Rheumatology Flashcards
Which seronegative spondylarthrioathies is most likely to cause enthesitis (inflammation of the joint capsules, tendons and ligaments join into the bone)?
Ankylosing spondylitis
What is the classical triad of primary Sjorgen syndrome?
Dry mucosa
Fatigue
Joint pain
(Active arthritis may be seen but arthralgia is more common)
Arthralgia VS arthritis?
In the strictest sense, arthralgia simply refers to joint pain. Arthritis is inflammation in the joints, which also causes symptoms such as pain and stiffness.
How is temporal arteritis diagnosed?
Biopsy, showing features of inflammation of which are typical of giant cell arteritis.
Normal biopsy does not r/o - skip lesions, suboptimal sample
What are the clinical features of polymyositis?
Proximal muscle weakness and pain
No skin involement
As disease progresses, and other muscles become involved:
Pharangeal or oesophageal muscles leading to dysphonia and dysphagia
Respiratory muscles can lead to poor ventilation with type 2 respiratory failure
What will be seen on biopsy of muscle affected by polymyositis (gold standard diagnostic investigation)?
Endomysial inflammatory infiltrates
Muscle necrosis and atrophy
What score is used to measure disease activity in RA?
DAS-28
Doctor looks at 28 joints to decide if they are tender or swollen
A patient global health assessment from 0 to 100
ESR and CRP can be added into the formula
Low score indicated remission, higher score suggests patient has more active disease
Bechet’s disease symptoms/features?
CT changes of an acute venous sinus thrombosis, on a background of recalcitrant oral ucleration
Recurrent ocular events (relapising anterior uveitis)
Genital ulceration may provide further support for the diagnosis
Features of anti-phospholipid syndrome?
Commonly occurs secondary to SLE
Causes arterial and vebous thromboembolism, thrombocytopenia and livedo reticularis (a mottled, lace-like appearence on the legs)
One or more of the follow positive blood tests on more than two ocassions, more than two weeks apart required to diagnose APS:
- Anti-cardiolipin antibodies
- Anti-beta 2-GPI antibodies
- Positive lupus anticoagulant assay
How does methotrexate work?
Folate antagonist, binds to dihydrofolate reductase impairing the synthesis of DNA and therefore cell replication (therefore common side effect is folic acid deficiency and subsequently a macrocytic anaemia)
How does cerebral lupus present?
Unremitting headache
Psychosis
Features of active lupus (prominent rash, raised ESR, low complement levels)
What is CREST syndrome?
Limited cutaneous form of systemic sclerosis
Calcinosis, Raynaud’s phenomenon, esophageal dysmotility, sclerodactyly, and telangiectasia (dilation of capillaries causing red marks on the skin)
Pulmonary hypertension presenting as right sided heart failure is a well known complication of systemic sclerosis associated with CREST syndrome subtype of systemic sclerosis
What lung complication does diffuse cutaneous SSc tend to cause?
Pulmonary fibrosis
as opposed to pulmonary HTN in limited SSc
How should you monitor for pulmonary HTN in systemic sclerosis?
Echocardiogram or diffusing capactiy on spirometery
Can be confirmed with right heart catherisation
What conditions is anterior uveitis associated with?
Associated with HLA-B7
Autoimmune disease: IBD, ankylosing spondylitis, reactive arthritis, Betchet’s disease
What is uveitis?
Inflammation of the anterior portion of the uvea, which includes the iris and ciliary body.
Patients present with a red and painful eye +/- photophobia, blurred vision, lacrimation and a hypopyon (inflammatory cells in the anterior chamber)
How do patients with reactive arthritis tend to present?
Dysuria
Iritis/conjunctivitis
Arthralgia
Pathophysiology of RA?
Citrullination of self antigens which are then recognised by T and B cells which then produce antibodies (rheumatoid factor (Fc portion of IgG), anti-CCP).
Stimulated macrophages and fibroblasts release TNFalpha.
Inflammatory cascade leads to proliferation of synoviocytes (boggy swelling)
These grow over the cartilage and lead to restriction of nutrients and cartillage is damaged.
Activated macrophages stimulate osteoclast differentiation contributing to bone damage.
Typical history for RA?
Female (3:1) 30-50 years Presents with progressive, peripheral and symmetrical polyarthritis. Affects MCPs/PIPs/MTPs Spares DIPs History of > 6 weeks Morning stiffness >30 mins duration Commonly c/o fatigue/malaise
What may be seen on examination of a patient with RA?
Soft tissue swelling and tenderness
Ulnar deviation/ Palmar sublucation of MCPs
Swan neck and Boutonniere deformity to digits
Rheumatoid nodules
Check median nerve for carpal tunnel association
Investigations for RA?
Rheumatoid factor Anti-CCP antibodies FBC (normocytic anaemia of chronic disease) WCC if concerned about septic arthritis ESR/CRP - elevated X-ray changes (established disease) USS/MRI (early disease) PFTs HRCT if chest and lung involvement (e.g. pulmonary fibrosis)
How does (progressed) RA appear on an X ray?
Loss of joint space
Erosions (periarticular)
Soft tissue swelling
Subluxation
Treatment of RA?
Initially DMARD monotherapy (methotrexate)
Combination DMARDs (leflunomide, hydroychloroquine, sulfasalazine)
Steroids (actutely) - PO/IM or intra articular
Symptom control with NSAIDs + PPI cover
If still severe after combination DMARDs, biologics (anti-TNFs such as entanercept)
OT/PT podiatry psychological
Extra-articular manifestations of RA?
3Cs - Carpal tunnel syndrome, elevated Cardiac risk (CVD), Cord compression (atlanto-axial subluxation)
3As- Anaemia (normochromic & normocytic), Amyloidosis (rare, can cause nephrotic syndrome and CKD), Arteritis (rare)
3Ps - Pericarditis (uncommon), Pleural disease (common), Pulmonary disease (common) e.g. bronchiectasis, bronchiolitis obliterans fibrosis
3Ss - Sjogren’s (common), Scleritis/episcleritis (uncommon), Splenic enlargement (together with neutropaenia = Felty’s syndrome, rare)
What is Giant cell arteritis and who is affected?
Chronic vasculitis of the large and medium sized vessels
Occurs among individuals over 50 years of age
Median age of onset is 72
Most commonly causes inflammation of arteries originating from the arch of the aorta
Occlusive arteries can result in anterior ischemic optic neuropathy
Visual symptoms are an opthalmic emergency
Inflammation of arteries supplying the muscles of mastication results in jaw claudication and tongue discomfort
GCA may present as CVA
Risk factors for GCA?
Increasing age 2-4 more times common in women Caucasion Strong association with PMR Genetic predisposition - HLA-DRA
How does GCA present?
