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MSK > Passmedicine Rheumatology > Flashcards

Passmedicine Rheumatology Flashcards

1
Q

What type of arthritis is gout?

A

Inflammatory

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2
Q

How do gout episodes typically present?

A

Episodes lasting several days
Often symptom free between episodes
Acute episodes develop maximal intensity within 12h

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3
Q

What are the symptoms of gout?

A

Pain
Swelling
Erythema

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4
Q

What joint is most affected in gout?

A

MTP (podagra = gout affecting this joint)

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5
Q

Apart from the MTP what joints are also commonly affected by gout?

A

Ankle
Wrist
Knee

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6
Q

What can untreated gout lead to?

A

Repeated acute episodes of gout can damage the joints –> chronic joint problem

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7
Q

What are the radiological features of gout?

A

Joint effusion
Punched out erosions with slcerotic margins in a juxta-articular distribution
Eccentric erosions
Soft tissue tophi

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8
Q

Differences between RA and OA: Aetiology

A

RA: autoimmune
OA: wear + tear –> localised loss of cartilage, remodelling of adjacent bone, assoc. inflammation

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9
Q

Differences between RA and OA: gender

A

RA: more common in women
OA: similar in men and women

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10
Q

Differences between RA and OA: age

A

RA: all ages
OA: elderly more common

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11
Q

Differences between RA and OA: typical joints affected

A

RA: MCP, PIP
OA: large wt bearing joints, CMC, DIP, PIP

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12
Q

Differences between RA and OA: typical hx

A

RA: morning stiffness, improves with use, systemic upset
OA: pain following use, improves with rest, unilateral symptoms, no systemic upset

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13
Q

Differences between RA and OA: x-ray findings

A

RA: loss of joint space, juxta-articular osteoporosis, periarticular erosions, subluxation

OA: loss of joint space, subchondral sclerosis, subchondral cysts, osteophytes forming at joint margins

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14
Q

What is the aetiology of systemic sclerosis?

A

Unknown

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15
Q

What is systemic sclerosis characterised by?

A

Hardened, sclerotic skin, and other connective tissues

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16
Q

In which gender is systemic sclerosis more common?

A

Females

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17
Q

What are the three patterns of disease of systemic sclerosis?

A
  1. Limited cutaneous systemic sclerosis
  2. Diffuse cutaneous systemic sclerosis
  3. Scleroderma (without internal organ involvement)
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18
Q

What are the features of limited cutaneous systemic sclerosis?

A

Can present with Raynaud’s

Scleroderma of face + distal limbs

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19
Q

What antibody is strongly associated with limited cutaneous systemic sclerosis?

A

Anti-centromere Ab

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20
Q

Name a subtype of limited cutaneous systemic sclerosis

A

CREST syndrome

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21
Q

What are the features of CREST syndrome?

A 
Calcinosis
Raynaud's
Oesophageal dysmotility
Sclerodactyly
Telangiectasia
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22
Q

What are the features of diffuse systemic sclerosis?

A

Scleroderma of the trunk + proximal limbs
Commonest cause of death: interstitial lung disease/pulmonary arterial hypertension
HAS POOR PROGNOSIS

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23
Q

What are the commonest complications associated with diffuse systemic sclerosis?

A

ILD, pulmonary arterial hypertension
Renal disease
HTN

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24
Q

What antibody is strongly associated with diffuse cutaneous systemic sclerosis?

A

scl-70 antibodies

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25
Q

What are the features of scleroderma (without internal organ involvement)?

A

Tightening + fibrosis of the skin

May manifest as plaques (morphoea) or linear

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26
Q

What antibodies are associated with systemic sclerosis?

A

ANA 90%

RF 30%

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27
Q

What is Paget’s disease of the bone?

A

Disease of increased but uncontrolled bone turnover

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28
Q

What is the aetiology of Paget’s disease?

A

Primary disorder of osteoclasts, with excessive osteoclastic resorption followed by increased osteoblastic activity

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29
Q

How does Paget’s normally present?

A

1 in 20 are symptomatic

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30
Q

What bones are most commonly affected by Paget’s disease?

A

Skull
Spine
Pelvis
Long bones of lower extremities

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31
Q

What are the predisposing factors for Paget’s?

A

Increasing age
Male
Northern latitude
Family history

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32
Q

What are the clinical features of Paget’s?

A

Tends to be older male with bone pain + isolated raised ALP

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33
Q

What are the classical features of Paget’s if it is left untreated?

A

Bowing of tibia

Bossing of skull

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34
Q

What does blood work for Paget’s usually show?

A

Normal Ca, phosp
Raised ALP
Other markers of bone turnover may be high (e.g. procollagen type 1, N-terminal propeptide, serum C-telopeptide, urinary N-telopeptide + urinary hydroproline)

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35
Q

X-ray of a Paget’s diseased skull would show…

A

Thickened vault

Osteoporosis circumscripta

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36
Q

What are the indications for the treatment of Paget’s?

A

Bone pain
Skull/long bone deformity
Fracture
Periarticular Paget’s

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37
Q

How is Paget’s treated?

A

Bisphosphonates (oral risedronate/IV zoledronate)

Calcitonin

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38
Q

What are the complications associated with Paget’s disease?

A 
Deafness (due to cranial nerve entrapment) 
Bone sarcoma 
Fractures
Skull thickening 
High output cardiac failure
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39
Q

What are the new recommendations for the treatment of RA?

A

Start DMARD ASAP and to include other Rx options, e.g. analgesia, physio + surgery

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40
Q

What is the initial therapy for RA?

A

DMARD monotherapy +/- bridging course of prednisolone

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41
Q

How do NICE recommend monitoring response to treatment in RA?

A

CRP + disease activity (e.g. DAS28)

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42
Q

What is the most commonly used DMARD?

A

Methotrexate

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43
Q

What must you do if you put a patient on methotrexate?

A

Monitor LFTs and FBC due to risk of myelosuppression and liver cirrhosis

Repeat weekly until stabilised, thereafter monitor every 2-3m

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44
Q

What are the three other DMARDs apart from methotrexate used for RA Rx?

A

Sufasalazine
Leflunomide
Hydroxychloroquine

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45
Q

When are TNF-inhibitors indicated for Rx of RA?

A

Inadequate response to 2+ DMARDs including methotrexate

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46
Q

Name 3 TNF-inhibitors

A

Etanercept
Infliximab
Adalimumab

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47
Q

What is etanercept?

A

Recombinant human protein, acts as a decoy for TNF-a

s/c administration

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48
Q

What are the side effectsof etanercept?

A

Demyelination

Reactivation of TB

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49
Q

What is infliximab?

A

Monoclonal Ab
Binds to TNF-a + prevents it fro binding with TNF receptors
IV administration

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50
Q

What risks are associated with infliximab use?

A

Reactivation of TB

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51
Q

What is adalimumab?

A

Monoclonal Ab

s/c administration

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52
Q

What is rituximab?

A

Anti-CD20 monoclonal Ab
RESULTS IN B CELL DEPLETION
Given as two 1g IV infusions 2 weeks apart
Infusion reactions common

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53
Q

What is abatacept?

A

Fusion protein that modulates a key signal required for activation of T lymphocytes
–> decreased T cell proliferation + cytokine production
Given as infusion

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54
Q

What is polyarteritis nodosa?

A

Vasculitis affecting medium sized arteries with necrotising inflammation leading to aneurysm formation

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55
Q

In which groups of people is polyarteritis nodosa most common?

A

In middle aged men

Associated with HEPATITIS B infection

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56
Q

What are the features of polyarteritis nodosa?

A 
Fever, malaise, arthalgia
Wt loss
HTN
Mononeuritis multiplex, sensorimotor polyneuropathy
Testicular pain 
Livedo reticularis
Haematuria, renal failure
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57
Q

What antibody is associated with polyarteritis nodosa?

A

pANCA

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58
Q

What is pseudogout?

A

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

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59
Q

What are the risk factors for pseudogout?

A 
Haemochromatosis
Hyperparathyroidism
Acromegaly 
Low mg, low phosp
Wilson's disease
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60
Q

Where does pseudogout tend to affect most?

A

Knee, wrist, shoulders most commonly affected

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61
Q

What investigations should you do in pseudogout and what will they find?

A

Joint aspiration: weakly positive birefringent rhomboid shaped crystals
X-Ray: chondrocalcinosis

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62
Q

What is the management of pseudogout?

A

Aspiration of joint fluid to exclude septic arthritis

NSAIDs/IA/IM/oral steroids

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63
Q

What is gout?

A

Form of microcrystal synovitis caused by deposition of monosodium urate monohydrate in the synovium

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64
Q

What causes gout?

A

Chronic hyperuricaemia (>450microm/l)

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65
Q

What is the acute management of gout?

