10 - Joint Rheumatology Flashcards

1
Q

What is giant cell arteritis and what is the typical aetiology?

A

- Chronic vasculitis of large and medium vessels in the scalp, neck and arms.

  • Occurs in people over 50 and associated with polymyalgia rheumatica
  • Usually inflammation of arteries originating from arch of aorta
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2
Q

What are some risk factors for GCA?

A
  • >50 years old (1 in 500)
  • Caucasian
  • Female
  • Polymyalgia rheumatica
  • Genetic Predisposition with HLA-DR4
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3
Q

What are the symptoms of GCA?

A
  • Headache
  • Scalp tenderness especially over temporal artery
  • Jaw/tongue claudication on mastication
  • Amaurosis fugax
  • Blindness, diplopia, blurring
  • Constitutional symptoms e.g malaise, weight loss
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4
Q

When is GCA an emergency?

A
  • Any visual symptoms as there is a risk of irreversible bilateral vision loss
  • Visual symptoms can present weeks-months after onset of other symptoms
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5
Q

What tests should you order if you suspect GCA?

A

- ESR/CRP: raised

- Platelets: raised

- Hb: lower

- Temporal artery biopsy: do not wait for this to start steroids, also may be negative biopsy due to skip lesions

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6
Q

How is GCA diagnosed?

A
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7
Q

How is GCA treated?

A

If acute visual symptoms

  • Immediate IV methylprednisolone for 1-3 days

If just GCA

- Prednisolone PO 60-100mg for at least 2 weeks then consider tapering

- Low dose aspirin to reduce thrombotic risk

- PPI, Adcal and Bisphosphonate if long term steroids

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8
Q

What is polymyalgia rheumatica?

A

Syndrome characterised by pain and stiffness of shoulder, hip girdles and neck

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9
Q

What is the aetiology of polymyalgia rheumatica?

A
  • Usually affects people >50 with peak incidence at 70-80
  • Associated with GCA
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10
Q

How does polymyalgia rheumatica present?

A
  • New sudden onset bilateral aching, tenderness and morning stiffness in shoulders, hips and neck of an elderly patient
  • Difficulty rising from chair or combing hair due to proximal limb involvement
  • Night time pain
  • Systemic symptoms e.g fatigue, weight loss, low grade-fever
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11
Q

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

A
  • Decreased ROM of shoulders, neck, hips
  • Muscle strength normal just limited by pain
  • Muscle tenderness
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12
Q

What investigations should you do if you suspect polymyalgia rheumatica?

A

- CRP and ESR: raised

- CK: normal, helps distinguish from myopathies

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13
Q

How can you diagnose polymyalgia rheumatica?

A

History and exam with raised inflammatory markers to support (need ESR and CRP)

Consider temporal artery biopsy if GCA symptoms

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14
Q

How is polymyalgia rheumatica treated?

A

- Prednisolone PO daily. Should have rapid response in week, if not then reconsider diagnosis.

- Bone protection for steroids

- Methotrexate if patient relapsing/prolonged therapy for steroid sparing treatment

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15
Q

What are some differential diagnoses for polymyalgia rheumatica?

A
  • Recent onset RA
  • Malignancy
  • Hypothyroidism
  • Polymyositis
  • OA
  • Spinal stenosis
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16
Q

What are spondylarthropathies?

A

Group of inflammatory conditions that tend to affect the axial skeleton. They all share clinical features of:

  • Seronegative (RF -ve)

- HLA-B27 association

- Axial arthritis in spine and SI joints

- Asymmetrical large joint oligoarthritis or monoarthritis

- Enthesitis

- Dactylitis

- Extraarticular features

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17
Q

What conditions are included in spondylarthropathies?

A
  • Ankylosing spondylitis
  • Psoriatic arthritis
  • Enteropathic arthritis
  • Reactive arthritis
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18
Q

What features suggest inflammatory back pain?

A

IPAIN

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19
Q

What is ankylosing spondylitis and who does it mainly affect?

A

Chronic inflammatory disease involving the spine and SI joints

Usually affects young men (15-30)

HLA-B27 association

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20
Q

What are the presenting symptoms of ankylosing spondylitis?