Headache: localised, unilateral, boring, lancinating in quality over the temple
Tounge or jaw claudication upon mastication
Constitutional symptoms
Visual symptoms (may develop weeks to months following the other symptoms): amaurosis fugax, blindness, diplopia and blurring
Scalp tenderness, especially over the temporal artery
How is GCA diagnosed?
Presence of 2 or more in patients over 50 years:
Raised ESR, CRP, or PV
New onset of localized headache
Tenderness or decreased pulsation of temporal artery
New visual symptoms
Biopsy revealing necrotizing arteritis
How is GCA treated
60-100mg prednisolone PO per day for at least 2 weeks, then consider tapering down
Methylprednisolone IV pulse therapy (1g) for 1-3 days IF ACUTE ONSET SYMPTOMS
Low dose asprin therapy to reduce thrombotic risks
Most common complication of GCA?
Permanent visual loss
20-50% of patients go blind if untreated
What is Polymyalgia Rheumatica?
Clinical syndrome characterized by pain and stiffness of the shoulder, hip girdles, and neck. Patients may use the term stiffness and pain interchangeably,
Primary impacts the elderly
Associated with morning stiffness
Elevated inflammatory markers
How is affected by PMR?
70-80 years
Very rare under 50
Association with GCA
Symptoms of PMR?
New sudden onset proximal limb pain and stiffness (neck, shoulders, hip)
Night time pain
Systemic symptoms (25%) fatigue, weight loss, low-grade fever
Difficulty rising from chair, combining hair (proximal muscle involvement)
How might the physical examination of a patient with PMR be?
Decreased ROM of shoulders, neck and hips
Muscle strength is usually normal - may be limited by pain/stiffness
Muscle tenderness
How is PMR diagnosed?
Examination
ESR or PV, CRP - will almost always be raised, although not proportional to severity of the symptoms
Consider temporal artery biopsy if symptoms of GCA
Dramatic response within 5 days of starting prednisolone
What other conditions may present with PMR symtpoms?
Cancer
RA
Treatment of PMR?
15mg of prednisolone daily, taper down slowly. Most patients require 18 months of treatment.
In relapsing patients methotrexate can be steroid-sparing
What is the presence of HLA-B27 associated with?
Spondyloarthropathies
What are the spondyloarthropathies?
Ankylosing spondylitis (most common)
Enteropathic arthritis
Psoratic arthritis
Reactive arthritis
Common clinical features of the spondyloarthropathies?
Sacroiliac/axial disease - back/buttock pain
Inflammatory arthopathy of peripheral joints
Enthesitis (inflammation at tendon insertions)
Extra-articular features (skin/gut/eye)
Ankylosing spondylitis clincal features
Usually presents in young men (teens to mid therties)
Presentation with bilateral buttock pain, chest wall and thoracic pain
Examination is often normal, loss of lumbor lordosis in later disease
Exaggerated thoracic kyphosis in later disease
Positive Schober’s test in later disease
Reduced chest expanison in later disease
Raised or normal CRP
How would you investigate Ankylosing Spndylitis?
CRP (may be normal)
MRI spine and SI joints
HLA-B27
How is ankylosing spondylitis managed?
NSAIDs
Physio
TNF inhibitors (e.g. infliximab)
IL-17 inhibitors (brodalumab,
Clinical features of psoriatic arthritis?
Psoriasis
Oligo-arthritis with dactylitis (sausage digit)
Symetrical or mono-arthritis
Severe disease: arthritis mutilans
Central erosions seen on USS or MRI, leading to pencil in cup x-ray appearence
How is psoriatic arthritis managed?
NSAIDs DMARDs TNF inhibitors IL-17 inhibitors IL 12/23 inhibitors
When does reactive arthritis occur?
Distant infection
Post dysentery (Salmonella/Shigella/Campylobacter)
Urethritis/cervicitis (Chlaymidya trachomatis)
How long after infection dose reactive arthritis occur?
Days-2 weeks post infection
What is reactive arthritis?
Sterile synovitis developing after a distant infection
Acute asymmetrical lower limb arthritis
Extra-articular features of reactive arthritis?
Skin: circinate balanitis, keratoderma blennorrhagica
Eye: conjunctivitis, uveitis
MSK: enthesitis
Urogential: urethritis
What investigations should be undertaken in suspected reactive arthritis?
Serology/microbiology
Raised inflammatory markers
Join asp to rule out septic arthritis/gout
HLA-B27
How should reactive arthritis be treated?
Treat underlying infection (this may not improve arthritis)
NSAIDs, joint injections
If not resolved in 2 years (most will) may need DMARDs
What is type 1 peripheral enteropathic arthritis?
Oligoarticular, asymmetric and has a correlation with IBD flares
What is type 2 peripheral enteropathic arthritis?
Polyarticular symettrical and has less correlation with IBD flares
10-20% of patients with IBD develop arthropathy. Which is more common, peripheral arthritis or axial disease?
Peripheral arthritis
What treatment should be considered in enteropathic arthritis?
Consider DMARDs (NSAIDs may flare IBD) TNF inhibitors will treat IBD and arthritis
Extra-articular manifestations of Ankylosing spondylitis?
Anterior uveitis Aortic incompetence AV block Apical lung fibrosis Amyloidosis
Features of inflammatory back pain?
Insidious onset Pain at night (improves on getting up) Age at onset <40 Improvement with exercise No improvement with rest
What is lupus?
Autoimmune disease
Inadequate T cell supressor activity with increased B cell activity
Most patients have antibodies to certain cell nucleus components
Complex multisystem disease with variable presentations
Characterized by remissions and flares
Can be famillial
Common signs and symptoms of SLE?
Serositis (pleurisy, pericarditis)
Oral ulcers, usually painless, palate is most specific
Arthritis - small joints, non errosive
Photosensitivity
Blood disorders: low WCC, lymphopenia, thrombocytopenia, haemolytic anemia
Renal invovlement - glomerularnephritis
Autoantibodies (90% of cases ANA +)
Immunologic tests e.g. low complements
Neurologic disorders - seizures, psychosis
What blood test abnormalities may be present in patients with SLE?
Most patients will have a raised ESR or plasma viscosity
Anaemia and leukopenia
ANA positive (90%)
Anti-Ro, Anti-La are common
Anti-dsDNA (rises with disease activity)
Maybe be antiphospholipid antibodies (these increase the risk of pregnancy loss and thrombosis)
C3 and C4 fall with disease activity
What can be used to monitor SLE?
Anti-dsDNA - titre rises with disease activity
C3 and C4 - both fall with disease activity
Urinalysis for detecting renal disease
Renal biopsy- diagnosis and prognosis
Skin biopsy - can be diagnostic
How is SLE treated?
