Ortho & Rheum Flashcards
Types of fracture (8)
Fissure Impaction Greenstick Transverse Avulsion Comminuted Oblique Spiral
Displacement of bones (3)
Translation (sideways movement, as % of bone diameter)
Angulation (bend in degrees)
Shortening (collapse, in cm)
Fractures causing avascular necrosis
Scaphoid fracture
Femoral head
Wrist fratures
Colles’ (distal radius with dorsal displacement fragments) - Forward fall. Dinner fork on lateral X ray
Smith’s (distal radius with volar displacement) - Backward fall. Garden spade on lateral x ray.
Scaphoid (*vulnerable blood supply)
NOF fracture
Types & Management (3)
Presentation
Complications
Intracapsular - Femoral neck between edge of femoral head and insertion to capsule
50% damage medial/lateral circumflex artery
May disrupt blood supply to femoral head - avascular necrosis - Surgery within 36 hours (Undisplaced - Internal fixation with screws. Displaced - hemiarthroplasty)
Extracapsular trochanteric # distal to insertion, involving or between trochanters - Nail/screw fixation
Extracapsular subtrochanteric # below lesser trochanter to 5cm distal - Nail/screw fixation
Pain in outer upper thigh or groin, radiate to knee, no wt bearing
Affected leg shortened, adducted and externally rotated
Pressure sores, DVT, bedbound, avascualr necrosis.
Total hip replacements dislocate more than hemis
Fracture healing time
Simple fractures take 3 weeks - Metaphyseal, closed, paediatric, upper limb.
Any complicating fracture doubles healing - Adult, diaphyseal, lower limb, open.
Stages of fracture healing
Haematoma formation *hours
MP and inflamm leukocytes move to area and begin secreting pro-inflammatory agents
Fibrocartilaginous callus formation (soft callus) *days
Inflammation leads to angiogenesis and increased number of chondrocytes. Secrete collagen and proteoglycans - fibrocartilage
Bony callus formation *weeks
Endochondral ossification and direct bone formation. Soft callus replaced by woven bone
Bone remodelling *months
Woven bone replaced by organised cortical bone. Continually remodelled therefore no scarring
NOF fracture grading
Gardens
- Incomplete #
- Complete but not dispisplaced
- Comp displaced <50%
- Comp, displaced > 50%
Femoral shaft fractures
High-velocity, and high-energy e.g. RTA
Joints in the ankle and pres of #
2 joints: ankle (tibia and fibula meet talus), syndesmosis joint (tibia to fib)
Similar to severe sprain: immediate severe pain, swelling (localised or along leg), bruising, tenderness - consider the mechanism
Ottawa ankle rules
When to X ray
>55
Inability to wt bear (4 steps) now and at time of injury
Bone tenderness at posterior edge or tip of lateral malleolus (6cm)
Bone tenderness at posterior edge or inf tip medial malleolus
(+ XR midfoot) bone tenderness at base of 5th metatarsal, cuboid or navicular
Preventing NOF#
Prevent falls - Good lighting, less sedation
Exercise and balance training - Tai Chi
Prevent osteoporosis - Bisphosphonates & Exercise
Vitamin D supplements
Management of ankle breaks
If neurovascular compromise or dislocation (obvious deformity) then reduce immediately
Reduce
Stabilise (4-6 weeks) moulded cast
Analgesia
Elevation
Re-assess neurovascular status
XR at reduction, 48 hours, 7 days, then 2 weekly
Ankle # Classifcation
Danis-Weber - Relative to the tibofibular syndesmosis
Below
At the level of
Above
Main complication of #
Compartment syndrome
6Ps - Pain out of proportion, parasthesia, pallor, paralysis, perishingly cold
When - Post fracture or reperfusion
Reduce risk by prompt fracture reduction and loose dressings
Treatment - Prompt fasciotomy
Post complications - Rhabdomyolysis -> renal failure (So give fluids)
Frozen shoulder
Thickening and contraction of glenohumeral joint capsule ± formation of adhesions - pain and loss of function either spont or post rotator cuff injury
40-65, Diabetes, thyroid
Loss of external rotation
Analgesia (paracetamol, NSAID), tens, activity, physio
Bone remodelling process
Osteocytes send signal to osteoclasts and osteoblasts
