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Ortho and Rheum > Arthritis - OA, RA, Gout, Spondyloarthritides > Flashcards

Arthritis - OA, RA, Gout, Spondyloarthritides Flashcards

1
Q

Two ways in which OA can arise

A

Abnormal biomechanical stress on a normal joint
OR
Normal stresses applied to an inherently compromised joint with abnormal physiology

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2
Q

What is a large risk factor for OA

A

Genetics!!!

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3
Q

How does bone density influence OA x2

A

High bone density is a RF for development of hand, hip and knee OA
Low bone density is a RF for more rapid progression of hip and knee OA

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4
Q

What is primary OA?

A

Involves characteristic locations and most likely due to genetic predisposition (abnormal joint physiology)

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5
Q

What is secondary OA?

A

When OA occurs at atypical joints (eg. ankle) suspect secondary OA - often abnormal joint stressors such as joint trauma, previous fracture, inflammatory arthropathy (gout)

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6
Q

When does joint trauma usually lead to OA and what sort?

A

15-20- years after the insult - can therefore be a cause of young-onset monoarticular or pauciarticular (less than 4 joints affected) OA

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7
Q

What type of hand OA is an indicator for subsequent knee OA etc

A

Multiple Heberden’s nodes - sign of primary OA therefore genetic predisposition to OA elsewhere

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8
Q

What can lead to a very severe form of OA?

A

Abnormal stresses on abnormal joint morphology - eg. meniscus tear in someone with hand OA, more likely to get severe knee OA

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9
Q

Risk factors for OA x8

A 
Genetics,
Race (hip OA especially prevalent in Caucasians)
Age 
Sex (women worse everywhere except hip)
Obesity (knee++)
Bone density 
Abnormal joint shape and alignment 
Joint trauma and usage
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10
Q

Common sites for primary OA

A

Spine, hip, knee, distal and intermediate IP joints

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11
Q

Presenting manifestations of OA x5

A

Pain, loss of joint motion and function, minimal morning stiffness, short-lived stiffness after resting
AND absence of systemic symptoms or other system involvement

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12
Q

Pathology behind joint stiffness in OA

A

Accumulation of hyaluronan and hylauronan fragments in deep layers of arthritic synovium during rest - pushes water out
Joint movement then mobilises hyaluronan from the tissue and improves stiffness symptoms

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13
Q

What do the cartilage changes of OA encourage?

A

Deposition of crystals (calcium and urate) - in the joints, therefore can have superadded acute pseudogout

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14
Q

What can lead to increased risk of secondary gout with OA

A

If on long-term thiazide diuretics or have chronic renal impairment - in combination with normal increased risk of deposition of crystals

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15
Q

Cause of pain with use in OA

A

Mechanical joint damage, enthesopathy (pain at tendon attachment to bone) from ligament or ligamentous attachments

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16
Q

Cause of pain at rest in OA

A

Inflammation with effusion and joint capsule distention

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17
Q

Cause of pain at night in OA

A

Intra-osseous hypertension

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18
Q

What causes structural changes in OA?

A

Bony enlargement, crepitus, deformity, instability and restricted movement

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19
Q

What muscle changes are common in OA?

A

Muscle weakness or wasting

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20
Q

What is seen on X-ray with OA? x4

A

Joint space narrowing, marginal osteophyte or “spur” formation and subchondral sclerosis of bone - also bone cysts in intra-articular bone

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21
Q

Lifestyle modifications for management of OA x6

A

Exercise - both quadriceps strengthening exercises and aerobic activity help
Pool exercise can help reduce joint loading in overweight people
Pacing out physically hard jobs throughout the day
Weight loss
Appropriate footwear
Walking aids

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22
Q

Medication to help OA x5

A

Analgesics - paracetamol followed by topic NSAIDs or capsaicin
Oral NSAIDs (highly selective COX inhibitors)
Weak opioids

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23
Q

Problems with NSAIDs for OA

A

GI ulceration risk with typical NSAIDs

Highly selective COX inhibitors - increase risk of MI and stroke you

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24
Q

Problems with weak opioids for OA

A

Good pain relief BUT CNS side effects eg. headache, constipation and confusion

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25
Q

What are alternative medications for older high-risk OA patients

A

Nutraceuticals - no renal or GI side effects

eg. Glucosamine or chondroitin sulphate

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26
Q

Injection treatment options for OA x2

A

Intra-articular steroid injection, quick pain relief that may last few weeks-months (may help for an important event eg. holiday)
Hylauronan preparations are also available - modest prolonged improvement

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27
Q

Surgical treatment for OA

A

Prosthetic joint replacements - hip and knee especially but now also shoulder, elbow and thumb base

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28
Q

Surgical treatment for mechanical locking in OA

A

Arthroscopic debridement and lavage - symptomatic improvement from lavage alone can last several months

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29
Q

What does the term “gout” include? x3

A

An acute attack, the propensity for repeated episodes and also for chronic gouty arthritis

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30
Q

What is the underlying pathology in gout?

