Rheumatology Flashcards
(44 cards)
1
Q
Which drugs can cause Rheumatoid diseases?
A
- Penicillin - cutaneous hypersensitivity
- B blocker - Raynauds
- Diuretics - Uric acid excretion
- Minocycline/ sulphasalazine - Lupus rashes
2
Q
What PMH history conditions are associated rheumatoid conditions?
A
- Seronegative spondyloarthropathy - anterior uveitis, psoriasis, IBD
- Sexually acquired infection / diarrhoea - indicate reactive arthritis or gonococcal arthritis
3
Q
What is gout?
A
- Gout is a type of crystal arthropathy associated with chronically high blood uric acid levels. Urate crystals are deposited in the joint causing it to become hot, swollen and painful.
- Gouty tophi are subcutaneous deposits of uric acid typically affecting the small joints and connective tissues of the hands, elbows and ears. The DIP joints are most affected in the hands.
4
Q
How does gout present and what joints does it affect?
A
- It typically presents with a single acute hot, swollen and painful joint. The obvious and extremely important differential diagnosis is septic arthritis.
- Typical Joints
- Base of the big toe (metatarsophalangeal joint)
- Wrists
- Base of thumb (carpometacarpal joints)
- Gout can also affects large joints like the knee and ankle.
5
Q
What are some RFs for gout?
A
- Male
- Obesity
- High purine diet (e.g. meat and seafood)
- Alcohol
- Diuretics
- Existing cardiovascular or kidney disease
- Family history
6
Q
How is gout diagnosed?
A
- Gout is diagnosed clinically or by aspiration of fluid from the joint. Excluding septic arthritis is essential as this is a potential joint and life-threatening diagnosis.
- Aspirated fluid will show:
- No bacterial growth
- Needle shaped crystals
- Negatively birefringent of polarised light
- Monosodium urate crystals
- Bloods: raised serum urate and uric acid
- X ray
- Typically the space between the joint is maintained
- Lytic lesions in the bone
- Punched out erosions
- Erosions can have sclerotic borders with overhanging edges
7
Q
How is gout managed?
A
- Acute
- 1st: NSAIDs (e.g. ibuprofen)
- 2nd: Colchicine. SE: GI upset: dose dependent diarrhoea. pt w renal impairment or significant heart disease
- 3rd: Steroids can be considered third-line
- Prophylaxis:
- Allopurinol: xanthine oxidase inhibitor which reduces the uric acid level - start 2/3 weeks after attack or continue through acute attack if taking it already
- Lifestyle: losing weight, staying hydrated and minimising the consumption of alcohol and purine-based food (meat and seafood).
8
Q
what is pseudogout?
A
- Pseudogout is a crystal arthropathy caused by calcium pyrophosphate crystals.
- Calcium pyrophosphate crystals are deposited in the joint causing joint problems. It is also known as chondrocalcinosis.
9
Q
How does pseudogout present?
A
- A typically presentation of pseudogout is an older adult with a hot, swollen, stiff, painful knee. Other joints that are commonly affected are the shoulders, wrists and hips.
- It can be a chronic condition and affect multiple joints. It can also be asymptomatic and picked up incidentally on an xray of the joint.
10
Q
How is pseudogout diagnosed?
A
Exclude septic arthritis needs to be excluded
Joint aspiration:
- No bacterial growth
- Calcium pyrophosphate crystals - Rhomboid shaped crystals
- Positive birefringent of polarised light
X ray
- Chondrocalcinosis is the classic xray change in pseudogout. It appears as a thin white line in the middle of the joint space caused by the calcium deposition. This is pathognomonic(diagnostic) of pseudogout.
- Others: LOSS of OA
11
Q
How is pseudogout managed?
A
- Chronic asymptomatic changes found on an xray do not require any action.
- Symptoms usually resolve spontaneously over several weeks. Symptomatic management involves: NSAIDs, Colchicine, Joint aspiration, Steroid injections, Oral steroids
- Severe: joint wash out
12
Q
How does rheumatoid arthritis present?
A
- Symetrical distal polyarthropathy
- Swollen, painful joints in hands and feet - worse after rest and improved with activity
- Stiffness worse in the morning (>30mins)
- Gradually gets worse with larger joints becoming involved
- Presentation usually insidiously develops over a few months
- Positive ‘squeeze test’ - discomfort on squeezing across the metacarpal or metatarsal joints
13
Q
What are the genetic and antibody associations of RF?