Osteoclasts resorb bone matrix: resorption pit - increases serum Ca
Osteoclasts undergo apoptosis and send signals to osteoblasts
Osteoblasts synthesise bone matrix
Bone matrix undergoes mineralisation
Hormones involved in bone remodeling (4)
PTH, 1,25-dihydroxyvitamin D, calcitonin, oestrogen
Osteoporosis
Definition
Location of #
Symptoms
T-score < -2.5 (s.d. below young healthy adult mean)
-2.5 < T
Risk factors for Osteoporosis
SHATTERED + FRAX (parental fracture) + SEDENTARY (decreased loading)
S - steroids + Cushing’s (>7.5mg for 3 months) - Decrease Ca absorption from gut, Increase osteoclast activity & Decrease muscle mass
H - hyperTh, hyperPTh, hypercalciuria
A - alcohol and tobacco
T - thin (BMI<19) or AN
T - testosterone decreased - primary hypogonadism, or anti-androgens @ PrCa
E - early menopause (<45)
R - renal/liver function - renal osteodystrophy in CKD, chronic liver disease
E - erosive/inflammatory disease: RA, multiple myeloma, metastasis
D - dietary Ca/T1DM - malabsorption, malnutrition
Osteoporosis managament
Lifestyle: smoking, alcohol, wt bearing exercise, balance (fall risk), calcium + vit D rich diet, fall prevention
Meds: Bisphosphonates + Ca + vit D supplements - AdCal D3, Accrete D3
Fall prevention: avoid polypharmacy
If low testosterone add testosterone
If intolerant bisphosphonates use denosumab (monoclonal aB to RANKL)
Raloxifene can be used for women (selective oestrogen receptor modulator)
Bisphosphonates
Egs
Mechanism
Side effects
Alendronic acid, risedronate, zoledronic acid
Inhibit osteoclastic bone resorption
Upper GI therefore take sitting upright with plenty of water first thing before food - crap absorption (1 hour before food)
Difficulty swallowing, oesophagitis, gastric ulcers
Osteonecrosis of the jaw
Osteoporosis blood tests
Ca, PO4, ALP, PTH all normal
Osteomalacia
Presentation
Blood test results
Widespread bone pain + tenderness (low back pain and hips)
Proximal muscle weakness - waddling gait (if severe)
Fatigue
Symptoms of underlying disease
Costochondral swelling, spinal curvature, hypocalcaemia (tetany, carpopedal spasm)
Ca - Decreased
PO4 - Decreased
ALP - Increased
PTH - Increased
Symptoms of low phosphate
Muscle weakness, parasthesia
Primary hyperPTH blood results
Ca - Increased
PO4 - Decreased
ALP - Increased
PTH - Increased
CKD (secondary hPTH) blood results
Ca - Decreased
PO4 - Increased
ALP - Increased
PTH - Increased
Pagets
2 Phases
Presentation
Complications (3)
Lytic phase - increased bone resorption by osteoclasts
Sclerotic phase - *Rapid bone formation by osteoblasts: disorganised and mechanically weaker and deformity/larger.
Bone pain and deformity with increased skin temperature. Fam history as AD mutation
Deformity: sabre tibia, kyphosis, skull bossing, enlarged maxilla/jaw
Pathological fracture (heavy bleeding as v.vascular)
Deafness/tinnitus compression of CN 8 by ear ossicles
Pagets Ix findings
X-ray
Bloods
Osteolysis and osteosclerosis (lytic and scleortic lesions)
Blade of grass lesion between healthy and sclerotic long bone
Cotton wool pattern of multifocal sclerosis in skull
Ca - Normal
PO4 - Normal
ALP - Increased
PTH - Normal
Nb further Ix - Isotope bone scans
Management of Pagets
Pain: NSAIDs and paracetamol
Antiresorptive: bisphosphonates
N.b. IV may give flu-like symptoms
Zoledronate popular as good with single IV dose
Monitor ALP
Ca and PO4 regulation by
VitD
PTH
Skin makes Cholecalciferol (D3) -> liver = 25 hydroxyvitamin D3 (inactive circulating) -> kidney = 1,25 dihydroxyvitamin D3 (active hormone)
To bone: increases Ca mobilisation, increases osteoclast function
To intestine: increases Ca absorption, increases PO4 absorption
To PTG: decreases PTH
Low Ca -> increased PTH
To bone -> increase osteoclast function
To kidney -> increases 1,25vD3 (1-alphahydroxylase), + decreases Ca excretion + increases PO4 excretion
Osteomalacia vs rickets
Disorder of mineralisation of bone matrix (osteoid) after fusion of epiphyses
Disorder of mineralisation of bone matrix prior to fusion of epiphyses
Causes of osteomalacia/rickets (8)
