pain
  • Kyphosis
  • Fractures
191
Q

what are the risk factors for osteoporosis?

A
  • Female
  • Older age
  • Low BMI
  • Postmenopause
  • Secondary amenorrhoea
  • Primary hypogonadism
  • Smoking and excessive alcohol use
  • Prolonged immobilisation
  • Low calcium intake
  • Vitamin D deficiciency
  • Steroids
  • PPIs
192
Q

how is osteoporosis diagnosed?

A

-DXA scan: T-score <2.5

193
Q

how is osteoporosis managed?

A
  • oral or IV bisphosphonates (risk >1%)
  • denosumab
  • raloxifene
  • teriparatide
194
Q

what are the clinical features of an osteoporotic spinal compression fracture?

A
  • Acute back pain from atraumatic activities
  • Kyphosis
  • Loss of lumbar lordosis
  • Localised tenderness
  • Loss of standing height
  • Loss of sagittal balance
195
Q

how is an osteoporotic spinal compression fracture diagnosed on x-ray?

A
  • lateral view shows wedging of anterior vertebral body and local kyphosis
  • AP may show interpedicular widening and/or spinous process malalignment suggesting posterior vertebral body involvement
196
Q

what are the clinical features of Sjogren’s syndrome?

A
  • Fatigue
  • Recurrent sensation of sand/gravel, itch or burning in eyes.
  • Redness of the eyes and sensitivity to wind and light
  • Dry mouth
  • Vasculitic skin disease
  • Dental caries
  • Arthralgia and myalgia
  • Corneal ulceration
  • Enlarged salivary glands
197
Q

what are the diagnostic criteria for Sjogren’s syndrome?

A
  • four out of six of dry eye symptoms
  • dry mouth symptoms
  • objective ocular dryness (Schirmer’s test ⩽5 mm in 5 min or van Bijsterveld score ⩾4)
  • objective oral dryness (unstimulated salivary flow rate ⩽0.1 ml/min or positive salivary scintigraphy and sialography)
  • positive anti-Ro/La antibodies
  • labial gland focus score ⩾1
198
Q

how should Sjogren’s eye disease be managed?

A
  • conservation of tears by humidification and avoidance of systemic medication that exacerbates dryness.
  • Recommend liposomal sprays
  • simple lubricating drops
  • Low dose steroid-containing eye drops
  • Ciclosporin-containing eye drops or ointments
  • Topical NSAIDs such as diclofenac and indomethacin
  • pilocarpine
199
Q

how is oral sjogrens managed?

A
  • humidify the environment.
  • good oral hygiene
  • pilocarpine
200
Q

how is systemic dryness in Sjogren’s syndrome managed?

A
  • pilocarpine

- topical oestrogen

201
Q

how are systemic symptoms of Sjogrens managed?

A
  • Regular exercise and a graded exercise programme
  • HCQ
  • AZA, CYC
  • Rituximab
  • IVIG
  • colchicine
  • dapsone
  • topical tacrolimus
202
Q

what are the clinical features of a soft tissue sarcoma?

A
  • Mass
  • Upper/lower GI bleed with GI stromal tumours
  • Erythematous or maculopapular lesion (haemangioma)
  • Purplish macular-papular lesions (Kaposi Sarcoma)
  • Dysfunctional uterine bleeding (leiomyosarcoma)
  • Increased abdominal girth
  • Weight loss and fatigue
  • Anorexia
  • Abdominal bloating, discomfort and pain
203
Q

how are soft tissue sarcomas managed?

A
  • Offer wide local excision of the tumour with adjunctive radiotherapy and chemotherapy with ifosfamide and mesna
  • For Ewing’s sarcoma, give vincristine, doxorubicin, cyclophosphamide, ifosfamide, etoposide and mesna
  • For rhabdomyosarcoma, give vincristine, dactinomycin and cyclophosphamide
  • Give imatinib for GIST
  • For high grade soft tissue sarcoma, give doxorubicin, ifosfamide and mesna
  • Trabectedin
204
Q

what are the clinical features of antiphospholipid syndrome?

A
  • History of vascular thrombosis
  • History of 3 or more consecutive pregnancy losses at <10 weeks’ gestation or unexplained fetal death >10 weeks gestation
  • Features of thrombocytopenia
  • Arthralgia/arthritis
  • Livedo reticularis
205
Q

what are the diagnostic criteria for anti-phospholipid syndrome?

