Flashcards in Rheumatology Deck (35)
What condition characteristically causes pain when brushing hair, jaw claudication and sudden loss of vision in one eye, and what needs to be done ASAP?
Giant cell arteritis (temporal arteritis).
Need to do an ESR, call ophthalmologist and give 40-60mg of prednisolone ASAP.
What level does the ESR rise to in GCA?
What two conditions are closely related (both cause high ESR)
GCA and polymyalgia rheumatica
PMR is not a true vasculitits but the two conditions often co-exist.
What are the symptoms of PMR?
<2weeks onet of symmetrical aching, tenderness and morning stiffness of the shoulders and proximal limb muscles.
Faitgue, fever, weight loss, anorexia and depression are often present.
When suspecting PMR what are you differential diagnoses?
Recent onset RA
Primary muscle disease
OA - cervical spondylosis, shoulder OA
bilateral subacromial impingement
What is the triad in Reiter's syndrome? (AKA reactive arthritis)
Urethritis, Arthritis, conjunctivitis
Which conditions are considered to be spondyloarthritides?
Reactive arthritis (Reiter's syndrome)
Enteropathic (associated with IBD)
What do spondyloarthripathies have in common?
Seronegative (Rh -ve)
HLA B27 association
Asymmetrical large joint arthritis
Enthesitis - inflammation of the site of insertion of tendons or ligaments into the bone (plantar fascitis, achilles tendonitis)
Dactylitis - inflammation of an entire digit due to soft tissue oedema and tenosynovial and joint inflammation
Extra-articular manifestations - iritis, psoriaform rashes, oral ulcers, aortic valve incompetence, IBD
What are the causes of gout?
Gout is caused by a build up of uric acid (the final product of endogenous and dietary purine metabolism).
The levels depend on a balance between purine synthesis and ingestion of dietary purine and the elimination of the urate (66% kidney, 33% intestine)
90% of patients have impaired excretion
chronic renal disease, drugs (diuretics, asprin), increased BP, lead toxicity, hyper PTH, hypo TSH, increased lactate production, G6PD
10% of patients have increased production
Increased purine synthesis (Lesch-nyan syndrome)
Increased turnover of purine (myeloproliferatiive disorders, lymphoproliferative disorders, carcinoma, psoriasis)
What finding is diagnostic for gout?
Synovial fluid showing negatively birefringent urate crystals on polarised light microscopy
How do you treat gout?
Acutely - NSAIDs or colchicine if CI
Prevention - loose weight, avoid: fasting, alcohol excess, high purine foods, and low dose aspirin.
Allopurinol can be used if recurrent attacks, tophi or renal stones, but it must not be started in an acute attack as may trigger a further attack, wait 3 weeks and then introduce. If have further attacks whilst on it do not stop it.
What are the differences between gout and pseudo-gout?
Gout = urate
Pseudo = calcium phosphate
Gout = -ve birefringent urate crystals
Pseudo = weakly +ve birefringent crystals
What are the common presentations of rheumatoid arthritis?
Slowly progressive, symmetrical polyarthritis, evolving over weeks - months.
Sero -ve or +ve for rheumatoid factor
+ve for Anti CCP (very specific)
Relapsing and remitting
Evolves over days and progresses over weeks.
Severe joint damage
Usually RF+ve and Anti CCP +ve
Lots of systemic manifestations
Acute monoarthritis, develops over 24-48hrs
50% progress to other types
Self limiting, <12 months, doesnt result in permanent joint damage
Describe the pathogenesis of rheumoatoid arthritis:
Synovitis is as a result of increased TNF
Chemoattractants in the joint recruit cirulating inflammatory cells
There is an inbalance of certain types of cells: synovial, abnormal fibroblasts, osteoclasts, B and T cells
Synovium becomes thickened, and results in a boggy swelling around the joints
Proliferation of the synvoium into folds and fronds
Presence of disorganised lymphoid follicles
Vascular proliferation with increased permeability
Hyperplastic synvoium moves onto cartilage surface and damages the cartilage by blocking nutrients
This leads to cartliage thinning and bone exposure with juxtaarticular oesteoporosis
What are the extra articular manifestations of rheumatiod arthritis?
