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Phase 3 > Week 11 > Flashcards

Week 11 Flashcards

1
Q

How does acute compartment syndrome present?

A

It is elevated interstitial pressure within a closed facial compartment resulting in microvascular compromise

Common sites are leg, forearm and thigh

CFs:

  • disproportionate pain, pain on passive stretching of the compartment, pallor, parasthesia, paralysis and pulselessness
  • swelling, shiny skin
  • autonomic responses- sweating, tachycardia

Mostly diagnoses clinical

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2
Q

Describe the pathophysiology of ACS:

A

Causes:

  • increased internal pressure
    • eg bleeding, swelling, iatrogenic infiltration
  • increased external compression
    • eg casts/bandages, full thickness burns
  • combination

Pressure within compartment exceeds pressure within the capillaries, muscle becomes ischaemic and develops oedema through increased endothelial permeability
Necrosis begins in the ischaemic muscles after 4 hours

Decreased perfusion
Muscle ischaemia
Muscle swelling
Increased permeability – fluid leaks into interstitial space
Increased pressure
Autoregulatory mechanisms overwhelmed
Muscle necrosis and myoglobin release
Loss of function , extremity or loss of life.
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3
Q

How is ACS managed?

A

Open any constricting dressings / bandages

Reassess

Surgical release:
- full length decompression of all compartments
- excise any dead muscle
- leave wounds open
- repeat debridement until pressure down and all dead muscle excised
Later wound closure
Skin grafting / Plastic surgery input

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4
Q

Describe the presentation and pathology of tendinopathy:

A

Chronic tendon injury of overuse, due to loss of balance between micro-damage from overuse and reparative mechanisms

Probably not inflamation – tendinosis not tendinitis

Deranged collagen fibres / Degeneration with a scarcity of inflammatory cells

Increased vascularity around the tendon

Failed healing response to micro tears

Inflammatory mediators released IL-1, NO, PG’s – cause apoptosis, pain and provoke degeneration through release of matrix metalloproteinases

CFs:

Pain
Swelling
Thickening
Tenderness

Diagnosed with imaging (Xray, US, MRI) also helps exclude other pathologies

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5
Q

Describe the management of tendinopathy:

A

Non-op:

NSAID’s
Activity modification
Physiotherapy – stretching , eccentric exercises
GTN patches (vasodilator so increased local perfusion)
PRP injection
Prolotherapy – irritant injection, dextrose
Extracorporeal Shockwave Therapy
Topaz – radiofrequency coblation

Op:

Debridement
Excision of diseased tissue
Possible to debride 50% of tendon without loss of function
(tendon transfers)

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6
Q

What is the clinical significance of ACS?

A

1 hour- nerve conduction normal, muscle viable

4 hours- neuropraxia in nerves (reversible) and reversible muscle ischaemia

8 hours- nerve axonotmesis and irreversible changes, irreversible muscle ischaemia and necrosis

End stage: stiff fibrotic muscle compartments, impaired nerve function, clawing of limbs, loss of function

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7
Q

Describe the presentation of septic arthritis:

A

Pain, fever, swollen joint, loss of function, acutely inflamed (<24 hours)
Caused by S. aureus, N, gonorrhoea, H. influenzae
Knee is affected in >50% of cases
RFs: pre-exisiting joint disease, DM, immunosuppression, CKD, recent joint surgery, prosthetic joints

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8
Q

Describe the presentation of reactive arthritis:

A

Sterile synovitis which occurs following an infection

Trigger organisms- salmonella, shigella, yersinia, chlamydia trachomatis

Preceding illness usually an urethritis or diarrhoeal

CFs: acute, asymmetrical lower limb arthritis, days-weeks post infection
Also presents with enthesisitis (plantar fasciitis), sacroilitits, spondylitis, anterior uveitis, conjunctivitis, keratoderma blenorrhgaica

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9
Q

Describe the presentation of gout:

A

Typically acute monoarthropathy with severe joint inflammation
>50% occur at the MTP joint of big toe
Other common joints are ankle, foot, knee, elbow, wrist or small joints of the hand
Can be polyarticular

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10
Q

What are the appropriate investigations for patients who present with acute joint pain and swelling?

