Revise Notes Msk Flashcards

1
Q

Acute Osteomyelitis
Pathophysiology

Infection of the bone
Adults - Usually contiguous spread
Children - Typically haematogenous spread

Most common cause: Staphylococcus aureus
Sickle cell patients - salmonella is the most common cause

A

Management

Investigation:
X-ray is often first port of call - soft tissue swelling, periosteal reaction and cortical destruction

MRI is considered gold standard (sensitivity 90%)

Antibiotics:
Flucloxacillin (clindamycin if pen all) - usually for 6 weeks minimum

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2
Q

Antiphospholipid syndrome (APS) is an autoimmune disorder that significantly impacts women’s reproductive health, being present in approximately 15% of women with recurrent miscarriage.

APS is characterised by the presence of lupus anticoagulant (LA) or anticardiolipin (aCL) antibodies.

The presence of a history of venous thromboembolism (VTE) in a patient with recurrent miscarriage strongly suggests APS.

Clinical Features

A

Clinical Features

Venous or Arterial Thrombosis:
Presenting with history of deep vein thrombosis (DVT), pulmonary embolism, or stroke.

Pregnancy Morbidity:
Recurrent Miscarriage: Women with APS are at higher risk of repeated pregnancy loss, particularly in the first trimester.

Premature Birth: APS can lead to premature delivery, often due to complications such as pre-eclampsia or eclampsia, which are linked to the syndrome.

Antibodies:
Lupus Anticoagulant (LA)
Anticardiolipin (aCL) Antibodies
Anti-β2-glycoprotein I Antibodies

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3
Q

Antiphospholipid syndrome

A

Management

Management focuses on preventing thrombotic events and managing pregnancy-related complications.

Anticoagulation: Long-term anticoagulation with warfarin is the mainstay of treatment for patients with a history of thrombosis.
The target INR is usually between 2.0 and 3.0, but it may be higher for recurrent events.

Antiplatelet Therapy: Low-dose aspirin is often considered, particularly in patients without a history of thrombosis but with positive antibodies, or in combination with anticoagulation for added protection.

Pregnancy Management: During pregnancy, women with APS are typically managed with low molecular weight heparin (LMWH) and low-dose aspirin to reduce the risk of miscarriage and other complications such as pre-eclampsia.

Warfarin must be avoided due to teratogenicity.

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4
Q

Autoantibodies
Table of high-yield autoantibodies and their associated conditions. These frequently crop up in the MSRA.

Autoantibody Condition
Anti-nuclear antibody (ANA)

Systemic Lupus Erythematosus (SLE), Mixed Connective Tissue Disease (MCTD), Sjögren’s Syndrome

Anti-dsDNA Systemic Lupus Erythematosus (SLE)

Anti-Smith (Anti-Sm) Systemic Lupus Erythematosus (SLE)

Anti-U1-RNP Mixed Connective Tissue Disease (MCTD)

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Anti-histone Drug-Induced Lupus

Anti-Ro (SS-A) Sjögren’s Syndrome
Anti-La (SS-B) Sjögren’s Syndrome

Anti-CCP Rheumatoid Arthritis

Anti-Scl-70 Diffuse Cutaneous Systemic Sclerosis

Anti-centromere Limited Cutaneous Systemic Sclerosis (CREST syndrome)

Anti-Jo-1 Polymyositis

Anti-phospholipid (aCL, LA) Antiphospholipid Syndrome

Anti-Mi-2 Dermatomyositis

Rheumatoid Factor (RF) Rheumatoid Arthritis

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5
Q

NICE guidance on referral following imaging

A

:

Adults

If X-ray is concerning for bone sarcoma OR if US suggests soft tissue sarcoma (or is uncertain and concern persists)

Refer via 2 week wait pathway
Children and young people

If X-ray is concerning for bone sarcoma OR if US suggests soft tissue sarcoma (or is uncertain and concern persists)

