Medicine - Rheumatology Flashcards
Features of RA on X-ray
SPADES soft tissue swelling periarticular erosions absent osteophytes deformity erosions subluxation
Features of OA on X-ray
LLOSS loss of joint space loss of articular cartilage osteophytes (bone lipping) subchondral cysts sclerosis
Side effects of methotrexate
ILD
Hepatitis
What is Felty’s syndrome?
RA
Splenomegaly
neutropenia/thrombocytopenia
Examples of anti-TNF drugs
Etanercept
Infliximab
Example of anti-CD20 drug
Rituximab
Example of JAK inhibitor
Tofacitinib
Example of anti-IL6 drug
Tocilizumab
Genetics involved in psoriatic arthritis?
HLA-B27 (one of the seronegative spondyloarthropathies)
How can PA be distinguished from RA at presentation?
PA has DIP involvement, and dactylitis
What nail changes are found in PA?
Hyperkeratosis
Onycholysis
Nail pitting
What is the CASPAR criteria used for?
Classifying Psoriatic arthritis
What is the PSARC criteria used for?
Monitoring response to treatments in PsA
Treatment options in PsA?
NSAIDs Joint injections (corticosteroid) DMARDs Anti-TNF drugs Biologics
Common causes of infection in septic arthritis:
Can be mono or polymicrobial:
- staph. aureus
- haemophilus influenza
- neisseria gonorrhoea
Risk factors for septic arthritis?
Prosthesis DM Steroids RA Alcohol/IVDU Ulcers Joint injections Surgery
What antibiotics are commonly used for septic arthritis treatment?
IV flucloxacillin + gentamicin (N)
IV vancomycin + gentamicin (P)
What are the contraindications to joint aspirations? (arthrocentesis)
Haemarthrosis Prosthetic joint Overlying skin infection Immunocompromised Clotting disorder
What type of crystals are found in gout?
Monosodium urate (negatively birefringent needle-shaped)
What type of crystals are found in pseudogout?
Calcium pyrophosphate (positively birefringent rhomboid-shaped)
Risk factors for gout?
DM Obesity HTN Haematological malignancy Diuretics Rich diet Chemotherapy
Risk factors for pseudogout?
Hypothyroidism
Hypophosphataemia
Hypomagnesaemia
Hyperparathyroidism Haemochromatosis FHx Older age Prior joint injury
What blood tests would you request if you suspected gout?
FBC, CRP, serum urate
What blood tests would you request if you suspected pseudogout?
FBC, CRP, (high) calcium and PTH, (low) Mg and PO4, (high) T3/4
What are the X-ray features of gout?
soft tissue swelling
tophi formation
rat-bite erosions in long-standing disease
What are the X-ray features of pseudogout?
chondrocalcinosis (almost diagnostic!)
What are the causes of GCA?
- primary = autoimmune issue (a type of large vessel vasculitis)
- secondary = to infection (hepatitis) or drugs
What is the definition of osteoporosis?
Reduction in bone mass (resorption > deposition)
matrix composition maintained but BMD reduced
What are the RFx for OP development?
S - steroids H - hyperthyroid/parathyroid/calciuria A - alcohol/smoking T - low testosterone T - thin (BMI <19) E - early menopause R - renal/liver failure E - erosive/inflammatory bone disease D - diet (low calcium/vit D, malabsorption, DM)
What is used to investigate OP and describe its results:
FRAX score (fracture risk assessment tool)
DEXA scan: gives a t-score
greater than -1 = normal
-1 to -2.5 = osteopenia
less than -2.5 = osteoporosis
less than - 2.5 with fractures = defined OP
Remember: T-score (compares to a healthy thirty year old), Z-score (compares to an age matched individual)
Name some of the pharmacological treatments for OP:
HRT
SERM e.g. raloxifene
Bisphosphonates e.g alendronate
Teriparatide (synthetic PTH)
Strontium ranelate (reduces OC and increases OB activity)
Denosumab (monoAb against RANK-L, stops OC recruitment)
Describe the signs/symptoms of ankylosing spondylitis
- lower back pain
- worse at night, better towards the end of the day
- pain better with exercise and worse with rest
- pain radiates from hip -> buttocks
- dyspnoea (if costochondral involvement)
- uveitis
- enthesitis (achilles tendonitis, plantar fasciitis)
How is Ank Spond diagnosed?
- clinical + radiological criteria
- MRI or X-ray used as imaging
- X-ray may show bamboo spine (syndesmophytes present)
What are three features of poor prognosis in Ank Spond?