Lack of sunlight
Lack of adequate diet
GI malabsorption: surgery, short bowel, pancreatic disease, CF, CD, coeliac
Renal disease: -> defective 1,25 form = renal osteodystrophy
Liver disease: -> cirrhosis
Drugs: anticonvulsants, rifampicin (liver, stop 25-hydroxy)
Rare:
Tumour induced hypophosphataemia
Fanconi syndrome (proximal renal tubule dysfunction)
Renal tubular acidosis
Genetic
Rickets presentation
Bony abnormalities:
Leg bowing - genu varum
Knock knees - genu valgum
In first few months: craniotabes (softening of skull), frontal bossing, rachitic rosary (enlarged end segment ribs) -> rachitis lung
Dental abnormalities (enamel)
Delayed walk/waddling gait, impaired gait
Symptoms of hypocalcaemia: convulsions, irritable, tetany, apnoa, cardiac arrest
Joint pain causes
ARTHRITIS
Arthritis, reactive arthritis, tendon/muscle damage, hyperuricaemia, referred pain, immune (e.g. SLE), tumour, ischaemia, sponyloarthtitides
Inflammatory vs Degenerative
Ease on use, stiffness worse in morning (>60 mins), hot and red (r/d/c/t/LoF), responds to NSAIDs, swelling *synovial and bony, young/psoriasis/fam Hx
Worse with use, morning stiffness (<30 mins), mainly evening, prior occ, sport, *no swelling, not inflamed.
Osteoarthritis Pathology Which joints RF Diagnostic triad
Deterioration of *articular cartilage and formation of new bone - osteophytes at joint margins
Knees, hips, small joints hands, spine
Age, female sex, obesity, occupation/hobbies, genetic (50%), joint laxity
Aged > 45 + activity related jt pain + no morning stiffness (<30 minutes)
Symptoms & Signs of OA
Joint swelling/synovitis - warmth + effusion
Reduced ROM
Crepitus
Pain on movement *may lead to disuse atrophy and weakness
Bony swelling and deformity - osteophytes: DIP (Heberden’s) + PIP (Bouchard’s)
No systemic features
X ray findings of OA
LOSS Loss of joint space Osteophytes Subchondral/subarticular sclerosis Subchondral cysts
Management of OA (3 tiers)
Patient education, weight loss, screen depression, *exercise for muscle strength, aids and devices (walking sticks, tap turners)
Local analgesia: capsaicin or topical NSAID (first line)
+ Paracetamol (2)
+ NSAIDs ± PPI (3)
Intra-articular steroid injections (methylpred) for acute exacerbation
Replacement (arthroplasty), fusion (arthrodesis)
RA
What
Who
Pathology
Chronic inflammatory autoimmune disease characterised by inflammation of synovial joints leading to symmetrical joint and periarticular tissue destruction
Women (especially pre menopause), Fam history, Smokers
Inflammation of synovium
Increased angiogenesis, influx inflammatory cells + CKs, cellular hyperplasia
Cells (MP, TCells, plasma cells) release IL1/IL6/TNF - promote proliferation -> joint destruction
Proliferation
Angiogenesis and hypertrophic synovium form pannus over articular cartilage
Serum antibodies in RA
Anti CCP
Rheumatoid factor (70%)
ANA (30%)
Clinical features of RA (7)
Morning stiffness Symmetrical swelling Swan neck Boutonniere Z-deformity thumb Ulnar/Radial deviation Muscle wasting hands
Extra articular manifestations of RA
Rheumatoid nodules @ extensor surface of tendons (palisade ring of MP and fibroblasts with necrotic core) and *lungs
Vasculitic lesions - commonly skin rashes, leg ulcers (@Feltys)
Pleuritic chest pain - pleuritis or pericarditis
Eye problems: secondary Sjogren’s: scleritis and episcleritis
Neurological: peripheral nerve entrapment, atlanto-axial subluxation (C1,C2) - soft tissue swelling within rigid tunnel
Respiratory system: rheumatoid nodules, Caplan’s syndrome, pulmonary fibrosis
Anaemia of chronic disease
Feltys syndrome
Triad of:
RA
Neutropenia - increased susceptibility to infection, lung and skin infections
Splenomegaly - LUQ pain and anaemia of chronic disease
Management of RA & Dug side effects
Physiotherapy, OR, psych services (depression), podiatry
DAS 28 - Severity scoring
DMARDS
Methotrexate (+ folic acid) - SE Neutropenia, pul fibrosis, cirhosi,s mouth ulcers
Sulfasalazine - SE Hepatits, Mouth ulcers, oligospermia. Can use in pregnancy.
