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Junior Medicine > Rheumatology conditions > Flashcards

Rheumatology conditions Flashcards

1
Q

What antibodies are involved in Rhematoid arthritis?

A
  • IgG Rheumatoid Factor
  • anti-CCP (citrullinated cyclic peptide)
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2
Q

What is the pathophysiology of RA?

A
  • Citrullation of self antigens which are then recognised by T&B cells
  • Macrophages are stimulated and release TNFalpha
  • There is an inflammatory cascade leading to proliferation of synoviocyes
  • Synoviocytes grow over cartilage and restrict nutrients
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3
Q

What is the typical history of a patient with RA?

A
  • Usually female
  • 30-50 years old
  • Stiffness is symmetrical, progressive and peripheral
  • Morning stiffness for >30mins duration
  • Usually involves with MCPs/PIPs/ MTPs (but spares the DIPs) but can affect any joint
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4
Q

What will you find on examination of a patient with RA?

A
  • Soft tissue swelling and tenderness
  • Ulnar deviation
  • Palmar subluxation of MCPs
  • Swan neck deformity
  • Boutonniere deformity
  • Rheumatoid nodules (at the elbow)
  • May have median nerve involvement
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5
Q

What investigations would you order to confirm RA?

A
  • RF and anti-CCP
  • FBC- may have normocytic aneamia (aneamia of chronic disease)
  • Inflammatory markers
  • Can request X-ray but changes only appear in more established disease
  • USS/MRI is more sensitive in early disease
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6
Q

What X ray findings will you find on a patient with RA?

A
  • Loss of joint space
  • Erosions (periarticular)
  • Soft tissue swelling
  • Subluxation
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7
Q

How do you treat RA?

A
  • Initially DMARD therapy - methotrexate
  • Can give combination DMARDs
  • Steroids for acute flares
  • Symptoms control with NSAIDs (+PPI cover)
  • Severe disease can consider biologics
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8
Q

Give some of the extra-articular manifestations of RA?

A

3 CAPS

3Cs

  • Carpal tunnel syndrome
  • Cord compression (atlanto-axial subluxation)
  • elevated Cardiac risk

3As

  • Anaemia (normocytic & normochromic)
  • Amyloidosis (rare now)
  • Arteritis (rare)

3Ps

  • Pericarditis (uncommon)
  • Pleural disease (common)
  • Pulmonary disease (common) e.g. bronchiectasis

3Ss

  • Sjögren’s
  • Scleritis/ episcleritis
  • Spenic englargement (if + neutropenia = Felty’s syndrome (rare))
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9
Q

What is Giant Cell Arteritis?

A

Chronic vasculitis of large and medium sized vessels

(also called temporal arteritis)

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10
Q

What are some of the risk factors for developing giant cell arteritis?

A
  • Age (greatest risk factor) >90% are older than 60
  • Increased prevalence in northern latitude
  • More common in women
  • Common in whites
  • Strong link with polymyalgia rheumatica
  • Genetic predisposition: HLA-DR4
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11
Q

What are some of the symptoms of giant cell arteritis?

A
  • Headache
    • often localised, unilateral over the temple
  • Tongue or jaw claudication on mastication
  • Visual symptoms are an emergency!
    • Amaurosis fugax
    • Blindness
    • Diplopia
    • Blurring
  • Scalp tenderness
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12
Q

How do you diagnose giant cell arteritis?

A

Presnce of any 2 or more of the following in patients >50yrs

  • Raised ESR, CRP or PV
  • New onset localised headache
  • Tenderness or decreased pulsation of temporal artery
  • New visual symptoms
  • Biopsy revealing necrotising arteritis
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13
Q

How do you treat Giant Cell Arteritis?

A
  • Prednisolone 60-100mg PO for at least 2 weeks before considering slow tapering
  • For acute onset visual symptoms:
    • consider 1g methyprednisolone IV pulse therapy for 1-3 days
  • Low dose aspirin reduces thrombotic risks
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14
Q

What is Polymyalgia Rheumatica?

A

Clinical syndrome of pain and stiffness in the shoulder, hip girdles and neck

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15
Q

Describe the typical history of a patient with polymyalgia rheumatica

A
  • Elderly patients with new sudden onset proximal limb pain and stiffness (neck, shoulders, hips)
  • Have difficulty rising from the chair or combin hair
  • Pain is worse at night
  • Systemic symptoms (25% cases): fatigue, weight loss, low grade fever)
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16
Q

What will you find on physical examination of a patient with polymyalgia rheumatica?