- smoking
- high ESR/CRP
- syndesmophytes present
What autoantibodies are found in SLE?
- ANA (sensitive but not specific)
- anti-ds-DNA (more specific)
What are the signs/symptoms of SLE?
S - serositis (pleuritis, pericarditis) O - oral ulcers A - arthritis P - photosensitivity B - blood (low WCC, RBC and plts) R - renal (glomerulonephritis) A - ANA Immunological - anti-ds-DNA N - neurological (confusion, seizures) M - malar rash (butterfly, non-scarring) D - discoid rash (scarring)
Name the large vessel vasculitides
- GCA
(- PMR) - Takayasu arteritis
Describe Takayasu arteritis
Large vessel vasculitis
aortic-arch syndrome/pulseless disease
inflammation of aorta and primary branches
common in females 15-25yrs
presents - fever, malaise, night sweats, weight loss, bruits, absent/reduced/assymmetrical pulses
Investigate with CT/MRI/angiography
Name the medium vessel vasculitides
PAN
Kawasaki disease
Describe PAN
Medium vessel vasculitis
Polyarteritis nodosa
a Necrotising vasculitis which causes aneurysms and thrombi
can cause infarction in all organ systems
Describe Kawasaki disease
Medium vessel vasculitis common in children and babies aneurysm formation in medium/large arteries, commonly affecting: - cardiac - axillary - iliac - popliteal arteries Presents with: - fever - conjunctivitis - mucositis (strawberry tongue) - peeling skin - lymphadenopathy
Describe the different types of ANCA:
Anti-neutrophil cytoplasmic antibodies
2 types:
- C-ANCA (cytoplasmic) = against proteinase 3 (PR3)
- P-ANCA (perinuclear) = against myeloperoxidase (MPO)
Describe the ANCA associated vasculitides
small vessel vasculitidies
- microscopic polyangitis: P-ANCA associated, necrotising inflammation in many organs including kidneys
- granulomatosis with polyangitis: C-ANCA associated, granulomatous inflammation, triad of upper respiratory/lower respiratory/kidney issues
- eosinophilic granulomatosis with polyangitis: P-ANCA associated, necrotising and granulomatous inflammation causing asthma, eosinophilia and peripheral neuropathy
Describe the immune-complex vasculitides:
HSP (Henoch Schonlein purpura)
- commonest childhood vasculitis
- median age ~4yrs
Cryoglobulinaemic vasculitis
- autoimmune where the cold triggers immunoglobulins called cryoglobulins reversibly precipitate at <37oC in serum
Describe reactive arthritis:
Seronegative spondyloarthropathy (RF-ve, HLA-B27 +ve) inflammatory arthropathy after infection (antigen cross reacts from infection to self-tissue in joint) Commonly pts have preceding venereal/diarrhoeal infection
What common infections can cause reactive arthritis
Venereal:
- shigella
- chlamydia
- salmonella
- yersinia
Diarrhoeal:
- campylobacter
What investigations would you want to carry out if reactive arthritis was suspected?
- bloods (ESR, CRP, RF, U&E)
- urinalysis and stool cultures
- joint aspirate
- STI check
- X-ray
Define Paget’s disease of bone
Also called ‘Osteitis deformans’
increased bone turnover (more OB and OC)
Rare <40yrs
bone remodelling and enlargement = deformity and weakness
Describe the pathophysiology of Paget’s disease of bone
3 distinct phases:
1) Initial short-lived burst of OC activity and bone resorption
2) Mixed phase of OC and OB activity (increased bone turnover and structurally abnormal bone)
3) Chronic sclerotic phase = bone formation > deposition
Describe primary and secondary bony lesions
Primary e.g. myeloma
- much more rare
- lytic usually
Secondary e.g. mets from lungs, breast, prostate, kidney, thyroid
- commoner
- usually sclerotic
Describe compartment syndrome and its causes
- increased interstitial pressure in a closed fascial compartment
- pressure can be increased due to internal cause (haematoma, iatrogenic cannula) or external cause (casts, burns, bandages)
What is the indication for a fasciotomy in compartment syndrome?
If myoglobin (released from ischaemic muscle) is high as this it toxic to the kidneys and can cause kidney damage
What are the important time points for managing compartment syndrome?
1-4hrs = reversible >8hrs = irreversible (muscle ischaemia and necrosis)
What genetic HLA type is common in RA?
