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Finals > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

What is the presentation of rheumatoid arthritis?

A

*Joint pain
*Tender, swollen joints
*Early morning stiffness ≥1 hour and joint gelling
*Symmetrical
*Typical sparing of the DIP joint

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2
Q

Investigations for rheumatoid arthritis

A

*Rheumatoid factor
*Anti CCP
*Radiograph
*Ultrasound
*CRP
*ESR

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3
Q

Criteria for rheumatoid arthritis

A

*EULAR - score of 6 or more
*2-10 large joints = 1
*1-3 small joints =2
*4-10 small joints=3
*>10 joints, at least 1 small = 5
*Low positive RF or anti CCP (≤3 time upper limit) = 2
*High positive RF or anti CCP = 3
*ongoing for ≥6 weeks = 1
*Abnormal CRP or ESR = 1

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4
Q

What should be checked before commencing treatment for rheumatoid arthritis?

A

*Hep B and C
*Purified protein derivative (PPD)
*FBC, LFTs

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5
Q

What is the management of rheumatoid arthritis?

A

*DMARD: sulfasalazine if low disease activity, consider oral prednisolone and NSAID
*DMARD: methotrexate if moderate/severe disease, oral prednisolone, NSAID, COX-2 inhibitor
*Second line: add another DMARD
*Third line: biological therapy (anti-TNF)
*Fourth line: methotrexate + rituximab

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6
Q

What are the complications of rheumatoid arthritis?

A

*Deformity: swan neck, ulnar deviation, z-thumb, boutonniére
*Work disability

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7
Q

What are the extra articular manifestations of rheumatoid arthritis?

A

*Pulmonary fibrosis with pulmonary nodules
*Felty’s syndrome
*Anaemia of chronic disease
*Cardiovascular disease
*Episcleritis and scleritis
*Carpal tunnel syndrome

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8
Q

What is Felty’s syndrome?

A

*Rheumatoid arthritis
*Neutropenia
*Splenomegaly

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9
Q

NAme two anti-TNF drugs

A

*Rituximab (monoclonal antibody against CD-20)
*Adalimumab

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10
Q

What is the presentation of osteoarthritis?

A

*Joint pain and stiffness worsened by activity
*Common joints: knee, hip, hand, spine
*Signs in the hands: Heberden’s nodes, Bouchard’s nodes, squaring at the base of the thumb

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11
Q

Investigation for osteoarthritis

A

*X ray of affected joints
*CRP and ESR (should be normal)

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12
Q

X ray of osteoarthritis

A

*Osteophytes
*Joint space narrowing
*Subchondral sclerosis
*Subchondral cysts

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13
Q

When can you diagnose osteoarthritis based on clinical history?

A

*If >45
*Typical activity related pain
*No early morning stiffness, or less than 30 mins of EMS

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14
Q

What is the management of oseteoarthritis?

A

*Patient education
*Weight loss
*Physio and occupational therapy and orthotics
*Oral paracetamol, topical NSAID
*Oral NSAID (+PPI)
*Consider opiates
*Intra-articualr steroid injection
*Join replacement (end stage, tried most non-operative)

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15
Q

What are the patterns of psioratic arthritis?

A
  • Symmetrical polyarthritis: hands, wrists, ankles, DIP joints
    -Spondylitic pattern: back stiffness, sacroilliitis, atlanto-axial joint involvement
    -Assymetrical pauciarthritis: fingers, toes, feet
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16
Q

What are the signs of psioratic arthritis?

A

*Plaques of psoriasis
*Pitting of the nails
*Onycholysis
*Dactylitis (inflammation of the full finger)
*Enthesitis (inflammation of the insertion point of the tendon into the bone)

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17
Q

What is the screening tool for psoriatic arthritis?

A

PEST

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18
Q

What are the associations of psoriatic arthritis?

A

*Eye disease
*Aortitis
*Amyloidosis

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19
Q

What is the presentation of septic arthritis?

A

*Hot, swollen, painful, restricted joint (knee most common)
*Acute presentation
*May have fever

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20
Q

What is the most common cause of septic arthritis?