A

First line: NSAIDs/colchicine + PPI if req.
Consider oral steroids (e.g. 15mg predn) if NSAIDs/colchicine CI
3rd line: IA steroids

Ensure patient continues on allopurinol if already taking

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66
Q

In treating an acute attack of gout, when should the patient be advised to stop taking NSAIDs?

A

1-2 days after symptoms have settled

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67
Q

What are the indications for urate lowering therapy?

A

All patients after their first attack of gout

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68
Q

In which patients is urate lowering therapy strongly indicated?

A 
>= 2 attacks in 12 months
Tophi
Renal disease
Uric acid renal stones
Prophylaxis if on cytotoxics/diuretics
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69
Q

What is used for urate lowering therapy?

A

First line: allopurinol (2w after attack) 100mg od initially titrating every few weeks to aim for serum uric acid of <300microm/l
Consider colchicine when starting allopurinol (or NSAID if colchicine not tolerated)
Second line: febuxpstat

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70
Q

How do allopurinol + febuxpstat work?

A

Xanthine oxidase inhibitors

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71
Q

What lifestyle modifications are helpful in gout?

A

Reduce alcohol intake
Lose wt
Avoid foods high in purines

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72
Q

What foods are high in purines?

A 
Liver
Kidney
Seafood
Oily fish
Yeast products
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73
Q

What drugs might you want to stop in someone with gout?

A

Precipitating drugs, e.g. thiazides

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74
Q

How does colchicine work?

A

Inhibits microtubule polymerization by binding to tubulin, interfering with mitosis. Also inhibits neutrophil motility and activity

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75
Q 
What are the expected values of serum:
Calcium 
Phosphate
ALP
PTH
in someone with osteoporosis?
A

Calcium - normal
Phosphate - normal
ALP - normal
PTH - normal

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76
Q 
What are the expected values of serum:
Calcium 
Phosphate
ALP
PTH
in someone with osteomalacia?
A

Calcium - decreased
Phosphate - decreased
ALP - increased
PTH - increased

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77
Q 
What are the expected values of serum:
Calcium 
Phosphate
ALP
PTH
in someone with primary hyperparathyroidism?
A

Calcium - increased
Phosphate - decreased
ALP - increased
PTH - increased

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78
Q 
What are the expected values of serum:
Calcium 
Phosphate
ALP
PTH
in someone with chronic kidney disease --> secondary hyperparathyroidism?
A

Calcium - decreased
Phosphate - increased
ALP - increased
PTH - increased

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79
Q 
What are the expected values of serum:
Calcium 
Phosphate
ALP
PTH
in someone with Paget's disease of the bone?
A

Calcium - normal
Phosphate - normal
ALP - increased
PTH - normal

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80
Q 
What are the expected values of serum:
Calcium 
Phosphate
ALP
PTH
in someone with osteopetrosis?
A

Calcium - normal
Phosphate - normal
ALP - normal
PTH - normal

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81
Q

How do bisphosphonates work?

A

Analogues of pyrophosphate (a molecule thatdecreases demineralisation in bone)
They inhibit osteoclasts by reducing recruitment + promoting apoptosis

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82
Q

What are bisphosphonates used to treat?

A

Prevention and treatment of osteoporosis
Hypercalcaemia
Paget’s disease
Pain from bone metatases

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83
Q

What are the AEs of bisphosphonates?

A

Oesophagitis, oesophageal ulcers (esp. alendronate)
Osteonecrosis of the jaw
Increased risk of atypical stress fractures of proximal femoral shaft
Acute phase response: fever, myalgia, arthalgia following administration
Hypocalcaemia (due to Ca efflux from bone)

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84
Q

How do bisphosphonate tablets need to be taken?

A

On empty stomach in the morning at least 30m before breakfast
Sitting upright/standing for 30m
Swallow with plenty of water

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85
Q

When should you co-prescribe vitamin D/Ca with bisphosphonates?

A

Vit D always

Ca if dietary intake is inadequate

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86
Q

When should you stop bisphosphonates?

A

After 5 years if the patient is <75, femoral neck T score of >2.5 + low risk according to FRAX/NOGG

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87
Q

What is temporal arteritis?

A

Large vessel vasculitis

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88
Q

What condition overlaps with temporal arteritis?

A

Polymyalgia rheumatica

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89
Q

What are the features of temporal arteritis?

A 
Patient usually >60
Rapid onset, <1m
Headache
Jaw claudication 
Visual disturbances (secondary to anterior ischaemic optic neuropathy)
Tender, palpable temporal artery 
50% have features of PMR
Lethargy, depression, low grade fever, anorexia, night sweats
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90
Q

What are features of PMR?

A

Aching

Morning stiffness in proximal limb muscles

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91
Q

What investigations should you do for temporal arteritis?

A

Inflammatory markers, expect ESR >50, elevated CRP
Temporal artery biopsy (NB skip lesions may be present)
CK and EMG normal

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92
Q

How do you treat temporal arteritis?

A

High dose prednisolone (should be dramatic response if not reconsider diagnosis)

Urgent ophthalmology review for those with visual symptoms (on the day)

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93
Q

What conditions are associated with cANCA antibodies?

A

Granulomatosis with polyangiitis (wegener’s)

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94
Q

What conditions are associated with pANCA?

A

Churg strauss syndrome, primary sclerosing cholangitiis, sometimes granulomatosis with polyangiitis

Others: UC, connective tissue dx (e.g. RA, SLE, Sjogren’s), autoimmune hepatitis

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95
Q

What is the most common target for cANCA?

A

Serine protease 3

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96
Q

What is the most common target for pANCA?

A

Myeloperoxidase

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97
Q

What is Marfan’s syndrome?

A

Autosomal dominant connective tissue disorder

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98
Q

What is the aetiology of Marfan’s syndrome?

A

FBN1 gene defect on chromosome 15 that encodes for the protein fibrillin 1

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99
Q

What are the features of Marfan’s?

A

Tall stature with arm span to height ratio >1.05
High arched palate
Arachnodactyly
Pectus excavatum
Scoliosis of >20 degrees
Heart: dilatation of aortic sinuses (may –> aortic aneurys, aortic dissection, aortic regurg, mitral valve prolapse)
Lungs: repeated pneumothoraces
Eyes: upward lens dislocation, blue sclera, myopia
Dural ectasia

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100
Q

What is dural ectasia?

A

Ballooning of the dural sac at the lumbrosacral level

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101
Q

What treatments have extended the life expectancy of those with Marfan’s?

A

Regular echos, beta-blockers, ACEi

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102
Q

What is osteomalacia?

A

Normal bony tissue but decreased mineral content

Rickets if growing, osteomalacia after epiphysis fusion

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103
Q

What can cause osteomalacia?

A 
Vit D deficiency, e.g. malabsorption, lack of sunlight, diet 
Renal failure
Drug induced, e.g. anticonvulsants 
Vitamin D resistant, inherited
Liver disease, e.g. cirrhosis
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104
Q

What are the features of Rickets?

A

Knock-knee, bow legs, features of hypocalcaemia

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105
Q

What are the features of osteomalacia?

A

Bone pain, fractures, muscle tenderness, proximal myopathy

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106
Q

What investigations should you do in suspected ostemalacia?

A

25(OH) vitamin D: low
Alk phos: raised
Ca, phos: low
X-Ray: children: cupped, ragged metaphyseal surfaces, adults: translucent bands (Looser’s zones or pseudofractures)

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107
Q

How do you treat osteomalacia?

A

Ca with vit D supplements

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108
Q

What does the histology of PMR show?

A

Vasculitis with giant cells

Characteristically skips certain sections of affected artery while damaging others

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109
Q

What arteries are most affected in PMR?

A

Muscle bed arteries

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110
Q

What are the typical features of PMR?

A

Patient typically >60
Usually rapid onset (<1m)
Aching, morning stiffness in proximal limb muscles
Also mild polyarthalgia, lethargy, depression, low grade fever, anorexia, night sweats

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111
Q

What investigations should you do in PMR?

A

ESR > 40 mm/hr

Note CK and EMG normal

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112
Q

How do you treat PMR?

A

Prednisolone e.g. 15mg od

Expect dramatic response

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113
Q

How does azathioprine work?

A

It is metabolised to the active compound mercaptopurine, a purine analogue that inhibits purine synthesis

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114
Q

How do you test for azathioprine toxicity?

A

Thiopurine methyltransferase test - TPMT deficiency predisposes to azathioprine related pancytopenia

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115
Q

What adverse effects are associated with azathioprine?

A 
Bone marrow depression 
NV
Pancreatitis 
Increased risk of non-melanoma skin cancer
Agranulocytosis/myelosupression
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116
Q

What drug should you be careful about prescribing alongside azathioprine?