Sun protection
Lifestyle risk reduction of CVD
Hydroxychloroquine is helpful for rash and arthralgia
Mycophenolate mofetil, azathioprine and rituximab are commonly used
Short courses of prednisolone for flares
When is the peak onset of SLE?
Early adulthood
Why is lupus 9x more common in women?
Estrogens are thought to be permissive for autoimmunity.
Estradiol may prolong the life of autoreactive B and T lymphocytes
How does UV light rigger SLE?
Alters the structure of DNA in the dermis which renders it more immunogenic
Examples of drugs which can trigger an SLE-like syndrome include?
Isoniazid
Minocycline
TNF inhibitors
What will the CRP in a patient with SLE be?
Normal
What will FBC be in most patients with SLE?
Abnormal
OA vs RA in terms of morning stiffness?
OA - no morning stiffness
RA - morning stiffness
OA vs RA in terms of effect of activity?
OA - worse with activity
RA - improves with activity
Most common joints effected by OA?
Knee
Hip
Hand
What joint is most commonly affected by gout?
First metatarsophalangeal joint
How do patients with gout typically describe the pain?
Anything touching the affected joint will cause discomfort
Inflammation develops within a few hours
Pain disturbs their sleep
What antibody is likely to be raised in drug induced lupus?
Anti-histone antibody
How does polymyositis initially present?
Bilateral, proximal (hip and shoulder girdle) muscle weakness, developing over weeks to months.
Muscle pain and tenderness sometimes present
Muscle bulk and reflexes are preserved (until very late)
What happens in progressive disease in polymyositis?
Pharyngeal or oesophogeal muscle involvement, leading to dysphonia and dysphagia
Respiratory muscles involvement, leading to poor ventilation and type 2 respiratory failure
What will be seen on joint aspiration in gout?
Negatively birefringent needle-shaped crystals
What arthritis can be caused by tumour lysis syndrome (renal involvement)?
Gout
A patient taking methotrexate for RA should be advised how when she wishes to become pregnant?
Wash out of at least 6 months before conception
Low dose steroids in the event of a disease flare
Classic signs of OA?
Heberden’s nodes
Bouchard’s nodes
What are Heberden’s nodes?
Swelling of the distal interpharangeal joint
What are Bouchard’s nodes?
Swelling of the proximal interpharangeal joints
What hand deformities may be seen in RA?
Ulnar deviation
Swan neck deformity
Boutinnieres deformity
Z deformity of the thumb
What are the most commonly affected joints in RA?
PIP: proximal interpharangeal joints
MCP: metacarpopharangeal joints of the fingers
What might be the caused of bilateral, proximal muscle pain and stiffness without a rise in CK levels?
PMR
What are the most commonly affected joints in ankylosing spondylitis?
Sacroilliac, hence the most common presenting complaint is lower back pain
What should be ruled out in a patient with dermatomyositis?
Mallignancy - dermatomyositis can present as a paraneoplastic phenominum
What is Anterior ischemic optic neuropathy and which rheumatological conditions is it associated with?
GCA/PMR with GCA
AION is infarction of the posterior cillary arteries which supply the optic nerve
Most common mechanism if visual loss in GCA
Classic findings: on fundus examination include a swollen, chalky white, optic disc
What findings indicate a diagnosis of Churg-Strauss sydnrome?
Esonophillia Poorly controlled asthma CXR findings indicative of granulomatous change Renal involvement Elevated ESR
What is Chaugg-Strass syndrome also known as?
Churg-Strauss vasculitis, eosinophilic granulomatosis with polyangiitis (EGPA), and allergic angiitis.
First line treatment for knee or hand OA?
TOPICAL NSAID
+ Paracetomol
Serious side effects of methotrexate?
Drug induced pulmonary fibrosis
Abortive/tetragenic
Liver chirrosis
Leucopenia
What is Schirmer’s test used to diagnose and how is it performed?
Sjorgen’s syndrome
Place filter paper on eye for 5 mins
Positive is less than 10 mm of moisture on the filter paper in 5 minutes
What rehumatological conditions is Raynaud’s phenomenon associated with?
Scleroderma
SLE
Dermatomyosis and polymoyositis
Sjorgen’s syndrome
Over what age should a patient developing symptoms of Raynaud’s phenomenon alert you to likely underlying disease?
30 years
What are the possible physical causes of raynauds phenomenon?
Use of heavy vibrating tools
Cervical rib
‘sticky’ blood - cryoglbuniaemia
What common drug class can induce Raynaud’s phenomenon?
Beta blockers
What is Raynaud’s phenomenon?
Condition caused by vasospasm of hand digits.
Painful
May be precipitated by stress
Characterized by a typical sequence of colour changes in response to a COLD STIMULUS: white, blue, red
What is the colour sequence and what is occuring at each stage in Raynaud’s phenomenon?
White - inadequete blood flow
Blue - venous stasis
Red - re-warming hyperaemia
What is Raynaud’s syndrome?
Idiopathic Raynaud’s phenomenon
Usually improves with age
May be familial
Treatment comprises measures including keeping warm, avoiding smoking
Pharmacological management of Raynaud’s phenonomenon?
Calcium-channel blockers are first line
Phosphodiesterase-5 inhibitors and prostacyclins are usually effective
Complications of RP?
Digital ulcers
Severe digital ischemia
Infection
Gangrene
Pattern of symptoms in Raynaud’s syndrome vs RP secondary to underlying disease?
RS: Pattern symettrical and bilateral, lasts minuites
RP: Asymettrical pattern, only a few digits affected, may last hours
What test can be used in the diagnosis of RP?
Nail-fold capilaroscopy
What is vasculitis?
Inflammatory blood vessel disorder
Clinical features result from the damage of blood vessel walls with subsequent thrombosis, ischemia, bleeding and/or aneurysm formation.
Important aspects of vasculitis history?
Age, gender, ethnicity
Comprehnesive drug history
FHx
Constitutional symptoms: fever, weight loss, malaise, fatigue, diminished apperitie, sweats
Glove and sweater approach
RP
MSK: arthralgia, myalgia, proximal muscle weakness
CNS/PNS: headaches visual loss, tinnitus, stroke seizure encephalopathy
Heart/lung: percarditis, cough, chest pain, hemoptysis, dyspnea
GI: abdominal pain
Renal haematuria
Limbs: Neuropathy. digital ulcers/ischemia
How should you examine a patient with suspected vasculitis?
Vital signs: BP ?HTN, Pulse ?irregular ?rate
Skin: palpable purpura, livedo reticularis, nodules, digital ulcers, gangrene, nail bed capillary changes
Neurologic: cranial nerve exam, sensorimotor exam
Ocular exam: visual fields, scleritis, uveitis episcleritis
Cardiopulmonary exam: Crackles, pleural rubs, murmurs, arrhythmias
Abdo exam: tenderness, organomegaly
What are the primary vasculitides (small-vessel)?