Nodules - elbows and lungs
Pleural and pericardial effusions
Carpel tunnel syndrome
Splenomegaly (RA + Splenomegaly + neutropenia = Felty's syndrome)
Episcleritis, scleritis, scleromalacia, keratoconjunctivitis sicca
What is the difference between a butoniere and a swan neck deformity?
Butoniere is a fixed flexion deformity of the PIP
Swan neck is a hyperextension of the PIP
What are the diagnostic criteria for rheumatoid?
>6 points = RA morning stiffness for >1hour +
1 med-large joint = 0
2-10 med-large joints = 1
1-3 small joints = 3
>10 joints at least one small = 4
-ve RF -ve antiCCP = 0
low +ve RF low +ve antiCCP = 2
high +ve RF high +ve antiCCP = 3
6 weeks = 1
What is osteoporosis?
reduced bone mass
What are the causes of osetoporosis?
primary - old age
secondary - steroid use, hyperthyroidism, alcohol, low BMI, low testosterone, early menopause, renal or liver failure, bone disease (myeloma, RA, OA) Dietary, DM
What scores on a DEXA scan would initiate treatment?
>0 = bone density is better than reference
0 to -1 = bone density is in top 84%, no evidence of osteoporosis
-1 to -2.5 = osteopenia, risk of #, life style advice
-2.5 or worse = osteoporosis, treat and repeat DEXA in 2 yrs
What are the different pharmacoloigcal measures used to treat osteoporosis?
Calcium Vit D
Raloxifene - selective oestrogen receptor modulator
Teriparatide - recombinant PTH
What are the diagnostic criteria for SLE?
need >4 out of the 11 below:
1. Butterfly rash
2. Discoid rash - affects the ears, cheeks, scalp, forehead and chest. Erythema -> pigmented hyperkeratotic oedematous papules -> atrophic depressed lesions
4. Oral ulcers (usually painless)
5. Non erosive arthritis (involving >2 peripheral joints, similar to RA
6. Serositis - pleuritis or pericarditis
7. Renal disorder a. persistent proteinuria >0.5g/d or b. cellular casts
8. CNS disorder a. seizures or b. psychosis
9. Haematological disorder a. haemolytic anaemia or b. leukopenia or c. lymphopenia, or d. thrombocytopenia
10. Immunological disorder a. Anti dsDNA or b. Anti Sm or c. Antiphospholipid antibody
11. Antinuclear antibody +ve
Which antibodies are found in SLE?
Extractable Nuclear Antigens (ENA): anti-Ro, anti-La, anti-Sm, anti-RNP
Anti histone antibodies (in drug induced lupus)
What us antiphospholipid syndrome?
Antiphospholipid antibodoes - anti-cardiolipin and lupus anticoagulant cause CLOTs:
Coagulation defects, Livedo reticularis, Obsetric complications and Thrombocytopenia.
What is the pathogeneis of SLE?
When cells die by apotosis, cellular remnants appear on the cell surface as small blebs (contain self antigens - including nuclear constituents that are normally hidden from the immune system)
In SLE the removal of these blebs my phagocytes is ineffectient so they are transferred to lymphoid tissue by APCs. These self antigens are then presented to T cells and B cells are stimulated to make autoantibodies against them.
What are the differentials of proximal muscle weakness and stiffness?
Polymyositis - will have raised CK
What are the red flags for back pain?
Acute onset in older people
Constant or progressive
Worse when supine
History of malignancy
Thoracic back pain
Bilateral or alternating leg pain
Current or recent infection
Leg claudication or exercise related weakness or numbness.
What is the difference between Heberden's nodes and Bouchard's nodes?
Heberden's are in the DIP joint
Bouchard's are at the PIP joint
What HLA is ankylosing spondylitis, associated with?