A
  • vascular thrombosis
  • pregnancy morbidity (preterm births or miscarriages)
  • Lupus anticoagulant, Anti-cardiolipin antibody and Anti-B2-glycoprotein I antibody, present on two or more occasions 12 weeks apart
206
Q

how is anti-phospholipid syndrome managed?

A
  • Offer vitamin k antagonists such as warfarin, with a target INR of 2.5
  • For pregnant women with APS, offer heparin and low dose aspirin throughout pregnancy
207
Q

what is catastrophic anti-phospholipid syndrome and how is it managed?

A
  • Acute onset of multi-organ failure as a result of massive microvascular thrombosis
  • Treatment includes anticoagulation with heparin and warfarin and immunomodulation with plasmapheresis, IVIG and corticosteroids
  • For refractory CAPS, offer rituximab
208
Q

what are the clinical features of a ganglion cyst?

A
  • Subcutaneous wrist mass
  • Aching discomfort
  • Increased mass size after activity
  • Transilluminating mass
209
Q

how is a ganglion cyst managed?

A
  • If there is no neurovascular compromise, advise observation of the cyst with analgesia
  • Cyst aspiration with an injection of corticosteroid can be given, but should be avoided with volar cysts due to the close association with the radial artery
  • If there is neurovascular compromise, offer surgical resection
210
Q

which organisms causes osteomyelitis in infants?

A
  • S aureus
  • Group B streptococci
  • Aerobic gram-negative bacilli (e.g., Escherichia coli)
  • Candida albicans.
211
Q

which organisms causes osteomyelitis in children 3 months to 5 years?

A
  • S aureus
  • Kingella kingae
  • Group A streptococcus
  • Streptococcus pneumoniae
  • Haemophilus influenzae
  • Pseudomonas (due to foot puncture wounds).
212
Q

which organisms causes osteomyelitis in children >5 years?

A
  • S aureus

- Group A streptococcus.

213
Q

which organisms causes osteomyelitis in adults?

A
  • S aureus
  • Coagulase-negative staphylococci
  • Aerobic gram-negative bacteria
  • Anaerobic gram-positive Peptostreptococcus species.
214
Q

which organisms causes osteomyelitis in older adults?

A

-Gram-negative bacilli.

215
Q

which organisms causes osteomyelitis in those with intravascular devices?

A
  • S aureus

- Candida species.

216
Q

which organisms causes osteomyelitis in IVDU?

A
  • S aureus

- Pseudomonas aeruginosa.

217
Q

which organisms causes osteomyelitis in sickle cell patients?

A
  • S aureus

- salmonella

218
Q

what are the clinical features of osteomyelitis?

A
  • Limp or reluctance to weight-bear
  • Non-specific pain at the site of infection
  • Malaise and fatigue
  • Local back pain with associated systemic symptoms
  • Paravertebral muscle tenderness and spasm
  • Local inflammation, tenderness, erythema or swelling
  • Fever
  • Reduced range of movement
  • Wound drainage or sinuses in chronic osteomyelitis
219
Q

how is osteomyelitis managed?

A
  • First line antibiotic therapy is flucloxacillin for 6 weeks
  • If penicillin allergic, give clindamycin for 6 weeks
  • If suspected MRSA, give vancomycin or teicoplanin for 6 weeks
  • consider adding fusidic acid or rifampicin in the initial 2 weeks
  • Surgical removal of bone sequestrum may be required
220
Q

what are the clinical features of plantar fasciitis?

A
  • Stabbing or knife like heel pain
  • pain relief with rest
  • Post static dyskinesia: pain with the first few steps after rising
  • Pain exacerbated by walking barefoot
  • Pain improves with NSAIDs
  • Positive dorsiflexion-eversion test
  • Pain with metatarsophalangeal joint extension (Windlass Test)
221
Q

how is plantar fasciitis managed?

A
  • self care advice
  • insoles
  • analgesia
  • corticosteroid injection
  • formal physiotherapy
  • extracorporeal shockwave therapy
  • surgery
222
Q

what are the clinical features of developmental dysplasia of the hip?

A
  • Positive Barlow test: Hip dislocates with posterior pressure
  • Positive Ortolani test: hip relocates with anterior pressure
  • Limited hip abduction
  • Abnormal positioning of the leg to delayed crawling/walking
  • Toe-walking
  • Asymmetrical thigh and skin folds
223
Q

what are the risk factors for developmental dysplasia of the hip?