A

Allopurinol
A significant reaction may occur
Use lower doses of azathioprine

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117
Q

What is Sjogren’s syndrome?

A

An autoimmune disorder affecting exocrine glands –> dry mucosal surfaces

Can be primary/secondary to RA/other connective tissue dx

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118
Q

In which gender is Sjogren’s syndrome more common?

A

Females

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119
Q

For what condition is there a marked increased in risk of in Sjogren’s syndrome?

A

Lymphoid malignancy

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120
Q

What are the features of Sjogren’s syndrome?

A 
Dry eyes (keratoconjunctivitis sicca)
Dry mouth 
Vaginal dryness
Arthalgia 
Raynaud's, myalgia 
Sensory polyneuropathy
Recurrent episodes of parotitis
Renal tubular acidosis
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121
Q

What antibodies are associated with Sjogren’s syndrome?

A

RF in nearly 100%
ANA 70%
AntiRo, AntiLa

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122
Q

What test can do you for Sjogren’s syndrome?

A

Schirmer’s test (filter paper near conjunctival sac to measure tear formation)

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123
Q

What does the histology show in Sjogren’s syndrome?

A

Focal lymphocytic infiltration

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124
Q

How do you manage Sjogren’s syndrome?

A

Artificial saliva + tears

Pilocarpine may stimulate saliva production

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125
Q

How does methotrexate work?

A

It is an antimetabolite that inhibits dihydrofolate reductase (an enzyme essential for the synthesis of purines and pyrimidines)

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126
Q

What are the indications for methotrexate use?

A

Inflammatory arthritis (esp. RA)
Psoriasis
ALL

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127
Q

What are the adverse effects of methotrexate?

A 
Mucositis
Myelosupression
Pneumonitis 
Pulmonary fibrosis
Liver fibrosis
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128
Q

What is the BNFs advice on methotrexate + pregnancy?

A

Avoid pregnancy for at least 6m after treatment cessation

Men should use effective contraception until 6m after treatment

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129
Q

What should you co-prescribe with methotrexate?

A

Folic acid 5mg

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130
Q

What is the recommended starting dose of methotrexate?

A

7.5mg

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131
Q

Only one strength of methotrexate should be prescribed - what is this?

A

2.5mg

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132
Q

What drugs should you avoid co-prescribing with methotrexate?

A

Trimethoprim
(increases risk of marrow aplasia as trimethoprim + methotrexate are both folate antagonists so –> pancytopenia/myelosuppression putting pt at risk of severe infection/bleeds)

Aspirin
(increases risk of methotrexate toxicity due t reduced excretion)

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133
Q

How do you treat methotrexate toxicity?

A

Folinic acid

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134
Q

Which HLA allele is reactive arthritis associated with?

A

HLA-B27

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135
Q

What is Reiter’s syndrome?

A

Triad of urethritis, conjunctivitis and arthritis

Was originally following dysenteric illness in WW2, but most commonly due to STIs now

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136
Q

What is reactive arthritis?

A

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

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137
Q

What are the features of reactive arthritis?

A

Develops after 4-6 weeks of initial infection
Symptoms generally last about 4-6m

Asymmetrical oligoarthritis of lower limbs
Dactylitis
Urethritis
Conjuncitivitis, anterior uveitis
Circinate balanitis, keratoderma blenorrhagica

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138
Q

What is keratoderma blenohagica?

A

Waxy brown/yellow papules on palms/soles

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139
Q

What HLA allele is ankylosing spondylitis associated with?

A

HLA-B27

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140
Q

In which group of people is ankylosing spondylitis most common?

A

Men, 20-30yo

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141
Q

What investigations can you use in ankylosing spondylitis?

A

ESR, CRP typically raised but normal levels do not exclude AS
HLA-B27 not useful as it is +ve in 10% of normal patients
Plain X-Ray of the SI joint is most useful for diagnosis

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142
Q

What are some later changes of ankylosing spondylitis you may see on X-Ray?

A

Sacroilitis - subchondral erosions, sclerosis
Squaring of lumbar vertebrae
Bamboo spine
Syndesmophytes (due to ossification of outer fibres of annulus fibrosus)
CXR - atypical fibrosis

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143
Q

What might spirometry show in ankylosing spondylitis?

A

Restrictive pattern due to pulmonary fibrosis, kyphosis, ankylosis of costovertebral joints

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144
Q

What is the management for ankylosing spondylitis?

A 
Regular exercise, e.g. swimming
NSAIDs 1st line
Physio
DMARDs if peripheral joint involvement 
Anti-TNF therapy should be given to patients with persistently high dx activity despite conventional Rx (e.g. etanercept)
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145
Q

What antibodies tend to be positive in SLE?

A

ANA 99%
RF 20%
anti-dsDNA very specific to SLE
Anti-Sm - even more specific

Others - anti-u1, SS-A (anti-Ro), SS-B (anti-La)

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146
Q

How do you monitor disease progression in SLE?

A

ESR (during active dx, CRP characteristically normal)
C3, C4 levels low during active disease (formation of complexes leads to consumption of complement)
Anti-dsDNA titres can be used to monitor disease

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147
Q

What is the different between Raynaud’s disease and Raynaud’s phenomenon?

A

Raynaud’s disease = primary

Raynaud’s phenomenon = secondary

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148
Q

In which group of people does Raynaud’s most commonly present?

A

Women in their 30s with bilateral symptoms

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149
Q

In someone presenting with Raynaud’s disease, what factors would suggest underlying connective tissue disease?

A 
Onset after 40 years
Unilateral symptoms
Rashes
Presence of Abs
Features which may suggest SLE, RA (e.g. recurrent miscarriages, arthritis) 
Digital ulcers, calcinosis
Chillblains
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150
Q

What are some secondary causes of Raynauds?

A 
Connective tissue dx (scleroderma, RA, SLE)
Leukaemia
Type 1 cyroglobulinaemia, cold agglutins
Use of vibrating tools
COCP, ergot 
Cervical rib
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151
Q

How do you manage Raynaud’s?

A

First line: CCB, e.g. nifedipine

IV prostacycline infusions

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152
Q

In which group of people is SLE more common?

A

Women

Afro-carribbean origin

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153
Q

What are the general features of SLE?

A

Fatigue
Fever
Mouth ulcers
Lymphadenopathy

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154
Q

What are the skin features of SLE?

A

Malar (butterfly) rash that spares the nasolabial folds
Discoid rash (scaly, erythematous, well demarcated in sun-exposed areas)
Photosensitivity
Raynaud’s phenomenon
Livedo reticularis
Non-scarring alopecia

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155
Q

What are the MSK features of SLE?

A

Arthalgia

Non-erosive arthritis

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156
Q

What are the CV features of SLE?

A

Pericarditis

Myocarditis

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157
Q

What are the respiratory features of SLE?

A

Pleurisy

Fibrosing alveolitis

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158
Q

What are the renal features of SLE?

A

Proteinuria

Diffuse proliferative GN

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159
Q

What are the neuropsychiatric features of SLE?

A

Anxiety, depression
Psychosis
Seizures

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160
Q

What is rheumatoid factor?

A

Circulating antibody (usually IgM) that interacts with the Fc portion of the patients own IgG

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161
Q

How can RF be detected?

A

Rose-Waaler test: sheep red cell agglutination

Latex agglutination test (less specific)

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162
Q

What % of RA patients have a +ve RF?

A

70-80%

High titre levels assoc. w. severe progressive dx

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163
Q

In which conditions is RF commonly +ve?

A 
Sjogren's 100%
Felty's syndrome 100%
Infective endocarditis 50%
SLE 20%
Systemic sclerosis 30%
General pop 5%
Rarely: TB, HBV, EBV, leprosy
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164
Q

When can you detect anti-cyclic citrullinated peptide antibody in those with RA?

A

May be detectable up to 10 years before development of RA

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165
Q

When should you test for anti-CCP antibodies?

A

In those with suspected RA but negative RF

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166
Q

What are the risk factors for osteoporosis as included in the FRAX risk assessment tool?

A 
Hx of glucocorticoid use
RA
Alcohol excess
Hx of parental hip fracture
Low BMI
Current smoking
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167
Q

Apart from the ones included on FRAX, what other risk factors are there for osteoporosis?

A 
Sedentary lifestyle
Premature menopause
Caucasians and asians
Endocrine disorders (e.g. hyperthyroidism, hypogonadism (e.g. Turner's), growth hormone deficiency, hyperparathyroidism, DM
Multiple myeloma, lymphoma
IBD, malabsorption, gastrectomy, liver disease
CKD
Osteogenesis imperfecta, homocystinuria
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168
Q

What medications can worsen osteoporosis?

