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Rheumatology Flashcards

1
Q

Vitamin D supplementation groups?

A
  1. All pregnant and breastfeeding women
  2. All children 6m - 5 y/o (babies formula milk >500ml dont need)
  3. Adults > 65 y/o
  4. People not exposed to much sun
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2
Q

Indications for testing Vitamin D?

A
  1. Bone disease e.g. osteomalacia/Paget’s
  2. Bone disease prior to specific treatment
  3. MSK problems possibly attributed to Vitamin D deficiency
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3
Q

Methotrexate MOA?

A

Antimetabolite that inhibitrs dihydrofolate reductase

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4
Q

Methotrexate indications?

A
  1. Inflammatory arthritis esp. RhA
  2. Psoriasis
  3. Some chemo e.g. ALL
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5
Q

Methotrexate adverse effects?

A
  1. Mucositis, myelosuppression
  2. Pneumonitis, pulmonary fibrosis
  3. Liver fibrosis
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6
Q

Methotrexate and pregnancy?

A
  1. Avoid pregnancy for 6m after treatment stopped
  2. Men need effective contraception for 6m after treatment
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7
Q

Methotrexate monitoring?

A

FBC, U&E, LFT before treatment, weekly until therapy stabilised, and then every 2-3 months

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8
Q

What needs to be coprescribed with methotrexate?

A

Folic acid 5mg OW, taken more than 24 hours after methotrexate dose

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9
Q

Methotrexate starting dose?

A

7.5mg OW

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10
Q

Methotrexate interactions?

A
  1. Trimethoprim/co-trimoxazole (increases risk of marrow aplasia)
  2. High dose aspirin increases risk of methotrexate toxicity secondary to reduced excretion
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11
Q

Methotrexate toxicity Rx?

A

Folinic acid

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12
Q

Lateral epicondylitis mushkies?

A
  1. Tennis elbow
  2. Most common 45-55 y/o, typically affects dominant arm
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13
Q

Lateral epicondylitis features?

A
  1. Pain and tenderness localised to the lateral epicondyle
  2. Pain worse on wrist extension against resistance with the elbow extended or supination of the forearm with the elbow extended
  3. Episodes typically last b/w 6m and 2y, pts tend to have acute pain for 6-12 weeks
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14
Q

Lateral epicondylitis Rx?

A
  1. Advice on avoiding muscle overload
  2. Simple analgesia
  3. Steroid injection
  4. Physiotherapy
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15
Q

Radial tunnel syndrome?

A
  1. Presents similarly to lateral epicondylitis however pain is typically distal to the epicondyle and worse on elbow extension/forearm pronation
  2. Common in gymnasts, racquet players and golfers who frequently hyperextend at the wrist or carry out frequent supination/pronation
  3. Pts can also complain of hand paraesthesia or acheing at the wrist
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16
Q

Cubital tunnel syndrome?

A

Tingling and numbness in the 4th and 5th finger

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17
Q

Temporal arteritis definition?

A

Large vessel vasculitis which overlaps with PMR, histology shows skip lesions

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18
Q

Temporal arteritis features?

A
  1. > 60 y/o
  2. Rapid onset (<1m)
  3. Headache
  4. Jaw claudication
  5. Tender, palpable temporal artery
  6. Vision testing is key Ix in all pts
  7. 50% have features of PMR
  8. Also constitutional symptoms
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19
Q

Vision testing in temporal arteritis?

A
  1. Anterior ischemic optic neuropathy accounts for the majority of ocular complications. It results from occlusion of the posterior ciliary artery (a branch of the ophthalmic artery) → ischaemia of the optic nerve head. Fundoscopy typically shows a swollen pale disc and blurred margins
  2. May result in temporary visual loss - amaurosis fugax
  3. Permanent visual loss is the most feared complication of temporal arteritis and may develop suddenly
  4. Diplopia may also result from the involvement of any part of the oculomotor system (e.g. cranial nerves)
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20
Q

Temporal arteritis Ix?

A
  1. Raised inflammatory markers (ESR > 50mm/hr, note ESR < 30 in 10% pts, CRP may be elevated)
  2. Temporal artery biopsy = skip lesions may be present
  3. Note CK and EMG normal
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21
Q

Temporal arteritis Rx?

A
  1. Urgent high dose glucocorticoids (if no visual loss high dose prednisolone, if visual loss IV methylprednisolone given prior to starting high-dose prednisolone)
  2. Urgent ophthalmology review
  3. Other = bone protection with bisphosphonates long term due to tapering steroid course, low dose aspirin also sometimes given
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22
Q

Anterior interosseous syndrome?

A

Caused by damage to the anterior interosseous nerve, a branch of the median nerve. It usually presents with pain in the forearm and weakness of flexion of the index finger and the distal phalanx of the thumb

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23
Q

Ankylosing spondylitis definition?

A

HLA-B27 associated spondylarthropathy, typically presents in males (3:1) aged 20-30 years old

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24
Q

Ankylosing spondylitis Ix?

A
  1. Raised ESR and CRP, normal levels don’t exclude Dx
  2. HLA B27 +ve in 90% AS, 10% normal patients (not that useful)
  3. Plain XR of sacroilial joints is most useful Ix in establishing Dx
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25
Q

Ankylosing spondylitis on XR?

A
  1. Sacroiliitis = subchondral erosions, sclerosis
  2. Squaring of lumbar vertebra
  3. Bamboo spine (late and uncommon)
  4. Syndesmophytes = due to ossification of outer fibres of annulus fibrosus
  5. CXR = apical fibrosis
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26
Q

If XR is -ve for sacroiliac joint involvement but AS suspicion remains high?