A
Genetic:
- HLA DR4 (a gene often present in RF positive patients)
- HLA DR1 (a gene occasionally present in RA patients)
Antibodies
- RF: 70% of RA patients: autoantibody that targets the Fc portion of the IgG antibody. It is mostly IgM
- Anti-CCP : more sensitive and specific to RA and often pre-date the development of RA
14
Q
A
15
Q
What joints are affected in RA?
A
- Proximal Interphalangeal Joints (PIP) joints NOT DIPS
- Metacarpophalangeal (MCP) joints
- Wrist and ankle
- Metatarsophalangeal joints
- Cervical spine - Atlantoaxial subluxation occurs in the cervical spine. Can cause spinal cord compression
- Large joints can also be affected such as the knee, hips and shoulders
16
Q
A
17
Q
What are the Signs in the Hands in RA?
A
- Z shaped deformity to the thumb
- Swan neck deformity (hyperextended PIP with flexed DIP)
-
Boutonnieres deformity (hyperextended DIP with flexed PIP)
- Due to a tear in the central slip of the extensor components of the fingers. This means that when the patient tries to straighten their finger, the lateral tendons that go around the PIP (called the flexor digitorum superficialis tendons) pull on the distal phalynx without any other supporting structure, causing the DIPs to extend and the PIP to flex.
- Ulnar deviation of the fingers at the knuckle (MCP joints)
18
Q
What are the extra articular manifestations of RA?
A
Pulmonary fibrosis with pulmonary nodules (Caplan’s syndrome)
Bronchiolitis obliterans (inflammation causing small airway destruction)
Felty’s syndrome (RA, neutropenia and splenomegaly)
Secondary Sjogren’s Syndrome (AKA sicca syndrome)
Anaemia of chronic disease
Cardiovascular disease
Episcleritis and scleritis
Rheumatoid nodules
Lymphadenopathy
Carpel tunnel syndrome
Amyloidosis
19
Q
How is RA diagnosed?
A
- Bloods: RBC (normocytic anaemia), WCC, raised CRP and ESR
- Imaging: USS - synovitis
- X ray of hands and feet: LESS
- Loss of joint space: destruction and deformity
- Erosions (bony)
- Soft tissue swelling
- Sublaxation
- Peri articular osteopenia
- Antibodies: RF, if -ve -> anti-CCP antibodies
- Scoring system: DAS 28: Disease Activity Score. It is based on the assessment for 28 joints and points are given for:
- Swollen joints
- Tender joints
- ESR/CRP result
20
Q
How is RA managed?
A
MDT team
1st presentation: NSAIDs/COX-2 inhibitors + PPIs
DMARDs
- 1st: monotherapy with methotrexate, leflunomide or sulfasalazine. Hydroxychloroquine can be considered in mild disease and is considered the “mildest” anti rheumatic drug.
- Methotrexate SE: Mouth ulcers and mucositis, Liver toxicity, Pulmonary fibrosis, Bone marrow suppression and leukopenia (low white blood cells), teratogenic
- Sulfasalazine SE: Temporary male infertility (reduced sperm count), Bone marrow suppression
- Leflunomide: Mouth ulcers and mucositis. Increased blood pressure, Rashes. Peripheral neuropathy. Liver toxicity, Bone marrow suppression and leukopenia, teratogenic (harmful to pregnancy)
- Hydroxychloriquine: skin pigmentation, liver toxicity, nightmares and reduced VA
- 2nd: 2 of these used in combination.
- 3rd: methotrexate + a biological therapy, usually Anti-TNF (adalimumab, infliximab, etanercept, golimumab and certolizumab pegol)
- 4th: methotrexate + rituximab
-
Pregnancy: Sulfasalazine + hydroxychloroquine
- Sulfasalazine: safe in pregnancy but give folic acid supplementation
21
Q
What is SLE?
A
- inflammatory autoimmune connective tissue disease.
- relapsing-remitting course, with flares and periods where symptoms are improved.
- The result of chronic inflammation means patients with lupus often have shortened life expectancy. Cardiovascular disease and infection are leading causes of death.
22
Q
What sx are present in SLE?
A
- Fatigue
- Weight loss
- Arthralgia (joint pain) and non-erosive arthritis
- Myalgia (muscle pain)
- Fever
- Photosensitive malar rash. This is a “butterfly” shaped rash across the nose and cheek bones that gets worse with sunlight.