A 
Glucocorticoids
SSRIs
Anti-epileptics
PPIs
Glitazones
Long term heparin therapy 
Aromatase inhibitors, e.g. anastrozole
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169
Q

Why should you investigate osteoporosis for secondary causes?

A

To exclude diseases that mimic osteoporosis (e.g. osteomalacia)
To identify the cause of osteoporosis + contributory factors
Assess the risk of subsequent fractures
To select the most appropriate form of treatment

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170
Q

What investigations are recommended for diagnosing osteoporosis?

A 
Hx, Ex 
FBC, ESR/CRP
Serum Ca, albumin, creatinine, phosphate, alk phos, liver transaminases
TFTs
DXA
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171
Q

What other investigations may be useful in osteoporosis for specific indications?

A

Lateral radiographs of lumbar and thoracic spine/DXA-based vertebral imaging
Protein immunoelectrophoresis and urinary Bence-Jones proteins
25OHD
PTH
Serum testosterone, SHBG, FSH, LH (in men),
Serum prolactin
24 hour urinary cortisol/dexamethasone suppression test
Endomysial and/or tissue transglutaminase antibodies (coeliac disease)
Isotope bone scan
Markers of bone turnover, when available
Urinary calcium excretion

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172
Q

What are the minimum baseline bloods that should be ordered for all patients with suspected osteoporosis?

A 
FBC
UE
LFTs
Bone profile
CRP
TFTs
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173
Q

What is Behcet’s syndrome?

A

A complex multisystem disorder associated with presumed autoimmune mediated inflammation of the arteries and veins

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174
Q

What is the aetiology of Behcet’s syndrome?

A

Unknown

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175
Q

What is the classic triad of Behcet’s syndrome?

A

Oral ulcers
Genital ulcers
Anterior uveitis

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176
Q

In which groups of people is Behcet’s most common?

A

Eastern Mediterranean countries
Men
20-40yos

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177
Q

What HLA allele is Behcet’s associated with?

A

HLA B51

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178
Q

What are the features of Behcet’s syndrome?

A 
1. oral ulcers, 2. genital ulcers, 3. anterior uveitis 
Thrombophlebitis and DVT
Arthritis
Neurological involvement 
Abdo pain, diarrhoea, colitis
Erythema nodosum
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179
Q

What is used to diagnose Behcet’s syndrome?

A

No definitive test
Based on clinical findings
Positive pathergy test is suggestive (puncture site following needle prick becomes inflamed with small pustule forming)

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180
Q

Where is the gene for HLA antigens found?

A

Chromosome 6

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181
Q

What diseases are strongly associated with HLA-A3 antigen?

A

Haemochromatosis

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182
Q

What diseases are strongly associated with HLA-B51 antigen?

A

Behcet’s disease

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183
Q

What diseases are strongly associated with HLA-B27 antigen?

A

Ankylosing spondylitis
Reiter’s syndrome
Acute anterior uveitis

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184
Q

What diseases are strongly associated with HLA-DQ2/8 antigen?

A

Coeliac disease

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185
Q

What diseases are strongly associated with HLA-DR2 antigen?

A

Nacrolepsy

Goodpasture’s

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186
Q

What diseases are strongly associated with HLA-DR3 antigen?

A

Dermatitis Herpetiformis
Sjogren’s syndrome
Primary biliary cirrhosis

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187
Q

What diseases are strongly associated with HLA-DR4 antigen?

A

T1DM

RA

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188
Q

What is chronic fatigue syndrome?

A

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

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189
Q

What are some other features of chronic fatigue syndrome?

A 
Sleep problems
Muscle/joint pains
Headaches
Painful lymph nodes without enlargement 
Sore throat
Cognitive dysfunction (e.g. difficulty thinking, inability to concentrate...)
Physical/mental exertion makes worse
General malaise, flu like symptoms
Dizziness
Nausea
Palpitations
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190
Q

What investigations should you do in chronic fatigue syndrome and why?

A

To exclude other pathology

FBC, UE, LFTs, TFTs, CRP, ESR, Ca, ferritin, coeliac screening, urinalysis

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191
Q

How do you manage chronic fatigue syndrome?

A

CBT
Graded exercise therapy
Pacing (organising activities to avoid tiring)
Low dose amitriptyline may be useful for poor sleep
Referral to pain management if it is a predominant feature

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192
Q

What is Ehler-Danlos syndrome?

A

AD connective tissue disorder that mostly affects type III collagen
Leads to tissue being more elastic than normal –> joint hypermobility + increased elasticity of skin

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193
Q

What are the features of Ehler-Danlos syndrome?

A

Elastic, fragile skin
Joint hypermobility + recurrent dislocation
Easy bruising
Aortic regurgitation, mitral valve prolapse, aortic dissection
SAH
Angioid retinal streaks

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194
Q

What is osteogenesis imperfecta?

A

Group of disorders of collagen metabolism resulting in bone fragility + fractures

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195
Q

How is osteogenesis imperfecta inherited?

A

AD

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196
Q

What is the aetiology of osteogenesis imperfecta?

A

Abnormality in type 1 collagen due to decreased synthesis of pro-alpha 1 or pro-alpha 2 collagen polypeptides

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197
Q

If the X-Ray is negative for SI joint involvement in AS but suspicion of AD is high what should be the next step in investigation?

A

MRI

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198
Q

What imaging findings confirm the diagnosis of AS?

A

Signs of inflammation in the SI joints (bone marrow oedema)

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199
Q

Name one of the most important risk factors for osteoporosis

A

Use of corticosteroids

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200
Q

The risk of osteoporosis is thought to rise significantly once an individual is taking what dose of steroids?

A

Equivalent of prednisolone 7.5mg a day for 3m+

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201
Q

If a patient is going t be taking steroids >3m and are at risk of osteoporosis when should bone protection start?

A

ASAP

202
Q

What are the two groups that patients at risk of corticosteroid induced osteoporosis are split into?

A
  1. > 65/previously had a fragility fracture –> offer bone protection
  2. <65 –> offer bone scan + results dependent on T score

> 0 - reassure; 0–>-1.5 - repeat bone density scan in 1-3y,

203
Q

What is the first line treatment for corticosteroid induced osteoporosis?

A

Alendronate

Ensure Ca and vit D replete

204
Q

When is treatment for osteoporosis indicated?

A

Following osteoporotic fragility fracture in a post-menopausal women confirmed to have osteoporosis (T score -2.5 or less)

(DEXA scan be not be necessary if clinician considers inappropriate/unfeasible)

205
Q

Who with osteoporosis should be offered vit D/Ca supplements?

A

All, expect those who are replete

206
Q

What is the first line treatment for osteoporosis?

A

Alendronate

207
Q

What % of pts cannot tolerate alendronate + why is this usually?

A

25%

Upper GI problems

208
Q

What is second line treatment for osteoporosis?

A

Risedronate or etidronate

209
Q

What treatments are recommended for those with osteoporosis who cannot take bisphosphonates?

A

Stronium ranelate

Raloxifene

210
Q

What evidence is there for alendronate/risedronate/etidronate?

A

Reduce risk of vertebral and non-vertebral fractures

211
Q

What is the option for a once a month oral bisphosphonate?

A

Ibandronate

212
Q

What kind of drug is raloxifene?

A

Selective oestrogen receptor modulator

213
Q

What is the evidence behind raloxifene?

A

Reduces vertebral fractures, prevents bone loss + increases bone density in spine + femur

214
Q

What are the AEs of raloxifene?

A

May worsen menopausal symptoms

Increases risk of TE events

215
Q

What is an additional benefit of raloxifene?

A

May reduce risk of breast cancer

216
Q

What is the action of strontium ranelate?

A

Increases deposition of new bone by osteoblasts (promotes differentiation of pre-osteoblasts to osteoblasts)
Reduces resorption of bone by inhibiting osteoclasts

217
Q

What is the issue with strontium ranelate?

A

Concerns re safety profile

Must only be prescribed by a specialist if there are no other treatments

218
Q

What are CIs for strontium ranelate?

A

Hx of CV dx or significant CV dx or prev. VTE

219
Q

What are the AEs of strontium ranelate?

A

Increased risk of CV event
Increased risk of TE events
Serious skin reactions, e.g. SJS

220
Q

What is the action of denosumab?

A

Human monoclonal antibody that inhibits RANK ligand, which in turn inhibits the maturation of osteoclasts

221
Q

How is denosumab given?

A

Single sc injection every 6m

222
Q

What is teriparatide?

A

Recombinant form of parathyroid hormone

223
Q

What is teriparatide good at?

A

Increasing bone mineral density

224
Q

What evidence does HRT have for osteoporosis management?

A

Reduces incidence of vertebral fractures + non-vertebral fractures

225
Q

When is the ONLY situation you would use HRT for osteoporosis management?