A

MRI

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27
Q

Ankylosing spondylitis spirometry?

A

May show restrictive defect due to combination of pulmonary fibrosis, kyphosis and AS of costovertebral joints

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28
Q

Ankylosing spondylitis Rx?

A
  1. Regular exercise e.g. swimming
  2. NSAIDs first line
  3. Physiotherapy
  4. DMARDs e.g. sulfasalazine only useful if peripheral joint involvement
  5. Anti-TNF if persistently high disease activity despite conventional treatments
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29
Q

CKD causes which type of hyperparathyroidism?

A

Secondary

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30
Q

Paget’s disease definition?

A

A disease of increased but uncontrolled bone turnover. It is thought to be primarily a disorder of osteoclasts, with excessive osteoclastic resorption followed by increased osteoblastic activity. Paget’s disease is common (UK prevalence 5%) but symptomatic in only 1 in 20 patients. The skull, spine/pelvis, and long bones of the lower extremities are most commonly affected.

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31
Q

Paget’s features?

A

Only 5% symptomatic
1. Older male with bone pain and isolated raised ALP
2. Bone pain = pelvis, lumbar, spine, femur
3. Classical untreated = bowing of tibia, bossing of skull

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32
Q

Paget’s Ix?

A
  1. Bloods = Raised ALP
  2. Bone turnover markers = PINP, CTx, NTx, urinary hydroxyproline
  3. XR = osteolysis in early disease –> mixed lytic/sclerotic lesions later
  4. Skull XR = thickened vault. osteoporosis circumscripta
  5. Bone scintigraphy = increased uptake seen focally at sites of active bone lesions
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33
Q

Paget’s indications for treatment?

A
  1. Bone pain
  2. Skull or long bone deformity
  3. Fracture
  4. Periarticular Paget’s
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34
Q

Paget’s Rx?

A
  1. Bisphosphonate (either oral risedronate or IV zoledronate)
  2. Calcitonin used less commonly now
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35
Q

Paget’s complications?

A
  1. Deafness (cranial nerve entrapment)
  2. Bone sarcoma (1% if affected for >10 years)
  3. Fractures
  4. Skull thickening
  5. High output cardiac failure
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36
Q

PMR features?

A
  1. > 60 y/o
  2. Rapid onset <1m
  3. Aching, morning stiffness in proximal limb muscles (weakness is not considered a symptoms of PMR)
  4. Constitutional
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37
Q

PMR Ix?

A
  1. Raised inflammatory markers e.g. ESR > 40 mm/hr
  2. CK and EMG normal
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38
Q

PMR Rx?

A

Prednisolone e.g. 15mg OD –> typically respond dramatically to steroids, failure to do so should prompt consideration of an alternative diagnosis

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39
Q

Most common cardiac manifestation of SLE?

A

Pericarditis

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40
Q

Most common glomerulonephritis in SLE?

A

Diffuse proliferative glomerulonephritis

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41
Q

Low calcium, low phosphate, raised ALP?

A

Osteomalacia

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42
Q

Bone pain, tenderness and proximal myopathy?

A

Osteoamalacia

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43
Q

Osteomalacia definition?

A

Softening of the bones secondary to low vitamin D levels that in turn lead to decreased bone mineral content

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44
Q

Osteomalacia causes?

A
  1. Vitamin D deficiency = malabsorption, lack of sunlight, diet
  2. CKD
  3. Drugs e.g. anticonvulsants
  4. Inherited e.g. hypophosphataemic rickets
  5. Liver disease e.g. cirrhosis
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45
Q

Osteomalacia features?

A
  1. Bone pain
  2. Bone/muscle tenderness
  3. Fractures = especially femoral neck
  4. Proximal myopathy = may lead to waddling gait
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46
Q

Osteomalacia Ix?

A
  1. Bloods = Low Vit D, low calcium, low phosphate, raised ALP
  2. XR = translucent bands (Looser’s zones or pseudofractures)
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47
Q

Osteomalacia Rx?

A
  1. Vitamin D supplementation (loading dose often needed initially)
  2. Calcium supplementation if dietary calcium inadequate
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48
Q

Gell and Coombs classification?

A
  1. Type I = Anaphylactic
  2. Type II = Cell bound
  3. Type III = Immune complex
  4. Type IV = Delayed hypersensitivity
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49
Q

Type I Reaction mushkies?

A
  1. Anaphylactic reaction
  2. Antigen reacts with IgE bound to mast cells
  3. E.g. anaphylaxis, atopy
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50
Q

Type II Reaction mushkies?

A
  1. Cell bound
  2. IgG or IgM binds to antigen on cell surface
  3. E.g. AIHA, ITP, Goodpasture’s, RhF, Pemphigus
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51
Q

Type III reaction mushkies?

A
  1. Immune complex mediated
  2. Free antigen and antibody (IgG, IgA) combine
  3. E.g. serum sickness, SLE, Post-streptococcal glomerulonephritis, Acute EAA
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52
Q

Type IV reaction mushkies?

A
  1. Delayed hypersensitivity
  2. T-cell mediated
  3. TB, GVHD, Allergic contact dermatitis, scabies, Chronic EAA, MS, GBS
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53
Q

Type V reaction mushkies?

A
  1. Antibodies that recognise and bind to cell surface receptors
  2. E.g. Graves’ disease, Myasthenia Gravis
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54
Q

Gout definition?

A

A form of microcrystal synovitis caused by the deposition of monosodium urate monohydrate in the synovium. It is caused by chronic hyperuricaemia (uric acid > 450 µmol/l)

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55
Q

Gout acute management?