Microscopic polyangitis
Granulomatosis with polyangitis - GPA (wegner’s granulomatosis)
Eosinophillic granulomatosis with polyangitis EGPA (churg-strauss syndrome
Iga vasculitis (Henoch-Schonlein purpura)
What are the primary vasculitides (medium-vessel)?
Polyarteritis nodosa (PAN) Kawasaki disease (KD)
What are the primary vasculitides (large-vessel)?
Takayasu arteritis (TAK) Ginat cell arteritis (GCA)
Vasculitis is normally secondary, what may it be caused by if this is the case?
Infection
Drugs
Mallignancy
Connective tissue disease
Why is urinalysis important in vasculitis?
Renal involvement often silent
Urinalysis to identify any underlying GN
What initial tests should be ran in suspected vasculitis?
FBC, U&Es, LFTs, CRP, PV< ESR Specific serology: ANA, ANCA, RF Complement levels: C3, C4 Hep screen for B and C HIV screen Cryoglobins Serum and urine protein elctrophoresis CK, blood cultures, ECG, CXR, CT scan, MRI arteriography
What is a common cause of skin vasculitis caused by medications?
Hypersensitivity vasculitis
Artial Myxomas can present with a vasculitis like syndrome, what test can exclude it?
ECHO
How is vasculitis managed?
R/o / treat any infection
Stop any offending drugs
1st line corticosteroids
2nd line cytotoxic medications, immunomodulatory or biologic agents (cyclophosphamide, methotrexate, azathioprine, leflunomide, mycophenolate mofetil, rituximab, IVIG
What are dermatomyositis and polymyositis?
Rare idiopathic muscle disease characterized by the inflammation of striated muscle.
M:F is smilar and peak age of onset is 40-50 years
How do dermatomyositis and polymyositis normally present?
INsideous onset of muscle proximal weakness
Ofetn painless
SOB/Rash
Often normal inflammatory markers, some raised
Normal FBC,
Kidney function not affected
Raised ALT from muscle but ALP and AST normal
80% antinuclear anitbody positive
Well demonstrated myositis on MRI
What is the diagnostic criteria for polymositis?
3 or more of Symetrical proximal muscle weakness Raised serum muscle enzyme levels Typical electromyographic changes Biopsy evidence of myositis
What is the diagnostic criteria for dermatomyositis?
Typical rash of dermatomyositis and 2 of
Symmetrical proximal muscle weakness
Raised serum muscle enzymes
Typical electromyographic changes
How are Dematomyositis and Polymyositis treated?
Mainstay of treatment for first few weeks are high dose corticosteroids.
Long term control with methotrexate or azathioprine.
Rituximab can be effective
IV immunoglobin also effective
Sun protection in DM is important HCQ may be required to reduce the rash
How are Dermatomyositis and Polymyositis monitored?
Monitoring and disease activity can be difficult but the inflammatory markers and CK are often used
EMG studies/MRI or biopsy may be needed
Complications of dermatomyositis and polymyositis?
Involvement of the striated muscle of the oesophogus - swallow difficulty and aspiration pneumonia
DIaphragmatic involvement - respiratory failure
Inflammatory lung disease
Increased risk of malignancy 2-3 years before and after diagnosis of dermatomyositis
DM: rash is photosensitive and often leads to post inflammatory hyper- or hypo- pigmentation in areas that are light exposed (scalp, face, neck)
Linear plaques on dorsal aspect of the hands (Gottron’s papules)
DIlated nail fold capillaries
Dry cracked palms and fingers
Periorbital oedema
Heliotrope rash to eye lids (violet rash)
What other rheumatological conditions can lead to myositis?
Scleroderma
SLE
What is systemic sclerosis?
Multisystem autoimmune disease
Also known as scleroderma
Increased fibroblast activity resulting in abnormal growth of conncective tissue which leads to vascular damage and fibrosis
What are the two main subtypes of SSc?
limited
diffuse
What is limited scleroderma normally preceded by?
Many years of Raynaud’s phenomenon
Which subtype of SSc is more common
Limited (CREST syndrome)
What complication often develops after aprox. ten years of the onset of symptoms of crest syndrome?
PA hypertension
What is diffuse scleroderma?
Less common subtype of SSc with higher mortality,
Characterised by the sudden onset of skin involvement and is proximal to the elbows and knees
How would you investigate SSc?
Inflamatory markers - usually normal X-ray hands - calcinosis CXR, HRCT, PFT - pulmonary disease ECG and ECHO - PA HTN, HF myocarditis and arrhythmias Antibody serology
What antibodies may be found in a patient with SSc?
Positive ANA (90%)
Anti-centromere antibody strongly associated with limited SSc
Scl-70 (topisomerase) and anti RNA polymerase III antibodies strongly associated with diffuse SSc
How is systemic sclerosis treated?
Calcium antagonist/sildenafil/iloprost infusion for Raynaud’s symptoms
Methotrexate and mycophenolae mofetil may reduce skin thickening
ACEi prevent HTN crisi and reduce mortality from renal failure
Short course of prednisolone for flares
Proton pump inhibitors for GI symptoms
Psychological support
What is the localized form of scleroderma called?
Morphoea
Which sex is more commonly affected by SSc?
Women 5 times more affected
What does vascular involvement of SSc invlude?
Raynaud’s phenomenon
Ischemic digital ulcer
HTN crisis
Pulmonary arterial HTN
How does SSc cause kidney problems?
Scleroderma renal crisis is a serious condition with features of accelerated HTN, which can lead to renal failure.
Seen early in the course of disease in patients with diffuse SSc
What is Sjogren’s syndrome?
Chronic autoimmune inflammatory disorder
Characterized by diminshed lacrimal and salivary gland secretion
Primary form - no association with other disease
Secondary form - association with another rheumatic disease
Most pts female
Common signs and symptoms
MADFRED Myalgia Arthralgia Dry mouth Fatigue Raynaud's phenomenon Enlarge parotids Dry eyes
What antibodies are positive in most patients with Sjorgen’s syndrome?
Anti Ro
Anti La
90%
What less common antibodies might be seen in a patient with Sjorgen’s syndrome?
RF and anti ds-DNA
What biopsy may be needed to diagnose Sjorgen’s syndrome and what will be seen?
Salivary gland
Focal lymphocytic infiltration
How is Sjorgen’s syndrome treated?
Avoid dry or smoky atmostpheres Dry eyes- artfical dear Dry mouth - artifical saliva Skin emoillents, vaginal lubricants Immunosupressents/Steroids rarely required
What are the most common diseases associated with Sjorgens syndrome?
RA
SLE
ALso: coeliac, primary bilary cirrhosis, autoimmune thyroid disease
What haemotological condition are patients with Sjogren’s syndrome more at risk of?