A

If pt also having vasomotor symptoms

226
Q

What non-medication treatments may be useful in the management of osteoporosis?

A

Hip protectors - compliance is an issue

Falls risk assessment - consider for high risk pts

227
Q

What is the most common organism causing septic arthritis?

A

Staph aureus

228
Q

What organism should be considered for causing septic arthritis in young sexually active individuals?

A

Neisseria gonorrhoea

229
Q

In adults, where is the most common location for septic arthritis?

A

Knee

230
Q

What criteria is used to assess the probability of septic arthritis in kids?

A 
Kocher's criteria - 
1 point for each of:
- Non wt bearing
- Fever >38.5
- WCC >12x10^9/L
- ESR >40mm/hr

(2 points = 40% risk, 3 = 93%, 4 = 99%)

231
Q

How is septic arthritis managed?

A 
IV antibiotics (flucloxacillin/clindamycin) for 6-12w 
Needle aspiration to decompress the joint
Athroscopic lavage may be req.
232
Q

What should be done before treating septic arthritis?

A

Take sample of synovial fluid before antibx are started!

233
Q

What is dermatomyositis?

A

Inflammatory disorder causing SYMMETRICAL, proximal muscle weakness + skin lesions

234
Q

What is the aetiology of dermatomyositis?

A

Idiopathic
Associated with connective tissue dx
Associated with underlying malignancy

235
Q

What malignancies are most commonly associated with dermatomyositis?

A

Ovarian, breast, lung

236
Q

What is polymyositis?

A

Variant of dermatomyositis where skin manifestations are not prominent

237
Q

What are the skin features in dermatomyositis?

A 
Photosensitive
Macular rash over back + shoulders
Helitrope rash in periorbital region
Gottron's papules
Mechanics hands - v. dry and scaly, with cracks on palmar + lateral aspects of fingers
Nail fold capillary dilatation
238
Q

What are Gottron’s papules?

A

Roughened red papules over extensor surface of fingers

239
Q

What are the non-skin manifestations of dermatomyositis?

A 
Proximal muscle weakness +/- tenderness
Raynaud's
Respiratory muscle weakness
Interstitial lung dx, e.g. fibrosing alveolitis/organising pneumonia
Dysphagia, dysphonia
240
Q

What antibody do 80% of those with dermatomyositis have?

A

ANA

241
Q

What antibody do 30% of those with dermatomyositis have?

A

Aminoactyl-tRNA synthases (e.g. Jo-1, Abs to signal recognition particle, anti-Mi-2 antibodies)

242
Q

What antibody is generally associated with RA?

A

Anti-CCP antibody

243
Q

What antibody is generally associated with SLE?

A

Anti-dsDNA

244
Q

What antibody is generally associated with diffuse systemic sclerosis?

A

Anti-Scl-70 antibodies

245
Q

What is anti-mitochondrial antibodies (AMAs) associated with?

A

Primary biliary cirrhosis

246
Q

What two conditions is hydroxychloroquine used in?

A

RA

Systemic/discoid lupus erythematosus

247
Q

What adverse effect is associated with hydroxychloroquine?

A

Bull’s eye retinopathy - my result in severe + permanent vision loss

248
Q

What 1 examination/investigation is required before starting a patient on hydroxychloroquine?

A

Baseline ophthalmological examination

thereafter annual screening

249
Q

Can hydroxychloroquine be used in pregnancy?

A

Yes

250
Q

What HLA allele is associated with ankylosing spondylitis?

A

HLA-B27

251
Q

What is the typical history of someone presenting with ankylosing spondylitis?

A

Young man who presents with low back pain + stiffness of insidious onset
Stiffness worse in morning + improves with exercise
Pt may experience pain at night, which improves on getting up

252
Q

What will you see on examination of someone with AS?

A

Reduced lateral flexion
Reduced forward flexion (Schober’s test)
Reduced chest expansion

253
Q

What is Schober’s test?

A

Draw line 10cm above + 5cm below back dimples (L5)

The distance between the two lines should increase by >5cm when the pt bends as far forward as possible

254
Q

What are other features associated with AS?

A 
The A's:
Apical fibrosis
Anterior uveitis (in 1/3rd)
Aortic regurgitation
Achilles tendonitis
AV node block
Amyloidosis

Cauda equina syndrome
Peripheral arthritis

255
Q

When is the typical onset of SLE?

A

20-40y

256
Q

What kind of hypersensitivity reaction is SLE?

A

Type 3

257
Q

What HLA alleles are associated with SLE?

A

HLA B8, DR2, DR3

258
Q

What is thought to cause SLE?

A

Immune system dysregulation leading to immune complex formation
Immune complexes can deposit in any organ incl. skin, joints, kidneys, brain

259
Q

What should all pts with OA be offered?

A

Help with wt loss

Advice re. local muscle strengthening exercises + general fitness

260
Q

What are the first line analgesics for OA?

A

Paracetamol + topical NSAIDs (for knee/hand)

261
Q

What are second-line analgesics for OA?

A

NSAIDs/COX-2 inhibitors, opioids, capsaicin cream, IA corticosteroids

262
Q

What must be co-prescribed with COX-2 inhibitors/NSAIDs?

A

PPI

263
Q

What drug that if the pt was already on would CI prescribing COX-2 inhibitors/NSAIDs?

A

Aspirin

264
Q

What are non-pharmacological treatments for OA?

A

Supports + braces
TENS
Shock absorbing insoles/shoes

265
Q

If all conservative measures for OA management fail what are the options?

A

Refer for consideration of joint replacement

266
Q

What is glucosamine?

A

Normal constituent of glycosaminoglycans in cartilage and synovial fluid

267
Q

What is the evidence re glucosamine use in treatment of OA?

A

Significant improvement in symptoms + reduces joint space narrowing
However NICE don’t recommend it

268
Q

What is osteoporosis?

A

Disorder characterised by loss of bone mass

269
Q

Define osteoporosis

A

Bone mineral density of less than 2.5 standard deviations below the young adult mean density

270
Q

What does osteoporosis put pts at risk of?

A

Fragility fractures (e.g. neck of femur fracture, which carries significant morbidity + mortality)

271
Q

What % of post-menopausal women will suffer an osteoporotic fracture at some point?

A

50%

272
Q

What are the major risk factors for osteoporosis?

A

Age, female sex

273
Q

What are other risk factors for osteoporosis?

A 
Corticosteroids use
Smoking
Alcohol
Low BMI
FH
274
Q

What screening tools can you use for osteoporosis? What do these assess?

A

FRAX/QFracture

Assess 10 year risk of pt developing a fragility fracture

275
Q

Which pts should be assessed for osteoporosis?

A

Those who have sustained a fragility fracture

276
Q

How is BMD assessed?

A

Dual energy X-Ray absorptiometry (DEXAscan) from which a T score can be worked out

277
Q

What bones does the DEXA scan use?

A

Lumbar spine

Hip

278
Q

What T score in either the hip or the lumbar spine warrants starting treatment for osteoporosis?

A
279
Q

What is the first line treatment for osteoporosis?

A

Bisphosphonate, e.g. alendronate

280
Q

When are bisphosphonates contraindicated?

A

If eGFR <35

281
Q

What are some respiratory extra-articular complications of RA?

A

Pulmonary fibrosis, pleural effusion, pulmonary nodules, bronchiolitis obliterans, methotrexate pneumonia, pleurisy

282
Q

What are some ocular extra-articular complications of RA?

A

Keratoconjunctivitis sicca, episcleritis, scleritis, corneal ulceration, keratitis, steroid induced cataracts, chloroquine retinopathy

283
Q

What is an MSK extra-articular complications of RA?

A

Osteoporosis

284
Q

What is a CV extra-articular complications of RA?

A

IHD (has similar risk as T2DM)

285
Q

What is a psychological extra-articular complications of RA?

A

Depression

286
Q

What is an immunological extra-articular complications of RA?

A

Increased risk of infection

287
Q

What two conditions are less commonly associated with RA?

A

Felty’s syndrome

Amyloidosis

288
Q

What are the features of Felty’s syndrome?

A

RA
Splenomegaly
Low WCC

289
Q

What organisms can cause the post-dysenteric form of reactive arthritis?

A 
Shigella flexneri
Salmonella typhimurium
Salmonella enteritidis
Yersinia enterocolitica
Campylobacter
290
Q

What organisms can cause the post-STI form of reactive arthritis?

A

Chlamydia trachomatis

291
Q

What is the management of reactive arthritis?

A

Analgesics, NSAIDs, IA steroids

Sulfasalazine, methotrexate sometimes used for persistent symptoms

292
Q

How long does it usually take for reactive arthritis to clear up?