A

The synovial fluid must be aspirated, Gram-stained and cultured prior to starting antibiotics, warfarin does not contraindicate needle aspiration

Neither the absence of organisms on Gram stain nor a negative subsequent synovial fluid culture excludes the diagnosis of septic arthritis

Specimens must be sent fresh to the laboratory and obtained prior to starting antibiotics

Polarising microscopy should always be carried out

Blood cultures should always be taken

The white cell count, erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) should be measured- inflammatory markers are useful for monitoring response to treatment

The serum urate level is of no diagnostic value in acute gout or sepsis

Electrolytes and liver function should be measured to detect end organ damage because renal function may influence antibiotic choice

If the history suggests non-articular infection, then appropriate cultures and swabs should be taken prior to starting antibiotics

Plain radiographs of the affected joint are of no benefit in diagnosing septic arthritis but may show chondrocalcinosis. They should be performed as a baseline investigation- usually MRI

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11
Q

What are the treatments for gout and when is urate lowering therapy introduced?

A

NSAIDs – high doses rapidly reduce pain and swelling
Alternatives – colchicine, corticosteroids
If attacks are repeated –
Allopurinol – xanthine oxidase inhibitor
Uricosuric agent (probenecid) – increases secretion of uric acid into urine

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12
Q

Describe the normal structure and function of bone:

A

Functions:
Structural; support, protection and movement
Mineral Storage; calcium and phosphate

Structure

Diaphysis (shaft)
Epiphysis (end)
Metaphysis (transitional flared area between diaphysis and epiphysis)

Cortical/compact outside with spongy/cancellous in the medullary cavity

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13
Q

Compare and contrast direct and indirect bone healing:

A

Indirect: formation of bone via a process of differential tissue formation until skeletal continuity is restored
INFLAMMATION, REPAIR, REMODELLING

Direct: surgical situation- direct formation of bone without the process of callus formation to restore skeletal continuity, relies on compression of the bone ends

Direct formation of bone via osteoclastic absorption and osteoblastic formation (cutting cones)

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14
Q

How can medication affect bone healing?

A

NSAIDs, steroids and bisphosphonates

NSAIDs reduce local vascularity at fracture site
Additional reduction in healing effect independent of blood flow

COX 2 NSAIDS inhibit fracture healing more than non-specific NSAIDS
Magnitude of effect is related to duration of treatment

Bisphosphonates:
Inhibit osteoclastic activity
Delay fracture healing as a result
Long half life

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15
Q

What factors compromise bone healing?

A

a

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16
Q

Describe avascular necrosis:

A

a

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17
Q

Describe secondary tumours in the bone:

A

Present in 60% of patients dying of cancer

Metastatic carcinoma: bronchus, breast, prostate, kidney, thyroid

Often mets to bones with good blood supply- long bones/vertebrae

CFs: often asymptomatic, bone pain, bone destruction, pathological fracture in long bones, hypercalcaemia
Spinal mets: vertebral collapse, spinal cord compression, nerve root compression, back pain

Can by lytic or sclerotic destruction

Lytic: osteoclast activity, stimulated by cytokines from tumour cells and inhibited by bisphosphonates

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18
Q

Describe myeloma:

A

Commonest malignant primary bone tumour

Monoclonal proliferation of plasma cells
Solitary: plasmacytoma or multiple myeloma

Orthopaedic and medical consequences

Medical: pancytopenia due to destruction of bone marrow

Orthopaedic: bone lesions (punched out lytic foci and generalised osteopenia)

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19
Q

What are the common radiological features of OA/DJD?

A

Joint space narrowing, characteristically asymmetric
Sclerosis: occur at joint margins and present unless severe OP is present
Osteophytosis; DIP, PIP and base of thumb should be bilateral
Joint erosions; temperomandiubular, acromioclavicular, sacroiliac and symphysis pubis joints
Sub-chondral cyst; DJD, RA, CPPD,

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20
Q

What are the common radiological features of RA?

A

Loss of joint space
Mild subarticular sclerosis
Lack of osteophyte

Symmetrical disease
   MCP joint erosions 
   MCP ulnar deviation 
   Deformed thumbs 
   Erosions distal ulna
   Erosive changes wrists  
   2o degenerative changes
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21
Q

What are the common radiological features of Paget’s disease?

A

Blade of grass or candle flame sign: begins as a subchondral area of lucency with advancing tip of V-shaped osteolysis, extending towards the diaphysis in long bones

Skull:
osteoporosis circumscripta: large, well-defined lytic lesion
cotton wool appearance: mixed lytic and sclerotic lesions of the skull

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22
Q

What are the common radiological features of ankylosing spondylitis?