B cell lymphoma
What are the risks pregnant women with Sjogren’s syndrome might need to know about?
anti Ro/SS A antibodies - higher risk of fetal loss, complete heart block in fetus, neonatal lupus syndrome of the newborn
What is Hypermobility Spectrum disorder?
This is a pain syndrome in people with joints that move beyond normal limits.
No precise definition - joint mobility is a graduated phenomenon.
Due to laxity of ligaments, capsules and tendons
Is thought that the origin of pain is from microtrauma
Complication of Hypermobility Spectrum Disorder?
Recurrent subluxations or dislocations
Symptoms and signs of hypermobility spectrum disorder?
Pain around the joints Worse after activity Genralized and fatigue Soft tissue rheumatism e.g. epicondylitis Abnormal skin: papyraceous scars, hyperextensible, thin, striae Marfanoid habitus Arachnodactlyly Drooping eyelids, myopia Hernias and uterine/rectal prolapses
Treatment of hypermobility spectrum disorder?
This is the mainstay of treatment is non drug therapy
Strengthening exercises to reduce joint subluxation
Work on posture and balance may also be needed
Splinting and even surgical interventions may be needed
Advice on pacing and goal setting
Specialist pain management input is often needed
Paracetamol should be mainstay
What score is used to measure extent of hypermobility spectrum disorder?
Beighton score
What are the heritable connective tissue disorders?
HSD
Marfan syndrome
Ehlers Danlos syndrome
What is osteoarthritis?
Degenerative joint disorder where there is a progressive loss of articular cartillage accompanied by new bone formation and capsular fibrosis
Aetiology of OA?
Failure of normal cartilage subject to abnormal or incongruous loading for long periods
Damaged or defective cartilage failing under normal conditions of loading
Break up of cartilage due to defective stiffened subchondral bone passing more load to it
Key features of cartillage in OA?
Loss of elasticity with a reduced tensile strength
Cellularity with proteoglycan content are reduced
What provokes pain in OA?
Pain
Weight baring
Activity
Starts intermittently, progresses to constant
X ray changes in OA?
Loss of joint space
Osteophytes
Subarticular sclerosis
Subchondral cysts
Pharmacological therapy?
Regular paracetomol is first choice NSAIDs short term orally Topical NSAIDs and topical rubefacients Capsaicin Intra-articular corticosteroids can be offered
Where may pain in OA emanate from?
Any tissue except cartilage which is avascular and aneural
It may be due to microfractures of the subchondral bone, or from low grade synovitis, capsular distention or muscle spasam
What is strongly associated with the development of knee OA?
Nodal OA
What is fibromyalgia?
Common disorder of central pain processing charcterized by chronic widespread pain in all 4 quadrants of the body - both sides, above and below the waist. Allodynia, as heightened, painful response to innoculous stimuli is often present.
Signs and symptoms of fibromyalgia?
Joint/muscle stiffness Profound fatigue Unrefreshed sleep Numbness Headaches Irritable bowel/bladder Depression and anxiety Poor concentration and memory Tender points on palpation of their muscles
What is the underlying pathogenesis of fibromyalgia?
Can be induced by deliberate sleep deprivation - reduced REM sleep and delta wave sleep.
Hyper-activation in response to noxious stimuli
Neural activation in brain regions associated with pain perception and response to non-painful stimuli
Risk factors for fibromyalgia?
Female (9:1)
Peak age of onset 40-50 years
Trigger - emotional distress, physcial pain e.g. arthritis, sleep deprivation
Treatment for fibromyalgia is based on pain intentsity, function, and associated features such as depression, fatigue, and sleep disturbance. What may it include?
Education - explanation of their symproms
Physical - exercise
CBT
Pharmacology - low dose amitryptiline, pregablin may be effective (OPIATES NOT RECCOMENDED)
What blood tests should be undertaken in a suspected diagnosis of fibromyalgia to exculde other pathologies?
ESR CRP FBC U&E LFT Ca CK TFT
What are the non modifiable risk factors for osteoperosis?
Advancing age (>65) Female gender Caucasion or south asian Family history History of low trauma fracture (fall from standing height or less at walking speed or less)
What are the modifiable risk factors for osteoperoisis?
Low body weight (58 kg or BMI<21) Premature menopause Calcium/vit D deficiency Inadequete physical activity Cigarette smoking Excessive alcohol intake (>3 drinks/day) Iatrogenic: e.g. corticosteroids, aromatase inhibitors
Gold standard to diagnose osteoperosis?
DEXA (Dual energy x-ray absorptiometry) of the lumbar spine and hip is considered the gold standard
Below what T score is considered osteoperosis?
2.5 or less
What is a normal bone marrow density T-score?
Greater than or equal to -1
What T score indicates osteopenia?
-1 and -2.5
What is T score?
Number of SDs from the mean bone density of persons of the same gender at age of peak density (25)
What is a Z score?
Z-score is a comparison of the patient’s BMD with an age- & gender matched population
What should a Z score of less than -2 prompt?
Evaluation for causes of secondary osteoperosis?
What are plain radiographs not used to diagnose osteoperosis? What might they show that is indicative of osteoperosis?
Lack sensitivity
May show rib fractures or vertebral compression fractures without trauma history - this prompts evaluation for osteoporosis
How is osteopenia treated?
Treatment should focus only on risk modification:
Weight bearing exercise
Vitamin D2 supplementation (800-2000 IU/day)
Limiting alcohol
Smoking cessatopm
Dietary advice regarding calcium intake
How is osteoperosis treated?
Vitamin D +/- calcium supplementation, AND
1st line: oral bisphosphonates - Alendronic Acid
2nd line: Denosumab or teriparatide
What are secondary causes of osteoperosis?
Coeliac disease Eating disorders Hyperparathyroidism Hyperthryoidism Multiple myeloma Men: hypogonadism
What instructions and advise should be given to patients who are taking bisphosphonates?
Take on empty stomach at least 30 mins before food with full glass of water
Serious side effects are very rare
Patients (or their carers) should be advised to stop taking alendronic acid and to seek medical attention if they develop symptoms of oesophageal irritation such as dysphagia, new or worsening heartburn, pain on swallowing or retrosternal pain.
What is gout?
Inflammatory arthritis related to a hyperuricemia (although this is not the only determining factor)
What complication is gout associated with?
High risk of CVD
What is the pathogenisis of gout?
Deposition of monosodium urate (MSU) crystals accumulate in joints and soft tissues
Result in chronic arthritis, tophi (soft tissue masses), urate nephropathy, and uric acid nephrolithiasis
Within what time period will most patients have a second flare of gout following the initial flare?
1 year
3/4 within 2
What are the non-modifiable risk factors for gout?
Age>40 years
Male gender
What are the modifiable risk factors for gout?