A
  • Decreased ROM of shoulders, neck, hips
  • Muscle stregnth is usually normal
  • Muscle tenderness
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17
Q

How do you treat polymyalgia rheumatica?

A
  • 15mg Prednisolone daily - will see rapid improvement within 5 days (confirms diagnosis too, if not seen reconsider diagnosis)
  • Dose can be tapered very slowly
  • Methotrexate can steroid sparing in relapsing patients
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18
Q

What are spondyloarthropathies?

A

Group of conditions that affect the spine and the peripheral joints

  • Ankylosing spondylitis (most common)
  • Enteropathic arthritis
  • Psoriatic arthritis
  • Reactive arthritis
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19
Q

Which gene is associated with spondyloarthropathies?

A

HLA-B27

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20
Q

What are the common features of all spondyloarthopathies?

A
  • Sacro-iliac/ axial disease (back/buttock pain)
  • Inflammatory arthropathy of peripheral joints
  • Entheisitis (inflammtio at tendon insertions)
  • Extra articular features (skin/gut/eye)
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21
Q

How does a patient with anklyosing spondylsis present?

A

Usually a young man (teens-mid thirties)

Presents with bilateral buttock , chest wall and thoracic pain

Examination is usually normal but will later lose lumbar lordosis and have an exaggerated kyphosis

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22
Q

What investigations can you do to help diagnose ankylosing spondylisis?

A
  • Schober’s Test - mark skin 10cm above and 5 cm below PSIS
    • ask patient to bend forward with straight legs, increase of >20 cm is normal
  • Will have reduced chest expansion
  • CRP may be raised by often normal
  • MRI of spine and SI joints
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23
Q

How do you treat ankylosing spondylsis?

A
  • NSAIDs and physio
  • TNF inhibitors
  • IL-17 inhibitors
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24
Q

What typical exam findings will you find on a patient with psoriatic arthritis?

A
  • Oligo-arthritis with dactylitis (sausage like fingers)
  • Can be symmetrical or mono-arthritis
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25
Q

How do you treat psoriatic arthritis?

A
  • NSAIDs
  • DMARDs
  • TNF inhibitors
  • IL-17 inhibitors
  • IL-12/23 inhibitors
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26
Q

What is reactive arthritis?

A
  • Sterile synovitis developing after a distant infection
  • Either post dysentry (Salmonella/ Shigella/ Campylobacter)
  • or, following urethritis/ cervicitis (Chlamydia trachomatis)
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27
Q

How does reactive arthritis present?

A
  • Usually presents 2 weeks post infection as acute asymmetrical lower limb arthritis
  • Skin: circinate balantitis - rash on penis
  • Keratoderma blennorrhagica
  • Eye: conjunctivitis
  • Enthesitis
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28
Q

How do you treat reactive arthritis?

A
  • Treat underling infection - may not improve the arthritis
  • NSAIDs and joint injections
  • Most resolve in 2 years- if not may need DMARDs
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29
Q

What is enteropathic arthritis?

A
  • 10-20% of patients with IBD develop arthropathy
    • 2/3 develop peripheral arthritis
    • 1/3 develop axial disease
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30
Q

What are the 2 types of peripheral disease in enteropathic arthritis?

A

Type 1: oligoarticular, asymmetric and has a correlation with IBD flares

Type 2: polyarticular, symmetrical and less correlation with IBD flares

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31
Q

How do you treat enteropathic arthritis?

A
  • Consider DMARDS
  • TNF inhibitors will treat both bowel disease and arthritis
  • Remember: NSAIDs may flare IBD so best to avoid
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32
Q

What are some of the extra- articular manifestations of ankylosing spondylitis?

A

All the A’s

  • Anterior uveitis
  • Aortic incompetence
  • AV block
  • Apical lung fibrosis
  • Amyloidosis
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33
Q

What are some of the features of inflammatory back pain?

A
  • Insidious onset
  • Pain at night (improves with waking)
  • Age of onset <40 years
  • Improves with exercise
  • No improvement with rest
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34
Q

What is Systemic lupus erythematosus?