Azathioprine
Adjunct: corticosteroid (low dose pred) + NSAID (lowest effective dose) short term
Second line: biologicals - Infliximab, etanercept
Methotrexate CI in which drugs
trimethoprim and phenytoin due to being folate inhibitors
Gout
What
Caused by
Protective
Arthritis due to deposition of monosodium urate (MSU) crystals within joint
Trauma + surgery (cell damage), starvation (increased insulin), infection (cell damage), diuretics (reduced renal excretion)
Alcohol (beer highest), purine rich foods (red meat/sea food), fructose (sugary drinks/cakes), diuretics, DM, CKD, CHD, HTN, hyperlipidaemia
Dairy, coffee, vitamin C
Hyperuricaemia ->
Gout and uric acid stones
Gout management
Acute
Chronic
First line: NSAIDs e.g. naproxen 10-14 days: high dose then reduce at 48 hours
If NSAIDs poorly tolerated use colchicine
Prophylactic drugs: allopurinol or febuxostat (xanthine oxidase inhibitors)
Start 2 weeks post attack
Co-prescribe NSAID or colchicine for acute attack for 3 months
Pseudogout
Calcium pyrophosphate deposition in articular and periarticular tissues
More commonly in the *elderly
No specific therapies therefore symptomatic:
SLE
What
Genetics
Presentation
Inflammatory, multisystem autoimmune disease with antinuclear antibodies
HLAB8/DR3
Multisystem disease with raised ESR but normal CRP
Criteria + systemic: fatigue, fever, weight loss, lymphadenopathy
Criteria for SLE
4/11 of DOPAMINE RASH
Discoid rash - over malar eminence
Oral ulcers - usually painless
Photosensitivity
Arthritis - 2 or more peripheral joints
Malar rash - fixed erythema, spares nasolabial folds
Immunological phenomena - anti-dsDNA, anti-Smith, antiphospholipid aBs
Neurological symptoms - seizures, migraines, polyneuropathy
ESR raised (*not CRP)
Renal disorder - proteinuria > 0.5g/day or +++, or casts
ANA +ve
Serositis - pleuritis (pleural rub on ausc or pleural effusion), pericarditis (on ECG, pericardial rub)
Haematological disorders - haemolytic anaemia (with reticulocytes) or leukopenia (<4x10^9), lymphopenia, thrombocytopenia
Ix for SLE
ESR/CRP - ESR raised, CRP normal
FBC - anaemia, leukopenia, thrombocytopenia
Autoantibodies: ANA (95%), anti-dsDNA (Dop specific) (60%), antiSmith (30%)
Complement levels: low C4 and C3 - active disease
Urinalysis: haematuria, casts, proteinuria
U+E (renal disease)
CXR: pleural effusions, cardiomegaly
ECG: pericarditis
Management of SLE
Joints - NSAID ± hydroxychloroquine ± steroids (GI and bone protection)
Mucocutaneous - Sunscreen, mouthwash (chlorhexidine), saliva, tears + oral hydroxychloroquine
Nephritis - cyclophosphamide + prednisolone + hydroxychloroquine
Antiphospholipid syndrome What Antibodies Diagnosis Presentation Treatment
AI disorder characterised by arterial/venous thrombosis and adverse pregnancy outcomes
Anticardiolipin, antiB2glycoprotein1, lupus anticoagulant
One clinical criteria and one lab criteria
Clin: vascular thrombosis, pregnancy morbidity (unexplained death beyond 10 weeks or x3 before 10 weeks)
Lab: Lupus antiocoagulant or anti-cardiolipin or anti-B2 glycoprotein 1 present on 2 occasions (12 weeks apart)
Thrombosis, DVT, pregnancy loss, pre-eclampsia, thrombocytopenia, livedo reticularis: violaceous lace like on trunk, stroke
Warfarin: target 2-3
Avoid clotting lifestyle: smoking, contraceptive pill, healthy diet, low alcohol
Sjogrens What HLA type Presentation Ix
AI condition with lymphocytic infiltration of exocrine glands
DR3 (SLE)
Dry eyes, dry mouth, enlarged parotid gland, dysphagia, alterter taste
May present alone or with SLE, RA, systemic sclerosis, CREST
Schirmer tear test (filter paper, +ve if less than 5mm in 5 mins)
Autoantibodies anti-Ro (SS-A), anti-La (SS-B) ± RF, ANA, APLS AAb
Sialometry/sialography
Artificial tears & Artificial saliva, drink plenty
Oral pilocarpine
Systemic sclerosis
What
Types
Multisystem AI disease with increased fibroblast activity -> *excessive collagen -> fibrosis -> *vascular damage + immune system activation.