Increased purine intake (meats, seafood) Alcohol intake (especially beer) High fructose intake Obesity Congestive HF Coronary artery disease Dyslipidemia Renal disease Organ transplantation HTN Smoking DM Urate-elevating medications e.g. thizazides, loop diruetics, Pyrazinamide
How is gout treated conservatively?
Maintain optimal weight
Regular exercise
Diet modification (purine-rich food)
Reduce alcohol consumption (beer and liquour)
Smoking cessation
Maitain fluid intake and avoid dehydration
First line treatment for acute gout?
NSAIDs
oral/IM steroids
colchcine if NSAIDs not tolerated
What medication is used to prevent gout, and how does it act?
Urate lowering therapy, after acute attack
Xanithine oxidase inhibitors (reduce urate formation): Allopurinol/febuxostat
Second line is benzbromarone and sulfinpyrazone are used less commonly as more side effects. They act to increase the renal excretion of uric acid.
How will the fluid aspirate contents of a joint viewed under polarised red light in gout?
Negatively birefringent, needle shaped crystals
How will the fluid aspirate contents of a joint viewed under polarised red light in pseudogout?
POsitively birefringent rhomboid shaped crystals
What are crystals in pseudogout composed of?
Calcium pyrophosphate
Who normally suffers from pseudogout?
Older women with OA
Does hyperuricemia need treatment if asymptomatic?
No
Within what time period should treatment begin for an acute gout flare?
within 24 hrs of onset
What type of pathology does worsening pain with particular movements indicate?
Peri-articular pathology
What MSK strucutres can pain arise from?
Synovium Join capsule Subchondral bone Peri-articular Skin
Where is pain from the glemohumeral joint or rotator cuff felt?
Upper arm
Where might hip pain radiate to?
Groin
Buttock
Thigh
Knee
What can cause radiculopathy?
Disc prolapse
What id pain during tenosynovitis triggered by?
Certain movements
Where is the pain from lateral epicondylitis felt? What makes it worse?
Outside of elbow joint
Worsened on resisted elbow extension
Where is the pain felt in Achilles tendinitis?
Just above the heel
Worse on active plantar flexion
Where is pain from De Quervain’s tensoynovitis felt? What makes it worse?
Snuffbox area of the wrist and is worse when pinching or using thumb to operate a smartphone
What rheumatological conditions have a proximal only patten of joint/muscle involvement?
PMR
What rheumatological conditions have a distal only patten of joint/muscle involvement?
OA
Gout
PsA
What rheumatological conditions have a small joint only patten of joint/muscle involvement?
RA (early stages)
What rheumatological conditions have a large joint only patten of joint/muscle involvement?
OA
What does monoarticular mean?
1 joint
What does oligoarticular mean?
2-4 joints
What does polyarticular mean?
More than 4 joints
Symetrical rheumatological conditions?
RA
Asymetrical rheumatological diseases?
PsA
Gout
Which rhematological diseases commonly involve the spine?
Main feature of AS
Sometimes PsA
Causes of acute monoarthritis?
Infections - Staph aureus and Streptococcal most common
Crystal induced - Gout (men), pseudogout (older women with OA)
Trauma - haemarthrosis
Septic arthritis until proven otherwise
Causes of chronic monoarthritis?
Infections - always consider TB
Inflammatory - Psoriatic arthritis, reactive arthritis, forigen body
Non-inflammatory - OA, Trauma (e.g. meniscal tare), osteonecrosis (associated with prednisolone use), neuropathic (Charcot’s joint)
Tumours - rare
Causes of acute polyarthritis?
Inflammatory arthritis - RA, PsA, reactive arthritis
Autoimmune - SLE, vasculitis
Viral infection - HIV, chikungunya, parovirus
Crystal arthritis - uncontrolled gout
Causes of chronic (>3 months) arthritis?
Inflammatory - RA, PsA, reactive
Autoimmune - SLE, vasculitis
Crystal arthrits - uncontrolled gout
Causes of arthritis of the DIPJs?
Psoratic arthritis: will also be nail dystrophy in the affected digit
OA commonest - Herberden’s nodes
What is early morning stiffness suggestive of?
Inflammatory arthritis e.g. RA PsA
What is generalised stiffness more likely to be suggestive of?
Inflammatory arthritis e.g. RA or PsA
Over what time period does swelling in gout tend to appear?
Over an hour - very actuely
What does swelling following injury suggest?
Haemarhtorsis
What kind of swelling is seen in OA?
Bony swelling (Heberden/Bouchard’s noads)
What does a swelling extruding chalky material indicate?
Gout tophi
What does a swelling exturding hard yellowish lumps indicate?
Calcinosis in systemic sclerosis
Inflammatory vs mechnical morning stiffness?
> 1 hour infammatory
>30 mins mechanical
Inflammatory vs mechnical effect of activity?
Better in inflammatory worse in mechanical
Inflammatory vs mechnical effect of resting?
Worse in inflammatory
Better in mechanical
Inflammatory vs mechnical fatigue?
Significant in inflammatory
Minimal in mechanical
Inflammatory vs mechnical systemic invovlement?
Yes in inflammatory
No in mechanical
What kind of vasculitis is caused by penicillin?
Cutaneous hypersensitivity (leucocytoclastic)
Exaggerated thoracic kyphosis and loss of lumbar lordosis may suggest what?
Longstanding AS
Exaggerated thoracic kyphosis and loss of lumbar lordosis may suggest what?
Osteoperotic fractures
Describe antalgic gait?
Pain causes the patient to reduce the time spent on the affected side
Describe Trendelenberg gait?
Due to poor hip abduction (weak gluteus medialis) the pelvis drops down on the opposite side when standing on the affected leg.
Seen in hip disease and after THR
Describe senory ataxia?
Wide based stamping gate, an attempt to compensate for lack of sensory input.
Sight also helps to compensate, hence worse with eyes shut.
Describe cerebellar ataxia?
Wide-based, staggering. Arms often flung out to try and improve balance.
Describe hemiplegic gait?
Narrow-based, leg swung forward and the toes scrape the ground
Festinant or projectile
Difficulty initiating walking, then a shuffling run.
Reduced arm swing.
What causes bow legs?
Usually medial compartment arthritis in OA as the medial compartment takes most of the load
How do you screen motor function of the hand?
The following to be performed against resistance
Wrist/finger extension - radial nerve
Finger ABduction of the index finger - ulnar nerve
Thumb ABduction - median nerve
What is Tinel’s test?
This is used to help diagnose carpal tunnel syndrome (CTS), the most common peripheral neuropathy of the upper
limb. Any type of arthritis at the wrist can predispose to this.
Tap over the carpal tunnel with your index and middle fingers for 30-60 seconds. If the patient develops tingling in
the thumb and radial two and a half fingers, this suggests median nerve irritation.