A

Build up of urate which is a breakdown product of purine

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31
Q

What do humans lack which would help with urate?

A

Uricase - in other mammals it oxidises urate to allantoin - which is readily soluble

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32
Q

What can increase urate levels?

A

Increased dietary purine intake and increased breakdown of endogenous proteins (cancer treatment or haematological malignancy)

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33
Q

How is urate excreted and how can this affect levels?

A

Urate is mainly excreted renally - therefore renal problems or drugs affecting renal function can slow down renal urate excretion

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34
Q

Urinary urate in causes of gout

A

If primarily an increased purine turnover cause then will be high urinary urate - if it is primarily a renal problem then will have low urinary urate

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35
Q

What is the serum concentration of urate needed for urine acid crystals to form?

A

> 0.42mmol/l (>7.0g/dl)

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36
Q

Upper limit of normal range of serum urate in a) men and post-menopausal women b) pre-menopausal women

A

a) 0.42mmol/l (>7.0g/dl)

b) 0.36mmol/l (>6.0g/dl)

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37
Q

Epidemiology of gout

A

Probably about 1% in caucasians
Rare in pre-menopausal women
Higher in pacific islands and new zealanders
Also Malaysia
May be higher in black afro-caribbean ethnic groups
More common in high social classes

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38
Q

Risk factors for gout x7

A 
Age (older)
Sex (male, rare in premenopausal women)
Obesity 
Diet (meat and fish increase risk, dairy products reduce risk)
Dietary fructose (sweeteners in US)
Drugs (thiazide diuretics) 
Alcohol (beer>>spirits>>wine)
Environmental lead exposure
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39
Q

Why is gout rare in pre-menopausal women?

A

Possibly due to the uricosuric effects of oestrogens

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40
Q

Relationship of alcohol and gout

A

Strong relationship between beer intake and gout (purines in yeast)
Weak relationship between spirit intake and gout
No relationship between wine intake and gout

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41
Q

What is the relationship between gout and hyperuricaemaia

A

Hyperuricaemia is needed for gout (crystals cannot form if serum not >0.42mmol) BUT not everyone with hyperuricaemia develops gout

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42
Q

Which joint is most commonly affected in gout?

A

First metatarsophalangeal joint (base of big toe)

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43
Q

Clinical features of acute gout

A

Rapid onset of monoarthritis - severe pain and inflammation in joint with overlying skin erythema
Also may have low-grade fever, general malaise and anorexia

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44
Q

What can onset of acute gout follow?

A

Drinking bout or local trauma

Infection, starvation, introduction or withdrawal of hypouricaemic agents

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45
Q

Progression of acute episode of gout?

A

Symptoms peak at 24hours

Can resolve sponteanously in 7-10 days if untreated but can also last for several weeks

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46
Q

What are the other most commonly affected joints in gout?

A

Foot, ankle, knee, wrist, finger and elbow - more commonly peripheral joints because crystals more likely to form in cooler joints

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47
Q

When in the day do gout attacks typically occur?

A

At night

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48
Q

Gold standard for diagnosing gout and the problem?

A

Urate crystals in synovial fluid BUT not many people with acute gout are going to want their joint aspirated

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49
Q

Appearance of urate and pyrophosphate crystals on polarising microscopy?

A

Urate crystals are strongly negatively birefringent on polarising microscopy
- Pyrophosphate are weakly positively birefringent

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50
Q

What DDX needs to excluded with gout?

A

Septic arthritis

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51
Q

What can chronic gout cause in older people?

A

Inflammatory arthritis - especially those on diuretics

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52
Q

What deposits can occur in chronic gout?

A

Crystal deposits (tophi) can develop around the joints or in the skin or cartilage - Chronic tophi gout can also have persistent low-grade fever

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53
Q

Common sites for tophi? x4

A

Develop around hands, feet, elbows and ears

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54
Q

In who are tophi particularly common?

