Rheumatology Flashcards
(143 cards)
1
Q
What is ankylosing spondylitis?
A
• Seronegative arthritis that predominantly affects the spine and sacro-iliac joints
• It is a chronic inflammatory condition that can eventually lead to fusion (ankylosis) of the intervertebral joints and SI joints
2
Q
What group tend to get ankylosing spondylitis?
A
More common in males and age of onset is typically between 20-40 year
3
Q
Symptoms in ankylosing spondylitis?
A
• Typically, patients complain of back pain which can be cervical, thoracic or lumbar
• Pain is inflammatory in nature – i.e. it gets worse with rest and better with movement
• There is significant early morning stiffness
4
Q
Examination in someone with suspected ankylosing spondylitis?
A
• On examination of spine schobers test would be done to show objectively that there is reduced lumbar spine flexion
• Schobers test involves measuring 5cm below PSIS and 10cm above whilst patient is upright and then get patient to bend forwards and you measure the distance, in normal situations the distance should extend beyond 20cm (so 5cm increase)
• In examination should also measure chest expansion as the costo-vertebral joints can sometimes be affected
• Will also see exaggerated lumbar lordosis and thoracic kyphosis on examination
5
Q
Question mark spine or bamboo spine?
A
Ankylosing spondylitis
6
Q
Investigations for ankylosing spondylitis?
A
• Bloods looking for increased inflammatory markers
• HLA testing (can be done by blood test) – ankylosing spondylitis and other seronegative arthritis are associated with HLA-B27
• X-rays of late disease may show sacroiliitis, syndesmophytes (bony growth inside ligaments), fusion of joints
• MRI is better for showing early disease changes
7
Q
Non-articular manifestations of ankylosing spondylitis?
A
• Uveitis
• Occasionally respiratory disease, aortic valve incompetence and renal impairment
8
Q
Management of ankylosing spondylitis?
A
• Key to management is early identification so preventative physiotherapy can be started before syndesmophyte formation and spinal mobility can be maintained
• NSAIDs can improve symptoms and signs of the disease
• DMARDs should only be given if peripheral joint involvement- they do not work in spinal disease
• Anti-TNF treatment (e.g. infliximab, certolizumab) are the only biologics that work and are only to be used in severe disease, they have been shown to reduce symptoms of spinal and peripheral joint inflammation and improve function
9
Q
Explain the difference between inflammatory and mechanical pain?
A
inflammatory pain - worse with rest, better with movement, significant morning stiffness i.e. lasts more than 30 minutes
mechanical pain - worse with movement, better with rest, little bit of morning stiffness but not for long
10
Q
What is the most prevalent seropositive polyarthropathy?
A
rheumatoid arthritis
11
Q
Pathogenesis of rheumatoid arthritis?
A
1) Presence of susceptibility genes
2) Environmental triggers cause changes to the way DNA is transcribed leading to conversion of amino acid arginine into citrulline
3) This results in protein unfolding and this unfolded protein can now act as an antigen
4) Antibodies to citrullinated peptides (i.e. this unfolded protein) are distributed throughout the circulation and form immune complexes with citrullinated proteins produced in an inflamed synovium
5) There is infiltration and activation of neutrophils
12
Q
What groups most commonly get rheumatoid arthritis?
A
• More common in women than men
• Most common age of onset is between 30 to 50yo
13
Q
Presentation of rheumatoid arthritis?
A
• There is a progressive, symmetrical, peripheral polyarthritis evolving over a period of a few weeks or months
• Pain is inflammatory in nature i.e. It gets worse with rest and better with movement
• There is prolonged morning stiffness (lasting more than 30 minutes)
• There is involvement of the small joints of the hands and feet – the MCPs, PIPs and MTPs – not the DIPs (DIPs are in osteoarthritis)
• Symmetric distribution
• Inflamed joints are soft and squishy and on examination there will be a positive compression test of MCPs and/ or MTPs (when you squeeze over the joints it causes pain)
14
Q
What are some deformities you can get later on in rheumatoid arthritis if it is not managed properly?
A
There can be ulnar deviation (fingers bend abnormally towards little finger), boutonniere deformity (fixed flexion of PIP and hyperextended DIP), swan-neck deformity (fixed flexion of the DIP, hyperextended PIP)
15
Q
Antibodies for rheumatoid arthritis?
A
Anti-CCP - very specific, sensitivity 66% (so about 34% of people with RA will not be picked up by this test)
rheumatoid factor - very sensitive, but not very specific (so almost everyone with RA will be picked up by this test but so will lots of people without RA)
16
Q
Imaging in rheumatoid arthritis?
A
• In early disease the XR may be normal however there may be some signs of soft tissue swelling or periarticular osteopenia
• In late disease may see erosions and subluxations
• Ultrasound can be good for showing synovitis in early disease and can detect MCP erosions
• MRI is occasionally used to show early disease
17
Q
List some non-articular manifestations of rheumatoid arthritis?