A

Usually within 1 y

293
Q

What would you expect to find of the synovial fluid in reactive arthritis?

A

Cloudy yellow colour
Culture negative
No crystals
WCC 20, 000/mm

294
Q

What is the most common Ig?

A

IgG

295
Q

What is the action of IgG?

A

Enhances phagocytosis of viruses/bacteria

Fixes complement + passes to foetal circulation

296
Q

What is the most predominant Ig in breast milk?

A

IgA

297
Q

Where is IgA mostly found?

A

Secretions of digestive, respiratory and urogenital tracts/systems

298
Q

What is the action of IgA?

A

Provides localised protection on mucous membranes

299
Q

What is the action of IgM?

A

First Ig to be secreted in response to an infection

Fixes complement b

300
Q

Does IgM pass to the foetal circulation?

A

No

301
Q

What is the role of IgD antibodies?

A

Largely unknown but involved in activation of B cells

302
Q

What is the action of IgE?

A

Mediates T1 hypersensitivity reactions by binding to Fc receptors on the surface of mast cells + basophils

Also provides immunity to parasite, e.g. helminths

303
Q

What is the least abundant Ig in the serum?

A

IgE

304
Q

What is the structure of IgE?

A

Monomer

305
Q

What is the structure of IgD?

A

Monomer

306
Q

What is the structure of IgM?

A

Penamer

307
Q

What is the structure of IgA?

A

Monomer/dimer

308
Q

What is the structure of IgG?

A

Monomer

309
Q

What can predispose to gout?

A

Decreased excretion of uric acid
Increased production of uric acid
Lesch-Nyhan syndrome

310
Q

What things can cause decreased excretion of uric acid?

A

Drugs, e.g. diuretics
CKD
Lead toxicity

311
Q

What things can cause increased production of uric acid?

A

Myeloproliferative/lymphoproliferative disorder
Cytotoxic drugs (e.g. chemotherapy)
Severe psoriasis

312
Q

What is the pathophysiology of Lesch-Nyhan syndrome?

A

Hypoxanthine-guanine phosphoribosyl transferase (HGPRTase) deficiency

313
Q

How is Lesch-Nyhan syndrome inherited?

A

X-linked recessive

314
Q

What are the features of Lesch-Nyhan syndrome?

A 
Gout
Renal failure
Neurological deficits
Learning difficulties
Self-mutilation
315
Q

What kind of muscle weakness do you get in PMR?

A

No true weakness of limb girdles

Weakness of muscles is due to myalgia (pain inhibition)

316
Q

How would you describe the pain in OA?

A

Exacerbated by exercise, relieved by rest

317
Q

What movement is affected first in hip OA?

A

Internal rotation

318
Q

What are risk factors for hip OA?

A

Age
Obesity
Prev. joint problems

319
Q

When is the pain from inflammatory arthritis most prominent?

A

Morning

320
Q

What other features will be present in inflammatory arthritis?

A

Systemic features, raised inflammatory markers

321
Q

What features may you see in referred lumbar spine pain?

A

Femoral nerve compression may cause referred hip pain

Femoral nerve stretch test +ve

322
Q

What is the femoral nerve stretch test?

A

Lie pt prone, extend hip joint with straight leg when bend the knee
This stretches the femoral nerve and causes pain if it is trapped

323
Q

What causes greater trochanteric pain syndrome (Trochanteric bursitis)?

A

Repeated movement of the fibroelastic iliotibial band

324
Q

What are the features of greater trochanteric pain syndrome (Trochanteric bursitis)?

A

Pain + tenderness over lateral thigh

325
Q

What people tend to get greater trochanteric pain syndrome (Trochanteric bursitis)?

A

Women aged 50-70

326
Q

What causes meralgia paraesthetica?

A

Compression of lateral cutaneous nerve of thigh

327
Q

What are the symptoms of meralgia paraesthetica?

A

Burning over anterolateral aspect of thigh

328
Q

What may avascular necrosis follow?

A

High dose steroid therapy or hip fracture or dislocation

329
Q

When is pubic symphysis dysfunction common?

A

In pregnancy - ligament laxity increases in response to hormonal changes

330
Q

What symptoms do you get in pubic symphysis dysfunction?

A

Pain over pubic symphysis with radiation to the groins + medial aspect of thighs

331
Q

What kind of gait may you see in pubic symphysis dysfunction?

A

Waddling

332
Q

When is transient idiopathic osteoporosis seen?

A

Uncommon condition but more seen in 3rd trimester of pregnancy

333
Q

How does transient idiopathic osteoporosis present?

A

Groin pain + limited range of movement in the hip
May be unable to wt bear
ESR may be elevated

334
Q

What is a T score based off of?

A

Bone mass of a young reference population

335
Q

What scores a T score of -1 mean?

A

Bone mass of one SD below the young reference population

336
Q

What is the Z score adjusted for?

A

Age, gender, ethnic factors

337
Q

T score >-1 =?

A

Normal

338
Q

T score of -1 to -2.5 =?

A

Osteopenia

339
Q

T score >-2.5

A

Osteoporosis

340
Q

What usually results in lateral epicondylitis?

A

Unaccustomed activity, e.g. playing tennis or house painting

341
Q

What are the features of lateral epicondylitis?

A

Pain/tenderness at lateral epicondyle

Worse on wrist extension against resistance/supination of forearm with elbow extended

342
Q

How long do bouts of lateral epicondylitis tend to last?

A

6m-2y

343
Q

What is involved in the management of lateral epicondylitis?

A

Advice re avoiding muscle overload
Simple analgesia
Steroid injection
Physio

344
Q

What are anti-jo antibodies also known as?

A

Ab against aminoacyl-tRNA

345
Q

What features are associated with antisynthase syndrome?

A

Myositis
Interstitial lung disease
Thickened + cracked skin of hands
Raynaud’s

346
Q

What is antisynthase syndrome?

A

Subtype of dermatomyositis

347
Q

What are poor prognostic features in rheumatoid arthritis?

A 
RF +ve
Poor functional status at presentation 
HLA DR4
X-ray - early erosions 
Extra-articular features, e.g. nodules
Insidious onset
Anti-CCP antibodies
Female gender
348
Q

What are the features of drug induced lupus?

A

Arthalgia
Myalgia
Skin (e.g. malar rash) + pulmonary involvement (e.g. pleurisy)

349
Q

What antibodies are positive in drug induced lupus?

A

ANA 100%
Antihistone in 80-90%
Anti-Ro/anti-Smith less commonly +ve

350
Q

What are the most common causes of drug induced lupus?

A

Procainamide

Hydralazine

351
Q

What are the less common causes of drug induced lupus?

A

Isoniazid
Minocycline
Phenytoin

352
Q

In which patients may you consider colchicine instead of NSAIDs for treating an acute attack of gout?

A

Elderly pts on warfarin (puts them at risk of GI haemorrhage)

353
Q

What are the rotator cuff muscles?

A 
SItS - small t for teres minor
Supraspinatus
Infraspinatus 
teres minor
Subscapularis
354
Q

What is the action of supraspinatus?

A

Abducts arm before deltoid (first 20 degrees)

355
Q

What is the action of infraspinatus?

A

Rotates arm laterally

356
Q

What is the action of teres minor?

A

Adducts + rotates arm laterally

357
Q

What is the action of subscapularis?

A

Adducts + rotates arms medially

358
Q

What does calcinosis look like?

A

White deposits

359
Q

What symptoms do patients get with oesophageal dysmotility?

A

Dysphagia

360
Q

What does sclerodactyly look like?

A

Thickened skin on tops of hands an inability to straighten fingers

361
Q

What is telangiectasia?

A

Excessive number of spider naevi

362
Q

What is the mechanism of type 1 hypersensitivity reactions?

A

Antigen reacts with IgE bound to mast cells

363
Q

Give examples of T1 HS reactions

A

Anaphylaxis

Atopy (e.g. asthma, hayfever, eczema)

364
Q

What is the mechanism of type 2 hypersensitivity reactions?

A

IgG or IgM binds to antigen on cell surface

365
Q

Give examples of T2 HS reactions

A 
Autoimmune haemolytic anaemia
ITP
Goodpasture's syndrome
Pernicious anaemia
Acute haemolytic transfusion reactions
Rheumatic fever
Pemphigus vulgaris / bullous pemphigoid
366
Q

What is the mechanism of type 3 hypersensitivity reactions?

A

Free antigen + antibody combine

367
Q

Give examples of T3 HS reactions

A

Serum sickness
Systemic lupus erythematosus
Post-streptococcal glomerulonephritis
Extrinsic allergic alveolitis (especially acute phase)

368
Q

What is the mechanism of type 4 hypersensitivity reactions?