Refer via very urgent referral pathway - for specialist assessment within 48 hours

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6
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7
Q

Recognition and Referral

Red flag symptoms - NICE guidance on recognition and urgent imaging

A

:

Adults

Unexplained lump increasing in size - concerning for soft tissue sarcoma
Urgent ultrasound within 2 weeks

Children and young people

Unexplained lump increasing in size - concerning for soft tissue sarcoma
Very urgent ultrasound (within 48 hours)
Unexplained bone pain OR bone swelling - concerning for bone sarcoma
Very urgent x-ray (within 48 hours)

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8
Q

Bone and soft tissue Sarcoma

Osteosarcoma

A

An aggressive, malignant bone tumour, most common in children and young adults (age 10-20 years)

Red flag symptoms for osteosarcoma - unexplained bone pain or swelling
Pain is commonly worse at night
Most commonly sites: end of long bones - particularly proximal femur, tibia and proximal humerus, or in the mandible
May present as low trauma fracture

Investigation: X-ray is 1st line
Sunburst appearance

Codman triangle - the malignant osteoid causes elevation of the cortex of the affected bone

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9
Q

Soft tissue sarcoma

A

A malignant tumour of soft tissue (muscles, ligaments, tendons, fat etc.)

Red flag symptoms for soft tissue sarcoma - unexplained lump that is increasing in size

Most commonly found in arms, legs, chest and abdomen
Investigations: US is 1st line

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10
Q

Malignant tumours

A

Ewing’s sarcoma
Most commonly occur in childhood or early adulthood
Usually present with severe pain +/- swelling in pelvis, chest wall or long bones

Chondrosarcoma
Malignant cartilage in axial skeleton

Osteosarcoma
The most common primary bone malignancy, presenting with unexplained bone pain or swelling +/- night time pain in children and young adults.

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11
Q

Benign tumours

A

Osteoma - a benign overgrowth, most often of the skull - seen in Gardner syndrome

Osteochondroma - most common - ‘cartilage-capped’ bony projections

Giant cell tumour - tumours most often at the epiphyses of long bones. Double bubble sign on XR.

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12
Q

Cauda Equina Syndrome

A

Pathophysiology

Compression of the nerve roots in the thecal sac of the lumbar spine.
The cauda equina is the collection of peripheral nerves (L1-S5) in the lumbar canal

Compression decreases blood flow/CSF diffusion resulting in reduced nutrient delivery, and intraneural compartment syndrome - this leads to nerve root ischaemia

Most common cause is acute lumbar disc herniation at L4/L5 - might be triggered by lifting a heavy object etc.

Lower motor neuron lesion

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13
Q

Management of CES

If any of the above red flags, arrange emergency referral to spinal surgery service

Imaging - 1st line: MRI - ideally obtained within 1-2 hours of presentation

Management - emergency surgical decompression within 24-48 hours

A

Clinical Features

Back pain

Sciatica - unilateral or bilateral - shooting/burning radiating pain into legs and feet

Lower limb weakness

Bladder dysfunction - disruption of the autonomic nervous system supply to the bladder leads to urinary retention (due to inability to initiate bladder muscle contraction), and overflow incontinence (no sensation of bladder filling)

Saddle anaesthesia
More rarely - bowel dysfunction or erectile dysfunction

Examination
Lower limb weakness - for example knee extension, ankle eversion or foot dorsiflexion

Sensory loss - absent/reduced sensation in legs

Reduced anal tone and absent pinprick sensation in perianal region (S2-S4)

Hyporeflexia of knee/ankle jerks -(remember, CES causes a LMN lesion)

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14
Q

Cervical Radiculopathy
Pathophysiology

Compression of cervical nerve root resulting in radicular pain along the corresponding dermatome in the upper limb

Causes: Degenerative changes including cervical disc herniation or spondylosis
C7 is the most common nerve root, then C6.

