rheumatology to work on COPY Flashcards
What investigations might you do in someone you suspect to have psoriatic arthritis?
X-ray
- Erosion in DIPJ + periarticular new-bone formation - Osteolysis - Pencil-in-cup deformity
Bloods
- ESR + CRP - normal or raised
- Rheumatoid factor -ve
- anti-CCP - negative
Joint aspiration - no bacteria or crystals
What investigations might you do in someone you suspect to have reactive arthritis?
ESR + CRP - raised ANA - negative RF - negative X-ray - sacroiliitis or enthesopathy Joint aspirate - negative (exclude septic arthritis + gout)
Give 4 properties of bone that contribute to bone strength
- Bone mineral density
- Bone size
- Bone turnover
- Bone micro-architecture
- Mineralisation
- Geometry
Give 5 risk factors for osteoporosis
- old age, women, FHx, previous fracture, smoking, alcohol, Asian/Caucasian
‘SHATTERED’
- Steroid use
- Hyperthyroidism, hyperparathyroidism, hypercalciuria
- Alcohol + tobacco use
- Thin (BMI < 18.5)
- Testosterone (low)
- Early menopause
- Renal or liver failure
- Erosive/inflammatory bone disease (e.g. myeloma or RA)
- Dietary low calcium /malabsorption or Diabetes type 1
what are is the clinical presentation of giant cell arteritis?
- Headache, typically unilateral over temporal area
- Temporal artery/scalp tenderness
- Jaw claudication
- Visual symptoms - vision loss (painless)
- Systemic symptoms - fever, malaise, lethargy
What are the investigations for giant cell arteritis?
- ↑ESR and/or CRP (=highly sensitive) ESR >50 mm/hr
- Halo sign on US of temporal and axillary artery
- Temporal artery biopsy = gold standard for Dx (show giant cells, granulomatous inflammation)
Describe the treatment for giant cell arteritis
- High dose corticosteroids - prednisolone ASAP
- DMARDs - methotrexate (sometimes)
- Osteoporosis prophylaxis is important - lansoprazole, alendronate, Ca2+, vit D
What is the pathophysiology of Wegener’s granulomatosis?
Necrotising granulomatous vasculitis affecting arterioles and venules
ANCAs can activate primed circulating neutrophils which leads to fibrin deposition in vessel walls and deposition of destructive inflammatory mediators
What investigations might you do in someone you suspect to have Wegener’s Granulomatosis?
ANCA testing - c-ANCA
Tissue biopsy - (renal biopsy best) - shows granulomas
CT - assessment of organ involvement
FBC - high eosinophils
What is the treatment for Wegener’s Granulomatosis?
- Glucocorticoids (prednisolone)
- Immunosuppresive drugs (cyclophosphamide OR rituximab)
- plasma exchange for specific complications
Give 5 risk factors for developing OA
- Genetic predisposition - females, FHx
- Trauma
- Abnormal biomechanics (e.g. hypermobility)
- Occupation (e..g manual labor)
- Obesity = pro-inflammatory state
- Old age
Describe the pathophysiology of osteoarthritis
Mechanical stress –> progressive destruction and loss of articular cartilage
exposed subchondral bone becomes sclerotic
cytokine mediated TNF/IL/NO involved
deficiency in growth factors
Describe the pathogenesis of SLE
Type 3 hypersensitivity reaction = immune complex mediated
Autoantibodies to a variety of auto antigens result in formation and deposition of immune complexes
What investigations might you do in someone who you suspect has SLE?
- Blood tests = anaemia, neutropenia, thrombocytopenia, RAISED ESR and NORMAL CRP
- Serum autoantibodies - ANA, anti-dsDNA
Describe the pharmacological treatment for SLE
● Avoid excessive sunlight and reduce CVS risk factors ● NSAIDs - ibuprofen ● Chloroquine and hydroxychloroquine ● Corticosteroids - prednisolone ● cyclophosphamide ● methotrexate ● Topical steroids
first line = hydroxychloroquine
Give 5 signs of limited scleroderma
CREST
1. Calcinosis - skin calcium deposits
2. Raynauds
3. Esophageal reflux/stricture
4. Sclerodactyly - thick tight skin on fingers/toes
5. Telangiectasia - dilated facial spider veins
Pulmonary arterial hypertension
Give 4 signs of diffuse scleroderma
Skin changes develop more rapidly and are more widespread than inlimited cutaneous scleroderma/CREST
- Proximal scleroderma
- Pulmonary fibrosis
- Bowel involvement
- Myositis
- Renal crisis
What is a diagnostic test for scleroderma?
Limited - ACAs
Diffuse - Anti-topoisomerase, Anti scl-70 ANAs ESR (normal)
If renal involvement, there may be anemia
Describe the management of scleroderma
avoid smoking, handwarmers
GI - PPIs, Antibiotics
Renal - ACEi
Pulmonary fibrosis - cyclophosphamide
Give 5 symptoms of sjögren’s syndrome
- Dry eyes and dry mouth
- dry skin and dry vagina
- Inflammatory arthritis
- Rash
- Neuropathies
- Vasculitis
- fatigue
- salivary and parotid gland enlargement
What investigations might you do in someone who you suspect to have sjögren’s syndrome?
Serum auto-antibodies –> anti-RO, anti-La, RF, ANA
Raised immunoglobulins and ESR
Schirmer’s test
- ability for eyes to self-hydrate - <10mm in 5 minutes
Rose bengal staining and slit lamp exam
What is the treatment for sjögren’s syndrome?