HLA DR4
Describe the features of RA (articular and extra-articular)
symmetrical deforming polyarthritis DIP sparing peak onset ~40yrs swan neck/boutonnieres deformities ulnar deviation swelling, heat, pain tenosynovitis
(Extra-articular) nodules lungs - ILD, fibrosis, pneumonia heart - IHC, pericarditis eyes (scleritis, episcleritis) kidneys - amyloidosis feltys syndrome
Describe the pathophysiology of RA
Genetics (DR4) + environmental (smoking increases PAD, increased anti-CCP antibodies, hormones and infections)
What common HLA type in seen in AnkSpond
HLA-B27, RF- (as it is a seronegative spondyloarthropathy!)
Describe GCA and how it presents
large vessel vasculitis (also called temporal arteritis)
affects extra-cranial branches of the carotid artery
can be primary (autoimmune) or secondary (drugs/infection e.g. hepatitis)
headache, temporal tenderness, jaw claudication, malaise, weight loss, depending on nearby nerves affected = amaurosis fugax, tongue tingling, confusion
How is GCA investigated and treated?
Bloods - high ESR/CRP
Temporal artery biopsy (beware of skip lesion)
Start steroids immediately = pred, or IV methyl-pred if visual changes
(usually need steroids for ~2yrs and then need to wean off)
Describe PMR and its presentation
polymyalgia rheumatica
Rare <60yrs
not a true vasculitis, can develop from GCA
presents with painful proximal myopathy (pelvic, neck, shoulder pain)
NO MUSCLE WEAKNESS! (helps to distinguish from myositis’)
What HLA type is PMR associated with?
HLA DRB1 (found in GCA-PMR concurrent cases, but NOT in PMR alone)
How is PMR investigated and treated?
High ESR/CRP
lots of other bloods! (CK should be normal to distinguish from myositis’)
Treat with steroids (but not needed as urgently as in GCA)
Use methotrexate for relapsing disease
Define polymyositis and its presentation
Idiopathic inflammatory myopathy characterised by striated muscle inflammation
Cause unclear
Presents: painful proximal myopathy + WEAKNESS
- malaise, weight loss, fever, dysphagia, palpitations, syncope
How is polymyositis investigated?
Clinical features
Lab findings: high platelets, high CRP, high CK (50-100x ULN), anti-Jo antibodies
MRI shows muscle inflammation and oedema
Define dermatomyositis and its presentation
Idiopathic inflammatory myopathy characterised by striated muscle inflammation (same as polymyositis) + rash
- heliotrope rash (eyelids), periorbital oedema and Gottron’s papules
Describe Sjogren’s syndrome and its associated HLA type
Systemic autoimmune disorder
presents with dry eyes and mouth
lymphocytic infiltration of lacrimal and salivary glands
9F : 1M
HLA B8/DR3
How does Sjogren’s syndrome present?
Sicca complex = reduced salivary and lacrimal gland excretion Dry eyes (keratoconjunctivitis), red itchy eyelids (blepharitis) Dry mouth (xerostomia) - pts often need to sip water to swallow food
How Sjogren’s syndrome diagnosed and how can it be managed?
Bloods: high ESR Schirmers test (filter paper) Salivary gland biopsy
lacrimal substitutes
artificial saliva/gels
chewing gum - stimulates saliva flow
How do primary and secondary bone growths/mets differ
Primary = lytic Secondary = more sclerotic
Describe compartment syndrome and its causes
Increased interstitial pressure in a closed fascial compartment
Causes nerve damage and cell death
causes:
increased internal pressure (bleeding/iatrogenic)
increased external pressure (burns, casts, bandages)
What are the S/Sx of compartment syndrome?
Pain Pallor Paraesthesia Paralysis Pulseless
shiny, swollen taught skin
increased autonomic responses (cause sweating and tachycardia)
What conditions are associated with carpal tunnel syndrome
RA, CKD, DM, acromegaly, pregnancy
What is the time at which the damage from compartment syndrome and the neuropraxia becomes irreversible
8hrs!
How is compartment syndrome investigated and managed?
Measure compartment pressure (?20-30mmHg above diastolic BP then this is a strong indicator for fasciotomy
Treatment: remove external constriction, fasciotomy, may need to remove dead muscle and get skin grafts
What is tendinopathy and common tendinopathes?
= general term for tendon degeneration with combination of: pain, swelling and impaired performance
Commonly: achilles, rotator cuff, tennis elbow (lateral) and golfers elbow (medial epicondyle)
How is tendinopathy managed?
NSAIDS/GTN patches Physio RICE Stretching and strengthening Extra-corporal shock wave therapy (causes microtrauma and increased healing in the local area?)
May need surgery