A

Management

If red flags are present, or there is severe progressive neurology, seek immediate specialist advice

If cervical radiculopathy has been present for < 4-6 weeks and there are no neurological signs on examination - conservative management, including simple analgesia.

Consider neuropathic analgesia if required.
If cervical radiculopathy has been present for > 4-6 weeks or in the presence of objective neurological

findings on examination:
Perform MRI imaging to confirm the

diagnosis
Refer for consideration of spinal injections / surgery (indicated if progressive motor weakness/unremitting pain despite 6-12 weeks of conservative management), where MRI confirms compression.

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15
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16
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17
Q

Spurling’s test positive:
Also known as a maximal cervical compression, Spurling’s test involves:
Extending the neck

Tilting and rotating the head to the affected side

Gently applying pressure to the head and neck

The test is considered positive if it reproduces radiculopathic pain, weakness or sensory changes

A

Figure 216: CT scan of a 52 year old man with left sided pain in his neck, as well as radicular pain in his left arm, with tingling sensation paresthesia in fingers 1-3.

Spurling’s test was positive. Triceps reflex was decreased. The scan shows spondylosis with osteophytes between the vertebral bodies C6 and C7 on the left side, causing foraminal stenosis at this level (lower arrow, also showing axial plane), thus explaining his symptoms by compression of C7 nerve.

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18
Q

Cervical Radiculopathy

A

Clinical Features

Neck pain
Pain along the corresponding dermatome in the arm, often shooting or burning
Night pain

Sensory symptoms - paraesthesia, loss or reduced sensation along affected dermatome

Motor symptoms - weakness
Examination
Restricted neck movements

C6 nerve root
Weakness in elbow flexion and wrist extension
Reflexes: Biceps and supinator affected
Sensory changes: Along lateral forearm, thumb and first finger

C7 nerve root

Weakness in elbow extension, wrist flexion and finger extension

Reflexes: Triceps reflex affected
Sensory changes: Middle finger

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19
Q

Compartment Syndrome

A

Key learning

Commonly due to lower limb trauma/surgery/crush injuries

Present with pain disproportionate to injury, tense compartments and paraesthesia

Pain with passive stretch of affected muscles
Clinical diagnosis

Compartment pressure measurement with manometry can aid diagnosis (>40mmHg diagnostic)

Definitive management is open fasciotomy

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20
Q

Compartment Syndrome

A

Pathophysiology

Increased pressure within a muscle compartment leads to compromised tissue perfusion and nerve function
Causes

Commonly due to trauma, including fractures, crush injuries, or muscle overuse.

Other causes include:
Ischemia-reperfusion injury
Burns
Vascular injuries

Bleeding disorders
Prolonged limb compression
Tight bandages

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21
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22
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23
Q

Clinical Features compartment syndrome

Commonly in lower limb
Classically severe pain disproportionate to injury
Tightness
Paraesthesia

Examination Findings

Tense compartments
Decreased sensation- particularly first web space of foot

Diminished pulses, and pallor or cyanosis.
Pain with passive stretch of affected muscles

Severe cases:
Paralysis
Absent pulses.

Investigations

Diagnosis is primarily clinical- Delayed diagnosis can lead to irreversible tissue damage.
Measurement of compartment pressures with a handheld manometer can aid diagnosis (> 40mmHg = diagnostic)
Imaging (MRI or CT) helps identify underlying causes.

