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
2
Q
What is a large risk factor for OA
A
Genetics!!!
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
4
Q
What is primary OA?
A
Involves characteristic locations and most likely due to genetic predisposition (abnormal joint physiology)
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)
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
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
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
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
10
Q
Common sites for primary OA
A
Spine, hip, knee, distal and intermediate IP joints
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
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
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
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
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
16
Q
Cause of pain at rest in OA
A
Inflammation with effusion and joint capsule distention
17
Q
Cause of pain at night in OA
A
Intra-osseous hypertension
18
Q
What causes structural changes in OA?
A
Bony enlargement, crepitus, deformity, instability and restricted movement
19
Q
What muscle changes are common in OA?
A
Muscle weakness or wasting
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
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
22
Q
Medication to help OA x5
A
Analgesics - paracetamol followed by topic NSAIDs or capsaicin
Oral NSAIDs (highly selective COX inhibitors)
Weak opioids
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
24
Q
Problems with weak opioids for OA
A
Good pain relief BUT CNS side effects eg. headache, constipation and confusion
25
What are alternative medications for older high-risk OA patients
Nutraceuticals - no renal or GI side effects
| eg. Glucosamine or chondroitin sulphate
26
Injection treatment options for OA x2
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
27
Surgical treatment for OA
Prosthetic joint replacements - hip and knee especially but now also shoulder, elbow and thumb base
28
Surgical treatment for mechanical locking in OA
Arthroscopic debridement and lavage - symptomatic improvement from lavage alone can last several months
29
What does the term "gout" include? x3
An acute attack, the propensity for repeated episodes and also for chronic gouty arthritis
30
What is the underlying pathology in gout?
Build up of urate which is a breakdown product of purine
31
What do humans lack which would help with urate?
Uricase - in other mammals it oxidises urate to allantoin - which is readily soluble
32
What can increase urate levels?
Increased dietary purine intake and increased breakdown of endogenous proteins (cancer treatment or haematological malignancy)
33
How is urate excreted and how can this affect levels?
Urate is mainly excreted renally - therefore renal problems or drugs affecting renal function can slow down renal urate excretion
34
Urinary urate in causes of gout
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
35
What is the serum concentration of urate needed for urine acid crystals to form?
>0.42mmol/l (>7.0g/dl)
36
Upper limit of normal range of serum urate in a) men and post-menopausal women b) pre-menopausal women
a) 0.42mmol/l (>7.0g/dl)
| b) 0.36mmol/l (>6.0g/dl)
37
Epidemiology of gout
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
38
Risk factors for gout x7
```
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
```
39
Why is gout rare in pre-menopausal women?
Possibly due to the uricosuric effects of oestrogens
40
Relationship of alcohol and gout
Strong relationship between beer intake and gout (purines in yeast)
Weak relationship between spirit intake and gout
No relationship between wine intake and gout
41
What is the relationship between gout and hyperuricaemaia
Hyperuricaemia is needed for gout (crystals cannot form if serum not >0.42mmol) BUT not everyone with hyperuricaemia develops gout
42
Which joint is most commonly affected in gout?
First metatarsophalangeal joint (base of big toe)
43
Clinical features of acute gout
Rapid onset of monoarthritis - severe pain and inflammation in joint with overlying skin erythema
Also may have low-grade fever, general malaise and anorexia
44
What can onset of acute gout follow?
Drinking bout or local trauma
| Infection, starvation, introduction or withdrawal of hypouricaemic agents
45
Progression of acute episode of gout?
Symptoms peak at 24hours
| Can resolve sponteanously in 7-10 days if untreated but can also last for several weeks
46
What are the other most commonly affected joints in gout?
Foot, ankle, knee, wrist, finger and elbow - more commonly peripheral joints because crystals more likely to form in cooler joints
47
When in the day do gout attacks typically occur?
At night
48
Gold standard for diagnosing gout and the problem?
Urate crystals in synovial fluid BUT not many people with acute gout are going to want their joint aspirated
49
Appearance of urate and pyrophosphate crystals on polarising microscopy?
Urate crystals are strongly negatively birefringent on polarising microscopy
- Pyrophosphate are weakly positively birefringent
50
What DDX needs to excluded with gout?
Septic arthritis
51
What can chronic gout cause in older people?