A
  1. NSAIDs or Colchicine first line
  2. Maximum dose NSAIDs until 1-2 days after symptoms have settled
  3. Oral steroids if NSAIDs or colchicine C/I, usually 15mg/d
  4. Intra-articular steroid injection
  5. If already on allopurinol, should be continued
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56
Q

Indications for urate-lowering therapy?

A
  1. To all patients after their first attack of gout
  2. Particularly recommended if: >=2 attacks in 12 months, tophi, renal disease, uric acid renal stones, prophylaxis if on cytotoxics or diuretics
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57
Q

Urate lowering therapy mushkies?

A
  1. Allopurinol first line
  2. Commencement of ULT is best delayed until inflammation has settled as ULT is better discussed when the patient is not in pain
  3. Initial 100mg OD, titrated every few weeks for serum uric acid of <300, lower initial doses used if pt has reduced eGFR
  4. Colchicine cover should be considered when starting allopurinol, NSAIDs can be used if cannot be tolerated
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58
Q

Second line ULT?

A

Febuxostat

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59
Q

Refractory gout cases ULT?

A
  1. Uricase
  2. Pegloticase can achieve rapid control of hyperuricaemia, given as infusion once every 2 weeks
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60
Q

Gout further management?

A
  1. Stop precipitating drugs e.g. thiazides
  2. Losartan has specific uricosuric action and may be particularly suitable for the many patients who have coexistent hypertension
  3. Increased vitamin C intake (either supplements or through normal diet) may also decrease serum uric acid levels
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61
Q

Bisphosphonate MOA?

A

Pyrophosphate analogue, a molecule which decreases demineralisation in bone. They inhibit osteoclasts by reducing recruitment and promoting apoptosis.

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62
Q

Bisphosphonate uses?

A
  1. Prevention and treatment of osteoporosis
  2. Hypercalcaemia
  3. Paget’s disease
  4. Pain from bone metastases
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63
Q

Bisphosphonates adverse effects?

A
  1. Oesophageal reaction = oesophagitis, ulcers (especially alendronate)
  2. Osteonecrosis of the jaw
  3. Increased risk of atypical stress fractures of the proximal femoral shaft in pts taking alendronate
  4. Acute phase response = fever, myalgia and arthralgia may occur following administration
  5. Hypocalcaemia due to reduced calcium efflux from bone, usually clinically unimportant
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64
Q

Oral bisphosphonate counselling?

A

Tablets should be swallowed whole with plenty of water while sitting or standing; to be given on an empty stomach at least 30 minutes before breakfast (or another oral medication); patient should stand or sit upright for at least 30 minutes after taking tablet

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65
Q

What needs to be corrected before giving bisphosphonates?

A

Hypocalcaemia/Vitamin D deficiency

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66
Q

When should you stop bisphosphonates at 5 years?

A
  1. < 75 y/o
  2. Femoral neck T score of >-2.5
  3. Low risk according to FRAX/NOGG§
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67
Q

Psoriatic arthritis mushkies?

A

An inflammatory arthritis associated with psoriasis and is classed as one of the seronegative spondyloarthropathies. It correlates poorly with cutaneous psoriasis and often precedes the development of skin lesions. Around 10-20% of patients with skin lesions develop an arthropathy with males and females being equally affected

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68
Q

Psoriatic arthritis patterns?

A
  1. Symmetrical polyarthritis = 30-40%, most common, similar to RhA
  2. Asymmetrical oligoarthritis = 20-30%, typically affects hands and feet
  3. Sacroiliitis
  4. DIP joint disease (10%)
  5. Arthritis mutilans (severe deformity fingers/hand, ‘telescoping fingers’)
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69
Q

Psoriatic arthritis other signs?

A
  1. Psoriatic skin lesions
  2. Periarticular disease = tenosynovitis and soft tissue inflammation resulting in enthesitis, tenosynovitis, dactylitis
  3. Nail changes = pitting, onycholysis
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70
Q

Psoriatic arthritis Ix?

A
  1. XR = often have the unusual coexistence of erosive changes and new bone formation, periostitis, ‘pencil-in-cup’ appearance
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71
Q

Psoriatic arthritis Rx?

A

Should be managed by rheumatologist, similar to Rx of RhA, however following differences are noted:
1. Mild peripheral arthritis/mild axial disease may be treated with ‘just’ an NSAID, rather than all patients being on disease-modifying therapy as with RA
2. Use of monoclonal antibodies such as ustekinumab (targets both IL-12 and IL-23) and secukinumab (targets IL-17)
3. Has a better prognosis than RA

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72
Q

Predominantly DIP disease?

A

Psoriatic arthritis

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73
Q

Predominantly MCP/PIP disease?

A

RhA

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74
Q

Antiphospholipid syndrome?

A

An acquired disorder characterised by a predisposition to both venous and arterial thromboses, recurrent fetal loss and thrombocytopenia. It may occur as a primary disorder or secondary to other conditions, most commonly systemic lupus erythematosus (SLE)

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75
Q

Antiphospholipid syndrome APTT effect?

A

Causes a pradoxical rise, due to ex-vivo reaction of lupus anticoagulant autoantibodies with phospholipids involved in the coagulation cascade

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76
Q

Antiphospholipid syndrome features?

A
  1. Venous/arterial thrombosis
  2. Recurrent foetal loss
  3. Livedo reticularis
  4. Thrombocytopenia
  5. Prolonged APTT
  6. Other features = pre-eclampsia, pulmonary HTN
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77
Q

Antiphospholipid syndrome Rx?