A

Management

Initial

Elevation
Analgesia
Avoid tight dressings

Definitive

Immediate decompression via open fasciotomy

Complications

Myoglobinuria
Nerve damage
Renal damage
Limb loss

Useful links

British Orthopaedic Association- Compartment Syndrome

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Vasculitis
Classification of Common Vasculitides Vasculitis can be classified according to the size of the vessels it primarily affects Large vessel vasculitis: Temporal arteritis, Takayasu’s arteritis Medium vessel vasculitis: PAN, Kawasaki, Beurger's Small vessel vasculitis: ANCA associated vasculitis - GPAA, EGPA Immune complex vasculitis - Goodpasture’s, SLE, HSP, cryoglobulinemia
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Large vessel vasculitis Temporal Arteritis
Temporal Arteritis Vasculitis of the superficial temporal artery (branch of the external carotid) Clinical Features Patients normally > 50 years of age 50% of patients have a history of polymyalgia rheumatica (suggested by pain and stiffness in the proximal muscles esp. in the mornings) Temporal headache Jaw claudication (chewing) Superficial tenderness (e.g. while showering/combing hair) Visual disturbance - due to anterior ischaemic optic neuropathy Diplopia Loss of vision Changes to colour vision O/E: Tender temporal artery which may be non pulsatile
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Takayasu's Arteritis large vessel arteritis Clinical features
Clinical features Classically occurs in young Asian females Systemic upset Intermittent claudication - exertional leg pain Angina Examination findings 1.Unequal blood pressures in upper limbs of > 10mmHg 2.Early diastolic murmur - aortic regurgitation 3.Carotid bruit and carotidynia (neck tenderness on palpation of carotids) Management Steroids
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Polymyalgia Rheumatica Clinical features Age > 60yrs Pain and stiffness in the shoulders, hips, and neck which develops acutely over a few days to weeks. Stiffness is worse in the mornings Low mood/ depression Night sweats Polyarthralgia
Investigations ESR > 40 (CK, EMG normal) Management Prednisolone 15 mg OD until symptoms are controlled (average 3-4 weeks), followed by a tapering dose for the following 3-6 months.
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Temporal arteritis investigation And management
Investigations Bloods: ESR raised, CRP raised Temporal artery biopsy - diagnostic investigation of choice Disadvantages: possibility of SKIP lesions Histology: Granulomatous arteritis with mononuclear cell infiltrates and GIANT CELLS Complications: CN7 palsy, auriculotemporal nerve injury. Management High dose steroids - e.g. prednisolone 60mg OD Urgent ophthalmology review - same day review if any visual symptoms
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Medium vessel vasculitis P. Polyarteritis Nodosa (PAN) K Kawasaki's Disease B Buerger's (thromboangiitis obliterans)
Polyarteritis Nodosa (PAN) Pathophysiology Necrotising inflammation of the 'medium' sized blood vessels, resulting in the formation of aneurysms Clinical Features Classically a middle aged man with a history of Hepatitis B Mononeuritis multiplex - painful, peripheral neuropathy affecting 2 or more peripheral nerves Hypertension Livedo reticularis Haematuria Acute renal failure Investigations pANCA (20% positive), Hepatitis B serology (30% positive) Angiogram: beading, microaneurysms
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Kawasaki's Disease Clinical features? Complications Coronary artery aneurysm Investigations Echocardiogram for ?coronary artery aneurysm Management High dose aspirin (risk of Reye's syndrome) and IV immunoglobulins
Kawasaki’s affects children, usually less than 5 years of age. Prolonged, unexplained fever (lasts at least 5 days), plus 1 or more of the following: Conjunctival injection Red/cracked lips Strawberry tongue Cervical lymphadenopathy Redness and desquamation of the skin of palms and soles Rash - varies between patients from morbilliform to maculopapular.
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Medium vessel vasculitis
Buerger's (thromboangiitis obliterans) Clinical Features Classically, a smoker develops symptoms of limb ischaemia (ulcers, claudication) Raynaud's Thrombophlebitis
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Small vessel vasculitis – ANCA associated Vasculitis
Microscopic Polyangiitis Eosinophilic Granulomatosis with Polyangiitis Granulomatosis with Polyangiitis