A
• Subcutaneous rheumatoid nodules- these are firm subcutaneous nodules that generally occur over pressure points, they can be removed surgically but tend to recur
• Lung Disease- range of conditions can occur, can get airways disease, pleural disease, pulmonary fibrosis, intrapulmonary nodules
• Heart Disease- raynauds, pericarditis, myocarditis, and endocarditis
• Nervous System Involvement- peripheral neuropathies
• Eye Disease- Scleritis and episcleritis
• Kidneys- amyloidosis causing proteinuria, nephrotic syndrome and CKD
• Anaemia
18
Q
Management of rheumatoid arthritis?
A
• First line treatment is DMARDs (disease modifying anti rheumatic drug) and first line DMARD is usually methotrexate (other examples include leflunomide or sulfasalazine)
• These should be started as soon as possible and ideally within 3 months of onset of persistent symptoms
• Offer additional DMARD in combination if remission/ low disease activity has not been reached
• If tried 2 DMARDs and still high disease activity biologics are offered, examples include infliximab, entanercept and rituximab
• Steroids can be used for managing flares
19
Q
Drug side effects in rheumatoid arthritis?
A
• Methotrexate is teratogenic and must be stopped in females at least 3 months before conception
• Side effects of DMARDS include bone marrow suppression, infection, LFT derangement, pneumonitis and nausea (blood tests need to be done regularly on these drugs)
• Side effects of biologics include increased risk of infection particularly tuberculosis and patients need to be screened for latent infections before they go on these drugs
20
Q
What type of crystals are there in gout?
A
monosodium urate crystals
21
Q
Explain what gout is and what causes it?
A
• An inflammatory arthritis that is associated with hyperuricaemia and presence of intra-articular urate crystals
• Uric acid is the final compound in the breakdown of purines in DNA metabolism
• Hyperuricaemia can be caused by increased urate production or decreased urate excretion
• Increased urate production may be due to inherited enzyme defects, malignancy, psoriasis, haemolytic disorders or high purine intake e.g. in alcohol, red meat or sea food
• 2 common causes of reduced urate excretion are diuretics and chronic renal impairment
22
Q
What groups is gout more common in?
A
• More common in men than women
• Generally, in older/ middle aged people
• (in young people it suggests some sort of genetic cause)
23
Q
Presentation of acute gout?
A
• 1st presentation is typically in the MTP joint in the foot
• Sudden onset of agonizing pain, swelling and redness
• The attack settles in 10 days without treatment and 3 days with treatment
• May have normal uric acid during the attack
24
Q
Presentation of chronic gout?
A
• Individuals with persistently high levels of uric acid can present with chronic tophaceous gout, as sodium urate forms smooth white deposits (termed tophi) in the skin and round joints, on the ear, fingers or the Achilles tendon
• There is chronic joint pain and sometimes acute attacks on top of the chronic pain
• It is often associated with renal impairment and/ or the long-term use of diuretics
25
What is polymyalgia rheumatica?
• This is a chronic inflammatory condition of muscles
• It is relatively common
26
What groups of patients tend to get polymyalgia rheumatica?
• It almost exclusively occurs in the elderly
• Thought to be associated with HLA-DR4, parvovirus and adenovirus
27
Presentation of polymyalgia rheumatica?
• Symmetrical myalgia of the proximal muscles (may start unilateral but becomes bilateral)
• Morning stiffness
• Reduced range of movement due to pain but the actual muscle strength is normal (this is in contrast to polymyositis where the muscle is weak)
• Fatigue anorexia, weight loss and low grade fever may occur
• PMR is associated with temporal/ giant cell arteritis and it is very important to ask about symptoms of GCA as it can result in loss of sight if untreated
28
What is polymyalgia rheumatica associated with?
giant cell arteritis - important to ask about symptoms as can result in loss of sight!!!
29
Diagnosis of polymyalgia rheumatica?
• No specific diagnostic test but most people have raised inflammatory markers
• Diagnosis is basically done by exclusion and response to steroids confirms the diagnosis
30
Treatment for polymyalgia rheumatica?
• Tends to respond very well to low dose steroids
• The condition generally lasts 18 months to 2 years before resolving
• If just PMR then start prednisolone 15 mg daily and gradually reduce the dose
• If GCA need to start at higher dose of steroids 40-60 mg daily and then reduce
31
Pathogenesis theory for SLE?
1) There is defect in the apoptosis mechanism meaning that when cells die their contents float around longer than normal so this causes the immune system to develop auto-antigens from the cells
2) Cells expressing these antigens are attacked by the immune system
3) There is formation of nucleosome/ anti-nucleosome complexes
4) These complexes are mainly deposited in the skin and kidneys (hence these are the areas most frequently affected by lupus)
32
What group of patients is SLE more common in?