A
  • Female sex
  • Positive family history
  • Breech presentation
224
Q

how is DDH diagnosed?

A
  • Perform hip USS in 6 week to 6 month olds with clinical features or risk factors: subluxation on provocative testing; abnormal relationship between femoral head and acetabulum
  • Perform hip x-rays: abnormal relationship between femoral head and acetabulum (assessed by acetabular index, Shenton’s line and ossification of femoral head)
225
Q

how is DDH managed?

A
  • For children <6 months, offer a dynamic flexion-abduction orthosis (Pavlik Harness)
  • Offer surgery: closed reduction with adductor or psoas tenotomy, followed by 3-4 months in a plaster cast or brace
  • Over the age of 18-24 months, an additional pelvic or femoral osteotomy is required
226
Q

what are the clinical features of Langerhans’ cell histiocytosis?

A
  • Bone pain and swelling
  • Papulosquamous rash that affects the scalp, skin folds and midline of the trunk
  • Single or multiple violaceous papulonodular and vesicular rash

0Polyuria and polydipsia due to DI secondary to craniofacial bone lesions and multi-system disease

  • Growth or sexual maturation failure
  • Vertebra plana: spondylitis with reduction of the vertebral body to a thin disc
  • Hepatosplenomegaly, jaundice and ascites
  • Cough, dyspnoea and chest pain
  • Orbital abnormalities including proptosis, periorbital swelling and erythema, diplopia or ophthalmoplegia
227
Q

how is langerhans cell histioytosis managed?

A
  • limited cutaneous disease, offer topical steroids, topical nitrogen mustard or psoralen combined ultraviolet A therapy
  • localised bone lesions, surgical curettage, radiotherapy, intralesional steroids, bisphosphonates and early chemotherapy with vinblastine and prednisolone
  • CBS: cladribine or cytarabine/radiotheraoy
  • For lymphadenopathy, offer surgical excision of single nodes, systemic steroids for regional nodes and chemotherapy for nodes resistant to treatment
  • For pulmonary LCH, offer corticosteroids or chemotherapy with vinblastine, methotrexate, cyclophosphamide, etoposide and cladribine. Lung transplant can be given in advanced disease
  • For multi-system LCH, offer prednisolone and vinblastine with 6-mercaptopurine added after 6 weeks in children. Adults should be offer cladribine or cytarabine. Should this treatment fail, other options include vemurafenib and stem cell transplant
228
Q

what are the clinical features of patellofemoral pain syndrome?

A
  • Ill-defined ache localised to the anterior knee behind the patella
  • Pain aggravated by compressive force
  • Increased Q angle (angle between the line connecting the ASIL to the centre of the patella and the line connecting centre of patella to anterior tibial tuberosity
  • Pain on palpation of the patellar retinaculum
  • Lateral patellar tilt
  • Reduced patellar mobility
  • Decreased muscle flexibility and muscle weakness
229
Q

what is seen on knee X-ray in patellofemoral pain syndrome?

A
  • trochlear dysplasia with the sulcus angle
  • patellar displacement with the bisect off angle
  • patellar tilt with the lateral tilt angle
230
Q

how is patellofemoral pain syndrome managed?

A
  • Advise relative rest and application of ice packs
  • Offer NSAIDs and paracetamol for analgesia
  • If there is no improvement with 6 weeks of conservative management, offer physiotherapy
231
Q

what are the clinical features of polymyalgia rheumatica?

A
  • Shoulder/hip girdle stiffness for >1 hour in the morning
  • Shoulder/hip girdle pain
  • Acute onset
  • Low grade fever
  • Anorexia
  • Weight loss
  • Malaise
  • Depression
  • Asthenia
  • Oligoarticular arthritis
232
Q

how is PMR managed?

A
  • initial standardized dose of prednisolone 15 mg daily orally
  • Intramuscular methylprednisolone (i.m. depomedrone) may be used in milder cases and may reduce the risk of steroid-related complications
  • bone protection
233
Q

what are the clinical features of psoriatic arthritis?

A
  • Inflammatory joint pain and stiffness
  • Peripheral arthritis
  • Dactylitis
  • Pain at the site of tendon attachment
  • Spinal stiffness (most severely cervical and lumbar)
  • Reduction of C-spine mobility
234
Q

what is seen on x-ray in psoriatic arthritis?