A

Bi-lateral sacro-iliitis
Squaring of vertebral bodies
Bamboo spine
Peripheral large joint arthritis

Romanus lesions and spinal fractures in spine

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23
Q

How can USS be used in early diagnosis of arthritis?

A

a

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24
Q

When are USS, MRI, CT and DXA indicated?

A

a

25
Q

When might interventional radiology be indicated in MSK disease?

A

a

26
Q

Define RA and describe its epidemiology:

A

Chronic multisystem autoimmune disease
Hallmark is synovitis affecting any synovial joint
More common in females, clusters in families and at high risk if 1st degree relative affected
Genetic factors and smoking influence aetiology, as well as infection (?)
Synovitis- immune cells invading an acellular synovium in the form of a pannus (hyperplastic invasive tissue leading to cartilage breakdown, erosions and reduced function)

27
Q

Describe the CFs if RA:

A

Synovitis – any synovial joint
Symmetrical
Small jts hands and feet early on; shoulder/hip at onset rare
MCPs/PIPs/wrists
Inflammatory – pain, erythema, swelling, EMS
Tenosynovitis, bursitis, CTS
Consitutional sx: fatigue, weakness, low grade fever, weight loss, anorexia

Extra-articular features:
Respiratory
Cardiac
Dermatological
Ophthalmic
Neurological
Haematological
28
Q

What might be in a differential diagnosis of new inflammatory arthritis?

A 
OA
SLE/other connective tissue disease
PMR
Psoriatic arthropathy
Sponyloarthropathies
Reactive arthritis
Sarcoid
CPPD (calcium pyrophosphate)
Lyme’s
29
Q

Which serological investigations to undertake in patients presenting with joint pain and swelling?

A

FBC
U+Es
LFTs
ESR/CRP
RF- not diagnostic, but part of assessment
ACPA- prognostic indicator and picks ups some RF-ve
(ANA)

30
Q

Describe pharmacological treatment of RA:

A

Symptomatic
- NSAIDs, Analgesia etc
Disease Modifying (DMARDs)
- Glucocorticoids (oral, IA, IM)
- MTX/SASP/LEF/Gold/HCQ
- MTX: dihydrofolate reductase inhibitor, anti-inflammatory, SEs GI, hair, skin and rashes more serious lungs, liver, BM. Pregnancy is total contraindication
- SASP: serious BM Sesames, safe in pregnancy
- Biologics (anti-TNF, anti-CD20, anti-IL6, etc)

31
Q

Describe MOA of biological RA therapies:

A

Anti-TNF
Etanercept, infliximab, adalimumab, golimumab, certolizumab
TB, Infection risk, MS, CHF

Anti-CD20
Rituximab
Infection, PML, Hypogammaglobulinaemia

Anti-IL6
Tocilizumab
Minimal CRP, infections, high lipids,

CTLA4-Ig
Abatcept
Infections,

(JAK inhibitors)
Tofacitinib and others e.g. Baricitinib
High lipids, infections esp VZV, reduced CRP

SEs:
High rate of infections (esp first 6 months)- TB, VZV, opportunistic infections (listeria, salmonella)
Should be vaccinated against influenza and pneumococcus annually- avoid live vaccines

32
Q

What is the role of the MDT in RA:

A

a

33
Q

Describe definition and presentation of SLE:

A

Definition:
Multi-system autoimmune disease in which autoantibodies are made against auto antigens. Immune pathology results from polyclonal B cell secretion of autoantibodies causing tissue damage by immune complex formation and deposition, complement activation and other direct effects.

Presentation:
Remitting and relapsing illness of variable presentation. Typically presents with malaise, fatigue, myalgia and fever.

Specific features are found in SLICC criteria

34
Q

Describe investigations and diagnosis of SLE:

A

Immunology: >95% are ANA positive, high double stranded DNA (highly specific but 60% sensitive)

With 4 or more diagnostic criteria and at least 1 immune feature

  1. Malar rash
  2. Discoid rash
  3. Photosensitivity
  4. Oral ulcers
  5. Non-erosive arthritis
  6. Serositis/pleuritis
  7. Renal disorder
  8. CNS disorder
  9. Haematological disorder
  10. Immunological disorder; anti-DsDNA antibody, anti-Sm antibody, antiphospholipid antibody
  11. ANA
35
Q

Describe treatment of SLE:

A

Mild Disease:

Cutaneous symptoms with topical steroids, prevent rashes with high factor sunblock
MSK- NSAIDs, IA/IM steroid, low dose oral prednisolone, HCQ ± MTX
Serositis- NSAIDs, MTX

Moderate disease:

treat as mild disease plus:

  • oral prednisolone
  • MTX, Aza, MMF, cyclosporine
  • belimumab
  • rituximab in refractory disease

Severe disease:

  • High dose steroid
  • DMARDs
  • B cell therapy
  • Cyclophosphamide
  • IVIg
  • Plasmapheresis
36
Q

Describe Sjorgen’s syndrome:

A

Chronic inflammatory autoimmune disease associated with CTD.
There is lymphocytic infiltration of exocrine glands, especially lacrimal and salivary
Decreased tear production and salivation, parotid swelling
Vaginal dryness, dyspareunia, dry cough, dysphagia
Measure conjunctival dryness
Treat sicca symptoms

37
Q

Describe systemic sclerosis:

A

Can be limited cutaneous or diffuse.

Limited- calcinosis, Raynaud’s, oesophageal and gut dysmobility, sclerodactyly and telangiactasia. Pulmonary hypertension is common

Diffuse: whole body, early organ fibrosis: lung, cardiac, GI and renal

Management: no cure, immunosuppressive regimens; IV cyclophosphamide in organ involvement or progressive skin conditions

38
Q

Describe myositis:

A

Insidious onset of progressive symmetrical proximal muscle weakness and auto-immune mediated striated muscle inflammation associated with myalgia and arthralgia

Myositis may be paraneoplastic, commonly from lung, pancreatic, ovarian or bowel malignancy

Management:

  • screen for malignancy
  • start prednisolone
  • immunosuppressives
39
Q

Describe the main vasculitides by vessel size and immunopathology:

A

See summary sheets for diagram

Large vessel vasculitis
- giant cell arteritis

Medium vessel vasculitis
- polyarteritis nodosa

Immune complex small vessel vasculitis

ANCA-associated small vessel vasculitis

  • microscopic polyangiits
  • granulomatosis with polyangitis
  • eosinophilic granulomatosis with polyangiitis
40
Q

Describe the presentation of GCA:

A
  • Thickened non-pulsatile temporal artery
  • Pain in upper legs and arms
  • Sudden blindness
  • Jaw claudication
  • Rarely, coronary or large-vessel involvement
41
Q

Describe the presentation of ANCA vasculitis:

A

GwP

  • ENT symptoms such as nose bleeds and deafness
  • pulmonary fibrosis or haemorrhage
  • glomerulonephritis
  • neuropathy

EGwP

  • late-onset asthma
  • eosinophilia in blood
  • rash
  • glomerulonephritis
  • peripheral neuropahty

Microscopic Polyangiits

  • pulmonary fibrosis
  • ENT symptoms
  • rash
  • glomerulonephritis
  • peripheral neuropathy
42
Q

Outline the investigations of vasculitis:

A

Diagnosis of GCA:

Clinical presentation:
- typical headache, age, other CFs
Clinical exam findings:
- temporal artery asymmetry, non-pulsatile
Acute phase response:
- ESR/CRP
Further investigations:
- temporal artery biopsy
- temporal artery USS
- MRI, PET CT

ANCA key points:

MUST be done in correct clinical setting

cANCA with PR3 very suggestive of GPA

pANCA with strong MPO suggestive of MPA (or EGPA)

Positive ANCA by indirect immunofluorescence but negative PR3/ MPO is of doubtful significance and does not support a diagnosis of AAV

Not all AAV has a +ve ANCA

43
Q

Describe the treatment of vasculitis:

A

ANCA:

  1. Achieve remission
    a. Prednisolone AND
    b. In severe disease
    i. Cyclophosphamide (PO/IV)
    1. SEs: infection, cytopenia, malignancy, infertility
    ii. Rituximab
    1. Anti-B cell biologic agent
    2. As effective and safer than CPO
    c. In moderate disease; methotrexate or mycophenylate
  2. Maintain remission
    a. Prevent relapse
    b. Lower drug toxicities
    c. More prolonged therapy (2+ years)
    d. Use azathioprine or methotrexate

GCA:

Maintain prednisolone 60mg for 1 month

Taper to 15mg by 12 weeks.

Aim to discontinue corticosteroids by 12- 18 months.