- Lymphadenopathy and splenomegaly
- Shortness of breath
- Pleuritic chest pain
- Mouth ulcers
- Hair loss
- Raynaud’s phenomenon
23
Q
How is SLE Ixd?
A
Autoantibodies: ANA, 2nd: anti DS DNA
Types of ANA Abs: Anti-Smith, Anti-centromere antibodies, Anti-Ro and Anti-La (Sjogren’s syndrome), Anti-Scl-70 (systemic sclerosis), Anti-Jo-1 (dermatomyositis)
Bloods: FBC (normocytic anaemia of chronic disease), C3 and C4 levels (decreased in active disease), CRP and ESR (raised)
Immunoglobulins (raised due to activation of B cells with inflammation)
Urinalysis and urine protein:creatinine ratio for proteinuria in lupus nephritis
Renal biopsy: lupus nephritis
Diagnosis:
24
Q
What are the complications/ sx of SLE?
A
- SOAP BRAIN
- Serositis - pleurisy, percarditis
- Oral ulcers
- Arthritis
- Photosesitivity / pericarditis
- Blood disorders
- Renal involvement
- Interstitial Lung Disease
- Neurological disorders: seizures, psychosis
25
How is SLE managed?
Lifestyle: NSAIDs, sun-block
## Footnote
1st: Hydroxychloroquine
2nd: One of the following: Methotrexate . Mycophenolate mofetil, Azathioprine, Tacrolimus, eflunomide, Ciclosporin
3rd: biological therapies
26
What is anklyosing spondylitis?
inflammatory condition mainly affecting the spine that causes progressive stiffness and pain. It is part of the seronegative spondyloarthropathy group of conditions relating to the HLA B27 gene.
27
How does ankylosing spondylitis present?
* young adult male in their late teens or 20
* Symptoms develop **gradually** over more than 3 months.
* lower back pain and stiffness and sacroiliac pain in the buttock region. pain and stiffness is worse with rest and improves with movement and pain is worse at night and in the morning and may wake them from sleep
* . **\>30 minutes** for the stiffness to improve in the morning and it gets progressively better with activity throughout the day.
* Symptoms can fluctuate with “flares” of worsening symptoms and other periods where symptoms improve.
* **Vertebral fractures** are a key complication of AS.
28
What are some of the extra articular manifestations of ank spond?
* Anterior uveitis
* Aortic incompetence
* AV block
* Apical lung fibrosis
* Amyloidosis
29
How is Ank Spond examined and investigated
Shober test
Ix:
* Inflammatory markers (CRP and ESR) may rise with disease activity
* **HLA B27** genetic test
* **Xray** of the spine and sacrum
* “Bamboo spine”
* Squaring of the vertebral bodies
* Subchondral sclerosis and erosions
* Syndesmophytes are areas of bone growth where the ligaments insert into the bone.
* Ossification of the ligaments, discs and joints. This is where these structures turn to bone.
* Fusion of the facet, sacroiliac and costovertebral joints
* **MRI** of the spine can show bone marrow oedema early in the disease before there are any xray changes
30
How is ankylosing spondylitis mxd?
* 1st: NSAIDs. If the improvement is not adequate after 2-4 weeks of a maximum dose then consider switching to another NSAID.
* 2nd: Steroids during flares
* 3rd: Anti-TNF medications: **etanercept**
* 4th: **Secukinumab** is a monoclonal antibody against interleukin-17.
* Lifestyle: Physiotherapy, Exercise and mobilisation, Avoid smoking, Bisphosphonates to treat osteoporosis, Treatment of complications
* Surgery: occasionally required for deformities to the spine or other joints
31
What is psoriatic arthritis?
* Psoriatic arthritis is an inflammatory arthritis associated with psoriasis. This can vary in severity. Patients may have a mild stiffening and soreness in the joint or the joint can be completely destroyed in a condition called arthritis mutilans.
* It occurs in 10-20% of patients with psoriasis and usually occurs within 10 years of developing the skin changes. It typically affects people in middle age but can occur at any age.
* It is part of the “seronegative spondyloarthropathy” group of conditions.
32
What are some of the patterns of psoriatic arthritis?
* Symmetrical polyarthritis presents similarly to rheumatoid arthritis and is more common in women. The hands, wrists, ankles and DIP joints are affected. The MCP joints are less commonly affected (unlike rheumatoid).
* Asymmetrical pauciarthritis affecting mainly the digits (fingers and toes) and feet. Pauciarthritis describes when the arthritis only affects a few joints.