• Lupus is 9x more common in females than males and commonly presents in childbearing years
• It is more common and there are more severe presentations in those of Afro-Caribbean, Hispanic American, Asian and Chinese ethnicity
33
Common presentations of SLE?
fatigue, skin problems (usually relating to sun exposure) and arthralgia
classic skin problems: malar butterfly rash, discoid lesions, photosensitivity, alopecia
also aphthous mouth ulcers and pleuritic chest pain can be complications
34
List some organ system manifestations of SLE?
• Renal- lupus nephritis, it should be noted that renal involvement is often asymptomatic until it is very serious so it is very important to do urine analysis in anyone suspected of SLE to check for proteinuria
• Haematological- leukopenia, lymphopenia, anaemia, thrombocytopenia
• Neuropsychiatric- seizures, psychosis, headache, aseptic meningitis
• Cardiac- pericarditis, pericardial effusion, pulmonary hypertension, endocarditis, accelerated ischaemic heart disease
• Respiratory- pleural effusions, rarely pulmonary fibrosis
• GI- less common but include autoimmune hepatitis, pancreatitis and mesenteric vasculitis
35
Describe antibody tests for lupus?
• Best antibody test is Anti-double stranded DNA (anti-ds-DNA), this is specific for lupus and the titre correlates with disease activity and is associated with lupus nephritis (however only present in 70% of people with SLE so if someone doesn’t have it that doesn’t rule out lupus)
• Anti-nuclear antibody – this is the “gateway” to connective tissue disease, i.e. will be positive in most people with any connective tissue disease which could be SLE or something else e.g. scleroderma or sjogrens. It has low specificity so doesn’t confirm SLE but if someone is negative they are unlikely to have SLE
• Anti-Ro and Anti-La is present in some with lupus and can be associated with neonatal lupus, these antibodies aren’t present in everyone with lupus and are also present in Sjogrens
• Anti-Sm is very specific for SLE but only 2/3 of people with SLE will be positive
36
What is antiphospholipid syndrome and what other condition is it related to?
• This condition can occur on its own but it is often secondary to SLE
• It is associated with recurrent venous and arterial thrombosis and recurrent miscarriages
37
Antibodies for antiphospholipid syndrome?
lupus anti-coagulant, anti-cardiolipin and anti-beta2glycoprotein
38
Management of antiphospholipid syndrome?
• If someone with this condition has had an episode of thrombosis they should be treated with anti-coagulation, those who have recurrent pregnancy loss can be put on LMWH during pregnancy, if someone is positive for the antibodies but never had an episode of thrombosis they do not require anti-coagulation
- note that DOACs have questions over if they are as effective as warfarin and LMWH in preventing thrombosis and are generally not used in APS
39
What do all patients with SLE need screened for?
Renal involvement:
All patients with SLE need a urine analysis done and if positive for protein then a kidney biopsy should be done to check for lupus nephritis
40
General measures for those with SLE?
• Education on fatigue
• Sun protection and advice on avoiding excessive exposure to sunlight
• Patients should be encouraged to reduce cardiovascular risk factors
41
Symptomatic treatment for SLE?
• Most patients don’t need oral corticosteroids or immunosuppressive agents
• Arthralgia, arthritis, fever and serositis all respond well to standard doses of NSAIDS
• Topical corticosteroids are effective for treating skin disease
• Antimalarial drugs such as hydroxychloroquinine also help mild skin disease, fatigue and arthralgias although patients require regular eye checks due to retinal toxicity
42
Treatment for SLE patients with Organ involvement?
• Corticosteroids and immunosuppressive drugs are given in organ involvement
• Examples of immunosuppressive agents include methotrexate or azathioprine (in moderate disease) or cyclophosphamide (in severe disease as very potent), cyclophosphamide is being increasingly replaced by mycophenolate mofetil
43
Monitoring for patients with SLE?
• It is important to monitor patients over time as new manifestations can develop
• Anti ds-DNA and complement levels are checked regularly (low levels of complement correspond to high disease activity because complement is consumed by the autoimmune disease process)
44
Management of gout?
Acute
• High dose NSAIDS e.g., diclofenac, naproxen
• Colchicine is an alternative medication for pain if the patient cannot tolerate NSAIDs
• Corticosteroids can be given if resistant pain
Chronic
• Xanthine oxidase inhibitors help lower urate levels (xanthine oxidase is an enzyme used in purine metabolism so inhibiting it lowers urate) the main one is allopurinol, another example would be febuxostat
• It is important that these are not given during an acute attack as they can make an acute attack worse
• They should be given after the attack has settled to prevent future attacks
• NSAIDs can potentially be used to try and stop attacks whilst hyperuricaemia is being corrected
45
What is pseudo gout?
• Inflammatory arthritis caused by deposition of calcium pyrophosphate crystals in the joint
46
Causes and groups of patients that tend to get pseudo gout?