Corticosteroid sparing therapy in patients with disease relapse on steroid sparing
Mycophenolate Mofetil
Methotrexate
Tocilizumab (anti-Il-6)

44
Q

Describe methotrexate MoA, indications and SEs:

A 
MoA: folate antagonism leading to impaired DNA synthesis and cell replication in chemotherapy
More subtle MoA in immunosuppression:
- adhesion molecules
- cytokines
- eicosanoids and MMPs
- methyl donors
- adenosine signalling

Indications:

  • rheumatological disease:
    • RA
    • psoriasis or psoriatic arthritis
  • steroid sparing agent in giant cell arteritis

SEs:

  • GI
    • N,D+V
    • hepatitis
    • stomatitis
  • Haematological
    • leukopenia
  • Others:
    • frequent infections
    • pulmonary fibrosis
45
Q

Describe azathioprine MoA, indications and SEs:

A

MoA:

  • converted into a nucleoside analogue in cells
  • incorporated into DNA and RNA leading to termination of nucleic acid strands
  • cell growth and metabolism halts
  • preferential action in lymphocytes as other cells have purine salvage pathway
  • given at too low a dose to prevent immune response through cytotoxic effect so other mechanisms must be in play
  • evidence that inhibits T-cell co-stimulation through interference with CD28

Indications:

  • most commonly used for inflammatory bowel disease
  • other severe autoimmune diseases
    • myasthenia gravis
    • eczema

SEs:

  • GI; NDV, hepatitis and cholestasis
  • haematological; leukopenia and thrombocytopenia
  • frequent infections
  • can accumulate in 0.2-0.6% who lack TPMT enzyme causing severe toxicity
46
Q

Describe cyclosporine MoA, indications and SEs:

A

MoA

  • small molecule inhibitor of calcineurin
  • effect of inhibiting signal transduction from the activated TCR complex
  • profound inhibition of T-cell activation

Indications

  • usually given for organ transplantation; liver, kidney, heart/lung
  • sometimes used for inflammatory conditions
  • can be used topically to skin/eye

SEs:

  • nephrotoxicity
  • hypertension
  • hepatotoxicity
  • anorexia and lethargy
  • hirsutism
  • parasthesia
47
Q

Describe broad categories of biologic drugs, and SEs associated with them:

A

TNF inhibitors

  • Increased risk of TB, particularly disseminated TB
  • Need to screen for latent TB before prescribing
  • Also increased risk of salmonella and listeria

Rituximab (anti CD20)

  • Generalised increased risk of serious infection
  • High risk of hepatitis B reactivation
  • Need to screen and prophylaxis if necessary

Abatacept (anti-CD86)

Increased risk of pneumonia and respiratory tract infection. Increased risk of TB but less than TNF blockade.

Anti-IL-1 therapy

Increased risk of respiratory tract infection and pneumonia.

SEs:
Hypersensitivity reactions
Infusion reactions
Mild gastrointestinal toxicity

48
Q

What are the features of mechanical back pain?

A
  • onset at any age
  • variable onset, may be acute
  • morning stiffness lasting <30 mins
  • exercise may worsen pain
  • often improves with rest
  • may improve overnight
  • generally worsens with movement or prolonged standing
  • most common cause is lumbar strain/sprain
  • examination aim is to exclude other pathologies
49
Q

What are the red flags for sinister causes of back pain?

A

Symptoms:

  • new onset age <16 or >50
  • following significant trauma
  • previous malignancy
  • systemic=fevers/rigor, general malaise, weight loss
  • previous steroid use
  • IV drug abuse, HIV or immunosuppressed
  • recent significant infection
  • urinary retention
  • non-mechanical pain (worse at rest/”night pain”)
  • thoracic spine pain

Signs:

  • saddle anaesthia
  • reduced anal tone
  • hip or knee weakness
  • generalised neurological deficit
  • progressive spinal deformity
50
Q

Describe the features, natural history and treatment of acute disc prolapse:

A

Radiculopathy:

  • may be acute, increase cough
  • typically leg > back pain, also known as sciatica
  • leg pain = dermatomal distribution
  • straight leg raising test +ve
  • reduced reflexes
  • most resolve spontaneously within 12 weeks
  • wait with investigations -> MRI (x-ray)
  • <10% need surgery (helps leg, not back pain)
51
Q

Describe the features of inflammatory back disease:

A
  • usually <40 years
  • insidious onset
  • morning stiffness lasting >30 mins
  • exercise improves pain/stiffness
  • no improvement with rest
  • may wake during second half of night

Symptoms in axSpA

  • fatigue
  • arthritis in other joints (hip/knees)
  • enthesitis; achilles tendon, plantar fasciitis
  • extra-articular inflammation; uveitis, psoriasis, IBD, other (heart/lungs/osteoP)
  • FHx of extra-articular arthritis
52
Q

Define spondylolisthesis, spondylosis and spinal stenosis:

A

Spondylolisthesis: slip of one vertebra onto the one below; pain may radiate to posterior thigh and increases with extension, only needs surgery if severe

Spondylosis: generalised degeneration of vertebral discs

Spinal stenosis: anatomical narrowing of spinal canna, congenital and/or degenerative

  • often presents with claudication in legs/calves
  • surgery is generally higher risk than no treatment
53
Q

Describe the presentation and pathology of OA:

A

The pathogenesis of OA involves a degradation of cartilage and remodelling of bone due to an active response of chondrocytes in the articular cartilage and the inflammatory cells in the surrounding tissues.

The release of enzymes from these cells break down collagen and proteoglycans, destroying the articular cartilage. The exposure of the underlying subchondral bone results in sclerosis, followed by reactive remodelling changes that lead to the formation of osteophytes and bone cysts.

Patients typically present with symptoms that are insidious, chronic, and gradually worsening. Clinical features include pain and stiffness in joints, worsened with activity* and relieved by rest. Prolonged OA results in deformity and a reduced range of movement.

Signs of osteoarthritis include localised swelling (e.g. Heberden’s nodes on the DIPJs, Fig. 2) or joint effusion, crepitus, muscle wasting (secondary to disuse), joint malalignment, fixed deformity, and a reduced range of movement.

54
Q

Describe treatment and management of OA:

A

Management
Stage 1- minimal treatment, lifestyle changes
Stage 2- physiotherapy, different non-pharmacological therapies, exercise and strength training, braces/knee supports and analgesia as required
Stage 3- NSAIDs, intra-articular injections of steroids, may consider prophylactic joint realignment surgery
Stage 4- surgery; realignment, replacement, excision, fusion

Surgery
Take away diseased surface
Replace with artificial material that sticks to bone
Can fix with uncemeted or cemented, hybrid or reverse hybrid

Post Op
Mobilisation, discharge, home exercise program

55
Q

Describe outcomes of OA surgery:

A

Outcomes

97% happy with surgery
General complications- DVT/PE, infection, neurovascular damage, swelling, stiffness, non/partial relief/recurrence
Anaesthetic problems
Specific hip- dislocation, fracture, leg length, discrepancy, hip noise, implant breakage/failure

56
Q

Describe juvenile idiopathic arthritis:

A

Presence of objective arthritis for at least 6 weeks under the age of 16

Most common chronic arthropathy of children
Includes several subtypes:
- Oligoarticular
- presents in one knee, though can be polyarthropathy
- Polyarticular
- fusion of bones in spine/neck
- Systemic onset
- systemic symptoms such as fever (high at night and settles in morning), pericarditis, serositis/pleurisy, organomegaly
- Psoriatic arthritis
- FHx of psoriasis/inflammatory conditions
- may have prolonged cradle cap

Diagnosis is made clinically; lab and radiography provide prognostic and classification information but not diagnostic

Around 10-20% present with asymptomatic uveitis, so must undergo regular ophthalmological examination

Treatment with methotrexate and biologics

57
Q

Describe paediatric vasculitis:

A 
Kawasaki disease:
Kawasaki disease (KD) is an acute, febrile, self-limiting, systemic vasculitis of unknown origin that almost exclusively affects young children

o Aneurysm formation in medium to large sized arteries
o Coronary arteries- myocardial infarction can also have in axillary, iliac and popliteal arteries
o Aneurysm formation, high fever, miserable, aseptic meningitis, red eyes and conjunctivitis, morbilliform rash, red, peeling skin
o IVIG treatment

Henoch-Schonlein purpura:

Henoch-Schonlein purpura (HSP) is the most common vasculitis of childhood and affects the small vessels. HSP is characterised by the classic tetrad of rash, abdominal pain, arthritis/arthralgia, and glomerulonephritis

o Palpable purpura, tends to be distal and
o Arthritis in same joints the rash is over

58
Q

Describe paediatric CTD:

A

a

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