A

T-cell mediated

369
Q

Give examples of T4 HS reactions

A 
TB/tuberculin skin reaction
Graft versus host disease
Allergic contact dermatitis
Scabies
Extrinsic allergic alveolitis (especially chronic phase)
MS
Guillain-Barre syndrome
370
Q

What is the mechanism of type 5 hypersensitivity reactions?

A

Antibodies that recognise and bind to cell surface receptors and stimulate them or block ligand binding

371
Q

Give examples of T5 HS reactions

A

Grave’s disease

Myasthenia gravis

372
Q

What drug should those with RA be given as soon as diagnosed?

A

DMARD + short dose of bridging prednisolone

373
Q

What are other treatment options for RA?

A

Analgesia
Physio
Surgery

374
Q

What should be used to monitor response to treatment in RA?

A

CRP and disease activity (e.g. DAS28)

375
Q

How are flares in RA managed?

A

Corticosteroids (oral/intramuscular)

376
Q

What is the most widely used DMARD in RA?

A

Methotrexate

377
Q

What monitoring is req. for pts on methotrexate?

A

LFTs + FBC (due to risk of liver cirrhosis + myelosuppression)

378
Q

What are 3 other DMARDs apart from methotrexate that may be used to treat RA?

A

Sulfasalazine
Leflunomide
Hydroxychloroquine

379
Q

If a pt with RA is having an inadequate response to DMARDs what is the next step in Rx?

A

If inadequate response to at least 2 DMARDs can start TNF-inhibitor

380
Q

What are the four TNF-inhibitors used in the treatment of RA?

A

Etanercept
Infliximab
Adalimumab
Abatacept

381
Q

How does etanercept work?

A

Recombinant human protein (anti-CD20 monoclonal Ab), acts as a decoy for TNF-a

382
Q

What are AEs of etanercept?

A

Demyelination

Reactivation of TB

383
Q

How is etanercept administered?

A

SC

384
Q

How does infliximab work?

A

Monoclonal Ab, binds to TNF-a and prevents it binding with TNF receptors

385
Q

How is infliximab administered?

A

IV

386
Q

What are the AEs of infliximab?

A

Reactivation of TB

387
Q

What is adalimumab?

A

Monoclonal Ab

388
Q

How is adalimumab administered?

A

SC

389
Q

What cell does rituximab lead to depletion in?

A

B cells

390
Q

How does abatacept work?

A

Fusion protein that modulates a key signal required for activation of T lymphocytes –> decreased T cell proliferation + cytokine production

391
Q

Does psoriatic arthritis tend to occur before or after the skin changes?

A

Tends to precede

392
Q

What % of pts with psoriasis skin lesions develop an arthropathy?

A

10-20%

393
Q

What are the types of psoriatic arthropathy?

A 
Rheumatoid like polyarthritis
Asymmetric oligoarthritis (typically affects hands/feet)
Sacroilitis
DIP joint disease
Arthritis mutilans
394
Q

What is arthritis mutilans?

A

Severe deformity of fingers/hands - ‘telescoping fingers’

395
Q

How should you treat psoriatic arthropathy?

A

Like RA

396
Q

What deformity may seen in hand x-ray of someone with psoaritic arthritis?

A

Pencil in cup deformity

Plantar spur

397
Q

When is it appropriate to start trying to use anti-TNFa drugs in someone with axial AS?

A

If they have tried and failed on 2 different NSAIDs and meets criteria for active disease on 2 occasions 12w apart

398
Q

List secondary causes of Raynaud’s

A

Connective tissue dx (e.g. scleroderma most common)
Leukaemia
Type 1 cryoglonulinaemia, cold agglutinins
Use of vibrating tools
Drugs, e.g. COCP, ergot
Cervical rib

399
Q

What kind of crystals are seen in gout?

A

Monosodium urate

Needle-shaped, negatively birefringent under polarised light

400
Q

What kind of crystals are seen in pseudogout?

A

Calcium pyrophosphate

Rhomboid positively birefringent under polarised light

401
Q

What crystals are seen in OA?

A

Calcium phosphate due to degeneration of cartilage no birefringence

402
Q

What crystals are see in RA?

A

Cholesterol crystals

Rhomboid + negatively birefringent

403
Q

What mnemonic can be used to remember some causes of gout?

A

DART - diuretics, alcohol, kidney disease, trauma

404
Q

If a patient on allopurinol for gout prophylaxis has an acute attack, should their allopurinol be stopped?

A

No - continue it

405
Q

List possible differentials for polyarthritis

A 
rheumatoid arthritis
SLE
seronegative spondyloarthropathies
Henoch-Schonlein purpura
sarcoidosis
tuberculosis
pseudogout
viral infection: EBV, HIV, hepatitis, mumps, rubella
406
Q

What are interferons and cytokines in the body released in response to?

A

Viral infections

Tumours

407
Q

INF-a and INF-b bind to what type of receptors?

A

Type 1

408
Q

What type of receptors does IFN-gamma bind to?

A

Type 2

409
Q

What cells produce INFa?

A

Leucocytes

410
Q

What is the action of INFa?

A

Antiviral action

411
Q

In which conditions is INFa helpful?

A

Hepatitis B and C
Kaposi sarcoma
Metastatic renal cancer
Hairy cell leukaemia

412
Q

What are adverse effects of INFa?

A

Depression

Flu like symptoms

413
Q

What cells produce INFb?

A

Fibroblasts

414
Q

What is the action of INFb?

A

Antiviral

415
Q

What condition is treated with INFb?

A

MS (can reduce freq. of exacerbations in RRMS)

416
Q

What cells produce INF-g?

A

Natural killer cells mostly + T helper cells

417
Q

What is the action of INF-g?

A

Antiviral action, but more of a role in immunomodulation, esp. macrophage activation

418
Q

In what diseases may INF-g be helpful?

A

Chronic granulomatous disease, osteopetrosis

419
Q

Why can TA cause visual symptoms?

A

Can cause occlusion of ophthalmic artery –> blindness (irreversible)
Transient visual problems may precede complete occlusion

420
Q

What is dactylitis?

A

Inflammation ofa digit

421
Q

What can cause dactylitis?

A

Spondyloarthritis: psoriatic/reactive
Sickle cell disease
Rarer - TB, sarcoidosis, syphillis

422
Q

What score is used to assess for hypermobility?

A

Beighton score

423
Q

What beighton score is +ve in kids?

A

6/9

424
Q

What beighton score is +ve in adults?

A

5/9

425
Q

Why might you get a single central radiodense line in the spine of someone with AS?

A

Ossification of the supraspinous and infraspinous ligaments

Known as dagger sign

426
Q

What is fibromyalgia?

A

Syndrome characterised by widespread pain throughout the body with tender points in specific areas

427
Q

What is the causes of fibromyalgia?

A

Unknown

428
Q

Which gender does fibromyalgia affect more?

A

Women

429
Q

What are the features of fibromyalgia?

A

Chronic pain - at multiple sites or sometimes all over
Lethargy
Cognitive impairment - ‘fibro fog’
Sleep disturbance, headaches, dizziness

430
Q

How is fibromyalgia diagnosed?

A

Clinically - American college of rheumatology classification criteria lists 9 pairs of tender points on body, if pt tendering at least 11 points fibromyalgia more likely

431
Q

What is involved in the management of fibromyalgia?

A

Explanation
Aerobic exercise
CBT
Medications - pregabalin, duloxetine, amitriptyline

432
Q

What two things are required for diagnosis of AS?

A

Radiological feature - sacroiliitis
Clinical feature

NOTE: squaring of vertebrae and bamboo spine are all signs but are not part of the diagnostic criteria

433
Q

How long may anti-CCP antibodies may detectable for before diagnosis of RA?

A

10 years

434
Q

What test can you do to differentiate between statin induced myopathy and PMR?

A

ESR -

Raised in PMR, normal in statin induced myopathy

435
Q

What ages tend to get Still’s disease?

A

Bimodal age distribution - 15-25y and 35-46y

436
Q

What are the features of Still’s disease?

A 
Arthalgia
Elevated serum derritin 
Salmon pink, maculopapular rash 
Pyrexia 
Lympadenopathy
RF and ANA -ve
437
Q

What is the pattern of the pyrexia in Still’s disease?

A

Typically rises in late afternoon/early evening in daily pattern + accompanies worsening of joint symptoms + rash

438
Q

What criteria can be used to help diagnose still’s disease?

A

Yamaguchi criteria

439
Q

What is the management of Still’s disease?

A

NSAIDs - first line to manage fever, joint pain + serositis
Trial at least a week before steroids added
If symptoms persist then consider methotrexate or IL-1/anti-TNF

440
Q

What is the mechanism of action of penicillamine?