A

Older women with secondary, diuretic-induced gout

They may develop without a history of acute gout

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55
Q

What is the composition of tophi?

A

Chalky deposits of urate embedded in matrix of lipid, protein and calcific debris

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56
Q

What renal complication can arise in gout? Incidence?

A

1 in 5 with gout over-excrete urate and may develop urate stones

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57
Q

What % of renal stones are pure urate?

A

5%

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58
Q

What can gout in childhood be a manifestation of?

A

Rare inherited disorders of metabolism such as Lesch-Nyhan syndrome, G6PD deficiency

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59
Q

Treatment of acute gout

A

NSAID’s/COX-2 inhibitor + PPI

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60
Q

Treatment of acute gout in those who can’t tolerate NSAIDs - problem with it

A

Colchicine - high doses can cause gastrointestinal upset such as diarrhoea
Lower doses are generally better tolerated

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61
Q

Other treatment of severe acute gout

A

Corticosteroids

Can be taken systemically or injected eg. directly into the joint

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62
Q

Lifestyle management for gout

A

Lose weight, reduce fish and meat intake, increase low-fat dairy intake, reduce alcohol intake and avoid beer

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63
Q

Main treatment for prevention of gout attack

A

Urate-lowering medication - Xanthine oxidase inhibitors eg. Allopurinol or Febuxostat

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64
Q

What can starting xanthine oxidase inhibitor cause

A

Can cause an acute attack of gout

Will also prolong an existing attack and therefore shouldn’t be given during one

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65
Q

Two other less common drugs used for preventing gout attacks

A

Benzbromarone, probenecid and sulfinpyrazone - are uricosuric drugs which work by inhibiting tubular reabsorption - only really used if people can’t take xanthine oxidase inhibitors

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66
Q

How do xanthine oxidase inhibitors work?

A

Prevent purine breakdown products xanthine and hypoxanthine being converted into urate

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67
Q

Which 4 drugs have been found to lower urate levels - but are not licensed for treatment of gout?

A

Losartan
Fenofibrate
Atorvastatin
Amlodipine

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68
Q

What happens in pseudogout?

A

Deposition of calcium pyrophosphate dihydrate (CPPD) crystals in cartilage

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69
Q

Which joints are most commonly affected in pseudogout?

A

Knees, ankles, shoulders, elbows, wrists or hands

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70
Q

Treatment of acute pseudogout episodes?

A

NSAIDs or intraarticular steroids

Lifestyle modifications similar to those for osteoarthritis

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71
Q

Prevention of pseudogout

A

Long-term NSAIDs or colchicine (oral daily for patients with >3 attacks annually)

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72
Q

What is the hypothesised pathology of rheumatoid arthritis?

A

An antigen in genetically predisposed individual initiates self-perpetuating immune response which cross-reacts with host tissue causing autoimmune synovitis and subsequent hypertrophy - this hypertrophy is the key factor that leads to cartilage and bone destruction - leading to progressive joint damage and disability

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73
Q

What is key effector cell in RA and how?

A

T-cell it mediates an immune response through a host of cytokines

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74
Q

What are the two key cytokines involved in pathogenesis of RA

A

TNF-alpha and Interleukin 1

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75
Q

Which genetic component has been found to be significant in RA

A

HLA-DR4 - established as a marker of prevalence as well as severity

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76
Q

When does RA commonly occur in men?

A

Rare before age of 30, increasing incidence with age

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77
Q

When does RA commonly occur in women

A

Steadily increases in incidence from mid-20s to peak incidence between 45 and 75 years

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78
Q

How are joints affected in common presentation of RA

A

Small joints of the hands and feet are affected symmetrically - predominantly the MCP joints, PIP joints and the wrists in the hand
And then MTP and forefoot joints in the feet

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79
Q

What are 3 less common forms of presentation of RA

A

Acute monoarticular, palindromic rheumatism and asymmetrical large joint arthritis

80
Q

What is palindromic rheumatism?

A

Rare episodic form of RA where pain and inflammation occurs in attacks and between attacks the joints are normal

81
Q

What is the spinal involvement of RA

A

Spine is rarely affected apart from cervical spine

82
Q

5 red flags in RA

A 
Atlanto-axial subluxatoin 
Amyloidosis
Pericarditis 
Monoarticular flare
Eye involvement
83
Q

What are warning signs of atlanto-axial subluxation in RA? x4

A

Pain around the occiput, radiating arm pain, numbness or weakness of the limbs and vertigo on neck movement

84
Q

What can happen if atlanto-axial subluxation is not picked up on in RA?