What is Phalen’s test?
If the history suggests carpal tunnel syndrome, Phalen’s test may be used..
Ask the patient to hold their wrist in complete and forced flexion (pushing the dorsal surfaces of both hands
together) for 60 seconds. If the patient’s symptom develop then the test is positive
Where is the sensory supply to the hand by the median nerve?
Skin over thenar eminence
Lateral 2/3 of palm
Palmar aspect of lateral 3 1/2 fingers
Dorsal fingertips of lateral 3 1/2 fingers (thumb, index, middle and half of ring finger)
Why is the skin over the thenar eminence spare in CTS?
Preservation of the palmar cutaneous branch
Motor supply to the hand: median nerve
All muscles of anterior compartment of forearm EXCEPT flexor carpi ulnaris and the medial two parts of flexor
digitorum profundus
pronator teres and pronator quadratus – pronate forearm
flexor carpi radialis – flexes and abducts wrist
palmaris longus – flexes wrist and tenses palmar aponeurosis
flexor digitorum superficialis – flexes fingers at PIPJs
lateral two parts of flexor digitorum profundus – flex index and middle fingers at DIPJs
flexor pollicis longus – flexes thumb at IPJ
intrinsic muscles of hand – LOAF muscles
lateral two lumbricals – flex MCPJs and extend IPJs of index and middle finger
opponens pollicis – opposes thumb
abductor pollicis brevis – abducts thumb
flexor pollicis brevis – flexes thumb at MCPJ
Clinical features of a median nerve palsy?
History of wrist trauma/pathology
Numbeness in the hand in a median nerve distribution (palm spared, unless damage in the arm)
Weakness of thumb opposition and abduction (move upwards away from palm, touch thumb to little finger)
Thenar eminance wasting (late feature)
If damage to arm: weak finger flexion put preservation of the ring finger and little finger DIPJs (ulnar nerve)
Sensory nerve supply to the hand - ulnar nerve?
Skin over the hypothenar eminence
Medial 1/3 of the hand
Palmar aspect of the lateral 1 1/2 fingers
medial 1/3 dorsum of the hand
dorsal aspect of the medial 1.5 fingers (little finger and half of ring finger)
Motor nerve supply to the hand: ulnar nerve
Two muscles of the forearm:
flexor carpi ulnaris - flexes and adducts wrist, medical two parts of flexor digitorum profundus
flex ring and little fingers at the DIPJs
Most of the intrinsic muscles of the hand - interossei and the adductor pollicis
Clinical features of ulnar nerve palsy?
These include numbness over the hypothenar eminence and in the ulnar nerve distribution of the hand
Paralysis of flexor carpi ulnaris causes weak wrist flexion and adduction
Paralysis of most of the intrinsic muscles of the hand results in weak MCPJ flexion and IPJ extension of the ring and little fingers, loss of finger abduction and adduction and loss of opposition of little finger
Paralysis of medial two parts of flexor digitorum profundus causes weak flexion of ring and little finger DIPJs
What is Froment’s test?
To test adductor pollicis, ask the patient to grip a piece of card between the thumb and the side of the
index finger
IN ulnar nerve palsy the IPJ and MCPJ of the thumb will flex as the patient tries to grib the card
WHat should be tested for un suspected ulnar nerve palsy?
To test adductor pollicis, ask the patient to grip a piece of card between the thumb and the side of the
index finger (Froment’s test). In ulnar nerve palsy, the IPJ and MCPJ of the thumb will flex as the patient
tries to grip the card. Test adduction by asking the patient to grip the card between the little and ring
fingers whilst holding the fingers extended. Test the first dorsal interosseus muscle by asking the patient to
abduct the extended index finger against resistance.
What is a Claw Hand deformity?
Present in ulnar nerve palsy
Fixed flexion of the IPJs and hyperextension of the MCPJs of the ring and little fingers, hyperextension of the MCPJs of the ring and little fingers due to unopposed median nerve function
Most pronounced when the nerve is injured at the wrist
Interpreting blood tests in rheumatic diseases?
Hb - anaemia of chronic disease most common in RA, Fe deficiency may be used to NSAIDs
Platelets - rise with inflammation or bleeding, fall in SLE
Neutrophils - rise with inflammation, sepsis and prednisolone usage, Fall in SLE or with DMARD toxicity
Lymphocytes - fall in SLE or DMARD induced
U&E - Rise due to NSAIDs, renal disease in lupus/vasculitis or gout
Uric acid - Elevated in gout, but falls with inflammation
LFTs - hepatitic rise due to DMARD toxicity
CK, ALT, LDH - rise in myositis
Which inflammatory marker is affected by anaemia?
ESR - rises
What can Anti-dsDNA antibodies suggest?
SLE
What can Anti RO and anti-LA antibodies indicate?
SLE
Sjorgren’s
What can anti centromere and anti Scl70 antibodies indicate?
Systemic scelrosis
What can anti Jo-1 antibodies indicate?
Polymyositis
Which antigen is associated with AS?
HLA-B27
What might C ANCA indicate?
GPA, infection, neoplasia
What might P ANCA indicate?
Microscopic polyangitis
Infection
Neoplasia
Potential side effects of methotrexate?
Nausea - most common Oral ulcers, hair thinning Hepatitis, cirrhosis Pneumonitis Bone marrow suppression
Potential side effects of hydroxychloroquine?
GI disturbance - most common
Retinal pigmentation and loss of vision – rare but
screening needed
No blood tests needed
Side effects of sulfasalazine?
GI upset -most common
Rash
Hepatitis
Bone marrow suppression
Side effects of azathioprine?
GI upset - most common
Bone marrow suppression
Side effects of cyclophosphamide?
Bone marrow suppression
Infertility
Increased cancer risk
Side effects of ciclosporin?
Renal impairment
HTN
Side effects of leflunomide?
GI Upset
HTN
Bone marrow suppression
Hepatitis
What is Schober’s test and what is a positive result?
To test for this decreased spine mobility, many doctors use the Schober Test, in which they draw two lines on the patient’s spine, 10 cm apart. Then, the patient leans forward and the doctor measures how much the distance increases between the two lines. An increase below 5 cm is positive and indicates AS, while an increase of 5 cm and above is negative and does not indicate AS.
Where does Paget’s disease of the bone typically affect?
The skull, spine/pelvis, and long bones of the lower extremities
What should patients with anti-phospholipid syndrome who haven’t had a thrombosis previously be treated with?
Low-dose aspirin
A positive femoral nerve stretch test in the context of hip pain?
Reffered lumbar spine pain
What treatment of osteoperosis may increase the risk of an atypical stress fracture of the proximal femoral shaft?
Bisphosphonates are associated with an increased risk of atypical stress fractures
What should be ruled out prior to commencing azathioprine?