A

Staph aureus

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21
Q

Investigation for septic arthritis

A

*Synovial fluid microscopy /culture/WCC
*Gram stain and polarising microscopy of synovial fluid
*Blood culture
*White cell count
*ESR and CRP

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22
Q

What is the management of septic arthritis?

A

*Joint aspiration
*IV antibiotics for 4-6 weeks
*Surgery if no response within 48 hours

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23
Q

What is gout?

A

Hyperuricaemia and deposition of urate crystals causing attacks of acute inflammatory arthritis, tophi around the joints, renal glomerular, tubular and interstitial disease and uric acid urolithiasis

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24
Q

What is the presentation of gout?

A

*Rapid onset of severe pain
*Joint stiffness
*Swelling and joint effusion
*Tenderness
*Tophi

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25
Q

What is the presentation of gout?

A

*Rapid onset of severe pain
*Joint stiffness
*Swelling and joint effusion
*Tenderness
*Tophi

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26
Q

What are the risk factors for gout?

A
  • Male
    *Age
    *Aspirin/ciclosporin/tacrolimus/pyrazinmide
    *Alcohol
    *Consumption of meat or seafood
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27
Q

What are the investigations for gout?

A

*Arthrocentesis with synovial fluid analysis: WBC>2x10^9, negatively birefringent needle shaped crystals under polarised light, monosodium urate crystals
*Serum uric acid level

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28
Q

What is the acute management of gout?

A

*NSAIDs, corticosteroid (intra-articular or parenterally) or colchicine
*Cold packs

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29
Q

What is the long term management of gout?

A

*Decreased purine and fructose intake
*Weight loss of max 1kg/month
*Exercise
*Decrease alcohol intake
*Allopurinol if ≥2 attacks in 12 months, presence of tophi, renal impairment, on diuretics, older than 40, urate>500micro mol/l

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30
Q

When would you prescribe allopurinol for gout?

A

≥2 attacks in 12 months, presence of tophi, renal impairment, on diuretics, older than 40, urate>500micro mol/l

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31
Q

What is the presentation of pseudogout?

A

*Hot, swollen, stiff joint (most often knee)
*Joint effusion

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32
Q

Investigation for pseudogout

A

*Arthrocentesis +synovial fluid analysis
*Rhomboid shaped positively birefringent crystal under polarised light
*X ray: chondrocalcinosis (thin white line in the middle of the joint space)
*Serum calcium: normal or elevated
*Serum parathyroid hormone: excludes hyperparathyroidism

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33
Q

What is the management of pseudogout?

A

*NSAIDs
*Colchicine
*Joint aspiration
*Steroid injection
*Oral steroids

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34
Q

What is giant cell arteritis?

A

*Temporal arteritis
*Systemic vasculitis of medium and large arteries

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35
Q

What are the risk factors for giant cell arteritis?

A

Female, >50

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36
Q

What is the presentation of giant cell arteritis?

A

*Headache, typically unilateral and around the forehead/temple
*Scalp pain or tenderness
*Aching, stiffness, claudication in extremities, tongue or jaw
*Blurred or double vision, painless sight loss
*May be associated with systemic symptoms
*Tenderness/thickening, or nodularity of superficial temporal arteries

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37
Q

Investigations for giant cell arteritis

A

*CRP
*ESR
*FBC
*Vascular ultrasonography or temporal artery biopsy (multi nucleated giant cells)

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38
Q

What is the management of giant cell arteritis

A

*Oral prednisolone 40-60mg per day straight away if suspected, taper this down with aim to stop steroids by 12-18 months
*Methotrexate or tocilizumab if relapse

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39
Q

What are the complications of giant cell arteritis?

A

*Vision loss
*cerebrovascular accident (stroke)

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40
Q

What is the presentation of polymyalgia rheumatica

A

*Bilateral shoulder pain that radiates to the elbow
*Bilateral pelvic girdle pain
*Worse with movement
*Interferes with sleep
*Stiffness for at least 45 minutes in the morning
*Constitutional symptoms: fever, anorexia, malaise, weight loss, low mood

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41
Q

Investigation for polymyalgia rheumatica

A

*Elevated CRP
*Elevated ESR
*FBC

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42
Q

What is the management for polymyalgia rheumatica?