Inflammatory arthritis - especially those on diuretics
52
What deposits can occur in chronic gout?
Crystal deposits (tophi) can develop around the joints or in the skin or cartilage - Chronic tophi gout can also have persistent low-grade fever
53
Common sites for tophi? x4
Develop around hands, feet, elbows and ears
54
In who are tophi particularly common?
Older women with secondary, diuretic-induced gout
| They may develop without a history of acute gout
55
What is the composition of tophi?
Chalky deposits of urate embedded in matrix of lipid, protein and calcific debris
56
What renal complication can arise in gout? Incidence?
1 in 5 with gout over-excrete urate and may develop urate stones
57
What % of renal stones are pure urate?
5%
58
What can gout in childhood be a manifestation of?
Rare inherited disorders of metabolism such as Lesch-Nyhan syndrome, G6PD deficiency
59
Treatment of acute gout
NSAID's/COX-2 inhibitor + PPI
60
Treatment of acute gout in those who can't tolerate NSAIDs - problem with it
Colchicine - high doses can cause gastrointestinal upset such as diarrhoea
Lower doses are generally better tolerated
61
Other treatment of severe acute gout
Corticosteroids
| Can be taken systemically or injected eg. directly into the joint
62
Lifestyle management for gout
Lose weight, reduce fish and meat intake, increase low-fat dairy intake, reduce alcohol intake and avoid beer
63
Main treatment for prevention of gout attack
Urate-lowering medication - Xanthine oxidase inhibitors eg. Allopurinol or Febuxostat
64
What can starting xanthine oxidase inhibitor cause
Can cause an acute attack of gout
| Will also prolong an existing attack and therefore shouldn't be given during one
65
Two other less common drugs used for preventing gout attacks
Benzbromarone, probenecid and sulfinpyrazone - are uricosuric drugs which work by inhibiting tubular reabsorption - only really used if people can't take xanthine oxidase inhibitors
66
How do xanthine oxidase inhibitors work?
Prevent purine breakdown products xanthine and hypoxanthine being converted into urate
67
Which 4 drugs have been found to lower urate levels - but are not licensed for treatment of gout?
Losartan
Fenofibrate
Atorvastatin
Amlodipine
68
What happens in pseudogout?
Deposition of calcium pyrophosphate dihydrate (CPPD) crystals in cartilage
69
Which joints are most commonly affected in pseudogout?
Knees, ankles, shoulders, elbows, wrists or hands
70
Treatment of acute pseudogout episodes?
NSAIDs or intraarticular steroids
| Lifestyle modifications similar to those for osteoarthritis
71
Prevention of pseudogout
Long-term NSAIDs or colchicine (oral daily for patients with >3 attacks annually)
72
What is the hypothesised pathology of rheumatoid arthritis?
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
73
What is key effector cell in RA and how?
T-cell it mediates an immune response through a host of cytokines
74
What are the two key cytokines involved in pathogenesis of RA
TNF-alpha and Interleukin 1
75
Which genetic component has been found to be significant in RA
HLA-DR4 - established as a marker of prevalence as well as severity
76
When does RA commonly occur in men?
Rare before age of 30, increasing incidence with age
77
When does RA commonly occur in women
Steadily increases in incidence from mid-20s to peak incidence between 45 and 75 years
78
How are joints affected in common presentation of RA
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
79
What are 3 less common forms of presentation of RA
Acute monoarticular, palindromic rheumatism and asymmetrical large joint arthritis
80
What is palindromic rheumatism?
Rare episodic form of RA where pain and inflammation occurs in attacks and between attacks the joints are normal
81
What is the spinal involvement of RA
Spine is rarely affected apart from cervical spine
82
5 red flags in RA
```
Atlanto-axial subluxatoin
Amyloidosis
Pericarditis
Monoarticular flare
Eye involvement
```
83
What are warning signs of atlanto-axial subluxation in RA? x4
Pain around the occiput, radiating arm pain, numbness or weakness of the limbs and vertigo on neck movement
84
What can happen if atlanto-axial subluxation is not picked up on in RA?
Sudden death - especially if patients undergo neck manipulation for intubation during surgical procedures
85
What can amyloidosis in RA cause?