A

Sudden death - especially if patients undergo neck manipulation for intubation during surgical procedures

85
Q

What can amyloidosis in RA cause?

A

Renal deposition of amyloid can be a features of long standing RA

86
Q

Signs of renal amyloid deposition in RA

A

Suspect if increasing leg oedema, proteinuria and worsening renal function

87
Q

What else can cause renal dysfunction in RA

A

Gold or penicillamine induced proteinuria

88
Q

What are signs of eye involvement in RA

A

Sudden onset of eye pain and increased lacrimation - possible scleritis

89
Q

What can untreated RA scleritis lead to?

A

Thinning of sclera and risk of perforation = scleromalacia perforans

90
Q

Indications of RA in the history

A

Progressive pattern of joint involvement, stiffness and increased pain after period of inactivity
History of joint swellings
FHx of rheumatological disease

91
Q

What are acute-phase haemotological responses associated with RA? x4

A

High ESR or CRP
High platelet count
High serum ferritin

92
Q

Significance of rheumatoid factor in RA

A

Can be used to support diagnosis but it is not conclusive as RF is present in a number of conditions

93
Q

What is a more specific marker for RA than RF?

A

Anti-cyclic citrullinated peptide (anti-CCP) - more specific and sensitive than RF

94
Q

What do you see radiologically with RA?

A

Classical periarticular erosions, joint space narrowing, osteopenia - characteristic and may appear within first 3 years of disease

95
Q

What can MRI pick up in RA?

A

Early synovitis and bone oedema - to pick up early disease

96
Q

DDX of RA x3

A 
Psoriatic disease (look for nail pitting or skin lesions)
Polyarticular gout (joint aspiration for crystals)
Malignant conditions such as leukaemia esp. in young people
97
Q

New favoured approach for treating RA?

A

More aggressive combination of drugs in early disease and then “step down” when disease is under control

98
Q

Use of NSAIDs in RA?

A

COX-1 inhibitors leads to GI problems
But selective COX-2 inhibitors have potential CV risks
However still used for symptomatic control - but little effect on joint damage or progression of disease

99
Q

Other symptomatic treatment of RA

A

Corticosteroids - mainstay for symptom control in RA
Multiple routes of administration are available, including local intra-articular injections and depot
Orally has quicker onset, can be used whilst waiting for DMARDs to have affect

100
Q

What is one of the oldest disease modifying anti-rheumatic drugs?

A

Gold - decline in popularity due to weekly injections, poor oral success and toxicity (skin rash or nephrotoxicity) problems

101
Q

What is the gold standard DMARD?

A

Methotrexate
All other DMARDs are compared against this
Excellent side effect profile except for post-dose nausea which can be controlled with folic acid

102
Q

How does methotrexate work in RA?

A

Believed to be due to induction of adenosine release to the inflammatory environment (different mechanism to its anti-malignancy effects)

103
Q

What was the first drug (DMARD) developed specifically for treatment of RA?

A

Sulfasalazine

104
Q

Side effects of Sulfasalazine x5

A

Minor GI upset or skin rashes can occur

As can drug induced hepatitis, cytopenias and Steven-Johnson syndrome. oligospermia

105
Q

What affects the half-life of sulfasalazine?

A

Acetylation status - therefore slow acetylators are more likely to develop toxicity

106
Q

What other drug is often used in combination with other DMARDs

A

Hydroxychloroquine - anti-malarial, effective in early and mild disease but no protection radiologically therefore often used in combination with other drugs

107
Q

What is the newest DMARD?

A

Leflunomide - inhibits de novo synthesis of pyrimidines

108
Q

When is Leflunomide used in RA?

A

May be useful in patients who have failed to respond to methotrexate - can be used in combination to improve response

109
Q

Problem with leflunomide in pre-menopausal women

A

Has recommended washout period of up to 2 years pre-conception therefore careful planning is needed in premenopausal women

110
Q

Anti-TNF alpha drugs in RA

A

Etanercept (human TNF receptor 2-immunoglobulin constant region fusion protein)
Then monoclonal Ab’s to human TNF - infliximab and adalimumab
Shown to be effectively clinically and on radiological progression

111
Q

Drug targeting interleukin 1 for RA

A

Anakinra - recombinant human IL-1 receptor antagonist

112
Q

Best benefit with Anakinra in RA

A

Modest clinical improvement but striking improvement in radiological progression

113
Q

Idea behind targeting B-cells in RA?