• More common in the elderly (wouldn’t generally consider in someone < 70yo)
• Causes include hyperparathyroidism, previous cartilage problems, hypothyroidism, haemochromatosis, hypomagnaesia
47
Presentation of pseudo gout?
• Tends to affect larger joints like the knee
• May get attacks of pain, swelling and stiffness
48
Diagnosis of pseudo gout?
• The radiological appearances are known as chondrocalcinosis
• Joint fluid microscopy shows rhomboidal weakly positive birefringement crystals
49
Management of pseudo gout?
• Unlike gout there are no prophylactic medications
• NSAIDs, colchicine or steroids can be given in acute attacks like in gout
50
What is osteoarthritis?
commonest disorder of joints
basic pathology is degeneration of the articular cartilage
51
Difference between primary and secondary osteoarthritis?
• Primary osteoarthritis has no obvious predisposing cause
• In secondary osteoarthritis there is a clear association with some predisposing condition which can be virtually any abnormality of a joint e.g. previous injury, abnormal stress on joint, previous inflammation
52
Groups more likely to get osteoarthritis?
• Prevalence increases with age
• Obesity predisposes to OA as putting more weight and therefore stress through the joints
• To some extent it runs in families
53
Presentation of osteoarthritis?
• Tends to affect the larger weight bearing joints e.g. the knee, hip, lumbar and cervical spine
• It can also affect the DIPs and PIPs in the hand but NEVER the MCPs (MCP involvement BUZZWORD for rheumatoid arthritis/ autoimmune condition!!!)
• Pain is mechanical – this means it is worse on activity but relieved by rest (this contrasts to inflammatory pain present in RA etc.)
• Can get stiffness in the morning but only lasts for 5-10 mins (stiffness is nowhere near as bad as RA)
54
Examination of osteoarthritis?
• May not see anything abnormal
• May be able to palpate crepitus (grating sensation over joints)
• May be hard swelling over affected joints (this is due to osteophyte formation)
• There may be reduced range of movement
• Joints may be tender and may be presence of effusions
• In OA affecting the hands may see Heberden’s nodes (swelling over the DIPs) and/ or Bouchard’s (swelling over the PIPs)
55
Diagnosis of osteoarthritis?
• Usually, a clinical diagnosis and XR is not needed to confirm
• However, if done features on XR include:
(LOSS)
- Loss of joint space
- Osteophyte formation
- Subchondral cysts
- Subchondral sclerosis
It should be noted that some patients with severe symptoms may have only small changes on XR and some patients with no symptoms may have substantial changes on XR.
56
Management of osteoarthritis?
There is no cure, all about managing symptoms
Step wise management:
1) Offer education and reassurance
2) Give advice on self-management in exercise, weight loss (if overweight) and suitable pacing
3) Refer to physiotherapy (can also refer to OT or podiatrist)
4) Analgesia (update from guidance 2022)- first should try topical NSAIDs, then oral NSAIDS, no longer meant to routinely prescribe paracetamol or weak opioids - only prescribe these for short term relief
5) Surgical treatment with joint replacement is a definitive solution however this is a big surgery with risk of complications and joint replacements only last for approximately 10-20yrs so other options should be tried first
57
Pathology of osteoarthritis?
• Degradation and damage to cartilage causes remodelling of bone due to active response of chondrocytes in the cartilage and inflammatory cells in the surrounding tissues
• Release of enzymes results in further degradation
• Initially there is flaking and fibrillation of the cartilage
• Then exposure of subchondral bone which gets harder (sclerotic) known as eburnation
• Remodelling changes lead to formation of osteophytes and subchrondral bone cysts
Used to be thought that osteoarthritis was purely a degenerative disease, but it is an inflammatory cycle in response to joint wear and tear that some people are more prone to than others
58
What is fibromyalgia?
• This is an unexplained condition that causes widespread muscle pain and fatigue
• It is not an inflammatory disorder but a functional disorder
(functional disorders are disorders where no obvious pathology is found and there is an assumed dysfunction of the organ or system – this includes conditions such as fibromyalgia, irritable bowel syndrome, chronic fatigue syndrome, chronic pain syndromes, non-epileptic attack disorder)
59
What is fibromyalgia associated with? Who tends to get it?
• It is more common in women
• There is association with emotional or physical trauma
• They may have other functional disorders too
• Can be associated with anxiety and depression
60
Presentation of fibromyalgia?
• Chronic and widespread pain
• Fatigue, disrupted and unrefreshing sleep
• Cognitive difficulties e.g., forgetfulness, concentration difficulties or mental slowness
• Multiple other unexplained symptoms, anxiety and/or depression and functional impairment of activities of daily living
61
Investigations for fibromyalgia?
• There is not an investigation for fibromyalgia, it is a diagnosis of exclusion so basically you have to rule out everything else first that could be causing the symptoms
• There are specific “tender points” that pressure on them may elicit pain on examination
62
Management of fibromyalgia?