A
  1. Primary thromboprophylaxis = low dose aspirin
  2. Secondary thromboprophylaxis = initial VTE (lifelong warfarin with INR 2-3), recurrent VTE (target INR 3-4, if happened while on warfarin then add aspirin), arterial thrombosis (lifelong warfarin INR 2-3)
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78
Q

Hip Osteoarthritis features?

A
  1. Pain exacerbated by exercise and relieved by rest
  2. Reduction in internal rotation is often the first sign
  3. Age, obesity and previous joint problems are risk factors
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79
Q

Hip Inflammatory arthritis features?

A
  1. Pain in the morning
  2. Systemic features
  3. Raised inflammatory markers
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80
Q

Referred lumbar spine pain to the hip featurs?

A

Femoral nerve compression may cause referred pain in the hip
Femoral nerve stretch test may be positive - lie the patient prone. Extend the hip joint with a straight leg then bend the knee. This stretches the femoral nerve and will cause pain if it is trapped

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81
Q

Greater trochanteric pain syndrome (Trochanteric bursitis) features?

A

Due to repeated movement of the fibroelastic iliotibial band
Pain and tenderness over the lateral side of thigh
Most common in women aged 50-70 years

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82
Q

Meralgia paraesthetica features?

A

Caused by compression of lateral cutaneous nerve of thigh
Typically burning sensation over antero-lateral aspect of thigh

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83
Q

Avascular necrosis of the hip features?

A

Symptoms may be of gradual or sudden onset
May follow high dose steroid therapy or previous hip fracture of dislocation

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84
Q

Pubic symphysis dysfunction features?

A

Common in pregnancy
Ligament laxity increases in response to hormonal changes of pregnancy
Pain over the pubic symphysis with radiation to the groins and the medial aspects of the thighs. A waddling gait may be seen

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85
Q

Transient idiopathic osteoporosis features?

A

An uncommon condition sometimes seen in the third trimester of pregnancy
Groin pain associated with a limited range of movement in the hip
Patients may be unable to weight bear
ESR may be elevated

How well did you know this?
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86
Q

Hydroxychloroquine uses?

A

RhA and SLE

87
Q

Hydroxychloroquine adverse effects?

A

Bull’s eye retinopathy = may result in severe and permanent visual loss –> baseline ophthalmological examination and annual screening

88
Q

Can HCQ be used in pregnant women?

89
Q

Allergic contact dermatitis reaction type?

A

Type IV hypersensitivity reaction

90
Q

Most important osteoporosis risk factors?

A
  1. Advancing age, female (2% at 50 years to 25% at 80 years in women)
  2. Steroid use, RhA, alcohol excess, history of parental hip fracture, low BMI, current smoking
91
Q

Medications that may worsen osteoporosis?

A
  1. SSRIs
  2. Antiepileptics
  3. PPIs
  4. Glitazones
  5. Long term heparin therapy
  6. Aromatase inhibitors e.g. anastrozole
92
Q

Is obesity associated with osteoporosis?

93
Q

Bisphosphonate renal contraindication?

A

If eGFR <35ml/min

94
Q

Secondary prevention of osteoporotic fractures in postmenopausal women?

A
  1. Vitamin D and calcium D supplementation
  2. Alendronate first line
  3. If cannot tolerate alendronate, Risedronate/Etomidate
  4. If cannot tolerate bisphosphonates, strontium ranelate/raloxifene
95
Q

Ibandronate?

A

Once-monthly oral bisphosphonate

96
Q

Raloxifene mushkies?

A

SERM
1. Prevents bone loss and reduce risk of vertebral fractures, not shown to reduce risk of non-vertebral fractues
2. Increases bone density in the spine and proximal femur
3. May worsen menopausal symptoms
4. Increased VTE risk
5. May decrease risk of breast cancer

97
Q

Strontium ranelate mushkies?

A
  1. Dual action bone agent = increases deposition of new bone by osteoblasts (promotes differentiation of pre-osteoblast to osteoblast) and reduces the resorption of bone by inhibiting osteoclasts
  2. Only used if no other options for osteoporosis
  3. Increased risk of cardiovascular events (CVS disease a contraindication)
  4. Increased VTE risk
  5. Can cause Stevens-Johnson syndrome
98
Q

Denosumab mushkies?

A
  1. Human mAb that inhibits RANK ligand, which in turn inhibits maturation of osteoclasts
  2. Given as single subcutaneous injection every 6m
  3. Initial trial data suggests that it is effective and well tolerated
99
Q

Teriparatide mushkies?

A
  1. Recombinant form of parathyroid hormone
  2. Very effective at increasing bone mineral density but role in the management of osteoporosis yet to be clearly defined
100
Q

HRT for osteoporosis?

A
  1. Has been shown to reduce the incidence of vertebral and non-vertebral fractures
  2. Due to concerns about increased rates of cardiovascular disease and breast cancer it is no longer recommended for primary or secondary prevention of osteoporosis unless the woman is suffering from vasomotor symptoms
101
Q

Rheumatoid arthritis poor prognostic features?

A
  1. RhF +ve
  2. Anti-CCP Abs
  3. Poor functional status at presentation
  4. X-ray: early erosions (e.g. after < 2 years)
  5. Extra-articular features e.g. nodules
  6. HLA DR4
  7. Insidious onset
  8. Female
102
Q

3 benign bone tumours?

A
  1. Osteoma
  2. Osteochondroma (Exostosis)
  3. Giant cell tumour
103
Q

Osteoma mushkies?

A
  1. Benign overgrowth of bone, most typically on skull
  2. Associated with Gardner’s syndrome
104
Q

Osteochondroma mushkies?