A

B-cells help T-cell activation and antigen presentation

114
Q

Drug targeting B cell in RA?

A

Rituximab - targets B cell surface marker CD20

Effective at suppressing inflammatory parameters and limiting joint damage in RA

115
Q

How does Abatacept work in RA?

A

Targets activation of T cells and disrupts T-cell contribution to inflammatory environment
Been proven to slow disease activity and joint damage in RA (not recommended for use in Britain yet)

116
Q

Coexisting problems in RA

A

Life expectancy can be reduced up to 7 years in men and 3 years in women but deaths not due to RA - therefore significant co-morbidities with RA - especially CV, therefore careful monitoring is needed

117
Q

What are the entheses?

A

Sites where tendons or ligaments insert onto the bone - inflammation = enthesitis and pathology = enthesopathy

118
Q

What is ankylosis?

A

Abnormal stiffening and immobility of a joint due to fusion of the bones

119
Q

What does spondylo- refer to?

A

The vertebrae of the spine

120
Q

What HLA are spondyloarthritides associated with?

A

HLA B27

121
Q

In what age human do spondyloarthrides occur in?

A

Occur in children and adults but spinal involvement is rare in children

122
Q

What is needed for a diagnosis of Spondyloarthritis (SpA)

A

Either
a) inflammatory spinal pain
or b) asymmetric or predominantly lower limb synovitis
plus c) any of following: psoriasis, IBD, alternating buttock pain, enthesopathy or sacroilitis

123
Q

Main SpA’s x6

A 
Ankylosing spondylitis 
Psoriatic arthritis 
Reactive arthritis (Reiter's syndrome) 
Enteropathic arthritis 
Undifferentiated SpA 
Childhood SpA
124
Q

Where are SpA more common?

A

North America and Europe - prevalence of HLA-B27 is higher here

125
Q

What is ankylosing spondylitis?

A

Aseptic inflammatory condition of the joints and entheses of the spine (attachment of ligaments to vertebral bodies) - preferentially affecting axial skeleton and large proximal joints

126
Q

Incidence of AS

A

0.2% of population
2% of HLA-B27 population
20% of HLA-B27 population with FHx

127
Q

Male:Female of AS

A

Male predominate
2.5-5:1
Males present earlier: 6:1 at 16 years and 2:1 at 30 years

128
Q

When does AS typically begin

A

Young adulthood

But symptoms can arise in adolescence or earlier

129
Q

What is the first symptom of AS usually?

A

Inflammatory back pain - insidious onset of lower back and/or buttock pain, present >3months, awakes from sleep, early morning stiffness and better with exercise

130
Q

What often accompanies inflammatory back pain with presentation of AS

A

Fatigue

131
Q

What does AS lead to?

A

Uncontrolled inflammation will lead to progressive stiffness and loss of spinal mobility due to reactive new bone formation from inflammation

132
Q

What clinical criteria are needed for AS

A

Inflammatory back pain
Limitation of spinal motion in both sagittal and frontal planes
Limitation of chest expansion

133
Q

What is seen on radiograph of sacroiliac joints in AS? x4

A

Erosions in the joint line, pseudowidening, subchondral sclerosis and finally ankylosis

134
Q

What is definite AS diagnosis

A

Radiological criteria + >1 clinical criteria

135
Q

Probable AS diagnosis

A

3 clinical criteria OR

Radiological criteria without any signs or symptoms of clinical criteria

136
Q

What is seen in radiograph of spine in AS?

A

Squaring and “shiny corners” of the vertebral bodies
Later - syndesmophytes and facet-joint fusion
Calcification of lateral and anterior spinal ligaments

137
Q

What is the incidence of peripheral arthritis with AS?

A

Up to 30% typically develop it

138
Q

What sort of peripheral arthritis do you get in AS?

A

Asymmetrical oligoarthritis affecting leg joints, most commonly the knee

139
Q

Other features of AS which cause heel pain

A

Enthesitis - at achilles tendon with associated bursitis and at plantar fascia - highly characteristic of AS but also in other SpA’s

140
Q

What else can occur in feet in SpA’s including AS

A

Dactylitis (can occur in hands but usually a toe - causing “sausage toe”) strongly suggestive of SpA

141
Q

What affects 40% AS patients at some time?