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Granulomatosis with Polyangiitis Pathophysiology An autoimmune disease resulting in necrotising, granulomatous inflammation of the vessels of the upper respiratory tract, lower respiratory tract and kidneys.
Clinical Features GPA affects the kidneys, upper and lower respiratory tracts. URT - sinusitis, epistaxis, nasal crusting, saddle nose LRT: haemoptysis, dyspnoea Renal: Rapidly progressive (crescentic) glomerulonephritis - Nephritic syndrome (HTN, haematuria, acute renal failure) Vasculitis rash, proptosis, cranial nerve lesions Investigations cANCA (PR3-ANCA) - 90% CXR: cavitations Renal biopsy: Epithelial crescents affecting Bowman's capsule Management Steroids Cyclophosphamide Plasma exchange Prognosis: survival 8-10 yrs
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Eosinophilic Granulomatosis with Polyangiitis Clinical Features Sinusitis Headache, runny nose, nasal congestion, facial pain Asthma like Dyspnoea, wheeze
Mononeuritis multiplex - peripheral neuropathy affecting at least 2 different nerves of the peripheral nervous system Burning pain, weakness, paraesthesia etc. Note: Symptoms can be worsened by leukotriene receptor antagonists (e.g. montelukast). Questions may describe a patient with presumed asthma, whose condition deteriorates after GP introduces montelukast. Investigations Bloods - eosinophilia Antibodies: pANCA (MPO-ANCA) - 60%
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Microscopic Polyangiitis
Clinical Features Fever Systemic upset Mononeuritis multiplex Renal impairment - raised creatinine, haematuria Rash - palpable, purpuric rash Investigations pANCA (70%), cANCA (40%)
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Small vessel vasculitis – Immune complex vasculitis
Henoch-Schonlein Purpura Goodpasture’s Syndrome Bechet’s disease – ulcers and uveitis
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Bechet’s disease – ulcers and uveitis
Pathophysiology Autoimmune mediated inflammation of the arteries and veins Clinical Features Commonly affects patients from middle-east (Turkey especially) with a positive family history, classic triad: 1. Oral ulcers 2. Genital ulcers (not usually on the penis) 3. anterior uveitis - pain, redness, photophobia, impaired vision Other features include thrombophlebitis, deep vein thrombosis, arthritis
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Goodpasture’s Syndrome Clinical Features
Renal - Rapidly progressive (crescentic) glomerulonephritis - nephritic syndrome.. Haematuria Proteinuria - frothy urine, peripheral oedema Acute renal failure Hypertension Pulmonary haemorrhage - haemoptysis, shortness of breath Systemic - fever, fatigue Investigations Antibodies - anti-GBM antibodies (IgG antibodies vs type 4 collagen (alveolar, GBM) Renal biopsy - Linear deposits of IgG along the basement membrane Management Plasma exchange Steroids Cyclophosphamide
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Henoch-Schonlein Purpura Pathophysiology IgA mediated small vessel vasculitis Clinical Features?
The most common vasculitis of childhood Age: Typically 2-10 years. Often triggered by infection: 50% of patients have a recent URTI Signs & symptoms: Palpable purpuric rash (with oedema), affecting the extensors and buttocks Abdominal pain Polyarthritis Nephritis due to IgA nephropathy - AKI, haematuria, proteinuria Management Supportive, analgesia Prognosis: Self-limiting. 1/3rd of patients will have relapse.
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Elbow fractures
Olecranon Fracture Radial head/neck fracture Supracondylar fracture
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Supracondylar fracture Clinical features Children following FOOSH Often complicated- displaced, angulated, rotated Swollen, deformed
Management MUA ORIF Immobilise with above elbow backslab Complications Displaced can cause damage to brachial artery
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Radial head/neck fracture Clinical features FOOSH/direct trauma Management Sling/backslab Supracondylar
Radial head/neck fracture Clinical features FOOSH/direct trauma Management Sling/backslab Supracondylar
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Elbow fractures XR if reduced ROM - fat pad sign= fracture (even if fracture not visible on XR) Olecranon Fracture Clinical features