A

*15mg prednisolone per day, if no response after 1 week, unlikely to be polymyalgia rheumatica
*Once symptoms are fully controlled, decrease to 12.5mg for 3 weeks then 10mg for 4-6 weeks, then reduce by 1mg every 4-8 weeks

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43
Q

What are the risk factors for osteoporosis?

A

*Older age
*Female
*Post menopausal (oestrogen protective)
*Decreased mobility
*Alcohol
*Smoking
*Long term corticosteroids
*SSRIs
*PPIs
*Anti-epileptics
*Aromatase inhibitors

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44
Q

Normal T score at hip

A

> -1

45
Q

Osteopenia T score

A

-1 to -2.5

46
Q

Osteoporosis T score

A

Less than -2.5

47
Q

FRAX tool

A

Predicts the risk of fragility fracture over the next 10 years

48
Q

Low risk FRAX score:

A

Reassure

49
Q

Medium risk FRAX

A

Offer DEXA

50
Q

High risk FRAX

A

treat

51
Q

What is the management of osteoporosis?

A

*Lifestyle: activity and exercise, healthy weight, stop smoking, reduce alcohol, avoid falls
*Vitamin D and calcium supplements
*Bisphosphonates (aledronate)
*HRT in women entering menopause early
*Raloxifene (selective oestrogen receptor modulator) as secondary prevention
*Denosumab (blocks osteoclast activity)

52
Q

What is ankylosing spondylitis?

A

Inflammatory condition mainly affecting the spine. Part of the seronegative spondyloarthropathy group relating to the HLA B27 gene
Radiological stage of axial spondyloarthritis

53
Q

Presentation of ankylosing spondylitis

A

*Inflammatory back pain (early morning stiffness, insidious onset, age<40, lasting >3 months)
*Iritis/uveitis
*Entethesitis -> plantar fasciitis, achilles tendonitis
*Presentation in late teens or early 20s
*Fatigue and sleep disturbance
*Schober’s test positive

54
Q

Schober’s test

A

*Find L5 and mark 10cm above and 5cm below
*Get patient to lean forwards
*If <20cm =lumbar restriction

55
Q

Investigations for ankylosing spondylitis

A

*Pelvic X ray: sacroiliitis
*HLA B27 genetic test
*CRP and ESR
*MRI: bone marrow oedema (allows early diagnosis)

56
Q

X ray changes of ankylosing spondylitis

A

*Bamboo spine
*Syndesmophytes - bone growth where ligaments insert into the bones
*Fusion and ossification

57
Q

What is the management of ankylosing spondylitis?

A

*NSAIDs
*Steroids for flare
*Anti-TNF
*Physio
*Exercise
*Avoid smoking
*Bisphosphonates

58
Q

What are the small vessel vasculitides?

A
  • Henloch scholein
  • Eosinophilic granulomatosis with polyangiitis
  • microscopic polyangiitis
  • granulomatosis with polyangiitis
59
Q

What are the medium vessel vasculitides?

A
  • Polyarteritis nodosa
  • eosinophilic granulomatosis with polyangiitis
  • kawasaki disease
60
Q

What are the large vessel vasculitides?

A
  • giant cell arteritis
  • Takayasu’s arteritis
61
Q

What is the presentation of giant cell arteritis?

A
  • headache: temporal, tender, subacute, constant, little relief from analgesia
  • Vision changes
  • Jaw claudication
  • constitutional symptoms
  • polymyalgia rheumatica symptoms (pelvic and shoulder girdle pain_
62
Q

Investigation for giant cell arteritis

A
  • Temporal artery biopsy
  • Temporal artery USS
  • ESR
63
Q

Presentation of henoch-schonlein purpura

A
  • palpable purpuric rash (and localised oedema) pn buttocks and extensor surfaces
  • abdominal pain
  • Polyarteritis
  • IgA nephritis
64
Q