A
  • autoimmune disease
  • inadequate T cell suppressory activity with increased B cell activity
  • complex multisystemic disease with variable presentations
  • characterised by remissions and flares
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35
Q

What are some of the signs and symtpoms of SLE?

A

SOAP BRAIN

  • Serositis - pleurisy, pericarditis
  • Oral ulcers - usually painless, palate is mores specific
  • Arthritis- of small joints (non erosive)
  • Photosensitivity - malar or discoid rash
  • Blood disorders- low WCC, lymphopenia, thrombocytopenia, haemolytic anaemia
  • Renal involvement - glomerulonephritis
  • Autoantibodies (ANA +)
  • Immunological test - low complement
  • Neurologic disorder - seizures or psychosis
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36
Q

What investigations can be done to investigate lupus?

A
  • ESR / plasma viscocity (will be raised)
  • 95% are ANA +
  • Anti-Ro, Anti La are common
  • Anti dsDNA titre rises with disease activity
  • Urinalysis - vital for detecting renal disease
  • Skin biopsy- can be diagnostic
  • Renal biopsy- can be diagnostic
37
Q

How do you treat lupus?

A
  • Sun protection
  • Healthy lifestyle to reduce CV risk
  • Hydroxychoroquine is helpful for rashes and arthralgia
  • Mycophenolate mofetil
  • Azathioprine
  • Rituximab
  • Short course prednisolone for flares
38
Q

What is Raynaud’s Phenomenon?

A

Painful condition due to vasospasm of the digits

Painful and characterised by colour changes in response to cold stimulus and stress

White> blue > red

39
Q

What is Raynaud’s syndrome?

A

Term used when Raynaud’s phenomenon is idiopathic

Common in young women, most improve with age

Advise to avoid smoking and keep warm

40
Q

What diseases are associated with raynaud’s phenomenon?

A
  • Scleroderma
  • SLE
  • Dermatomyositis and Polymyositis
  • Sjogren’s syndrome
41
Q

What are some physical causes of Raynaud’s?

A
  • Smoking
  • Use of heavy vibrating tools
  • Sticky blood e.g. cryoglbulinaemia
  • Drug induced: beta blockers
42
Q

How do you treat Raynaud’s Phenomenon?

A
  • Keep warm
  • stop smoking
  • CCB can be used first line
  • Phosphodiesterase-5-inhibitors usually effective
43
Q

What are some of the complications of Raynaud’s phenomenon?

A
  • Digital ulcers
  • Severe digital ischemia
  • Infection
44
Q

What is vasculitis?

A

An inflammatory blood vessel disorder

45
Q

How do you take a history to diagnose vasculitis?

A
  • Consider age, gender, ethnicity
  • Comprehensive drug history
  • Family history of vasculitis
  • Consitutional symptoms : fever, weight loss, malaise, fatgue, diminished appetite, sweats
  • Ask about Raynaud’s
  • MSK: arthralgia, myalgia, proximal muscle weakness?
  • CNS/PNS: headaches, visual loss, tinnitus, stroke, seizure, encephalopathy
  • Nose bleeds, crusts, ulcers
  • Heart lung: pericarditis, cough, chest pain, haemoptysis, dyspnoea
  • GI: abdo pain
  • Renal: haematuria
  • Limbs: neuropathy, digital ulcers/ ischemia
46
Q

What should you look for on examination of a patient with vasculitis?

A
  • Vital signs: hypertension, pulse regularity and rate
  • Skin: palpable purpura, livedo reticularis nodules (mottled skin), digiatal ulcersm gangrene, nail bed capillary changes
  • Neurologic: CN exam, sensorimotor exam
  • Ocular exam: visual fields, scleritis, uveritis, episcleritis
  • Cardiopulmonary exam: crackles, pleural rubs, murmurs, arrhythmias
  • Abdo exam: tenderness, organomegaly
47
Q

What are the primary vasculitides (small, medium and large vessels)?

A

Small vessel vasculitis

  • Microscopic polyangiitis (MPA)
  • Granulomatosis with polyangiitis (GPA)
  • Eosinophilic granulomatosis with polyangiitis (formerly Churg Strauss)
  • IgA vasculitis

Medium vessels

  • Polyarteritis nodosa
  • Kawasaki disease

Large vessel vasculitis

  • GCA
  • Takatasu arteritis
48
Q

What tests should you do if suspecting vasculitis?