Olecranon Fracture Clinical features Falls onto point of elbow Tenderness, swelling around elbow Management Backslab- elbow flexed 90 degrees
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Hand fracture Scaphoid fracture Colles fracture
Hand fractures FOOSH- fall onto the outstretched hand Occurs with forced dorsiflexion Younger patients: Scaphoid fracture Older patients: Colles’ fracture
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Colles fracture Distal radial fracture Results in dorsal displacement of distal fragment ‘Dinner-fork’ deformity Risk factors Older patients Osteoporosis Clinical features Neurovascular compromise Median nerve- thumb abduction Radial artery Tenderness, swelling, and ecchymosis over the wrist
Investigations X-rays- dorsal angulation and displacement of the distal radius fragment CT or MRI may be required for complex fractures or to assess for associated injuries Management 1.Immobilise in dorsal backslab cast and elevate with sling 2.Manipulation under anaesthetic (MUA) if above does not results in satisfactory position 3.If complex (comminuted, intra-articular, re-displaced) or above fails- surgical fixation
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Scaphoid fracture Clinical features Pain and swelling radial aspect wrist Poor grip Pain when telescoping thumb Tender anatomical snuffbox / palmar aspect scaphoid Radiology XR- specialist views: AP, lateral, right and left obliques (scaphoid views) Can consider MRI
Management Treat if suspect fracture clinically OR radiologically as can be missed on XR and risk of complications (see below) Scaphoid plaster (beer glass position) or Futuro splint Follow up in 2 weeks for repeat imaging Specific complications Higher risk in proximal or displaced fractures Non-union Avascular necrosis 1.Impairment of vascular supply to involved bone fragment 2.Stiff and painful wrist 3.Later on: loss of strength, reduced ROM wrist and osteoarthritis Management: Surgical: Open reduction internal fixation (ORIF)
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Finger injuries
Finger injuries Mallet finger Clinical features Extensor tendon avulsed from distal phalanx Mechanism: ball striking tip of finger causing hyperextension Investigation XR to ensure no avulsion fracture Management Splint for 6 weeks
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Systemic Sclerosis Systemic Sclerosis Systemic sclerosis is an autoimmune condition characterised by thickening and hardening of the skin (sclerosis) and other connective tissues. 90% of patients with any form are ANA positive.
There are 3 distinct patterns of systemic sclerosis, including: Limited cutaneous SS Diffuse cutaneous SS Scleroderma
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Limited cutaneous systemic sclerosis Clinical Features
Clinical Features Typically women aged 30-50 years of age Sclerosis affects the face & distal limbs Raynaud’s phenomenon is common Used to be referred to as CREST syndrome. Features of LCSS therefore include: Calcinosis, Raynaud’s, Esophageal dysfunction, Sclerodactyly, Telangiectasia Antibody Anti-centromere antibodies ANA
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Diffuse cutaneous systemic sclerosis Clinical Features Typically women aged 30-50 years of age Sclerosis affects the trunk & proximal limbs
Complications Interstitial lung disease (up to 8/10 patients) - SSc-ILD (Scleroderma-related ILD) - pulmonary fibrosis with progressive respiratory failure Pulmonary hypertension Hypertension, CKD Antibody SCL-70 antibodies ANA
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Scleroderma Clinical Features
Hardened, thickened areas of skin. Tightening of the skin gives a 'shiny' appearance. Plaque morphoea - oval patches of discoloured, hardened skin which might be shiny Linear morphoea: thickened lines of skin along the arms and legs No organ involvement
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Systemic Lupus Erythematosus Systemic lupus erythematosus (SLE) is a chronic multisystem disorder of autoimmune aetiology, affecting approximately 1 in 1000 people in the UK.
Investigations Antibodies: ANA – 95% sensitivity Anti-dsDNA – 95% specific Anti-smith – 98% specific Monitoring disease activity: In active disease CRP can be normal - so a high CRP might suggest infection ESR and anti-dsDNA levels can be used for monitoring disease activity Low C3 and C4 levels may also reflect active disease due to consumption
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