Presentation of eosinophilic granulomatosis with polyangiitis

A
  • asthma
  • blood eosinophilia
  • paranasal sinusitis
  • mononeuritis multiplex
  • pANCA positive in 60%
65
Q

Presentation of microscopic polyangiitis

A
  • renal impairment: raised creatinine, haematuria, proteinuria
  • fever
  • lethargy, malaise, weight loss
  • rash: palpable purpura
  • cough, dyspnoea, haemoptysis
  • mononeuritis monoplex
  • pANCA/cANCA
66
Q

Presentation of granulomatosis with polyangiitis

A
  • URT: epistaxis, sinusitis, nasal crusting
  • LRT: dyspnoea, haemoptysis
  • Pauci-immune, rapidly progressive glomerulonephritis
  • Saddle shaped nose deformity
  • Vasculitic rash
  • eye involvement, cranial nerve lesion
  • cANCA (>90%), pANCA(25%)
  • X ray (can show cavitating lesions
67
Q

Presentation of polyarteritis nodosa

A
  • fever, malaise, arthralgia
  • weight loss
  • hypertension
  • mononeuritis multiplex
  • livedo reticularis (rash)
  • Hep B serology is positive in 30%
68
Q

Presentation of kawasaki disease

A
  • high grade fever lasting >5 days
  • Conjunctival injection
  • Bright red, cracked lips
  • Strawberry tongue
  • Cervical lymphadenopathy
  • Red palms and soles which then peel
69
Q

Presentation of takayasu’s arteritis

A
  • systemic features
  • unequal blood pressure
  • carotid bruit and tenderness
  • absent/weak peripheral pulse
  • Upper and lower limb claudication on exertion
  • aortic regurgitation
70
Q

Investigation takayasu arteritis

A

MRA or CTA for vascualr imaging

71
Q

What is Paget’s disease of the bone?

A

Chronic localised bone remodelling, resulting in overgrowth of poorly organised bone -> osseous deformity, nerve compression, and pathological fractures.
Disorder of osteoclasts with excessive osteoclastic activity followed by increased osteoblastic activity

72
Q

Presentaiton of Paget’s disease of the bone

A
  • asymptomatic
  • long bone or back pain
  • pathological fracture
  • Bony deformities
  • hearing loss
  • isolated rise in alkaline phosphate
73
Q

Investigation for paget’s disease of the bone

A
  • x ray
  • bone scan
  • total serum alkaline phosphatase or bone specific
  • serum calcium (usually normal)
74
Q

What are the benign bone tumours?

A
  • osteoma
  • osteochondroma
  • giant cell tumour
75
Q

What are the malignant bone tumours?

A
  • osteosarcoma
  • Ewing’s sarcoma
  • Chondrosarcoma
76
Q

What is the most common benign bone tumour?

A

Osteochondroma

77
Q

What is the msot common malignant bone tumour?

A

Osteosarcoma

78
Q

X ray osteosarcoma

A
  • codman triangle and sunburst pattern
79
Q

X ray Ewing’s sarcoma

A

Onion skin appearance

80
Q

X ray Giant cell tumour

A

Double bubble or soap bubble appearance

81
Q

Where does osteosarcoma occur most frequently?

A

in the metaphyseal region of long bones prior to the epiphyseal closure (femur, tibia, humerus)

82
Q

Where does Ewing’s sarcoma most frequently occur?

A

Pelvis and long bones

83
Q

Where does Chondrosarcoma most commonly occur?

A

Axial skeleton

84
Q

Where does osteoma more commonly occur?

A

Skull

85
Q

Which tumours most commonly cause bone metastases?

A
  • prostate
  • lung
  • breast
86
Q

Starting with the most common, where are the common sites of bone mets?

A
  • spine
  • pelvis
  • ribs
  • skull
  • long bones
87
Q

What are the features of bone mets?