Limited cutaneous (70%) - face, forearms and lower legs Diffuse cutaneous (30%) - rest of skin + *organ fibrosis
Autoimmune Rheumatic disease
RA SLE Sjogrens Systemic sclerosis Antiphospholipid
Limited cutaneous systemic sclerosis features
CREST syndrome though usually raynauds for many years then followed by skin changes Calcium deposits in fingers Raynords eSophageal refulx/reduced motility Sclerodactially Telangecasia
Diffuse cutaneous systemic sclerosis features (4)
Skin changes happen more rapidly and are more widespread. Early involvement of organs
Gastrointestinal involvement - Heartburn + reflux oesophagitis, bowel pseudo obstruction.
reduced motility
Renal involvement - Scleroderma renal crisis: accelerated HTN, headache, oliguria
Lung disease - Pul fibrosis & Pul Hypertension
Myocardial fibrosis - Arrhythmias
Ix of Systemic sclerosis
FBC (microcytic if GI bleed, haemolytic in renal crisis), ESR/CRP,
U+E (elevated Ur + Cr @ renal crisis)
LuFT + diffusing capacity (restrictive) - disproportionate drop in DLCO to FVC - pul HTN
ECG - arrhythmia
CXR - lung disease = infiltrate, heart disease = cardiomegaly + heart failure
Barium swallow = oesophageal disorders and delayed emptying
*Serum autoantibodies
ANA - 90%
Anti-Scl70 - diffuse disease
Management of systemic sclerosis
Raynauds = *Nifedipine (only drug licensed) - could try PDE5 inhibitors (sildenafil)
GI - PPI for life
Pulmonary = Cyclophosphamide (fibrosis), sildenafil (PAH) + O2
Joints = Prednisolone
Skin = Topical emollient ± topical corticosteroid (for itch) ± cyclophosphamide (for thickening)
Renal = AKI, HTN use ACEI ± other antihypertensives
Ehler Danlos
What?
Presentation (5 system)
Management
Defect in structure, production or processing of collagen
Women > men x 8
Skin: increased elasticity + fragility
Joints: laxity, hypermobility, pes planus, prone to dislocation
CV: dizziness, palpitations, heart valve abnormalities, mitral valve prolapse, aortic root dilatation
Ocular: abnormal globe, cornea
Hearing: tinnitus due to ossicle laxity
Physiotherapy, regular gentle exercise, genetic counselling
Periodic echo for floppy mitral valve or aortic root dilatation
Marfan’s
What
Presentation (6 systems)
Signs (2)
AD disorder of decreased extracellular microfibril formation.
Skin: striae
CV: aortic dilatation, dissection, mitral regurgitation
Lungs: pleural rupture - pneumothorax
Eyes: lens dislocation, closed angle glaucoma
Skeleton: arachnodactyly, hypermobility, pectus excavatum
Facial: retrognathia, high arched palate, enopthalmos
Walker’s sign - encircles wrist with overlapping pinky and thumb
Steinberg’s - Thumb extends past fingers when held in closed fist.