• Patient education, it is important to validate the symptoms and explain what fibromyalgia is, there is a lot of stigma around the condition
• Should give advice on graded exercise and fatigue management
• Cognitive behavioural therapy can be helpful at changing the patient’s way of thinking about their pain
• Atypical analgesics can help some with pain e.g. tricyclics, gabapentin, SSRIs, pregabalin
• In some people complementary medicine such as acupuncture is helpful
63
What is juvenile idiopathic arthritis?
• Autoimmune arthritis that primarily affects children (typical onset before 16)
• Causes pain and swelling in joints
64
What are the 3 major types of juvenile idiopathic arthritis?
• Oligoarticular JIA (fewer than 6 joints)
• Polyarticular JIA (multiple joints)
• Systemic JIA (wild variety of systemic symptoms)
65
Describe oligoarticular juvenile idiopathic arthritis?
• Approx. 50% of cases
• Females > males
• 2-3 years range - very rare to present after 10
• < 5 joints
• Medium and large joints, asymmetric, rarely the hips, non-destructive arthritis
• Usually, no systemic features
• If the child is ANA positive more likely to get uveitis
66
Describe polyarticular juvenile idiopathic arthritis?
• Approx. 33%
• F >M
• Peaks in ages 2-5 years and 10-14 years
• Any joints, usually symmetric, destructive arthritis
• Less frequent uveitis
67
Describe systemic juvenile idiopathic arthritis?
• Approx. 10%
• F=M
• Any age really under 17
• Any joints, destructive arthritis
• Sometimes no joint involvement
• Daily high fevers, evanescent salmon-pink rash, Hepatosplenomegaly , lymphadenopathy , heart lung liver
68
Presentation of juvenile idiopathic arthritis?
• Joint pain
• Morning stiffness or stiffness after still for a period (gelling)
• Limp
• 25% may report no pain, only swelling is observed, massage doesn’t help
• Systemic symptoms with systemic JIA e.g. rash, daily fevers, hepatosplenomegaly and lymphadenopathy
69
Clinical diagnosis of juvenile idiopathic arthritis?
• No one lab is totally diagnostic
• Elevated ESR, CRP, WBC, platelets
• Most children do not have positive rheumatoid factor
• RF positive predicts chronic erosive joints in polyarticular JIA
• ANA positive is associated with increased risk of uveitis (refer these patients to ophthalmologist)
• HLAB27 increases risk of enthesitis associated JIA
70
Management of juvenile idiopathic arthritis?
MAIN MANGEMENT
• NSAIDs should be tried first
• Steroids (joint injections)
• Methotrexate in some children if other treatments not working (follow CBC and LFTs every few months for neutropenia, transaminitis)
TREATING COMPLICATIONS
Treating complications
• Leg length discrepancy – special shoes or operative
• Uveitis – requires frequent ophthalmologist screening if ANA pos
• Contractures – physical therapy, Botox injections and muscle relaxants
• Growth problems – careful monitoring
71
Prognosis of juvenile idiopathic arthritis?
• Oligoarticular – highest rate of remission
• RF pos oligoarticular has lowest likelihood of remission persist into adulthood as other forms of arthritis
• Prognosis for systemic depends on extent of arthritis and systemic symptoms after 6 months
72
What is septic arthritis and how does it occur?
• Joint infection
• Can be caused by direct invasion, blood stream infection or less commonly from an infectious focus from cellulitis abscess or spread from osteomyelitis
73
With any mono-arthritis you must rule out?
septic arthritis as this is surgical emergency and needs treated within 24 hours to stop irreversible damage
74
Presentation of septic arthritis?
• Inflammation
• Warmth
• Redness
• Joint effusion
• Agonizingly painful
• Decreased function or ROM
75
Main causative agents for septic arthritis?
• Staph aureus
• Group A streptococci
• Neisseria gonorrhoea if sexually active
• Only staph epi if infection is in relation to a prosthetic joint
76
Investigations for septic arthritis?
• Aspirate joint and send fluid to microbiology
• Blood cultures
• Swabs
• Must check for crystals to rule out gout
• Ultrasound and XR may be helpful
77
Management for septic arthritis?
• This is a surgical emergency
• May need to do joint drainage/ arthroscopic drainage
• Broad spectrum IV antibiotics then tailor when results back
78
XR shows pencil in cup appearance
explain what this means
psoriatic arthritis
(arthritis mutilans subtype)
this is because the erosions are central, i.e. close to the joint so the end of the bone is eroded into a sharp pencil shape and the surface of the adjoining bone is worn away by the pencil into a smooth cup. In rheumatoid arthritis the erosions are juxta-articular meaning they are further away from the joint so this deformity does not occur. Hence pencil in cup appearance is characteristic of psoriatic arthritis only.
79
What is psoriatic arthritis?
• A seronegative arthritis that occurs in up to 30% of people affected by skin psoriasis
80
Who tends to get psoriatic arthritis?