A
  • Urine dip (renal involvement is usually silent)
  • FBC, U&E, LFTs, CRP, PV, ESR
  • Complement levels
  • Hepatitis screen for B, C, HIV
49
Q

How do you treat vasculitis?

A
  • Rule out infection
  • Stop any offending drugs
  • 1st line: Corticosteroids
  • 2nd line: Cytotoxic medications, immunomodulatory or biologics
50
Q

What are Dermatomyositis and polymyositis?

A

Rare idiopathic muscle diseases that are characterised by inflammation of striated muscles

51
Q

What is the diagnostic criteria for dermatomyositis and polymyositis?

A
  • Symmetrical proximal muscle weakness
  • Raised serum muscle enzyme markers
  • Electromyographic changes
  • Biopsy evidence of myositis
  • Typical rask of dermatomyositis
  • PM if > 3 of first 4 above
  • DM if rash and _>_2 of the first 2
52
Q

How do you treat dermatomyositis and polymyositis?

A
  • High dose corticosteroids main stay for first few weeks
  • Monitor CK and inflammatory markers
  • Long term control with MTX and AZA or Rituximab
  • Use sun protection in DM to reduce the rash
53
Q

What is the link between dermatomyositis and malignancy?

A
  • Patients with DM have increased risk of malignancy in 2-3 years before and after DM diagnosis
  • Usually followed for 5 years
54
Q

Why are patients with dermatomyositis and polymyositis at risk of aspiration pneumonia or respiratory failure?

A

The upper oesophagus has striated muscle therefore swallowing may be affecting increasing risk of aspiration pneumonia

The diaphragm involvement may lead to respiratory failure

55
Q

What visual features do you see in dermatomyositis

A
  • Gottron’s papules (linear plaques on the dorsal aspect of hands)
  • Dilated nail fold capillaries
  • Periorbital oedema - violet rask to eye lids (heliotrope rash)
56
Q

What medications should you consider stopping in patients with recurent flares of gout?

A

Thiazides

e.g. indapamide

bendroflumothiazide

57
Q

What are the crystal differences between gout and pseudogout?

A

Gout: monosodium urate cystals

  • negatively birefringent
  • needle shaped

Pseudogout: Calcium pyrophosphate crystals

  • positively birefringent
  • rhomboid shaped
58
Q

How do you diagnose polymyalgia rheumatica?

A
  • Typically based off history and exam supported by raised inflammatory markers
  • Check ESR, PV and CRP
  • Consider temporal artery biopsy if there are symptoms of GCA
59
Q

What is hypermobility spectrum disorder?

A

A pain syndrome in people with joints that move beyond normal limits

May affect a number of joints

Due to the laxity of ligaments, capsules and tendons. though the origin of pain is from microtrauma

60
Q

What are some of the signs and symptoms of hypermobility spectrum disorder?

A
  • Pain around the joints worse after activity
  • General pain and fatigue
  • May have
    • soft tissue rheumatism e.g. epicondylitis
    • abnormal skin: scars, hyperextensible, thin, straie
    • marfanoid habitus
    • arachnodactyly
    • drooping eyelids/ myopia
    • hernia
    • uterine/ rectal prolapse
61
Q

What treatment is offered for hypermobility spectrium disorder?

A

Mainstay is non-drug treatment

  • strengthening exercises to reduce joint subluxation
  • work on posture and balance
  • splinting or surgical intervnetions
  • specialist pain management

Pharmacologically: paracetamol is the main stay

62
Q

Give some heritable connective tissue disorders

A
  • Marfan’s syndrome
  • Ehler’s Danlos syndrome
63
Q

What is defective in marfan’s sydrome?

A
  • Fibrillin
64
Q

What is osteoarthritis?

A

A degenerative joint disorder with progessive loss of articular cartilage accompanied by new bone formation and capsular fibrosis

65
Q

What happens to cartilage in OA?

A
  • Loss of elasticity with reduced tensile stregnth
  • Cellularity and proteoglycan content are reduced
66
Q

What are some of the risk factors for developing OA?

A
  • Age main factors - present in 80% of people age 65+
  • Women > men
  • Obesity
  • Trauma and joint malalignment
67
Q

Which joints are most commonly affected by OA?

A
  • Hip
  • Knee
  • Spine
68
Q

What are the signs and symptoms of OA?