- Artificial tears, artificial saliva, vaginal lubricants
- Hydroxychloroquine
- NSAID
- M3 agonist - pilocarpine
Give 3 symptoms of dermatomyositis
- Rash
- Muscle weakness
- Lungs are often affected too (e.g. interstitial lung disease)
What investigations might you do in someone who you suspect has dermatomyositis?
- Muscle enzymes raised
- Electromyography (EMG)
- Muscle/skin biopsy
- Screen for malignancy
- CXR
What is the treatment for dermatomyositis?
Steroids - prednisolone
Immunosuppressants
which organisms can cause septic arthritis?
- Staphylococcus aureus
- Streptococci
- Neisseria Gonorrhoea
- Gram negative = E. coli, pseudomonas aeruginosa
what are the risk factors for septic arthritis?
Pre-existing joint disease (OA or RA) Joint prostheses IVDU Immunosuppression Alcohol misuse Diabetes Intra-articular corticosteroid injection Recent joint surgery
Describe the treatment for septic arthritis
Aspirate joint Empirical Abx - flucloxacillin - if allergic to penicilin = clindamycin - if MRSA = vancomycin - if gram negative = cefotaxime Analgesia - NSAIDS
What organisms can cause osteomyelitis?
- Staph. aureus
- Coagulase negative staph (s. epidermidis)
- Aerobic gram negate bacilli (salmonella)
- haemophilus influenza
- Mycobacterium TB
Name 2 predisposing conditions for osteomyelitis
- Diabetes
2. PVD
Give 4 host factors that affect the pathogenesis of osteomyelitis
- Behavioural (risk of trauma)
- Vascular supply (arterial disease, DM)
- Pre-existing bone/joint problems (RA)
- Immune deficiency
Acute osteomyelitis: what changes to bone might you see histologically?
- Inflammatory cells
- Oedema
- Vascular congestion
- Small vessel thrombosis
Chronic osteomyelitis: what changes to bone might you see histologically?
- Necrotic bone - ‘squestra’
- New bone formation ‘involucrum’
- Neutrophil exudates
- Lymphocytes and histiocytes
Why does chronic osteomyelitis lead to sequestra and new bone formation?
- Inflammation in BM increase intramedullary pressure exudate into bone cortex which rupture through periosteum
- this causes interruption of periosteum blood supply which results in necrosis and sequestra
- therefore new bone forms
What is acute osteomyelitis associated with?
Associated with inflammatory bone changes caused by pathogenic bacteria
What is chronic osteomyelitis associated with?
Involves bone necrosis
what are the signs of acute osteomyelitis?
- Tender
- Warm
- Red swollen area around OM
what are the signs of chronic osteomyelitis?
- Acute OM signs
- Draining sinus tract
- Non-healing ulcers/fracture
What is the differential diagnosis of osteomyelitis?
- Cellulitis
- Charcot’s joints (sensation loss –> degeneration)
- Gout
- Fracture
- Malignancy
- Avascular bone necrosis
What investigations might you do on someone who you suspect may have osteomyelitis?
- Bloods - raised inflammatory markers (CRP, ESR) and WCC
- X-rays (cortical erosion, sequestra, sclerosis) and MRI (delineates inflammatory layers, marrow oedema)
- Bone biopsy - gold standard
- Blood cultures
Describe the usual treatment for osteomyelitis
Large dose IV antibiotics tailored to culture findings (S. aureus = flucloxacillin)
immobilisation
Surgical treatment = debridement +/- arthroplasty of joint involved
Name 3 risk factors of RA
- Smoking
- Women
- family history
- Other AI conditions
- genetic factors - HLA-DR4 and HLA-DRB1
Describe the pathophysiology of RA
- Chronic inflammation - B/T cells and neutrophils infiltrate
- Proliferation –> pannus formation (synovium grows out and over cartilage)
- Pro-inflammatory cytokines –> proteinases –> cartilage destruction
what are the symptoms of RA?
- Early morning stiffness (>60 mins)
- Pain eases with use
- Swelling
- General fatigue, malaise
- Extra-articular involvment
what are the signs of RA?
- Symmetrical polyarthorpathy
- Deforming –> ulnar deviation, swan neck deformity, boutonniere deformity
- Erosion on X-ray
- 80% = RF positive
RA extra-articular involvement: describe the effect on soft tissues
Nodules
Bursitis
Muscle wasting
RA extra-articular involvement: describe the effect on the eyes
Dry eyes
Scleritis
Episcleritis
RA extra-articular involvement: describe the pulmonary effects
Pleural effusion
Fibrosing alveolitis
RA extra-articular involvement: describe the effects on the heart
Pericardial rub
Pericardial effusion
RA extra-articular involvement: describe the effects on the skin
Vasculitis - infarcts in nail bed
What is seen on an X-ray of someone with RA?
LESS:
- Loss of joint space (due to cartilage loss)
- Erosion
- Soft tissue swelling
- Soft bones = osteopenia
Describe the pathophysiology of gout
Purine –> (by xanthine oxidase) xanthine –> uric acid –> monosodium rate crystals OR excreted by kidneys
Urate blood/tissue imbalance –> rate crystal formation –> inflammatory response through phagocytic activation
Overproduction/under excretions of uric acid causes build up and precipitated out in joints
Give 3 causes of gout
= Hyperuricaemia
- Impaired excretion - CKD, diuretics, hypertension
- Increased production - hyperlipidaemia
- Increased intake - high purine diet = red meat, seafood, fructose, alcohol