A

- Gradual onset lower back pain that is worse in the night. Early morning stiffness

  • Pain relieved with exercise/improves throughout the day
  • Pain radiates from SI joints to bilateral buttock
  • May have thoracic or chest pain
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21
Q

What might you find on examination of a patient with ankylosing spondylitis?

A
  • Normal
  • Loss of lumbar lordosis
  • Exaggerated thoracic kyphosis
  • Reduced chest expansion
  • Decreased lumbar flexion (Schober’s test <20cm)
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22
Q

What are some extraarticular features that ankylosing spondylitis is associated with?

A
  • Enthesitis (achilles tendonitis, plantar fascitis)
  • Anterior uveitis
  • Aortic valve incompetence
  • AV block
  • Pulmonary apical fibrosis
  • Amyloidosis
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23
Q

How is ankylosing spondylitis investigated and diagnosed?

A

Diagnosis is clinical with support from imaging

- MRI spine and SI joints(more sensitive than X-ray)

- X-Rays

- Raised CRP/ESR

- Normocytic anaemia

- HLA-B27 positive in 90% cases

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24
Q

What do MRI and X-ray’s show in ankylosing spondylitis?

A

MRI:

- Active inflammation with bone marrow oedema

- Destructive changes like erosions, sclerosis, ankylosis

X-Ray

  • SI joint space narrowing due to fusion, sclerosis, ankylosis/fusion

- Vertebral syndesmophytes due to enthesitis between ligaments and vertebrae

- Bamboo spine due to calcification of ligaments

- Dagger spine

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25
Q

How is ankylosing spondylitis managed?

A

- Physiotherapy with intense exercise to maintain posture

- NSAIDs

- TNF-a inhibitors (adalimumab)

- IL-17 inhibitors

  • Can have local steroid injections and hip replacements if severe
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26
Q

How does psoriatic arthritis present?

A

Occurs in 10% of psoriasis patients and can occur before skin changes. Often have nail changes, enesthesis and rashes with lots of patterns:

  • Oligoarthritis with dactylitis in DIPJs
  • Symmetrical
  • Monoarthritis
  • Psoriatic arthritis mutilans (rare severe deformity where osteolysis occurs around the phalanx, leading to a telescoping finger)
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27
Q

What radiological investigations are done for psoriatic arthritis and what are the findings?

A

- CRP raised

- X-Ray: central joint erosions with mouse ears and pencil in cup deformity

- MRI: central joint erosions

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28
Q

How is psoriatic arthritis managed?

A

- NSAIDs

- DMARDS (Sulfasalazine and Methotrexate)

- TNF-a inhibitors

  • IL-17 inhibitors
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29
Q

What is the pathophysiology of reactive arthritis?

A

Condition where arthritis and other features occur as an autoimmune response to an infection elsewhere in the body, e.g GI or GU infection

- Post dysentry: Salmonella, Shigella, Campylobacter

- Post Urethritis: Chlamydia Trachomatis

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30
Q

How does reactive arthritis present?

A
  • Up to 2 weeks after initial infection

- Acute monoarthritis of lower limb

- Reiter’s: urethritis, uveitis/conjunctivitis and arthritis

- Other features: uveitis, keratoderma blenorrhagica, circinate balanitis, mouth ulcers, enthesitis

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31
Q

What is Reiter’s syndrome?

A

Triad of:

  • Arthritis
  • Conjunctivitis
  • Urethritis

Can’t see, Can’t pee, Can’t climb a tree!!!!

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32
Q

How is reactive arthritis investigated?

A

- Take joint aspirate to rule out septic arthritis/gout!!!!!!!!!!!!!!!

- Serology

- STI screening

- Stool culture if diarrhoea

- Raised CRP/ESR

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33
Q

How is reactive arthritis managed?

A

- Treat underlying infection (may not improve arthritis)

- NSAIDs or local steroid injections

  • If not resolving in 6 months consider DMARDs (often HLA-B27+)
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34
Q

What is enteropathic arthritis?

A

Chronic inflammatory arthritis associated with IBD and Coeliac’s. 10% of IBD patients will get.

Can be peripheral arthritis (2/3) or axial arthritis (1/3)

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35
Q

What are the two different types of peripheral disease for enteropathic arthritis?

A

Type 1: oligoarticular, asymmetric, associated with IBD flares

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

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36
Q

How is enteropathic arthritis managed?