A
  • Pain provoked by movement and weight bearing
    • starts intermittently but can become constant
  • Feeling joint may give way (knee)
  • Joints feel ‘stuck’ after inactivity
69
Q

What are the X-ray findings of OA?

A
  • Loss of joint space
  • Osteophytes
  • Subchondral cysts
  • Subarticular sclerosis
70
Q

What non drug therapy can be offered for OA?

A

Should be offered to all

  • Strengthening exercises
  • Weight loss
  • Use of laterally wedged insoles reduces joint loading
  • Walking sticks
71
Q

What is the pharmacological management of OA?

A
  • Regular paracetamol (1st line)
  • NSAIDs should only be used short term
  • Topical NSAIDs
  • Intraarticular corticosteroid injections can be offered
72
Q

When are surgical options to OA offered?

A
  • If conservative management fails
  • Young patient have higher change of revision surgery so best to wait as long as possible
73
Q

What is fibromyalgia?

A

Chronic widespread pain in all 4 quadrants of the body

74
Q

What are some of the triggers for fibromyalgia?

A
  • Sleep disturbance is main cause
    • causes hyper-activation in response to noxious stimulation
75
Q

Give some of the signs and symptoms of fibromyalgia

A
  • Pain- heightened to innocuous stimuli
  • joint/muscle stiffness
  • profound fatigue
  • unrefreshed sleep
  • numbness
  • headaches
  • irritable bowel/bladder
  • depression and anxiety
  • poor concentration and memory
76
Q

What will you find on examination in fibromyalgia?

A

There should be no physical abnormalities or neurological signs

Examine for tender points on palpation of muscles

(no specific diagnostic test)

77
Q

Give some risk factors of fibromyalgia

A
  • Female: male 9:1
  • Peak onset 40-50yrs
  • May have ovious trigger (emotional or physical)
78
Q

How is fibromyalgia treated?

A

Tailor to pain intensity, function and associted features (sleep distubance, depression, fatigue)

Simple meausures to improve sleep and physical activity levels.

Most patients improve with explanation of symtpoms

Drugs: low dose amitryptyline (opiates are not reccommended)

CBT is effective

79
Q

What is osteoperosis?

A

Skeletal condition of low bone mass, deterioration of bone tissue and disruption of bone architecture

Leads to compromised bone stregnth and increased risk of fracture

80
Q

What are some of the non modifiable risk factors for OA?

A
  • Age >65 yrs
  • Female
  • Caucasian or south asian
  • FHx of osteoporosis
  • History of low trauma fracture
81
Q

What are some of the modifiable risk factors of osteoporosis?

A
  • Low BMI <21
  • Premature menopause (<45)
  • Calcium/ vitamin D deficiency
  • Inadequate physical activity
  • Cigarette smoking
  • Excessive alcohol intake (>3 drinks/day)
  • Iatrogenic e.g. corticosteroids, aromatase inhibitors
82
Q

How do you diagnose osteoporosis?

A
  • DEXA scan (dual energy x-ray absorptiometry) of lumbar spine and hip is gold standard
  • T score <-2.5 = osteoperosis
    • normal T score is > -1
    • osteopenia if t score between -1 and -2.5
  • Plain radiographs lack sensitivty to diagnose OP but can show rib fractures of vertebral compression fractures without history of trauma which should warrant investigation
83
Q

How is osteopenia managed?

A
  • weight bearing exercises
  • Vitamin D3 supplements
  • limit alcohol
  • smoking cesation
  • dietary advice (calcium intake)
84
Q

How is osteoperosis managed?

A

Vitamin D3 + calcium supplements plus:

  1. First line: oral bisphosphonates (or IV if oral not tolerated)
  2. Second line : Denosumab or terparatide
85
Q

What adive should you give someone taking alendronic acid?

A
  • Take once a week
  • Take first thing in the morning before having anything to E+D to avoid GI upset
  • Sit upright for at least 30 minutes after taking
86
Q

What are some of the secondary causes of osteoporosis?

A
  • Coeliac disease
  • Eating disorders
  • Hyperparathyroidism
  • Hyperthyroidism
  • Multiple myeloma
  • Hypogonadism in men
87
Q

What is one of the main risks of taking bisphosphonates e.g. alendronic acid?

A

Osteonecrosis of the jaw

88
Q

The Z score on DEXA scans is adjusted for which parameters?

A
  • Age
  • Gender
  • Ethnic factors

Junior Medicine (6 decks)

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