Renal deposition of amyloid can be a features of long standing RA
86
Signs of renal amyloid deposition in RA
Suspect if increasing leg oedema, proteinuria and worsening renal function
87
What else can cause renal dysfunction in RA
Gold or penicillamine induced proteinuria
88
What are signs of eye involvement in RA
Sudden onset of eye pain and increased lacrimation - possible scleritis
89
What can untreated RA scleritis lead to?
Thinning of sclera and risk of perforation = scleromalacia perforans
90
Indications of RA in the history
Progressive pattern of joint involvement, stiffness and increased pain after period of inactivity
History of joint swellings
FHx of rheumatological disease
91
What are acute-phase haemotological responses associated with RA? x4
High ESR or CRP
High platelet count
High serum ferritin
92
Significance of rheumatoid factor in RA
Can be used to support diagnosis but it is not conclusive as RF is present in a number of conditions
93
What is a more specific marker for RA than RF?
Anti-cyclic citrullinated peptide (anti-CCP) - more specific and sensitive than RF
94
What do you see radiologically with RA?
Classical periarticular erosions, joint space narrowing, osteopenia - characteristic and may appear within first 3 years of disease
95
What can MRI pick up in RA?
Early synovitis and bone oedema - to pick up early disease
96
DDX of RA x3
```
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
New favoured approach for treating RA?
More aggressive combination of drugs in early disease and then "step down" when disease is under control
98
Use of NSAIDs in RA?
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
Other symptomatic treatment of RA
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
What is one of the oldest disease modifying anti-rheumatic drugs?
Gold - decline in popularity due to weekly injections, poor oral success and toxicity (skin rash or nephrotoxicity) problems
101
What is the gold standard DMARD?
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
How does methotrexate work in RA?
Believed to be due to induction of adenosine release to the inflammatory environment (different mechanism to its anti-malignancy effects)
103
What was the first drug (DMARD) developed specifically for treatment of RA?
Sulfasalazine
104
Side effects of Sulfasalazine x5
Minor GI upset or skin rashes can occur
| As can drug induced hepatitis, cytopenias and Steven-Johnson syndrome. oligospermia
105
What affects the half-life of sulfasalazine?
Acetylation status - therefore slow acetylators are more likely to develop toxicity
106
What other drug is often used in combination with other DMARDs
Hydroxychloroquine - anti-malarial, effective in early and mild disease but no protection radiologically therefore often used in combination with other drugs
107
What is the newest DMARD?
Leflunomide - inhibits de novo synthesis of pyrimidines
108
When is Leflunomide used in RA?
May be useful in patients who have failed to respond to methotrexate - can be used in combination to improve response
109
Problem with leflunomide in pre-menopausal women
Has recommended washout period of up to 2 years pre-conception therefore careful planning is needed in premenopausal women
110
Anti-TNF alpha drugs in RA
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
Drug targeting interleukin 1 for RA
Anakinra - recombinant human IL-1 receptor antagonist
112
Best benefit with Anakinra in RA
Modest clinical improvement but striking improvement in radiological progression
113
Idea behind targeting B-cells in RA?
B-cells help T-cell activation and antigen presentation
114
Drug targeting B cell in RA?
Rituximab - targets B cell surface marker CD20
| Effective at suppressing inflammatory parameters and limiting joint damage in RA
115
How does Abatacept work in RA?
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
Coexisting problems in RA
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
What are the entheses?
Sites where tendons or ligaments insert onto the bone - inflammation = enthesitis and pathology = enthesopathy
118
What is ankylosis?
Abnormal stiffening and immobility of a joint due to fusion of the bones
119
What does spondylo- refer to?
The vertebrae of the spine
120
What HLA are spondyloarthritides associated with?
HLA B27
121
In what age human do spondyloarthrides occur in?
Occur in children and adults but spinal involvement is rare in children
122
What is needed for a diagnosis of Spondyloarthritis (SpA)
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
Main SpA's x6
```
Ankylosing spondylitis
Psoriatic arthritis
Reactive arthritis (Reiter's syndrome)
Enteropathic arthritis
Undifferentiated SpA
Childhood SpA
```
124
Where are SpA more common?
North America and Europe - prevalence of HLA-B27 is higher here
125
What is ankylosing spondylitis?