A
  • pathological fractures
  • hypercalcaemia
  • raised ALP
88
Q

Calcium, phosphate, ALP and PTH in osteoporosis

A
  • Calcium: normal
  • Phosphate: normal
  • ALP: normal
  • PTH: normal
89
Q

Calcium, phosphate, ALP and PTH in Osteomalacia

A
  • Calcium: decreased
  • Phosphate: decreased
  • ALP: Increased
  • PTH: Increased
90
Q

Calcium, phosphate, ALP and PTH in Primary hyperparathyroidism

A
  • Calcium: increased
  • Phosphate: decreased
  • ALP: increased
  • PTH: Increaesd
91
Q

Calcium, phosphate, ALP and PTH in chronic kidney disease (secondary hyperparathyroidism)

A
  • Calcium: decreased
  • Phosphate: increased
  • ALP: increased
  • PTH: increaesd
92
Q

Calcium, phosphate, ALP and PTH in Paget’s disease

A
  • Calcium: normal
  • Phosphate: normal
  • ALP: Increased
  • PTH: normal
93
Q

What is the mechansim of bone destruction in cancer?

A

OSteoclasts stimulated by cytokines from tumour cells

94
Q

What is the presentation of osteosarcoma?

A
  • bone pain
  • swelling
  • pathological fracture
95
Q

Where does osteosarcoma metastasise to?

A

Lungs- early

96
Q

What is the presentation of osteoma?

A
  • Pain, worse at night
  • pain releived by aspirin
  • scoliosis
  • juxta-articualr tumours can cause sympathetic synovitis
97
Q

What is SLE?

A

Autoimmune disease (type 3 hypersensitivity reaction) associated with HLA B8, DR2, DR3. Immune complex deposition can affect any organ including the skin, joints, kidney and brain

98
Q

Epidemiology of SLE

A
  • more common in women
  • afro-carribbeans and asian communities
  • onset aged 20-40
99
Q

Presentation of SLE

A
  • General: fatigue, fever, mouth ulcers, lympahadenopathy
  • Sking: malar or discoid rash, photosensitivity, raynaud’s, livedo reticularis, non scarring alopecia
  • MSK: arthralgia, non-erosive arthritis
  • CV: pericarditis, myocarditis
  • Resp: Pleurisy, fibrosing alveolitis
  • Renal: proteinuria, glomerulonephritis
  • Neuro/psych: anxiety and depression, psychosis, seizure
100
Q

Investigation of SLE

A
  • ANA (99% positive)
  • 20% rheumatoid factor positive
  • anti-dsDNA
  • anti-smith
  • ESR (CRP during active disease may be normal so if raised, may suggest infection)
  • C3 and C4 may be low during active disease
101
Q

What is Sjogren’s syndrome?

A

Autoimmune disorder affecting the exocrine glands resulting in dry mucosal surfaces

102
Q

What are the features of Sjogren’s?

A
  • Dry eyes
  • dry mouth
  • vaginal dryness
  • arthralgia
  • raynauds, myalgia
  • sensory polyneuropathy
  • recurrent episodes of parotitis
  • renal tubular acidosis
103
Q

Investigations for Sjogrens

A
  • Rheumatoid factor
  • ANA positive
  • Anti Ro (70%), Anti la (30%)
  • Schirmer’s test
104
Q

What is Polymyositis?

A

Inflammatory disorder causing symmetrical, proximal muscle weakness, thought to be t cell mediated against muscle fibres

105
Q

What are the features of polymyositis?

A
  • proximal muscle weakness ± tenderness
  • Raynaud’s
  • respiratory muscle weakness
  • interstitial lung disease
  • dysphagia, dysphonia
106
Q

Investigations for polymyositis

A
  • elevated creatinine kinase
  • elevated muscle enzymes e.g. LDH, AST and ALT
  • EMG
  • muscle biopsy
  • Amti-synthetase antibodies (Anti-Jo-1)
107
Q

What is dermatomyositis?

A

Variant of polymyositis in which skin manifestations are prominent e.g. purple (helitrope) rash on the cheeks and eyelids

108
Q

what class of HLA rheumatoid

A

DR4

109
Q

What are the signs of osteoarthritis in the hands?

A
  • Heberdens nodes
  • squaring of the base of the thumb
  • Bouchard’s nodes

Finals (37 decks)

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