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Flashcards in Rheumatology Deck (35)
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1
Q

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?

A

Giant cell arteritis (temporal arteritis).

Need to do an ESR, call ophthalmologist and give 40-60mg of prednisolone ASAP.

2
Q

What level does the ESR rise to in GCA?

A

> 50 mm/hr

3
Q

What two conditions are closely related (both cause high ESR)

A

GCA and polymyalgia rheumatica

PMR is not a true vasculitits but the two conditions often co-exist.

4
Q

What are the symptoms of PMR?

A

<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.

5
Q

When suspecting PMR what are you differential diagnoses?

A
Recent onset RA
Polymyositis 
Hypothyroidism 
Primary muscle disease 
Malignancy 
Infection 
OA - cervical spondylosis, shoulder OA
neck lesions 
bilateral subacromial impingement 
Spinal stenosis
6
Q

What is the triad in Reiter’s syndrome? (AKA reactive arthritis)

A

Urethritis, Arthritis, conjunctivitis

7
Q

Which conditions are considered to be spondyloarthritides?

A

Ankylosing spondylitis
Psoriatic arthritis
Reactive arthritis (Reiter’s syndrome)
Enteropathic (associated with IBD)

8
Q

What do spondyloarthripathies have in common?

A

Seronegative (Rh -ve)

HLA B27 association

Axial arthritis

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

9
Q

What are the causes of gout?

A

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)

10
Q

What finding is diagnostic for gout?

A

Synovial fluid showing negatively birefringent urate crystals on polarised light microscopy

11
Q

How do you treat gout?

A

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.

12
Q

What are the differences between gout and pseudo-gout?

A
Gout = urate 
Pseudo = calcium phosphate 
Gout = -ve birefringent urate crystals 
Pseudo = weakly +ve birefringent crystals
13
Q

What are the common presentations of rheumatoid arthritis?

A
Typical:
Slowly progressive, symmetrical polyarthritis, evolving over weeks - months. 
Sero -ve or +ve for rheumatoid factor 
\+ve for Anti CCP (very specific)
Relapsing and remitting 
Rapidly progressing:
Evolves over days and progresses over weeks. 
Severe joint damage 
Usually RF+ve and Anti CCP +ve 
Lots of systemic manifestations 

Pallindromic:
Acute monoarthritis, develops over 24-48hrs
50% progress to other types

Transient
Self limiting, <12 months, doesnt result in permanent joint damage

14
Q

Describe the pathogenesis of rheumoatoid arthritis:

A

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

15
Q

What are the extra articular manifestations of rheumatiod arthritis?

A
Nodules - elbows and lungs 
Lymphadenopthy 
Vasculitis 
Fibrosisng aveolitis 
Obliterative bronchiolitis 
Pleural and pericardial effusions 
Raynauds
Carpel tunnel syndrome
Peripheral neuropathy 
Splenomegaly (RA + Splenomegaly + neutropenia = Felty's syndrome)
Episcleritis, scleritis, scleromalacia, keratoconjunctivitis sicca
osteoporosis 
amyloidosis
16
Q

What is the difference between a butoniere and a swan neck deformity?

A

Butoniere is a fixed flexion deformity of the PIP

Swan neck is a hyperextension of the PIP

17
Q

What are the diagnostic criteria for rheumatoid?

A

> 6 points = RA morning stiffness for >1hour +

Joints:
1 med-large joint = 0
2-10 med-large joints = 1
1-3 small joints = 3
>10 joints at least one small = 4

Serology:
-ve RF -ve antiCCP = 0
low +ve RF low +ve antiCCP = 2
high +ve RF high +ve antiCCP = 3

Duration
6 weeks = 1

18
Q

What is osteoporosis?

A

reduced bone mass

19
Q

What are the causes of osetoporosis?

A

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

20
Q

What scores on a DEXA scan would initiate treatment?

A

> 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

21
Q

What are the different pharmacoloigcal measures used to treat osteoporosis?