A
  1. Most common benign bone tumour
  2. More in males, usually diagnosed <20 y/o
  3. Cartilage-capped bony projection on external surface of a bone
105
Q

Most common benign bone tumour?

A

Osteochondroma

106
Q

Giant cell tumour mushkies?

A
  1. Tumour of multinucleated giant cells within a fibrous stroma
  2. Peak incidence: 20-40 years
  3. Occurs most frequently in the epiphyses of long bones
  4. X-ray shows ‘double bubble’ or ‘soap bubble’ appearance
107
Q

3 malignant tumours of bone?

A
  1. Osteosarcoma
  2. Ewing’s sarcoma
  3. Chondrosarcoma
108
Q

Most common primary malignant bone tumour?

A

Osteosarcoma

109
Q

Sunburst pattern?

A

Osteosarcoma

110
Q

Osteosarcoma mushkies?

A
  1. Most common primary malignant bone tumour
  2. Seen mainly in children and adolescents
  3. Occurs most frequently in the metaphyseal region of long bones prior to epiphyseal closure, with 40% occuring in the femur, 20% in the tibia, and 10% in the humerus
  4. XR = Codman triangle (from periosteal elevation) and ‘sunburst’ pattern
  5. Mutation of Rb gene significantly increases risk of osteosarcoma (hence association with retinoblastoma)
  6. Other predisposing factors include Paget’s disease of the bone and radiotherapy
111
Q

Ewing’s sarcoma mushkies?

A
  1. Small round blue cell tumour
  2. Seen mainly in children and adolescents
  3. Occurs most frequently in the pelvis and long bones, tends to cause severe pain
  4. Associated with t(11;22) translocation which results in an EWS-FLI1 gene product
  5. X-ray shows ‘onion skin’ appearance
112
Q

Chondrosarcoma mushkies?

A
  1. Malignant tumour of cartilage
  2. Most commonly affects the axial skeleton
  3. More common in middle age
113
Q

Food high in purines that cause gout?

A

Liver, kidneys, seafood, oily fish, yeast products

114
Q

Osteoarthritis clinical diagnosis without investigations if?

A
  1. Pt >45 y/o
  2. Has exercise related pain
  3. No morning stiffness or morning stiffness lasting >30 mins
115
Q

Heberden’s nodes?

116
Q

Bouchard’s nodes?

117
Q

Methotrexate s/e?

A
  1. Myelosuppression
  2. Liver cirrhosis
  3. Pneumonitis
118
Q

Sulfasalazine s/e?

A
  1. Rashes (SJS)
  2. Oligospermia
  3. Heinz body anaemia, megaloblastic anaemia, myelosuppression
  4. Interstitial lung disease
  5. May colour tears –> stained contact lenses
119
Q

Leflunomide s/e?

A
  1. Liver impairment
  2. Interstitial lung disease
  3. HTN
120
Q

HCQ s/e?

A
  1. Retinopathy
  2. Corneal deposits
121
Q

Gold s/e?

A

Proteinuria

122
Q

Penicillamine s/e?

A
  1. Proteinuria
  2. Exacerbation of Myasthenia Gravis
123
Q

Etanercept s/e?

A
  1. Demyelination
  2. Reactivation of TB
124
Q

Infiliximab, Adalimumab s/e?

A

Reactivation of TB

125
Q

Rituximab s/e?

A

Infusion reactions are common

126
Q

Osteoarthritis X-ray changes?

A
  1. Loss of joint space
  2. Osteophytes forming at joint margins
  3. Subchondral sclerosis
  4. Subchondral cysts
127
Q

Ankylosing spondylitis night pain?

A

Yes, improves on getting up

128
Q

Ankylosing spondylitis clinical examination?

A
  1. Reduced lateral flexion
  2. Reduced forward flexion (Schober’s test) = a line is drawn 10 cm above and 5 cm below the back dimples (dimples of Venus). The distance between the two lines should increase by more than 5 cm when the patient bends as far forward as possible
  3. Reduced chest expansion
129
Q

Ankylosing spondylitis ‘other’ features?

A

8 A’s
1. Apical fibrosis
2. Anterior uveitis
3. Aortic regurgitation
4. Achilles tendonitis
5. AVN block
6. Amyloidosis
7. Arthritis (peripheral, 25%, more common in females)
8. And Cauda Equida Syndrome

130
Q

RhA drug oligospermia?

A

Sulfasalazine

131
Q

Prednisolone eye effect?

132
Q

Raynaud’s phenomenon?

A

Exaggerated vasoconstrictive response of the digital arteries and cutaneous arteriole to the cold or emotional stress. It may be primary (Raynaud’s disease) or secondary (Raynaud’s phenomenon)

133
Q

Secondary causes of Raynaud’s phenomenon?

A
  1. CTD = Scleroderma (most common), RhA, SLE
  2. Leukaemia
  3. Type I Cryoglobulinamia, cold agglutinins
  4. Use of vibrating tools
  5. Drugs: OCP, Ergot
  6. Cervical rib
134
Q

Factors suggesting underlying CTD in Raynauds?

A
  1. > 40 y/o
  2. Unilateral symptoms
  3. Rashes
  4. Autoantibodies
  5. Digital ulcers, calcinosis
  6. Very rarely: chillblains
135
Q

Raynaud’s management?

A
  1. All pts with suspected secondary Raynaud’s phenomenon should be referred to secondary care
  2. 1st line = CCB e.g. nifedipine
  3. IV Prostacyclin (epoprostenol) infusions: effects may last several weeks/months
136
Q

Osteoarthritis management?