A

- Treat bowel symptoms and will improve arthritis

- Do not use NSAIDs as this can flare IBD

  • Consider TNF-a inhibitors for bowel and arthritis symptoms
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37
Q

What is hypermobility spectrum disorder and who does it commonly affect?

A

Pain syndrome where joints move beyond normal limits due to laxity of ligaments, capsules and tendons

More common in women, Asian people, family history and presents in childhood

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38
Q

What are some signs and symptoms of hypermobility spectrum disorder?

A
  • Pain around joints is worse after activity
  • Fatigue
39
Q

How is hypermobility spectrum disorder treated?

A

NO CURE

Non-Pharmacological

  • Physiotherapy to strengthen and reduce subluxation
  • Splinting

Pharmacological

  • Paracetamol
  • Specialst pain management
40
Q

What are the different types of arthritis?

A

- Inflammatory: seronegative, seropositive (RA and lupus), septic/infectious, crystal induced

- Non-inflammatory: OA

Also think if mono or polyarthritis

41
Q

What is the pathophysiology of the most common type of arthritis, OA?

A

Progressive loss of articular cartilage accompanied by new bone formation and capsular fibrosis

42
Q

What are some risk factors for OA?

A
  • Age
  • Female
  • Obesity
  • Trauma
  • Joint malalignment
43
Q

What are some signs and symptoms of OA?

A
  • Monoarticular joint pain
  • Crepitus
  • Reduced ROM
  • Early morning stiffness <30mins
  • Inacitivity gelling in knee
  • Feeling that joint is going to ‘give way’
44
Q

How is OA diagnosed and what will this show?

A

X-RAY

Loss of joint space

Osteophytes

Subarticular sclerosis

Subchondral bone cysts

45
Q

How is OA managed conservatively, medically and surgically?

A

Conservatively: physiotherapy for strengthening, weight loss to decrease joint loadning, walking stick

Medically: regular paracetamol, oral or topical NSAIDs, topical capsaicin, intrarticular corticosteroid injections

Surgically: joint replacements

46
Q

What is nodal OA?

A

OA affecting the PIPJs (Bouchard’s), DIPJs (Herbeden’s), thumb CMCs and knees

More common in post menopausal women

47
Q

What is fibromyalgia? (diagnosis of exclusion)

A
  • Chronic (>3months) widespread pain in all 4 quadrants of the body involving left and right side, above and below the waist and the axial skelton

- Fatigue and unrefreshing sleep

  • Can also be low mood, stiffness and disturbe sleep
48
Q

What is the possible pathogenesis of fibromyalgia?

A
  • Deliberate sleep deprivation
  • Reduced REM and delta-wave sleep so hyperactivatin in response to noxious stimulation and neural activation of pain perception sensors in response to non-painful stimuli
49
Q

What are some of the symptoms of fibromyalgia?

A

- Joint/muscle stiffness

- Fatigue

- Unrefreshed sleep

  • Headaches
  • IBS
  • Depression and anxiety
  • Poor concentration

- Widespread tender points

50
Q

What are some risk factors for fibromyalgia?

A
  • Female
  • Middle aged 40-50
  • Low household income
  • Low educational status
  • Trigger e.g emotional or physical
51
Q

How is fibromyalgia diagnosed?

A
  • Clinical diagnosis
  • Clinical tests rule out other diagnoses

- No MSK or neurological abnormalities on examination

- Tender points on palpation of muscles

52
Q

How is fibromyalgia treated?

A

- Patient education (pacing, exercise, relaxation, physio)

- CBT

- Low dose amitriptylline can help pain and improve sleep

- Pregabalin can be used if amitriptylline not useful

- Duloxetine or SSRIs for concurrent depression

  • DO NOT GIVE STEROIDS, NSAIDS OR OPIATES
53
Q

What blood tests are recommended in fibromyalgia to rule out other pathology?

A
  • ESR/CRP
  • FBC
  • U+Es
  • LFTs
  • Ca
  • CK
  • TFT
54
Q

What is osteoporosis?

A

Low bone mass that leads to compromised bone strength and increased risk of fracture

Cortical bone affected then long bone fractures, if trabeculae ten cresh fractures

55
Q

What are some risk factors for osteoporosis?