A
Bisphosphonates 
Calcium Vit D
Stontium renelate 
HRT 
Raloxifene - selective oestrogen receptor modulator 
Teriparatide - recombinant PTH
22
Q

What are the diagnostic criteria for SLE?

A

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
  3. Photosensitivity
  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
23
Q

Which antibodies are found in SLE?

A

Anti dsDNA
Extractable Nuclear Antigens (ENA): anti-Ro, anti-La, anti-Sm, anti-RNP
Rheumatoid factor
Anti histone antibodies (in drug induced lupus)

24
Q

What us antiphospholipid syndrome?

A

Antiphospholipid antibodoes - anti-cardiolipin and lupus anticoagulant cause CLOTs:
Coagulation defects, Livedo reticularis, Obsetric complications and Thrombocytopenia.

25
Q

What is the pathogeneis of SLE?

A

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.

26
Q

What are the differentials of proximal muscle weakness and stiffness?

A
Polymyositis - will have raised CK
Systemic vasculitis 
SLE
Parkinsonism 
Hypo/hyper thyroidism 
Osteomalacia
27
Q

What are the red flags for back pain?

A
Aged 55yrs 
Acute onset in older people 
Constant or progressive 
Nocturnal pan 
Worse when supine 
History of malignancy 
Abdominal mass
Thoracic back pain 
Morning stiffness 
Bilateral or alternating leg pain 
Neurological disturbance 
Sphincter disturbance
Current or recent infection 
Immunosupressed
Leg claudication or exercise related weakness or numbness.
28
Q

What is the difference between Heberden’s nodes and Bouchard’s nodes?

A

Heberden’s are in the DIP joint

Bouchard’s are at the PIP joint

29
Q

What HLA is ankylosing spondylitis, associated with?

A

HLA B27

30
Q

What are the 5 As of ankylosing spondylitis?

A
Achilles tendonitis 
Anterior uveitis 
Apical fibrosis 
Aortic regurg
Amyloidosis
31
Q

What is the difference between limited systemic sclerosis and diffuse systemic sclerosis?

A

Limited systemic sclerosis:
Skin involvement limited to the face, hands and feet.
Anti centromere antibodies
CREST syndrome is part of it: Calcinosis, Raynaurds, Esophageal and gut dysmotility, Sclerodactyly and Telangiectasia

Diffuse systemic sclerosis:
Can be whole body, and organ fibrosis.
Anti topoisomerase 1 (Scl70) antibodies and anti RAN polymerase.

32
Q

What is the difference between polymyositis and dermatomyositis?

A

Polymyositis is progressive symmetrical proximal muscle weakness from striated muscle inflammation.
The muscle weakness can cause dysphagia and dysponia but NEVER dysphasia.

Dermatomyositis is myositis that is associated with skin signs. 
Macular rash (shawl sign if over back and shoulders), helliotrope rash on eyelids, nailfold erythema, roughed red papules on knuckles, knees and elbows (Gottron's papules) 

Both with have raised muscle enzymes and associated with anti-Mi2 and anti Jo1 antibodies.

EMG shows spontaneous fibrillation potentials at rest, polyphasic potentials on contraction.

33
Q

Which vasculitis are ANCA +ve?

A

Microscopic polyangitis,
Wegener’s granulomastosis: airways disease (nasal obstruction, epistaxis) renal disease( haemtauria with crescent formation) pulmonary involvement
Churg-strauss syndrome: late onset asthma, eosinophilia, and granulomatous small vessel vasculitis affecting the lungs, nerves heart and skin

34
Q

Which vasculitis are ANCA -ve?

A

HSP,

Goodpastures: Pulmonary renal syndrome, acute glomerulonephritis plus pulmonary symptoms.

35
Q

What is polyarteritis nodosa?

A

It is a medium vasculitis causing aneurysms and thrombosis leading to infarction of the affected organs.
May be associated with Hep B