* Spondylitic pattern is more common in men. It presents with:
* Back stiffness
* Sacroiliitis
* Atlanto-axial joint involvement
* Other areas can be affected:
* Spine
* Achilles tendon
* Plantar fascia
33
What are some of the signs of psoriatic arthritis?
* **Plaques** of psoriasis on the skin
* **Pitting** of the nails
* **Onycholysis** (separation of the nail from the nail bed)
* **Dactylitis** (inflammation of the full finger)
* **Enthesitis** (inflammation of the entheses, which are the points of insertion of tendons into bone)
* Other associations
* **Eye disease** (conjunctivitis and anterior uveitis)
* **Aortitis** (inflammation of the aorta)
* **Amyloidosis**
34
What screening tools and investigations are used for psoriatic arthritis?
PEST screening tool
Xray Changes
* **Periostitis** is inflammation of the periosteum causing a thickened and irregular outline of the bone
* **Ankylosis** is where bones joining together causing joint stiffening
* **Osteolysis** is destruction of bone
* **Dactylitis** is inflammation of the whole digit and appears on the xray as soft tissue swelling
* **Pencil-in-cup** appearance
35
What is arthritis mutilans?
This is the most severe form of psoriatic arthritis. This occurs in the phalanxes. There is osteolysis (destruction) of the bones around the joints in the digits. This leads to progressive shortening of the digit. The skin then folds as the digit shortens giving an appearance that is often called a “telescopic finger”.
36
How is psoriatic arthritis managed?
1. NSAIDs for pain
2. DMARDS (methotrexate, leflunomide or sulfasalazine)
3. Anti-TNF medications (etanercept, infliximab or adalimumab)
4. Ustekinumab is last line (after anti-TNF medications) and is a monoclonal antibody that targets interleukin 12 and 23
37
How does reactive arthritis present?
* Bilateral conjunctivitis (non-infective)
* Anterior uveitis
* Circinate balanitis is dermatitis of the head of the penis
* TOM TIP: These features of reactive arthritis (eye problems, balanitis and arthritis) lead to the saying “can’t see, pee or climb a tree”.
38
What is reactive arthritis
* Reactive arthritis is where synovitis occurs in the joints as a reaction to a recent infective trigger. It used to be known as Reiter Syndrome.
* Typically it causes an **acute monoarthritis**, affecting a single joint in the lower limb (most often the knee) presenting with a warm, swollen and painful joint.
* Common infections that trigger reactive arthritis are gastroenteritis or STIs : **Chlamydia**. Gonorrhoea commonly causes a gonococcal septic arthritis.
* **HLA B27** gene: part of the seronegative spondyloarthropathy group of conditions.
39
How is reactive arthritis managed?
* Rule out septic arthritis: acute warm, swollen, painful joint need to be treated according to the local “hot joint” policy. This will involve giving antibiotics until the possibility of septic arthritis is excluded. Aspirate the joint and send a sample for gram staining, culture and sensitivity testing to exclude septic arthritis.
* The aspirated fluid can also be sent for crystal examination to look for gout and pseudogout.
40
How is reactive arthritis mxd?
* NSAIDs
* Steroid injections into the affected joints
* Systemic steroids may be required, particularly where multiple joints are affected
41
What are polymyositis and dermatomyositis
* Polymyositis and dermatomyositis are autoimmune disorders where there is inflammation in the muscles (myositis).
* **Polymyositis** is a condition of chronic inflammation of muscles
* **Dermatomyositis** is a connective tissue disorder where there is chronic inflammation of the skin and muscles.
42
What are some of the sx of dermatomyositis?
* **Gottron lesions** (scaly erythematous patches) on the knuckles, elbows and knees
* **Photosensitive erythematous rash** on the back, shoulders and neck
* **Purple rash** on the face and eyelids
* Periorbital oedema (swelling around the eyes)
* **Subcutaneous calcinosis** (calcium deposits in the subcutaneous tissue)
43
How does polymyositis present?
Muscle pain, fatigue and weakness
Occurs bilaterally and typically affects the proximal muscles
Mostly affects the shoulder and pelvic girdle
Develops over weeks
44
How is polymyositis/ dermatomyositis diagnosed?
* * Clinical presentation
* Elevated **CK**
* Autoantibodies
* Polymyositis: **Anti-Jo-1** antibodies: (but often present in dermatomyositis)
* Dermatomyositis: **Anti-Mi-2 + ANA**
* Electromyography (**EMG**)
* Muscle biopsy can be used to establish a definitive diagnosis.