A

Modifiable and Non-modifiable

SHATTERED

Steroids

Hyperthyroidism, hyperparathyroidism, hypercalcuria

Alcohol

Thin

Testosterone low

Early menopause

Renal or liver failure

Erosive/Inflammatory bone disease

Diet low in Ca

56
Q

What are some secondary causes of osteoporosis?

A
  • Celiac
  • Eating disorders
  • Hyperparathyroidism
  • Hyperthyroidism
  • Multiple myeloma
57
Q

How is a diagnosis of osteoporosis made?

A

Gold standard: DEXA of lumbar spine and hip. See image for numbers

Other investigations: X-ray, Ca, PO4

58
Q

What is a Z-Score for osteoporosis?

A

Comparison of the patients BMD with other people of the same age and gender

If <2 then consider secondary osteoporosis

59
Q

What fractures should make you suspect osteoporosis?

A
  • Non trauma vertebral compression fracture
  • Non-trauma rib fracture
60
Q

How is osteopenia treated? (T of -1 to -2.5)

A

RISK MODIFICATION

  • Weight bearing exercise
  • Vitamin D3 supplements
  • Limit alcohol
  • Smoking cessation
  • Diet advice (increase Ca and Vit D)
61
Q

What is the pharmacological treatment for osteoporosis?

A

Lifestyle changes, Vitamin D and Ca supplementation PLUS

1st line: oral bisphosphonates (e.g alendronic acid) but can give IV if oral not tolerated

2nd Line: Denosumab or Teriparatide

Can give HRT to prevent osteoporosis and testosterone to hypergonadal men

62
Q

What instructions should you give to patients on how to take alendronic acid?

A
  • Take on empty stomach
  • Take with full glass of water
  • Remain upright for 30 minutes after taking
  • Wait 30 minutes before eating or taking other drugs
63
Q

What are some side effects of oral bisphosphonates such as alendronic acid?

A
  • Photosensitivity
  • GI upset
  • Oesophageal ulcers
  • Jaw osteonecrosis
64
Q

What are some indications for a DEXA scan?

A
  • Low trauma fracture
  • Women >65 with one or more risk factors for osteoprosis
  • Before giving long term steroids

Do not need pretreatment for women >75 years

65
Q

What is gout?

A

Deposition of monosodium urate crystals in joints (usually first MTJ) leading to inflammatory mono-arthritis. Due to hyperuricaemia

Long term can get urate deposits (tophi) and renal disease

66
Q

What are some things that can trigger a gout attack?

A
  • Trauma
  • Surgery
  • Starvation
  • Infection
  • Diuretics
67
Q

What are some risk factors and differentials for gout?

A

Need to rule out septic arthritis!!!

DD: haemarthrosis, reactive arthritis

68
Q

What investigations are done to diagnose gout and what do they show?

A

- Serum urate: raised

- Xray of joint: soft tissue swelling, punched out erosions

- Joint aspiration of synovial fluid: negatively birefringent needle shaped crystals under polarised light microscopy

69
Q

What are the general management principles of gout?

A
  • Treat acute attack
  • Prevent recurrences by lowering serum urate with medication and lifestlye
  • Lower CVD risk as gout associated with CVD
70
Q

How do we treat and acute attack of gout?

A
  • RICE
  • NSAIDs or Colchicine
  • IM or oral steroids
71
Q

How is chronic gout treated?

A

Lifestyle changes:

  • Lose weight
  • Regular exercise
  • Purine rich foods
  • Reduce alcohol consumption
  • Increase fluid intake

Pharmacology (ULT if >1 attack in a year)

- Allopurinol or Febuxostat

- Cover allopurinol with NSAID as can cause acute attack

  • Can use benzbromarone and sulfinpyrazone as renal excretion of uric acid but more side effects
72
Q

What is pseudogout?

A

Deposition of calcium pyrophosphate crystals in a joint causing inflammatory arthritis. Usually in knees or wrist

73
Q

What are some risk factors of pseudogout?

A
  • Old age
  • OA
  • Hyperparathyroidism
  • Haemochromotosis
74
Q

What are some investigations for pseudogout and what do they show?

A

- X-ray: calcium deposition (chondrocalcinosis)

- Synovial fluid analysis: positively birefringent rhomboid shaped crystals

75
Q

How is pseudogout treated?

A

Acute: RICE, NSAIDs, intraarticular steroid injections

Prevention: possible colchicine

76
Q

What is the pathophysiology of rheumatoid arthritis?