• Those with psoriatic nail disease are more likely to get psoriatic arthritis
• Joint problems can precede the skin problems (so you shouldn’t rule out psoriatic arthritis because no skin disease)
81
Explain the 5 main patterns of psoriatic arthritis?
1) Mono or oligoarthritis
2) Polyarthritis- this often begins with asymmetrical pattern and progresses to be virtually indistinguishable from RA
3) Spondylitis- disease with spinal involvement, there is usually sacroiliitis and involvement of the cervical spine
4) DIP arthritis- this is the most typical pattern and there is often adjacent nail dystrophy, reflecting enthesitis (inflammation where the tendons or ligaments insert into the bone) extending into the nail root. Dactylitis in which an entire finger or nail is swollen with joint and tendon sheath involvement is characteristic of this condition.
5) Arthritis Mutlians- this is the most aggressive but only affects about 5% of those with psoriatic arthritis and causes marked periarticular osteolysis and bone shortening
82
Diagnosis of psoriatic arthritis?
• Rheumatology exam but also look for skin disease
• Bloods- check for inflammatory markers and check for anti-CCP and rheumatoid factor etc. to rule out other seropositive inflammatory arthritis
• Can check for HLA-B27
• X-rays
83
Management of psoriatic arthritis?
• NSAIDs and/ or analgesics can help pain although sometimes can worsen the skin lesions
• Physiotherapy, OT, orthotics and chiropodist can be used
• Corticosteroid injections into joints can help with localized synovitis
• DMARDs e.g. methotrexate, sulfasalazine or leflunomide can be used in patients with persistent peripheral joint synovitis
• Anti-TNF can be used in severe disease that is unresponsive to NSAIDs and methotrexate
84
What is reactive arthritis?
• Seronegative arthritis that occurs in response to an infection in another part of the body most common GU (chlamydia, Neisseria) or GI infections (salmonella, campylobacter)
• The infection triggers an autoimmune inflammatory arthritis
• It usually occurs 1-3 weeks following the infection
85
What groups is reactive arthritis more common in?
• HLA-B27 is thought to increase susceptibility as it can cause a person to respond to infection differently
• Most common in ages 20-40
86
Presentation of reactive arthritis?
• Large joints e.g. the knee become inflamed 1-3 weeks following the infection (should be noted that the infection may have been mild and although important to ask about, patients may not be aware that they have recently had an infection)
87
What is Reiters syndrome?
• Rarely some patients have a triad of symptoms known as Reiter’s syndrome: urethritis, uveitis (or conjunctivitis) and arthritis
88
Investigations for reactive arthritis?
• Take bloods to check for inflammatory markers and HLA-B27
• May do joint fluid analysis to check for septic arthritis (should be noted that reactive arthritis is sterile unlike septic arthritis where the actual joint is infected)
89
Management and prognosis of reactive arthritis?
• Most patients recover fully in 6 months, but some can have a relapse
• In susceptible individuals, reactive arthritis, sacroiliitis and spondylitis may develop
• Treatment is aimed at the underlying infectious cause and symptomatic relief
• Pain responds well to NSAIDs and locally injected or oral corticosteroids
• Relapsing cases are sometimes treated with sulfasalazine or methotrexate
• TNF alpha blocking agents are the drugs of choice in severe or persistent disease but are rarely necessary
90
What is enteropathic arthritis?
• Arthritis associated with patients who have ulcerative colitis or Crohn’s disease
91
Presentation of enteropathic arthritis?
• Joint symptoms may predate the development of bowel symptoms and lead to diagnosis
• Or patient may present with symptoms of crohns or UC
• The arthritis is usually present in several joints, is asymmetrical and predominantly affects lower limb joints
• Generally, there is worsening of arthritis symptoms during flare ups of IBD
92
Investigations of enteropathic arthritis?
• Investigations to look for Crohns or UC e.g. colonoscopy, endoscopy, stool sample
• Bloods to check for raised inflammatory markers and HLA-B27
• X-ray/ MRI can show sacroiliitis
• Ultrasound can show synovitis/ tenosynovitis
93
Management of enteropathic arthritis?
• Generally, management involves treating the inflammatory bowel disease as this helps control the arthritis
• For pain relief NSAIDs are generally not used as they can exacerbate the IBD, paracetamol and cocodamol are used instead
• If mono-arthritis then can use intra-articular steroid injections
• DMARD sulfasalazine is often used as this helps both the bowel and joint disease
• Anti-TNF e.g. infliximab can also help both the bowel disease and the arthritis
94
Explain how most antibody tests are reported and what this means?