A
  • erosion in the DIPJ joint and periarticular new bone formation resulting in an irregular fuzzy appearance
  • joint subluxation and interphalangeal ankylosis
  • ivory phalanx
  • osteolysis and pencil-in-cup deformity in advanced disease
235
Q

how is psoriatic arthritis managed?

A
  • Offer NSAIDs and/or local intra-articular steroid injections
  • offer a DMARD (e.g. methotrexate), offering a second DMARD if this fails to control the disease
  • The choice of first line anti-TNF includes: etanercept, infliximab, adalimumab and golimumab
  • Second line biologics include: certolizumab pegol and secukinumab
  • For patients requiring rapid control of skin disease, infliximab or adalimumab are preferred
236
Q

what are the clinical features of thoracic outlet syndrome?

A
  • Repetitive job or overhead activities
  • Pain, paraesthesias and circulatory changes in the arm, hands and fingers
  • Upper extremitiy fatigue
  • Motor weakness
  • Thenar eminence atrophy
  • Positive Adson’s test
  • Positive costoclavicular test
  • Decreased radial pulse with hyperabduction
  • Positive Roos’ test
  • Positive stretch test
  • Positive Wright’s Manoeuvre
237
Q

how is thoracic outlet syndrome managed?

A
  • Offer conservative management with analgesia and occupational/physiotherapy
  • Offer corticosteroid injection into trigger points and associated muscles
  • Offer surgical decompression of the thoracic outlet
  • If there is arterial or venous thrombosis, offer catheter directed thrombolysis and anticoagulants if there is residual ischaemia
238
Q

what are the clinical features of rotator cuff injuries?

A
  • Shoulder pain
  • Shoulder weakness
  • Loss of active range of movement
  • Pain and weakness on resisted external rotation indicates infraspinatus tear
  • Pain and weakness of empty can test suggests supraspinatus tear
  • Deltoid fatigue
  • Pain and weakness on lift off test suggests subscapularis tear
  • Pain and weakness on belly-press test: subscapularis tear
  • Positive Neer impingement test
  • Positive Hawkins’ impingement test
239
Q

how is a rotator cuff injury managed?

A
  • Offer analgesia with paracetamol and NSAIDs
  • Refer for physiotherapy
  • Consider a subacromial corticosteroid injection
  • Refer to orthopaedic surgeon if there is no improvement
240
Q

what are the clinical features of a tendinopathy?

A
  • Insidious onset
  • Well-localised tenderness on palpation of the affected tendon
  • Pain during activity
  • Tendon thickening and nodularity
  • Crepitus
241
Q

what is seen on USS in tendinopathy?

A
  • thickened, blurred tendon

- possible hypoechoic foci within the tendon

242
Q

how is tendinopathy managed?

A
  • Advise rest, ice therapy to affected area and NSAIDs with paracetamol
  • Offer bracing or splinting of the affected area
  • Offer a corticosteroid injection around the affected area
  • Offer heal lifts with Achilles’ tendinopathy
  • If these methods fail, offer extracorporeal shock wave lithotripsy for calcific tendinitis
243
Q

what are the clinical features of tenosynovitis of the hand and wrist ?

A
  • Symptoms localised over and around a retinacular sheath
  • Pain increased with motion
  • Painful popping sensation with finger flexion and extension (trigger finger)
  • Palpable nodule at the level of the metacarpal head (trigger finger)
  • Pain, tenderness and swelling localised to the radial side of the wrist, aggravated by thumb movement and ulnar deviation while the thumb is clasped in the palm/Finkelstein test (de Quervain’s disease)
  • Pain and swelling 4cm proximal to the wrist joint, with redness and palpable crepitus (intersection syndrome)
  • Pain, swelling and tenderness at Lister’s tubercle (extensor pollicis longus tenosynovitis)
  • Ulnar sided wrist pain (extensor carpi ulnaris tenosynovitis)
  • Pain at palmar wrist crease over scaphoid tubercle and along the length of the tendon (flexor carpi radialis tenosynovitis)
244
Q

how is tenosynovitis of the hand and wrist managed?

A
  • Advise the patient to rest, apply intermittent ice treatment and take regular paracetamol and NSAIDs
  • Offer a splint to ease rest during the day
  • Refer for physiotherapy
  • Offer a steroid injection into the area if this is ineffective
245
Q

what are the clinical features of Ehlers-Danlos?