A

Autoimmune disease causing symmetrical polyarthritis and increased CVD risk

Antibodies to Fc portion of IgG RF and anti-CCP. Made due to cirullination of self antigens that are then recognised by B and T cells so produce antibodies RF and anti-CCP.

Stimulated macrophages release TNFa and stimulate osteoclast differentiation so bone damage. Inflammatory cascade leads to proliferation of synviocytes that grow over cartilage and restrict nutrients to cartilage

77
Q

What is the typical history of RA?

A
  • Woman aged 30-50
  • Progressive symmetrical polyarthritis
  • Affects MCPs, PIPs, MTPs and spares DIPJs
  • Can affect hips, knees, shoulders, C-spine
  • >6 weeks
  • Morning stiffness >30 minutes
  • Malaise
  • Low grade fever
78
Q

What signs can you see on examination with RA?

A

- Early: soft tissue swelling and tenderness

- Hands: ulnar deviation and subluxation of fingers, swan-neck and Boutonniere deformity, Z-deformity of thumbs

- Rheumatoid nodules: elbow

- Median nerve: may be compressed at carpal tunnel

79
Q

What are some extra-articular manifestations of ra?

A

- Fatigue, fever weight loss

- Nodules: elbows, lung, cardiac, lymphadenopathy

- Lungs: pleural disease, intersitial fibrosis

- Cardiac: IHD, pericarditis

  • Osteoporosis
  • Carpal tunnel syndrome
  • Frozen shoulder
  • De Quervian’s tenosynovitis
80
Q

What is a pneumonic to remember the extra-articular manifestations of RA?

A
  • 3 Cs
  • 3 As
  • 3 Ps
  • 3 Ss
81
Q

What are some investigations you should do if you suspect RA?

A

- FBC: anaemia of chronic disease

- RF and Anti-CCP: positive, high titres associated with severer disease and extra-articular manifestations

- Inflammatory markers: raised

- Xray: see image

- USS/MRI: early disease has greater sensitivity for synovitis

- HRCT: if lung disease

82
Q

What is the criteria for diagnosing RA?

A

EULAR

  • Joint involvement
  • Serology
  • Acute phase reactants
  • Duration of symptoms
83
Q

What is the management for RA?

A

Non-Pharmacological: OT, physio, psychotherapist

Pharmacological:

1st line us Methotrexate monotherapy helps improve long term outcomes.

- Consider combination with HCQ, leflunomide, sulfasalazine

  • If disease still severe after combination DMARDs consider biologics (TNF-a inhibitors)

- Steroids for acute flares

- NSAIDs or symptoms relief with PPI cover

84
Q

How should you start DMARDs for RA?

A
  • Give methotrexate weekly with folic acid
  • Give steroid cover for first 3 months
85
Q

What tool can you use to measure if RA is improving or getting worse?

A

DAS28 helps to tell you the disease activity

Looks at how many swollen joints, how many tender joints, inflammatory markers and patient as a whole

86
Q

If a patient is complaining of swelling in the small joints of the hand but you cannot see or palpate this on examination, what investigation should you order?

A

US to look for synovitis. MRI also

87
Q

A DEXA scan produces a T-Score. Although this can determine bone mass, it cannot predict the risk of fractures. What can be used to predict the risk of fractures?

A

FRAX tool can calculate 10 year risk of hip fracture and osteoporotic fracture

88
Q

What is the definition of an osteoporotic/fragility/low trauma fracture?

A

Fracture as a result of a fall from standing height or less, at walking speed or less

89
Q

What test is needed next?

A

URINE DIPSTICK

90
Q

What might a temportal artery biopsy show in GCA?

A
  • Granulomas
  • Necrotizing arteritis
  • Skip lesions
91
Q

What is seen on muscle biopsy with polymyositis and dermatomyositis?

A
92
Q

What is the most common side effect of methotrexate and alendronic acid?

A

Methotrexate: nausea

Alendronic acid: indigestion/epigastric pain

93
Q

What is the inheritance pattern of HLA-B27 gene?

A

Autosomal dominant

94
Q

What are some of the complications of ankylosing spondylitis?

A
  • Increased risk of CVD
  • Osteoporosis
  • IBS
  • Anterior uveitis