A

Thought to reduce IL-1 synthesis and prevent maturation of newly synthesized collagen

441
Q

When might penicillamine be used?

A

RA Mx

442
Q

What are adverse effects of penicillamine?

A

Rashes
Taste disturbance
Proteinuria

443
Q

What can penicillamine cause in patients with Wilson’s disease?

A

Membranous glomerulonephropathy

444
Q

Offer prophylactic bisphosphonates to those with a T score of _____ if they are on steroids/going to be on steroids for 3+ months (even if <65y)

A

1.5

445
Q

What does joint aspirate in RA show?

A

High WCC (predominantly PMNs)
Yellow and cloudy
No crystals

446
Q

What are typical features of RA?

A

Swollen, painful joints in hands + feet
Stiffness worse in morning
Gradual gets worse with larger joints becoming involved
Presentation usually insidious over a few m
Positive squeeze test

447
Q

What is a squeeze test?

A

Discomfort on squeezing across the metacarpal or metatarsal joints

448
Q

What deformities are late features of RA?

A

Swan neck deformity and boutonniere deformities

449
Q

What is palindromic rheumatism?

A

Relapsing/remitting monoarthritis of different large joints

450
Q

What is chondrocalcinosis?

A

Calcification of the cartilage

451
Q

What is antiphospholipid syndrome?

A

Acquired disorder characterised by predisposition to both venous and arterial thromboses, recurrent foetal loss, thrombocytopenia

452
Q

What is the aetiology of antiphospholipid syndrome?

A

Primary disorder

Secondary to other conditions, e.g. SLE

453
Q

Antiphospholipid syndrome causes a paradoxical increase in what?

A

APTT + low platelets - due to ex-vivo reaction of lupus anticoagulant autoantibodies with phospholipids involved in the coagulation cascade

454
Q

What are the features of antiphospholipid syndrome?

A 
Venous/arterial thrombosis
Recurrent foetal loss
Livedo reticularis
Thrombocytopenia
Prolonged APTT
Pre-eclampsia, pulmonary HTN
455
Q

What conditions are associated with antiphospholipid syndrome?

A

SLE - most common
Other autoimmune disorders
Lymphoproliferative disorders
Phenothiazines

456
Q

How should you manage antiphospholipid syndrome?

A

Initial VTE: warfarin with INR target of 2-3 for 6m
Recurrent VTE - lifelong warfarin (increase target INR to 3-4 if VTE occur while on warfarin)
Arterial thrombosis treat with lifelong warfarin aiming for INR 2-3

457
Q

What might you see on the skull x-ray of someone with paget’s?

A

Thickening of calvarium

Ill-defined sclerotic and lucent areas

458
Q

What antibody is associated with antiphospholipid syndrome?

A

Anti-cardiolipin antibody and lupus anticoagulant (La)

459
Q

What is sulfasalazine used to treat?

A

IBD

RA

460
Q

What kind of drug is sulfasalazine?

A

5-ASA

461
Q

How does sulfasalazine work?

A

Decreases neutrophil chemotaxis alongside supressing proliferation of lymphocytes + pro-inflammatory cytokines

462
Q

What are cautions for sulfasalazine use?

A

G6PD deficiency

Allergy to aspirin/sulphonamides (e.g. co-trimoxazole)

463
Q

What adverse effects are associated with sulfasalazine?

A

Olgiospermia
SJS
Pneumonitis/lung fibrosis
Myelosupression, Heinz body anaemia, megaloblastic anaemia
May colour tears –> stained contact lenses

464
Q

Is sulfasalazine safe to use in pregnancy and breastfeeding?

A

Yes

465
Q

When does OI tend to present?

A

Childhood

466
Q

What are the features of OI?

A

Fractures following minor trauma
Blue sclera
Deafness secondary to otosclerosis
Dental imperfections common

467
Q

What things do you have to take into consideration when a patient with RA is undergoing surgery under GA?

A

Do lateral and anteroposterior cervical spine radiographs to screen for alantoaxial subluxation - to ensure pt goes into surgery with a Cspine collar and spine is not hyperextended on intubation

468
Q

Why might you get a normal temporal biopsy in TA?

A

Skip lesions

469
Q

What should be prescribed in RA to reduce need for NSAIDs/COX2 inhibitors?

A

Simple analgesia, e.g. paracetamol, codeine

470
Q

What two blood tests must be negative to diagnose Still’s disease?

A

RF and ANA

471
Q

What is a very common SE of colchicine?

A

Diarrhoea

472
Q

What are vasculitides?

A

Group of conditions characterised by inflammation of BV walls

473
Q

What vasculitides affect the aorta and its branches?

A

Takayasu’s arteritis
Buergers disease
Giant cell arteritis

474
Q

What vasculitides affect large and medium sized arteries?

A

Buergers disease
Giant cell arteritis
Polyarteritis nodosa

475
Q

What vasculitides affect medium sized muscular arteries?

A

Polyarteritis nodosa

Wegeners granulomatosis

476
Q

What vasculitides affect small muscular arteries?

A

Wegeners granulomatosis

Rheumatoid vasculitis

477
Q

What is Takayasu’s arteritis?

A

Inflammatory, obliterative arteritis affecting aorta and its branches

478
Q

What are features of Takayasu’s arteritis?

A

Upper limb claudication
Diminished/absent pulses
ESR raised in acute phase

479
Q

What is Buergers disease?

A

Segmental thrombotic occlusions of small and medium sized lower limb vessels

480
Q

Who is Buergers disease most common in?

A

Young male smokers

481
Q

What are the features of Buergers disease?

A

Proximal pulses usually present but pedal pulses loss

Acute hypercellular occlusive thrombus often present

482
Q

What might you see on angiography in Buergers disease?

A

Tortuous corkscrew shaped collateral vessels

483
Q

What kind of lesions might you see in GCA temporal artery biopsy?

A

Granulomatous lesions

484
Q

What might you see on angiography in polyarteritis nodosa?

A

Saccular/fusiform aneurysms and arterial stenoses

485
Q

What is Wegeners granulomatosis?

A

Systemic necrotising granulomatous vasculitis

486
Q

What cutaneous lesions might you see in Wegeners granulomatosis?

A

Ulceration
Nodules
Purpura

487
Q

What might you see in sinus imaging in Wegeners granulomatosis?

A

Mucosal thickening and air fluid levels

488
Q

What are the main treatments for vasculitides?

A

Immunosupression

489
Q

What HLA allele is associated with seronegative spondyloarthropathies?

A

HLA-B27

490
Q

What does seronegativemean in seronegative spondyloarthropathies?

A

RF -ve

491
Q

What are the common features of seronegative spondyloarthropathies?

A

Peripheral arthritis, usually asymmetrical
Sacroilitis
Enthensopathy, e.g. Achilles tendonitis, plantar fasciitis
Extra-articular manifestations e.g. uveitis, pulmonary fibrosis (upper zone), amyloidosis, aortic regurg

492
Q

What are the seronegative spondyloarthropathies?

A

ankylosing spondylitis
psoriatic arthritis
Reiter’s syndrome (including reactive arthritis)
enteropathic arthritis (associated with IBD)

493
Q

What kind of hearing loss do you get in Paget’s?

A

Sensorineural

494
Q

After someone is on bisphosphonates for how many years can you consider stopping them?

A

5 years or 3 for IV zolendronate - reassess need for ongoing treatment, if T score >-2.5 can stop and review in 2y

495
Q

What things would make you keep someone on bisphosphonates indefinitely?

A 
Age >75
Glucocorticoid therapy
Previous hip/vertebral fractures
Further fractures on treatment
High risk on FRAX scoring
T score
496
Q

What criteria can be used to diagnose RA?

A

2010 American College of Rheumatology criteria

497
Q

Who should you consider a diagnosis of RA in?

A

Those with:

  1. At least 1 joint with definite clinical synovitis
  2. synovitis is not better explained by another disease
498
Q

What score is needed on the 2010 American College of Rheumatology criteria for a diagnosis of RA?

A

6/10

499
Q

What is the 2010 American College of Rheumatology criteria for a diagnosis of RA?

A 
A) JOINT INVOLVEMENT
1 large joint = 0
2-10 large joints = 1
1-3 small joints = 2
4-10 small joints = 3
10 joints (at least 1 small) = 5

B. SEROLOGY
-ve RF + ACPA = 0
low +ve RF or ACPA = 2
high positive RF or ACPA = 3

C. ACUTE PHASE REACTANTS
Normal CRP + ESR = 0
Abnormal CRP or ESR = 1

D. DURATION OF SYMPTOMS
<6w = 0
>6w = 1

500
Q

What investigation should you do before starting someone on TNF inhibitors?

A

CXR - TNF inhibitors can cause reactivation of TB

MSK (27 decks)

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