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
Incidence of AS
0.2% of population
2% of HLA-B27 population
20% of HLA-B27 population with FHx
127
Male:Female of AS
Male predominate
2.5-5:1
Males present earlier: 6:1 at 16 years and 2:1 at 30 years
128
When does AS typically begin
Young adulthood
| But symptoms can arise in adolescence or earlier
129
What is the first symptom of AS usually?
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
What often accompanies inflammatory back pain with presentation of AS
Fatigue
131
What does AS lead to?
Uncontrolled inflammation will lead to progressive stiffness and loss of spinal mobility due to reactive new bone formation from inflammation
132
What clinical criteria are needed for AS
Inflammatory back pain
Limitation of spinal motion in both sagittal and frontal planes
Limitation of chest expansion
133
What is seen on radiograph of sacroiliac joints in AS? x4
Erosions in the joint line, pseudowidening, subchondral sclerosis and finally ankylosis
134
What is definite AS diagnosis
Radiological criteria + >1 clinical criteria
135
Probable AS diagnosis
3 clinical criteria OR
| Radiological criteria without any signs or symptoms of clinical criteria
136
What is seen in radiograph of spine in AS?
Squaring and "shiny corners" of the vertebral bodies
Later - syndesmophytes and facet-joint fusion
Calcification of lateral and anterior spinal ligaments
137
What is the incidence of peripheral arthritis with AS?
Up to 30% typically develop it
138
What sort of peripheral arthritis do you get in AS?
Asymmetrical oligoarthritis affecting leg joints, most commonly the knee
139
Other features of AS which cause heel pain
Enthesitis - at achilles tendon with associated bursitis and at plantar fascia - highly characteristic of AS but also in other SpA's
140
What else can occur in feet in SpA's including AS
Dactylitis (can occur in hands but usually a toe - causing "sausage toe") strongly suggestive of SpA
141
What affects 40% AS patients at some time?
Acute anterior uveitis (iritis) - typically unilateral - causing pain, photophobia and if untreated impaired visual acuity
142
Radiological progression in AS as recorded with Modified Stoke AS Spinal Score
```
0 = normal
1 = erosion, sclerosis or squaring
2 = syndesmophyte
3 = bridging syndesmophyte
```
143
What bone condition can develop in AS?
Osteoporosis - predisposing to spinal fractures
144
Key features of psoriatic arthritis?
Psoriasis, inflammatory arthritis, enthesitis, dactylitis and in minority sacroiliitis or spondylitis
145
What differentiates the arthritis psoriatic arthritis from the other SpA's?
It is the only SpA in which the small joints of the hands are frequently affected
146
What is arthritis mutilans?
Osteolysis resulting in destruction of the small joints of the digits with shortening
147
Features of arthritis in psoriatic arthritis x5
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
What % of psoriasis sufferers have some form of arthritis?
5-15%
149
What are psoriatic nail changes
Pitting, onycholysis and hyperkeratosis - seen in 80% of patients
150
Features of skin lesions in psoriatic arthritis
Can be subtle - look in scalp and natal cleft
151
What is reactive arthritis (ReA)?
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
How long after infection does ReA typically occur?
Usually 1-3 weeks
153
Pattern of arthritis in ReA?
Asymmetrical oligoarthritis especially affecting the leg joints
154
What else can you get in ReA?
Enthesitis (achilles tendonitis or plantar fasciitis - as with AS)
Dactylitis
Sacroiliitis
155
What is Reiter's syndrome?
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
What is keratoderma blennorrhagicum?
A painless papulosquamous eruption on palms or soles -which is a mucocutaneous lesion in Reiters
157
What other mucocutanous lesions can be seen in Reiters
Circinate balanitis, keratoderma blenorrhagicum and painless lingual or oral ulcers
158
What is enteropathic arthritis?
Inflammatory arthritis + IBD (esp. UC and Crohns)
159
How do bowel and peripheral joint problems usually occur in enteropathic arthritis?
Usually occur independently and arthritis may wax and wane over years
160
What is type 1 arthropathy?
Affects 5% of IBD patients
Oligoarticular arthritis typically affecting the knees - self-limiting without joint deformities, may precede onset of IBD symptoms
161
What can also occur in type 1 arthropathy?
Enthesitis of achilles tendon and plantar fascia and dactylitis
162
What is type 2 arthropathy?