Marfans management
Annual ECHO - aortic root width
CV MRI - every 5 years
MDT: geneticist, ophthalmologist, cardiologist, orthopaedics
Avoid maximal exertion: scuba diving, weight lifting
Prophylactic beta-blockers - propanolol
Reduce MAP and pulse rate
Polymyositis + dermatomyositis What? Which muscles Cause Blood tests (3)
AI connective tissue disorders characterised by inflammation of striated muscles
Proximal muscles
Virus implicated: HIV, coxsackie
CK elevation, LDH, aldolase
AAb: anti-Jo1
Polymyositis
Presentation
Not painful
Progressive symmetrical proximal muscle weakness - pelvic girdle
Difficulty rising from chair, climbing stairs, combing hair
Pharyngeal weakness - dysphagia
Interstitial lung disease and AV nodal disease
Dermatomyositis
Rash: (may be UV related) Heliotrope violaceous eyelid Gottron’s papules - purple scaly patches on extensors Nailfold erythema Shawl sign - macular rash Systemic upset: fever, arthralgia, malaise, weight loss AV conduction defects Interstitial lung disease 50% GI ulcers
Seronegative arthropathies Diseases Associations HLA number? Criteria
Ankylosing spondylitis, Reiter’s syndrome, enteropathic arthritis, psoriatic arthritis, Behcet’s disease, JIA
Anterior uveitis, IBD (similar to Crohn’s)
HLA B27
Inflammatory spinal pain or synovitis (in lower extremities) +
Fam Hx: anky spon, psoriasis, reactive arthritis, IBD
Past or present psoriasis
Past or present IBD
Past or present pain alternating between buttocks
Past or present pain spontaneous pain and achilles or plantar fascia
Diarrhoea one month before arthritis
Ankylosing spondylitis
What?
Presentation (6)
Seronegative spondyloarthropathy of axial skeleton sacroiliitis and spondylitis (vertebral inflammation)
Inflammatory back pain + enthesitis
Stiffness and pain waking in early morning
Gradual onset
Improvement with movement, no improvement with rest
Age at onset < 40
Tenderness at sacroiliac region (felt in buttocks) or limited spinal motion
Extra articular features of Ank spond (6)
The As of association (6) Apical fibrosis - LuFT Apical fibrosis Anterior uveitis Aortic regurg Achilles tendonitis AV node block Amyloidosis
Ank spond management
No cure: symptomatic control and control of complications
Physiotherapy + rehabilitation + exercise
First line: NSAIDs (± analgesics - paracetamol)
If pain refractory to NSAIDs (2) - TNFalpha inhibitor
-Methotrexate doesnt work
Local enthesitis - intra-articular corticosteroid injection
Peripheral arthalgia - DMARD: sulfasalazine
Reactive arthritis What? Organisms? Reiter’s (Most common) Ix Management
Occurs 1-4 weeks post exposure to GI and GU infections
Campylobacter/salmonella/shigella or chlamydia
Can’t see, can’t wee, can’t bend your knee (typically lower limb)
Conjunctivitis, non-gonococcal urethritis + post-infectious arthritis
Acute asymmetrical, lower extremity oligoarthritis
Lower back pain + heel pain (enthesitis)
ESR/CRP very high, FBC - WCC
Joint aspiration - rule out septic or crystal arthropathies
Culture: stool, throat UG tract - for causative organism
Serology chlamydia: PCR or NAAT and contract tracing
NSAID + rest ± intra-articular steroids ± ABX chlamydia (azithromycin injx single or doxy week)
Vasculitis egs.
Large vessel
Medium
Small
Large vessel: PMR, GCA, Takyasu’s arteritis
Medium vessel: PAN, Kawasaki’s
Small vessel: Wegener’s/GPA, Churg-Strauss (non-ANCA = HSP)
LVV - Giant Cell arteritis What? Main serious complication? Who? Presentation? Diagnosis?
Inflammatory granulomatous arteritis of aorta and large cerebral arteries (extracranial branches of carotid)
Women > 50 & associated with PMR - 50%
Recent onset temporal headache + scalp tenderness + transient visual symptoms (diplopia) + jaw claudication (on chewing) + malaise + myalgia + fever
Abnormality on palpation of temporal artery (absent pulse, beaded, tender)
ESR > 50mm/hr + temporal artery tenderness + *temporal artery biopsy
Granulomatous inflammation, multinucleated giant cells, intimal hypertrophy and inflammation
LVV - GCA complications
Anterior ischaemic optic neuritis
Stenoses of branches of aortic arch - subclavian and axillary arteries - 20%
Aortic aneurysm (x17)
Subclavian steel - Retrograde blood flow in vertebral artery due to proximal stenosis of subclavian artery
LVV - GCA management
High dose oral prednisolone 1mg/kg/day for 4 weeks then taper
LVV - Polymyalgia rheumatica
What?
Diagnosis?
Treatment?
Severe bilateral pain and morning stiffness: shoulders, neck, pelvic girdle (>2 weeks) with systemic features at onset (malaise, fever, fatigue)
Age > 50
Symp > 2w
Morning stiffness > 45 mins
Evidence of acute phase response ESR/CRP
Prednisolone - see improvement in 24-48 hours for 2 years (tapering dose down to minimum.