Azathioprine - check thiopurine methyltransferase deficiency (TPMT) before treatment
What type of hypersensitivity reaction is SLE?
Type 3
Type 3 is characterised by antigen-antibody complexes. The pathogenesis of SLE involves cellular remnants containing nuclear material being transferred to lymphatic tissues. They are then presented to T cells which in turn stimulate B cells to produce autoantibodies. IgG autoantibodies are primed to attack DNA and other nuclear material which results in antigen-antibody complexes causing damage in various areas.
What is trochantaric bursitis also known as?
Greater trochanteric pain syndrome is now the preferred term for trochanteric bursitis.
What is trochanteric bursitis?
Due to repeated movement of the fibroelastic iliotibial band
Pain and tenderness over the lateral side of thigh
Most common in women aged 50-70 years
Course of reactive arthritis?
Reactive arthritis is not typically acute - it can develop up to 4 weeks after precipitating infection and can run a relapsing-remitting course over several months
What other rheumatology drug does azathioprine severely interact with?
Azathioprine and allopurinol have a severe interaction causing bone marrow suppression
Why should visual acuity be monitored for patients taking hydroxycholoroquine?
May result in severe and permananent retinopathy
Why might corticosteroids cause a patient to have reduced power of the shoulders, biceps and hip flexors/extensors
A patient is complaining of a proximal muscle weakness that matches a proximal myopathy. The prolonged course of steroids could be causing this.
What common rheumatological treatment can induce neutrophillia?
Corticosteroid treatment (e.g. prednisolone)
Why must a chest X-ray be performed before starting biologicS?
Can cause chest infection
How should GCA be managed if there is visual loss?
IV methylprednisolone 500mg-1g three days OD
A patient with osteoperosis, who has an intermidate risk but has not have a DEXA scan, should be managed how?
FRAX score recalculated with a dexa scan
When diagnosing PMR, what does normal CK rule out?
Myopathy
MND
What should be prescribed alongside long term steroids?
Bisphosphonates
PPI
Psoratic arthritis features
Joint pain DIP involvement - random distribution, oligoarthritis Skin changes Nail changes Enthesis (AT) - pains around the joints SERONEGATIVE HLAB-27 associated
DIstrubution of AS?
axial mainly
peripheral + illiosacral joints
How can Ankylosing spondylitis lead to heart block?
Fibrosis of the conductive system of the heart
Ankylosing spondylitis X ray findings?
Bamboo spine
Dagger spine (fusion of spinous processes)
Sacroilitis
(Apical chest fibrosis - bad prognosis)
When can DMARDs be considered in Ankylosing spondylitis?
In peripheral disease - no evidence for axial disease
What are the seronegative arthritis’?
Psoratic artheritis
Enteropathic arthritis (alongside IBD)
Ankylosing spondylitis
Reactive arthritis
Which gene are serongeatives arthritis’ associated with?
HLA B27
Poor prognostic factors for RA?
RF positive anti-CCP antibodies poor functional status at presentation X-ray: early erosions (eg after less than two years) extra articular factors e.g. nodules HLA DR4 insideous onset
What X-ray features might be present in a joint affected by gout?
Joint effusion - early sign
well defined ‘punched out’ errosions with sclerotic margins in a juxta-articular distribution, often with overhanging edges
relative preservation of joint space until late disease
eccentric errosions
soft tissue tophi may be seen
What might be seen on x-ray of a joint affected by pseudogout?
Chondrocalcinosis
in the knee this may be seen as linear calcifications of the meniscus and articular cartilage
What are risk factors for pseudogout?
Haemochromatosis
Hyperparathyroidism
Low magnesium, low phosphate
Acromegaly, Wilson’s disease
What is P ANCA associated with
P-ANCA is most strongly associated with microscopic polyangiitis and ulcerative colitis.
Ankylosing spondylitis - x-ray findings
subchondral erosions, sclerosis
and squaring of lumbar vertebrae
Features of stills disease?
arthralgia
elevated serum ferritin
rash: salmon-pink, maculopapular
pyrexia
typically rises in the late afternoon/early evening in a daily pattern and accompanies a worsening of joint symptoms and rash
lymphadenopathy
rheumatoid factor (RF) and anti-nuclear antibody (ANA) negative
Epidemiology of stills disease?
has a bimodal age distribution - 15-25 yrs and 35-46 yrs
Joint aspitrate in RA?
Joint aspirate in rheumatoid arthritis shows a high WBC count, predominantly PMNs. Appearance is typically yellow and cloudy with absence of crystals
Ankylosing spondylitis - x-ray findings
subchondral erosions,
sclerosis
and squaring of lumbar vertebrae
What is used in a new diagnosis of RA?
Methotrexate and pred
For the methotrexate monitor every 3 months - FBC U&Es and LFTs (nephrotoxic, myelosupression and heaptoxicity)
Special insturctions methotrexate
Once a week injection
Folate 5mg every day (methotrexate competitively inhibits dihydrofolate reductase (DHFR), an enzyme that participates in the tetrahydrofolate synthesis) BUT NOT ON DAY OF METHOTREXATE
3 monthly monitoring of U&Es (nephrotoxic), LFTs (hepatotoxicity) and FBC (myelosupression)
First line imperial abx in suspected septic arthritis?
IV flucloxacillin
Gout management in severe renal disease?
Steroids
Polymyocitis vs PMR?
Polymyositis: raised CK, Raised LDH AST ALT, weakness and tenderness
In PMR tenderness only and raised CRP
How many criteria to diagnose SLE?
4/11 of the criteria
What is livedo reticularis associaed?
Rash associated with antiphospholipid syndrome (can be 2 to lupus)
Mottled appearance
What is antiphospoholipid synydrome?
Primary disorder or associated with SLE Coagulation defect - raised APTT Livedo reticularis Obestertic complications 1st trimester miscarriage - pre eclampsia Thrombocytopenia
Anti-coagulation in antiphospholipid syndrome?
Initial VTE (INR) 2-3, 6 months warfarin Recurrent VTE, INR 2-3, lifelong Recurrent VTE on warfarin INR target 3-4
If pregnant LMWH+aspirin
DOACs no licsensed in this syndrome
Most SPecific marker for RA?
Anti-CCP
OA vs mallignsncy
Malignancy - radiolucent lesions
Gout vs pseudogout?
Crystals: Gout uric acid, pseudogout calcium phosphate
Crystial shape: Gout - needle like Pseudogout rhomboid like
Bifringency; Gout - Negative Pseudogout - weaklypositive
Joint affected: Gout - 1st MCP Pseudogout - Knee
Radiography Gout - rat bite erosions, pseudogout - white lines of chondocalcinosis
What DMARD requires visual acuity testing?
Hydroxychloroquine - may result in a severe and permanent retinopathy