A
  1. Conservative
  2. 1st line = Paracetamol and topical NSAIDs (topical indicated for OA of knee or hand)
  3. 2nd line = Oral NSAIDs/COX-2 inhibitors, opioids, capsaicin cream and intra-articular corticosteroids (PPI with NSAID and COX-2, avoid these drugs if also taking aspirin)
  4. Non-pharm = Supports and braces, TENS, shock-absorbing insoles or shoes
  5. If conservative methods fail then refer for consideration of joint replacement
137
Q

Pseudogout definition?

A

A form of microcrystal synovitis caused by the deposition of calcium pyrophosphate dihydrate crystals in the synovium

138
Q

Pseudogout risk factors?

A
  1. Strongly associated with increasing age
  2. If <60 y/o usually have some underlying risk factor e.g. haemochromatosis, hyperparathyroidism, low magnesium, low phosphate, acromegaly, Wilson’s disease
139
Q

Pseudogout features?

A
  1. Knee, wrist and shoulders most commonly affected
  2. Joint aspiration = weakly positively birefringent rhomboid shaped crystals
  3. XR = linear calcifications of the meniscus and articular cartilage
140
Q

Pseudogout management?

A
  1. Aspiration of joint fluid to exclude septic arthritis
  2. NSAIDs or intra-articular, intra-muscular or oral steroids as for gout
141
Q

When does risk of osteoporosis increase with steroids?

A

If patient taking equivalent of prednisolone 7.5mg a day for 3 or more months

142
Q

Management of patients at risk of corticosteroid-induced osteoporosis?

A
  1. > 65 y/o OR those with previous fragility fracture should be offered bone protection
  2. < 65 y/o should be offered a bone density scan, with further management dependent on score –> (>0 = reassure, 0 - -1.5 = repeat bone density scan in 1-3 years, < -1.5 = offer bone protection)
143
Q

RhA drug causing demyelination?

A

Etanercept

144
Q

Sjogren’s syndrome?

A

An autoimmune disorder affecting exocrine glands resulting in dry mucosal surfaces. It may be primary (PSS) or secondary to rheumatoid arthritis or other connective tissue disorders, where it usually develops around 10 years after the initial onset. Sjogren’s syndrome is much more common in females (ratio 9:1). There is a marked increased risk of lymphoid malignancy (40-60 fold).

145
Q

Sjogren’s syndrome features?

A
  1. Dry eyes = keratoconjunctivitis sicca
  2. Dry mouth
  3. Vaginal dryness
  4. Arthralgia
  5. Raynaud’s, myalgia
  6. Sensory polyneuropathy
  7. Parotitis
  8. Renal tubular acidosis (usually subclinical)
146
Q

Sjogren’s syndrome Ix?

A
  1. RhF +ve in 50%
  2. ANA +ve in 70%
  3. Anti-Ro (SSA) in 70% with PSS
  4. Anti-La (SSB) in 40% with PSS
  5. Schirmer’s test = filter paper near conjunctival sac to measure tear formation
  6. Histology = focal lymphocytic infiltration
  7. Also: Hypergammaglobulinaemia, low C4
147
Q

Sjogren’s syndrome Rx?

A
  1. Artificial saliva and tears
  2. Pilocarpine may stimulate saliva production
148
Q

Reactive arthritis?

A

One of the HLA-B27 associated seronegative spondyloarthropathies. It encompasses what was formerly called Reiter’s syndrome (Nazi), a term which described a classic triad of urethritis, conjunctivitis and arthritis following a dysenteric illness during the Second World War. Later studies identified patients who developed symptoms following a sexually transmitted infection (post-STI, now sometimes referred to as sexually acquired reactive arthritis, SARA)

149
Q

Reactive arthritis definition?

A

An arthritis that develops following an infection where the organism cannot be recovered from the joint

150
Q

Reactive arthritis features?

A
  1. Typically develops within 4w of initial infection
  2. Arthritis is typically an asymmetrical oligoarthritis of lower limbs
  3. Dactylitis
  4. Urethritis
  5. Eye = conjunctivitis, anterior uveitis
  6. Skin = circinate balanitis, keratoderma blenorrhagicum
151
Q

Is azathioprine safe to use in pregnancy?

152
Q

Azathioprine mushkies?

A

Metabolised to the active compound mercaptopurine, a purine analogue that inhibits purine synthesis. A thiopurine methyltransferase (TPMT) test may be needed to look for individuals prone to azathioprine toxicity.

153
Q

Azathioprine major interaction?

A

Allopurinol

154
Q

Azathioprine adverse effects?

A
  1. Bone marrow depression
  2. N&V
  3. Pancreatitis
  4. Increased risk of non-melanoma skin cancer
155
Q

Paget’s disease definitive treatment?

A

Bisphosphonate (either oral risedronate or IV zoledronate)

156
Q

Bowing of tibia, bossing of skull?

A

Paget’s disease

157
Q

When are topical NSAIDs indicated for osteoarthritis?

A

OA of knee or hand

158
Q

Dermatomyositis mushkies?

A
  1. Inflammatory disorder causing symmetrical, proximal muscle weakness and characteristic skin lesions
  2. May be idiopathic or associated with connective tissue disorders or underlying malignancy (typically ovarian, breast and lung cancer, found in 20-25% - more if patient older). Screening for an underlying malignancy is usually performed following a diagnosis of dermatomyositis
  3. Polymyositis is a variant of the disease where skin manifestations are not prominent
159
Q

Dermatomyositis skin features?