Affects 3% of IBD patients
| Usually polyarticular arthritis affecting MCP joints but also other joints - usually in migratory fashion
163
What occurs in 20% of IBD patients
Sacroiliitis and spondylitis
164
What is undifferentiated spondyloarthritis?
Inflammatory back pain or peripheral large joint arthritis in HLA-B27 positive - without fullfilling criteria for a subtype
165
What is 1st line treatment for sacroiliitis and spondylitis?
Regular physio and exercise
NSAIDs - naproxen or diclofenac
or COX-2 inhibitors - etoricoxib or celecoxib
166
What is 2nd line treatment for sacroiliitis and spondylitis?
Oral and IM corticosteroids - should be avoided longterm
| Or local into sacroiliac joints
167
What is 3rd line treatment for sacroiliitis and spondylitis?
Anti-TNF alpha agents
168
Adjunctive treatment for sacroillitis and spondylitis?
Bisphosphonates, calcium and vit D - improve bone density
| Low dose amitriptyine at night to improve sleep and reduce pain
169
What is 1st line treatment for oligoarthritis and/or enthesitis? x4
Analgesics - paracetamol or codeine-based drugs
Intra-articular or intra-lesional corticosteroid (not weight-bearing tendons)
NSAIDs
Orthotics
170
What is 2nd line treatment for oligoarthritis and/or enthesitis? x3
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
What is 3rd line treatment for oligoarthritis and/or enthesitis?
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
What is a neuropathic joint?
Due to diabetes, syphilis - charcot joint - rapid degeneration of bones secondary loss to loss of sensory input
173
What causes neuropathic joint?
Any disease causes reduced sensation in the foot
174
Main xray signs of neuropathic joint
Multiple losses of joint space
175
What part of spine is affected first in AS
Lumbar first and then progress to thoracic and cervical regions
176
When can you get chest pain with AS
Pleuritic chest pain from involvement of costovertebral joints
177
When do you get posture changes in AS and what sort?
Later in the disease
| Thoracic kyphosis and spinal fusion leading to question mark posture
178
Cardiac consequence of AS
Aortic regurge
179
Lung complication of AS
Apical fibrosis - would show on CXR
180
Pneumonic for raised urea levels related to gout
CAN'T LEAP
Cyclophosphamide/ciclosporin
Aspirin (low dose)
Nicotine/nicotinic acid
Thiazides
Loop diuretics
Ethambutol (TB)
Alcohol
Pyrazinamide (TB)
181
Pathology of psuedogout
Excessive cartilage pyrophosphate production leading to local calcium pyrophosphate supersaturation and CPPD crystal formation/deposition
182
What causes acute attack of pseudogout arthritis
Shedding of crystals into joint cavity
183
What predisposes to pseudogout
Most causes of joint damage eg. osteoarthritis trauma
| More rarely - haemachromatosis, hyperparathyroidism, hypomagnesiumia, hypophosphatasia
184
Provoking factors for pseudogout
Intercurrent illness, surgery, local trauma
185
Who is pseudogout more common in
Women (2:1) and in the elderly > 60
186
Acute presentation of pseudogout
Painful swollen joint - red hot and tender with restricted ROM and fever
187
Features of chronic arthropathy
Pain, stiffness and functional impairment similar to osteoarthritis - bony swelling, crepitus, deformity
188
Investigations in pseudogout
Microscopy - weak positive bifringent crystals
| Plain radiograph - chondrocalcinosis or signs of osteoarthritis
189
What type of nodes do you get in OA?
```
Heberdens nodes (DIPs)
Bouchards nodes (PIPs)
```
190
Later hand features of RA x7
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
Surgical options in RA x4
Synovectomy, arthrodesis, arthroplasty or tendon repair
192
HLA associated with reactive arthritis
HLA-B27 identified in 70-80% of patients
193
Gender ratio for reactive arthritis
20:1 M:F
194
Management of arthritis of reactive arthritis
Initially rest with NSAIDs - aspirate effusions then when articular infection excluded give intra-articular steroids if NSAIDs haven't worked
195
If initial arthritis management doesn't work?
Can try sulfasalazine or etanercept (if CI or intolerance to sulfasalazine)
196
Management of circinate balanitis
1% hydrocortisone cream
197
Prognosis of reactive arthritis
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