• Most antibody tests are reported as either absolute values in international units or as a titre
• A titre gives a value for the number of dilutions before activity is lost, the higher the titre the greater the concentration of the antibody, e.g. 1/80 is lower than 1/640 because the antibody had to be diluted 640 to lose activity vs 80
95
ANA is reported as a __1_____ It is very __2___ but not ____3_____
Low titres are commonly seen in ____4______
1 titre
2 sensitive
3 specific
4 elderly patients and hypothyroidism
96
Anti-dsDNA is highly specific for ____ and titres vary ________ so _________
SLE
vary with time and disease activity so it is good for monitoring disease
97
Why is anti CCP of prognostic significance?
positivity is Associated with more severe and extra articular disease
98
What is ANCA associated with and what are 2 types?
small vessel vasculitis
c-ANCA and p-ANCA
99
What do you need for true positivity with anti-phospholipid antibodies and why?
Have to be positive on two occasions 12 weeks apart for true positivity because they can be transiently raised in infection/ inflammation
100
What is serum complement measurement useful for?
useful for measuring disease activity in some conditions like lupus
C3 and C4 are low in active lupus because the disease consumes complement
101
Explain ways to distinguish, joint pain, muscle pain and soft tissue pain?
Joint Disease
• Pain
• Swelling
• Stiffness (lasts longer then more likely to be inflammatory)
• Limitation of movement
Soft tissue problem
• More localised
• Only certain movements of the joint are affected
• Examples are rotator cuff problems, epicondylitis, trochanteric bursitis etc.
Muscle diseases
• Pain in affected muscles
• Weakness
• Wasting
• No stiffness
102
If stiffness lasts longer is the condition more likely to be inflammatory or non-inflammatory?
inflammatory
103
It is very rare for women to get gout before ____
menopause even after menopause it is much less likely
104
What is the classical symmetrical poly arthritis?
rheumatoid arthritis
105
What is classically an asymmetrical oligoarthritis?
psoriatic arthritis
106
Asymmetrical inflammatory disease tends to be _____
a seronegative spondylarthopathy
107
Explain how vasculitis can be classed?
• Vasculitis can be categorised into small and large vessel
• Large vessel include giant cell arteritis which affects older people and takayasus which affects younger people
• Small vessel vasculitis can be ANCA positive or ANCA negative
• ANCA positive small vessel vasculitis include GPA, EGPA and MPA
• ANCA negative includes Henoch schonlein vasculitis
• There are also medium vessel types of vasculitis but these arent taught in much detail e.g. polyarteritis nodosa
108
What is GCA?
• A large vessel vasculitis of the vessels supplying the head
• It is granulomatous
109
What groups tend to get GCA?
• Very rare under 50 yo and occurs in association with polymyalgia rheumatica
110
Presentation of GCA?
• Severe headaches, tenderness of the scalp or of the temple
• May get claudication of the jaw when eating
• Tenderness or swelling of one or more temporal or occipital arteries (despite prominent arteries there is reduced pulsation)
• In bad disease arteries are non pulsatile because they are blocked, if you can feel someone’s temporal artery pulse then they are unlikely to have GCA
• Reason why it is so important to pick up is because it can involve the ophthalmic artery and cause painless loss of vision in an eye which can be permanent (hence those with PMR need to be warned of these symptoms!)
111
Investigations for GCA?
• Bloods to check for raised inflammatory markers
• The most definitive diagnosis is with temporal artery biopsy (although shouldn’t wait for results to start steroids), should also be noted that vasculitis may be patchy and that the whole length of the biopsy needs examined
• Can also do an ultrasound
112
Management of GCA?
• If there is new visual loss (transient or permanent) or double vision need same day referral to ophthalmologist
• For everyone else suspected of GCA should get a urgent referral to rheumatology
• Shouldn’t delay steroids until confirmation, give steroids straight away if suspected as it is a medical emergency
• 40-60 mg prednisolone and reduce gradually
113
What is takayaus arteritis?
• This is a large vessel vasculitis that occurs in younger people
• It affects the aortic arch and other major arteries
• It is rare
114
What is GPA?
• ANCA positive (anti-neutrophil cytoplasm antibodies) small vessel vasculitis
• There is granulomatous inflammation of the respiratory tract, small and medium vessels
• Glomerulonephritis can also occur
115
Presentation of GPA?
• Constitutional symptoms of fever and weight loss may precede the onset of organ specific symptoms
• ENT symptoms are common including nosebleeds, deafness, recurrent sinusitis, nasal crusting and over time there can be collapse of the nose known as saddle nose deformity
• Can also get lung involvement with haemoptysis and cavitating lesions
• Can present with a rapidly progressive glomerulonephritis > nephritic syndrome
116
Investigations for GPA?
• Bloods looking for anaemia of chronic disease and raised inflammatory markers
• Check for ANCA (specifically c-ANCA)
• U and Es and urine analysis to check for renal involvement
• Chest X-ray to look for lung lesions
• Biopsy of kidney or skin can help confirm diagnosis (presence of granulomas- no eosinophils)
117
Management of GPA?
• Most cases require IV steroids and cyclophosphamide due to aggressive disease course
118
What is EGPA?