A
  1. Photosensitive
  2. Macular rash over back and shoulder
  3. Heliotrope rash in periorbital region
  4. Gottron’s papules = roughened red papules over extensor surfaces of fingers
  5. ‘Mechanic’s hands’ = extremely dry and scaly hands with linear ‘cracks’ on the palmar and lateral aspects of the fingers
  6. Nail fold capillary dilatation
160
Q

Dermatomyositis ‘other’ features?

A
  1. Proximal muscle weakness +/- tenderness
  2. Raynaud’s
  3. Respiratory muscle weakness
  4. Interstitial lung disease e.g. Fibrosing alveolitis or organising pneumonia
  5. Dysphagia, dysphonia
161
Q

Dermatomyositis Ix?

A
  1. Majority of pts (80%) are ANA positive
  2. 30% have Abs to anti-synthetase Abs incl. anti-Jo1, anti Mi2, anti-SRP
162
Q

Anterior groin pain in active young adult?

A

Femoroacetabular impingement

163
Q

Femoracetabular impingement (FAI) mushkies?

A

One of the most common causes of persistent hip pain in active young adults. It commonly presents with hip/groin pain worse on prolonged sitting and associated with snapping, clicking or locking of the hip. There is an association between FAI and prior hip pathology eg Perthes in childhood. It is caused by a variant in hip anatomy leading to abnormal contact between the femur and acetabulum rim. Over time this can lead to soft tissue damage including labral tears

164
Q

Snapping hip syndrome?

A

Patients experience a snapping or clunking as tendons e.g the iliotibial band, move over the hip bones during flexion and extension. The snapping sound occurs either due to subluxation of a tendon or catching of a thickened tendon on the greater trochanter. In most cases, this is painless unless there is associated labral tear

165
Q

What needs to be checked before AZA treatment?

A

Thiopurine methyltransferase is the enzyme required to metabolism azathioprine, a small proportion of the population had reduced activity or deficiency of this enzyme putting them at risk of azathioprine toxicity. Accordingly. levels should be tested prior to commencing the drug with cautious dosing or an alternate therapy used if TPMT is found

166
Q

Marfan’s syndrome mushkies?

A

An autosomal dominant connective tissue disorder. It is caused by a defect in the FBN1 gene on chromosome 15 that codes for the protein fibrillin-1. It affects around 1 in 3,000 people.

167
Q

Marfan’s syndrome mushkies?

A
  1. Tall stature with arm span to height ratio > 1.05
  2. High arched palate
  3. Arachnodactyly
  4. Pectus excavatum
  5. Pes planus
  6. Scoliosis of > 20 degrees
  7. Heart = dilation of the aortic sinuses (seen in 90%) which may lead to aortic aneurysm, aortic dissection, aortic regurgitation, mitral valve prolapse (75%)
  8. Lungs = repeated pneumothoraces
  9. Eyes = upwards lens dislocation, blue sclera, myopia
  10. Dural ectasia = ballooning of the dural sac at the lumbosacral level
168
Q

Marfan’s prognosis?

A

The life expectancy of patients used to be around 40-50 years. With the advent of regular echocardiography monitoring and beta-blocker/ACE-inhibitor therapy this has improved significantly over recent years. Aortic dissection and other cardiovascular problems remain the leading cause of death however

169
Q

Sulfasalazine MOA?

A

A prodrug for 5-ASA which works through decreasing neutrophil chemotaxis alongside suppressing proliferation of lymphocytes and pro-inflammatory cytokines

170
Q

Sulfasalazine cautions?

A
  1. G6PDD
  2. Allergy to aspirin or sulphonamides (cross-sensitivity)
171
Q

Pt allergy to aspirin caution?

A

Sulfasalazine

172
Q

Is sulfasalazine safe in pregnancy and breastfeeding?

173
Q

Septic arthritis pathophysiology?

A
  1. Most common overall S. aureus (although in young adults who are sexually active Neisseria gonorrhoeae is the most common organism (disseminated gonococcal infection)
  2. Most common cause is haematogenous spread (this may be from distant bacterial infections e.g. abscesses)
  3. In adults, the most common location is the knee
174
Q

Septic arthritis features?

A
  1. Acute, swollen joint = restricted movement in 80%, examination findings (warm to touch/fluctuant)
  2. Fever = present in the majority of patients
175
Q

Septic arthritis Ix?

A
  1. Synovial fluid sampling is obligatory (should be done prior to Abx if necessary, may need to be done under radiographic guidance)
  2. Blood cultures (most commonly haematogenous spread)
  3. Joint imaging
176
Q

Septic arthritis Rx?

A
  1. IV Abx which cover gram +ve cocci, flucloxacillin first line (clindamycin if penicillin allergic), usually given for 4-6 weeks, typically switched to oral after 2 weeks
  2. Needle aspiration to decompress joint
  3. Arthroscopic lavage may be required
177
Q

Anti-histone antibodies?

A

Drug induced lupus

178
Q

Drug induced lupus features?

A
  1. Arthralgia
  2. Myalgia
  3. Skin (malar rash) and pulmonary involvement (pleurisy) are common
  4. ANA +ve in 100%, dsDNA -ve
  5. Anti-histone antibodies in 80-90%
  6. Anti-Ro, anti-Smith in 5%
179
Q

Anti Jo-1?

A

Polymyositis

180
Q

Anti Scl70?

A

Diffuse systemic sclerosis

181
Q

Anticentromere Ab?

A

Limited systemic sclerosis

182
Q

Causes of drug-induced lupus?

A
  1. Most common = procainamide, hydralazine
  2. Less common = isoniazid, minocycline, phenytoin
183
Q

Highest specificity for RhA?

A

Anti-CCP, may be detected up to 10 years prior. Allowing early detection of patients suitable for aggressive anti-TNF therapy

184
Q

Rheumatoid factor mushkies?