A

Acute anterior uveitis (iritis) - typically unilateral - causing pain, photophobia and if untreated impaired visual acuity

142
Q

Radiological progression in AS as recorded with Modified Stoke AS Spinal Score

A 
0 = normal 
1 = erosion, sclerosis or squaring
2 = syndesmophyte
3 = bridging syndesmophyte
143
Q

What bone condition can develop in AS?

A

Osteoporosis - predisposing to spinal fractures

144
Q

Key features of psoriatic arthritis?

A

Psoriasis, inflammatory arthritis, enthesitis, dactylitis and in minority sacroiliitis or spondylitis

145
Q

What differentiates the arthritis psoriatic arthritis from the other SpA’s?

A

It is the only SpA in which the small joints of the hands are frequently affected

146
Q

What is arthritis mutilans?

A

Osteolysis resulting in destruction of the small joints of the digits with shortening

147
Q

Features of arthritis in psoriatic arthritis x5

A

Any type can occur - can be asymmetrical oligoarthritis (50%), predominately small joint (5-10%), rheumatoid pattern (25%), arthritis mutilans (1-5%) or spondyloarthritis (20%)

148
Q

What % of psoriasis sufferers have some form of arthritis?

A

5-15%

149
Q

What are psoriatic nail changes

A

Pitting, onycholysis and hyperkeratosis - seen in 80% of patients

150
Q

Features of skin lesions in psoriatic arthritis

A

Can be subtle - look in scalp and natal cleft

151
Q

What is reactive arthritis (ReA)?

A

Aseptic arthritis occur subsequent to an extra-articular infection, typically of GI or GU tract
Initial activation of immune system followed by autoimmune reaction

152
Q

How long after infection does ReA typically occur?

A

Usually 1-3 weeks

153
Q

Pattern of arthritis in ReA?

A

Asymmetrical oligoarthritis especially affecting the leg joints

154
Q

What else can you get in ReA?

A

Enthesitis (achilles tendonitis or plantar fasciitis - as with AS)
Dactylitis
Sacroiliitis

155
Q

What is Reiter’s syndrome?

A

ReA accompanied by urethritis, conjunctivitis or mucocutaneous lesions — although ReA is commonly being used to describe all of this
- can’t see, can’t pee, can’t climb a tree

156
Q

What is keratoderma blennorrhagicum?

A

A painless papulosquamous eruption on palms or soles -which is a mucocutaneous lesion in Reiters

157
Q

What other mucocutanous lesions can be seen in Reiters

A

Circinate balanitis, keratoderma blenorrhagicum and painless lingual or oral ulcers

158
Q

What is enteropathic arthritis?

A

Inflammatory arthritis + IBD (esp. UC and Crohns)

159
Q

How do bowel and peripheral joint problems usually occur in enteropathic arthritis?

A

Usually occur independently and arthritis may wax and wane over years

160
Q

What is type 1 arthropathy?

A

Affects 5% of IBD patients
Oligoarticular arthritis typically affecting the knees - self-limiting without joint deformities, may precede onset of IBD symptoms

161
Q

What can also occur in type 1 arthropathy?

A

Enthesitis of achilles tendon and plantar fascia and dactylitis

162
Q

What is type 2 arthropathy?

A

Affects 3% of IBD patients

Usually polyarticular arthritis affecting MCP joints but also other joints - usually in migratory fashion

163
Q

What occurs in 20% of IBD patients

A

Sacroiliitis and spondylitis

164
Q

What is undifferentiated spondyloarthritis?

A

Inflammatory back pain or peripheral large joint arthritis in HLA-B27 positive - without fullfilling criteria for a subtype

165
Q

What is 1st line treatment for sacroiliitis and spondylitis?

A

Regular physio and exercise
NSAIDs - naproxen or diclofenac
or COX-2 inhibitors - etoricoxib or celecoxib

166
Q

What is 2nd line treatment for sacroiliitis and spondylitis?

A

Oral and IM corticosteroids - should be avoided longterm

Or local into sacroiliac joints

167
Q

What is 3rd line treatment for sacroiliitis and spondylitis?

A

Anti-TNF alpha agents

168
Q

Adjunctive treatment for sacroillitis and spondylitis?

