Rheumatology Flashcards
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)