A

Rheumatoid factor (RF) is a circulating antibody (usually IgM) that reacts with the Fc portion of the patients own IgG.. It is recommended as the first-line antibody test for patients with suspected rheumatoid arthritis.
1. Detected by either Rose-Waaler test (sheep red cell agglutination) or Latex agglutination test (less specific)

185
Q

High titre levels in RF?

A

Associated with progressive disease but NOT a marker of disease activity

186
Q

RhA XR indication?

A

XRs of all hands and feet

187
Q

What needs to be given when starting allopurinol?

A

NSAID or Colchicine cover

188
Q

CREST syndrome?

A

Subtype of Limited Systemic Sclerosis
1. Calcinosis
2. Raynaud’s phenomenon
3. Oesophageal dysmotility
4. Sclerodactylyl
5. Telangiectasia

189
Q

3 types of systemic sclerosis?

A
  1. Limited Cutaneous SS
  2. Diffuse Cutaneous SS
  3. Scleroderma
190
Q

Systemic sclerosis M:F?

191
Q

Limited cutaneous SS mushkies?

A
  1. Raynaud’s may be first sign
  2. Scleroderma affects face and distal limbs predominantly
  3. Anti-centromere antibodies
  4. CREST is a subtype
192
Q

Diffuse cutaneous SS mushkies?

A
  1. Scleroderma affects trunk and proximal limbs predominantly
  2. Anti Scl 70 antibodies
  3. Most common cause of death is respiratory involvement, seen in 80% (ILD and PAH)
  4. Other complications include renal disease and HTN
  5. Poor prognosis
193
Q

Sclerodema mushkies?

A

No internal organ involvement
1. Tightening and fibrosis of skin
2. May be manifest as plaques (morphoea) or linear

194
Q

RhA XR?

A
  1. Early = Loss of joint space, juxta-articular osteoperosis, soft-tissue swelling
  2. Late = Periarticular erosions, subluxation
195
Q

Pre-HCQ eye Ix?

A

Colour retinal photography and spectral domain optical coherence tomography

196
Q

How long are bisphosphonates typically given for?

A

5 years (or 3 years for IV zoledronate)

197
Q

After 5 year bisphosphonate therapy Ix?

A

Treatment should be re-assessed for ongoing treatment, with an updated FRAX score and DEXA scan –> stratifies in to high and low risk groups

198
Q

High risk group post 5 years bisphosphonates?

A

Age >75
Glucocorticoid therapy
Previous hip/vertebral fractures
Further fractures on treatment
High risk on FRAX scoring
T score <-2.5 after treatment

199
Q

High vs. low risk actions?

A
  1. High = continue indefinitely or until criteria no longer apply
  2. Low = discontinue and re-assess after 2y or if a further fracture occurs
200
Q

Chronic fatigue syndrome Dx?

A

Diagnosed after at least 4 months of disabling fatigue affecting mental and physical function more than 50% of the time in the absence of other disease which may explain symptoms

201
Q

Chronic fatigue syndrome epidemiology?

A

More common in females

202
Q

CFS Rx?

A
  1. CBT
  2. Graded exercise therapy
  3. Pacing (organising activities to avoid tiring)
  4. Low-dose amitryptiline may be useful for poor sleep
  5. Referral to pain management clinic if pain is a predominant feature
203
Q

Anti-synthetase antibodies?

A

Dermatomyositis

204
Q

Secondary sjogrens as what % of RhA?

A

Occurs in about 50% of cases of RhA

205
Q

Dactylitis causes?

A
  1. Spondyloarthritis = Psoriatic and reactive arthritis
  2. Sickle cell disease
  3. Others = TB, Sarcoid, syphilis
206
Q

Gout drug causes?

A
  1. Diuretics = thiazides, furosemide
  2. Ciclosporin
  3. Alcohol
  4. Cytotoxic agents
  5. Pyrazinamide
  6. Aspirin
207
Q

What needs to be done prior to starting biologics for RhA?

A

CXR to look for TB

208
Q

RhA Rx?

A

Evidence of joint inflammation should start DMARD ASAP
1. Initial = DMARD monotherapy +/- short course of bridging prednisolone
2. Use CRP and DAS28 to assess response to Rx
3. Flares managed with corticosteroids (oral or IM)

209
Q

RhA drug options?

A
  1. DMARD
  2. TNF inhibitors
  3. Rituximab
  4. Abatacept
210
Q

DMARD examples?

A
  1. Methotrexate
  2. Sulfasalazine
  3. Leflunomide
  4. HCQ
211
Q

TNF inhibitor mushkies for RhA?

A
  1. Indication = inadeuqate response to at least 2 DMARDs including methotrexate
  2. Etanercept = recombinant human protein, acts as a decoy receptor for TNF-α, subcutaneous administration, can cause demyelination, risks include reactivation of tuberculosis
  3. Infliximab = monoclonal antibody, binds to TNF-α and prevents it from binding with TNF receptors, intravenous administration, risks include reactivation of tuberculosis
  4. Adalimumab = monoclonal antibody, subcutaneous administration
212
Q

Rituximab mushkies for RhA?

A
  1. Anti-CD20 mAb, results in B cell depletion
  2. 2x 1g IV infusions are given 2 weeks apart
  3. Infusion reactions are common
213
Q

Abatacept mushkies for RhA?

A
  1. Fusion protein that modulates a key signal required for activation of T lymphocytes
  2. Leads to decreased T cell proliferation and cytokine production
  3. Given as an infusion
  4. Not currently recommended by NICE

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