Steroid induced osteoporosis - DEXA + bisphosphonate + Ca + Vit D
LVV - Takyasus arteritis
What
Stages & Symptoms
Chronic, progressive, inflammatory, occlusive disease of aorta and branches
Systemic stage + occlusive stage
Systemic: fever, fatigue, wt loss, arthralgia, tenderness on arteries
Occlusive: Limb claudication Cardiac: angina, dyspnoea (CHF) Neurological: dizziness, headache, TIA, visual disturbance, stroke Vascular: claudication of jaw, back pain (aortic arch), *HTN Pulmonary: haemoptysis GI: abdo pain from ischaemia/infarction Renal: haematuria
LVV - Takyasus
Signs
Managment
*Difference in SBP of >10mmHg between arms
Impalpable peripheral pulse
High BP - renal artery stenosis
Arterial bruits on all arteries and aortic regurgitation
ESR > 50 CRP elevated with active disease
Glucocorticoids + aspirin + bone protection
If persistent use TNF alpha antagonist
MVV - Polyarteritis nodosa
What?
Presentation
Necrotising inflammation of medium sized or small arteries without glomerulonephritis
Any organ BUT spares pulmonary and glomerular arteries
Nerves and skin most common
Nerves: *mononeuritis multiplex
Skin: purpura, subcutaneous nodules, necrotic ulcers, *livedo reticularis
Systemic symptoms: fever, wt loss, headache, myalgia
MVV - Polyarteritis nodosa
Management
Complications
Prednisolone ± DMARD (cyclophosphamide) - if relapse
Renal failure - not due to glomerulonephritis - due to microaneurysms and infarcts - accelerated HTN - requires regular renal monitoring - poor prognosis = half die within 3 months
MVV - Kawasaki’s
What?
Symptoms?
Management?
Idiopathic self-limiting systemic vasculitis in children 6M - 5Y (mainly asian)
CRASH and BURN
Conjunctivitis (bilateral + non-purulent)
Rash - non vesicular
Adenopathy (cervical + unilateral)
Strawberry tongue + inflammation of lips and mouth (cracked lips)
Hands/feet - palmar erythema/swelling/desquamation (2-5 days after onset)
Fever > 5 days
First line IVIg + high dose aspirin
Coronary artery aneurysm and dilatation - echo
SVV - ANCA - Wengers presentation
Upper resp: otorrhoea, sinus pain, nasal discharge, hoarseness, stridor
-Saddle nose deformity, nasal septal perforation, subglottic stenosis
Lower resp: SOB, cough, haemoptysis, chest pain, dyspnoea, rhonchi, reduced air entry
Renal: oedema, HTN, haematuria (later)
SVV - ANCA - Wengers management
Life threatening/organ involvement
Remission with IV methylpred (3d) + pred oral + cyclophosphamide
Non-life threatening:
Remission with IV methylpred (3d) + oral prednisolone + methotrexate
Maintain remission with oral pred + methotrexate + folic acid
SVV - Non ANCA - IgA vascultits
What?
Presentation
Management
HSP
Young man with previous URTI - GpA strep (pyogenes)
IgA immune complexes deposited in small vessels
Low grade fever, *abdominal pain and vomiting, purpuric rash on buttocks and extensor, joint pain
Arthralgia, abdo pain, rash
In 40%-> nephrotic syndrome
Urinalysis: proteinuria, RBC, casts, 24 hour urine protein
Joint or abdo pain: ibuprofen or paracetamol
Kidney function: steroids
SVV - ANCA - Churg-Strauss
What?
Presentation
Tissue eosinophilia, granulomatous inflammation, vasculitis
Asthma (wheeze), eosinophilia in peripheral blood, paranasal sinusitis, pulmonary infiltrates, histological confirmation vasculitis, *mononeuritis multiplex
Anti-GBM disease
What?
Ix
Management
Lungs and kidneys: pulmonary renal syndrome -> glomerulonephritis and pulmonary haemorrhage -> haemoptysis and renal failure
Renal function: abnormal
Renal biopsy: crescentic glomerulonephritis - perform *urgently
Anti-GBM - positive
If reversible renal or any pulmonary involvement - oral prednisolone + cyclophosphamide + plasmapheresis
Septic arthritis
What?
Oragnisms?
Risk factors?