A
  • Joint hypermobility established by the Beighton 9-point score
  • Joint or spine pain, exacerbated by unaccustomed physical activity
  • Motor delay in infancy
  • Chronic pain
  • Fatigue
  • Recurrent joint dislocation or subluxation
  • Muscle pain or spasm
  • Soft, silky skin texture, or semi-transparent skin
  • Thin and stretchy double fold of skin
  • Stretch marks
  • Easy bruising
  • Atrophic scars
  • Poor wound healing
  • Hernias or organ prolapse
  • Orthostatic hypotension or POTS
  • Blue sclera
246
Q

how is Ehlers-Danlos managed?

A
  • Offer pain management with analgesia
  • Refer for physiotherapy and occupational therapy to improve quality of life
  • Offer CBT for chronic, unremitting pain with deconditioning
  • Offer splints and orthotics to support movement
247
Q

what are the clinical features of Perthes’ disease?

A
  • Limp
  • Limited range of movement at the hip joint: flexion deformity initially, and with progression adduction in flexion, internal rotation and abduction in extension are limited
  • Short stature
  • Muscle wasting
  • Hyperactivity
  • Trendelenberg’s sign
  • Synovitis
248
Q

what is seen on x-ray in Perthes’ diseas?

A
  • Perform AP and frog lateral view pelvic x-rays
  • femoral head collapse and fragmentation
  • subchondral fracture
249
Q

how is perthes’ disease managed?

A
  • For children aged 2 to 6, active monitoring is required
  • Offer analgesia with paracetamol and NSAIDs, and advise limited activity while disease is active
  • Refer for physiotherapy
  • If there is a developing deformity, offer casting/bracing with a Petrie cast
  • Surgery may be required: osteotomy
250
Q

what are the clinical features of equinovarus foot deformity?

A
  • Foot is fixed equinus and cannot be dorsiflexed
  • Hindfoot in varus and adducted
  • Forefoot adducted
251
Q

what is seen on x-rays in equinovarus foot deformity?

A

-parallelism between talus and calcaneus

252
Q

how is equinovarus foot deformity managed?

A
  • Offer the ponsetti casting method: stretching the foot, repositioning and then casting weekly, before performing Achilles tenotomy
  • Offer the French functional method: stretched and taped by specialist physiotherapist
  • Offer surgery: selective medial release and posteromedial release, with or without subtraction osteotomy
253
Q

what are the clinical features of discoid lupus?

A
  • Disc shaped, erythematous maculopapular scaly lesions, typically on the face, neck, scalp, ears and extensor surfaces of the arms
  • Telangiectasia, hyperpigmentation and hypopigmentation
  • Permanent scarring alopecia
254
Q

what is seen on skin biopsy in discoid lupus?

A
  • prominent hyperkeratosis
  • follicular plugging
  • vacuolar degeneration
  • thickened epidermal basement membrane
  • periappendageal inflammation
255
Q

how is discoid lupus managed?

A
  • Offer treatment with medium strength topical corticosteroids e.g. 0.1% triamcinolone for lesions on the body, or 0.5 to 2.5% hydrocortisone for lesions on the face and scalp
  • Consider intralesional triamcinolone acetonide
  • Offer hydroxychloroquine if there is no response to topical treatment
  • If disease is refractory, offer methotrexate, azathioprine or mycophenolate mofetil or topical tacrolimus
  • Surgical excision can be used to treat scarred lesions
256
Q

what are the clinical features of slipped capital femoral epiphysis?

A
  • Gait with affected leg externally rotated
  • Groin or knee pain
  • Bilateral hip pain
  • Trendelenburg’s gait
  • Restricted range of movement
257
Q

what are the risk factors for developing slipped capital femoral epiphysis?

A
  • Puberty
  • Obesity
  • Endocrine disorders
  • Male
258
Q

what is seen on x-ray in slipped capital femoral epiphysis?

A
  • AP x-rays: Klein’s line does not intersect the femoral head
  • frog-leg lateral x-rays: Klein’s line does not intersect the femoral head and blurred or widened physis (Bloomberg’s sign)
259
Q

how is slipped capital femoral epiphysis managed?

A
  • Activity restriction with analgesia

- SCFE is treated with centre-to-centre screw fixation across the growth plate or an open osteotomy of the femoral neck

FINALS (18 decks)

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