A

Bisphosphonates, calcium and vit D - improve bone density

Low dose amitriptyine at night to improve sleep and reduce pain

169
Q

What is 1st line treatment for oligoarthritis and/or enthesitis? x4

A

Analgesics - paracetamol or codeine-based drugs
Intra-articular or intra-lesional corticosteroid (not weight-bearing tendons)
NSAIDs
Orthotics

170
Q

What is 2nd line treatment for oligoarthritis and/or enthesitis? x3

A

DMARDs may be effective if aggressive, erosive or polyarticular disease
Methotrexate may be effective for both skin and joint disease
Sulphsalazine - for both joint and bowel disease in IBD

171
Q

What is 3rd line treatment for oligoarthritis and/or enthesitis?

A

If inadequate response to conventional DMARDs - Anti-TNF with etanercept, infliximab or adalimumab - can be very effective for skin and joint disease but not been proven as effective for IBD

172
Q

What is a neuropathic joint?

A

Due to diabetes, syphilis - charcot joint - rapid degeneration of bones secondary loss to loss of sensory input

173
Q

What causes neuropathic joint?

A

Any disease causes reduced sensation in the foot

174
Q

Main xray signs of neuropathic joint

A

Multiple losses of joint space

175
Q

What part of spine is affected first in AS

A

Lumbar first and then progress to thoracic and cervical regions

176
Q

When can you get chest pain with AS

A

Pleuritic chest pain from involvement of costovertebral joints

177
Q

When do you get posture changes in AS and what sort?

A

Later in the disease

Thoracic kyphosis and spinal fusion leading to question mark posture

178
Q

Cardiac consequence of AS

A

Aortic regurge

179
Q

Lung complication of AS

A

Apical fibrosis - would show on CXR

180
Q

Pneumonic for raised urea levels related to gout

A

CAN’T LEAP

Cyclophosphamide/ciclosporin
Aspirin (low dose)
Nicotine/nicotinic acid
Thiazides

Loop diuretics
Ethambutol (TB)
Alcohol
Pyrazinamide (TB)

181
Q

Pathology of psuedogout

A

Excessive cartilage pyrophosphate production leading to local calcium pyrophosphate supersaturation and CPPD crystal formation/deposition

182
Q

What causes acute attack of pseudogout arthritis

A

Shedding of crystals into joint cavity

183
Q

What predisposes to pseudogout

A

Most causes of joint damage eg. osteoarthritis trauma

More rarely - haemachromatosis, hyperparathyroidism, hypomagnesiumia, hypophosphatasia

184
Q

Provoking factors for pseudogout

A

Intercurrent illness, surgery, local trauma

185
Q

Who is pseudogout more common in

A

Women (2:1) and in the elderly > 60

186
Q

Acute presentation of pseudogout

A

Painful swollen joint - red hot and tender with restricted ROM and fever

187
Q

Features of chronic arthropathy

A

Pain, stiffness and functional impairment similar to osteoarthritis - bony swelling, crepitus, deformity

188
Q

Investigations in pseudogout

A

Microscopy - weak positive bifringent crystals

Plain radiograph - chondrocalcinosis or signs of osteoarthritis

189
Q

What type of nodes do you get in OA?

A 
Heberdens nodes (DIPs) 
Bouchards nodes (PIPs)
190
Q

Later hand features of RA x7

A

Ulnar deviation as a result of subluxation at MCP joints
Swan-neck deformity (hyperextented PIP and flexed DIP)
Radial deviation of wrist
Z deformity of thumb
Boutonniere deformity (flexion of PIP and hyperextension of DIP)
Trigger finger
Wasting of small muscles in hands and palmar erythema

191
Q

Surgical options in RA x4

A

Synovectomy, arthrodesis, arthroplasty or tendon repair

192
Q

HLA associated with reactive arthritis

A

HLA-B27 identified in 70-80% of patients

193
Q

Gender ratio for reactive arthritis

A

20:1 M:F

194
Q

Management of arthritis of reactive arthritis

A

Initially rest with NSAIDs - aspirate effusions then when articular infection excluded give intra-articular steroids if NSAIDs haven’t worked

195
Q

If initial arthritis management doesn’t work?

A

Can try sulfasalazine or etanercept (if CI or intolerance to sulfasalazine)

196
Q

Management of circinate balanitis

A

1% hydrocortisone cream

197
Q

Prognosis of reactive arthritis

A

Most remit completely or have little active disease 6 months after presentation
May still get occasional pain in joints, entheses or spine
Some may get chronic arthritis rarely and some develop ank spon

Ortho and Rheum (13 decks)

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