Bacterial infection of a joint - can destroy a joint in under 24 hours - Usually in the knee
S.aureus
Streptococci e.g. GBS (staph and strep account for 90%), gonococcal in sexually active (tends to be with pustules, remember Reiter’s is chlamydia)
*Prosthetic joint (x10), RA, OA, IV drug abuse, alcoholism, diabetes, immunosuppression, skin infection
Nb. Suspect in anyone with a swollen red joint
Septic arthritis
Ix
Management
Urgent joint aspiration - synovial fluid Gram stain and culture
Blood culture x2 ± gonococcal cultures (rectal, urethral, pharyngeal)
Acute phase markers: ESR, CRP, WCC raised
Surgical drainage and lavage (wash) + high dose IV abx
IV abx 2/3 weeks then oral 3/4 weeks - 6 total
If suspect G+ use vancomycin, if suspect G- use 3rd gen cephalosporin
When cultures back
For staph flucloxacillin
If suspect MRSA vancomycin
If gonococcal arth or G- cefotaxime or ceftriaxone
Osteomyelitis
What?
Organisms?
Infection of bone marrow, may spread to cortex and periosteum via Haversian canals, leading to inflammatory destruction of bone.
Commonly s.aureus (or MRSA risk if diabetes or immunocompromised or IVDU)
Potts disease - vertebral osteomyelitis from haematogenous spread of TB
Osteomyelitis
Ix
Management
FBC (WCC) Blood cultures (+ve) Acute phase markers: ESR + CRP + WCC Plain radiograph - Areas appear dark, soft tissue swelling, periosteal thickening (at 7 days), patchy osteopenia (lytic changes are late) Cultures from debrided bone
Analgesia and limb splinting if long bone
Initial broad spec: vancomycin + cefepime (IV)
Culture directed ABX + debridement
IV for 2 weeks then oral for 4 weeks
Back pain fed flags
TUNA FISH
Trauma
Unexplained weight loss, loss of appetite - cancer/myeloma
Neurological symptoms including bowel bladder dysfunction - cauda equina
Age > 50 or < 20
Fever and night sweats - osteomyelitis/cancer
IVDU/immunosuppression - osteomyelitis
Steroid use - immunocompromise + osteoporotic fracture
History of cancer (prostate, breast, lung, renal)
Cervical back pain
Common cause?
Presentation?
Cervical spondylosis - chronic disc degeneration (CERVICAL OSTEOARTHRITIS)
Simple neck pain + radiculopathy (pain, numbness, tingling, weakness in upper limbs) + myelopathy (spinal cord)
Worse on movement
Cervical stiffness (limited all movements)
C5 - C7 -> diminished reflex (biceps + supinator = C5/C6, triceps = C7)
Plain XR - osteophytes, narrowing of disc space, encroachment of intervertebral foramen
If neuropathy -> require MRI
Lower back pain DDx 15-30yrs 30-50yrs 50+yrs Ix
Trauma, fracture, pregnancy, anky spon, prolapsed disc, mechanical
Degenerative spinal disease, prolapsed disc, malignancy (breast, bronchus, prostate, kidney)
Degenerative, osteoporotic collapse, myeloma, spinal stenosis, malignancy, Paget’s (pelvis 70%, lumbar 50%)
FBC, ESR, CRP, UE, Alk phos, serum/urine electrophoresis, PSA
Osteosarcoma Who? Associations? Where? Presentation? Course X ray
Most common malignant in children (15-19)
Paget’s
In epiphyses of long bones - knee (75%) or proximal humerus
Painless
Destroys bone and spreads locally, rapidly *mets to lung
Combined bone destruction and formation. Soft tissue calcification = sunburst/hair on end + Codman’s triangle (area of new subperiosteal bone created when tumour raises periosteum from bone
Ewigs sarcoma What? Who? Presentation? Xray
Primitive neuroectodermal tumour
15 yo boy
Mass or swelling, long bones of arms or legs, pelvis, chest
Pain, redness, malaise, fever
Bone destruction with onion skin layers of periosteal bone formation + Codman’s triangle
NSAID side effects (5)
Increase in BP Oedema Gastric/Duodenal ulcer Headaches Liver and Kidney damage through decrease of prostaglandins
Cauda equina syndrome
Signs (4)
Causes
Saddle anaesthesia + Sciatica Upgoing plantars, Loss of reflexes Reduced anal tone Urinary retention
Degenerative - Slipped disk
Inflamatory - Ank spond
Infective - Potts, Abcess
Trauma - Fractures/ Haematoma from spinal