• ANCA positive small vessel vasculitis
• There is eosinophilic granulomatous inflammation of the respiratory tract, small and medium vessels and an association with asthma
119
Presentation of EGPA?
• Constitutional symptoms of fever and weight loss
• Allergic rhinitis and asthma that is difficult to control
• May be involvement of skin with vasculitic rash
• Can get heart, GI and kidney involvement
120
Investigations for EGPA?
• Bloods looking for anaemia of chronic disease and raised inflammatory markers
• Check for ANCA (specifically p-ANCA)
• U and Es and urine analysis to check for renal involvement
• Chest X-ray to look for lung lesions
• Biopsy of kidney or skin can help confirm diagnosis (presence of granulomas and eosinophilic infiltration)
121
Management of EGPA?
• Most cases require IV steroids and cyclophosphamide due to aggressive disease course
122
What is HSP?
IgA Vasculitis
ANCA negative small vessel vasculitis
This is a generalized vasculitis involving the small vessels of the skin, the GI tract, the kidneys and joints (rarely the lungs and CNS) and it is due to deposition of IgA complexes in these places
123
What groups does HSP affect?
• About 75% of cases occur in children aged 2-11
• More than 75% of patients have had a preceding URTI, Pharyngeal or GI infection (1-3 weeks before)
• Commonly infection with group A strep
124
Presentation of HSP?
• Purpuric rash over buttocks and lower limbs
• Colicky abdo pain
• Bloody diarrhea
• Joint pain with or without swelling
• Renal involvement
125
Management of HSP?
• There is no proven treatment of benefit
• It is usually self limiting with symptoms resolving in 8 weeks
• Relapses can occur for months to years
• MUST PERFORM URINE ANALYSIS TO SCREEN FOR RENAL INVOLVEMENT AS HENOCH SCHONLEIN CAN POTENTIALLY CAUSE RAPIDLY PROGRESSIVE GLOMERULONEPHRITIS
126
What is a point to remember about pulmonary fibrosis in rheumatoid arthritis?
PF can be caused both by the rheumatoid arthritis but also by the treatment as methotrexate can cause PF!
127
What is the pharmacological treatment of choice for raynauds?
nifedipine
128
What is polyarteritis nodosa?
medium sized vasculitis with necrotising inflammation that can result in aneurysm formation - associated with hepatitis B infection
129
Synovial fluid colour in normal, RA and septic?
normal - light slightly straw coloured
Ra- more yellow
septic - cloudy opaque
130
What is Feltys syndrome?
RA, splenomegaly, low white blood cells
131
When a patient is on steroids what is important to consider?
DONT STOP pnemonic
DONT - after 3 weeks you are steroid dependent, do not stop them suddenly
S- sick day rules, when unwell need a bigger dose of steroids
T - need to carry a steroid treatment card
O- osteoporosis prevention (calcium, vitamin D and bisphosphonate)
P - PPI - steroids can cause increased acid/ reflux
132
What is Behcets disease ?
this is a complex vasculitis that affects vessels of all sizes, small, medium and large both arterial and venous
133
What is Behcets associated with?
HLA B51
potential link to H. pylori
134
Presentation of Behcets
mouth ulcers and genital ulcers
erythema nodosum, papule and pustules similar to acne, vasculitic like rashes
anterior and posterior uveitis
arthralgia and oligoarthritis
inflammation can also affect GI tract, CNS, lungs and cause thrombosis in different places
135
How are mouth ulcers in Behcets different from aphthous ulcers?
they are more painful and larger
tend to take weeks to heal
sharply circumscribed erosions with a red halo
136
Test for Behcets?
pathergy test - sterile needle to create a subcutaneous abrasion, which doesn't heal well and then develop a skin lesion or ulcer when checked in 24-48 hours
137
Analgesia for osteoarthritis?
Analgesia (update from guidance 2022)- first should try topical NSAIDs, then oral NSAIDS, no longer meant to routinely prescribe paracetamol or weak opioids - only prescribe these for short term relief
138
NICE guidelines pharma mechanical backpain?
oral NSAIDs consider 1st
consider weak opioids with or without paracetamol only if NSAID contraindicated or not effective. Do not offer paracetamol alone.
139
By what mechanisms can temporal arteritis cause loss of sight and how does this appear on fundoscopy?
Most common mechanism is (anterior) ischaemic optic neuropathy which appears as swollen and pale disc with blurred margins
Second most common mechanism is a CRAO which appears as a pale retina with a cherry red spot
140
Apart from visual loss what is another important complication of GCA?
stroke
141
Will you always be able to diagnose GCA based on temporal artery biopsy?
no as it can appear as skip lesions so may be areas not affected and you happen to biopsy one of those areas
142
What parameters should be monitored frequently in those with henoch schnolein purpura?
hypertension and urinalysis
143
Patients with Sjrogens syndrome have an increased risk of what?
lymphoid malignancies
