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Phase 3 > Musculoskeletal > Flashcards

Musculoskeletal Flashcards

1
Q

Define Acute Compartment Syndrome

A

‘an orthopaedic emergency resulting from elevated interstitial pressure within a closed fascial compartment resulting in microvascular compromise, most commonly in the leg, forearm or thigh which could lead to loss of function, limb or life’

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2
Q

Describe the pathology of Acute Compartment Syndrome

A

Increased Internal Pressure (Bleeding, Swelling)

Increased External Compression (Casts, Bandages)

Pressure within the compartment exceeds the pressure within the capillaries

Muscles become ischaemic and develop oedema through increased endothelial permeability

Necrosis begins in the ischaemic muscles after four hours

Ischaemic nerves become neuropraxic (loss of motor and sensory function)

This may recover if relieved early, however permanent damage may result after only four hours

In the later stages, there is a compromise of the arterial supply

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3
Q

Describe the clinical features of Acute Compartment Syndrome

A

Pain (out of proportion to that expected from the injury and on passive stretching of the compartment)

Pallor

Paraesthesia

Paralysis

Pulselessness

Swelling

Shiny Skin

Autonomic Response - Sweating, Tachycardia

Reduced Consciousness Level

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4
Q

Describe the management of Acute Compartment Syndrome

A

Open any constricting dressings/bandages

Surgical Release:

Full length decompression of all compartments

Excise any dead muscles

Leave wounds open

Repeat debridement until pressure is down and all dead muscle has been excised

Later, close the wound and graft the skin if needed

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5
Q

Define Tendinopathy

A

‘chronic tendon injury of over use due to repetitive loading, characterised by degeneration and disorganisation of collagen fibres, increased cellularity and only little inflammation’

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6
Q

Describe the pathology of Tendinopathy

A

Tendinopathy is likely not an inflammatory process

Deranged collagen fibres and degeneration with a scarcity of inflammatory cells

Increased vascularity around the tendon

Failed healing response to micro-tears

Inflammatory mediators including IL-1, NO and Prostaglandins are released which cause apoptosis, pain and provoke degeneration through release of Matric Metalloproteinases

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7
Q

Describe the management of Tendinopathy

A

Pharmacological:

NSAIDs

GTN Patches

PRP Injection

Prolotherapy

Steroid Injection

Non-Pharmacological:

Activity Modification

Physiotherapy

Extracorporeal Shockwave Therapy

Radiofrequency Coblation

Operative Management:

Debridement

Excision of Diseased Tissue

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8
Q

Describe the presentation, diagnosis and management of large vessel vasculitis

A
  • Takayasu’s Arteritis
    • Pulseless disease or aortic arch syndrome
    • Systemic features include fever, malaise, night sweats, weight loss, myalgia, arthralgia and fatigue
    • Late features include bruits, absent/reduced pulses, claudication, ischaemic heart disease, headaches, BP variability
    • Diagnosed by CT/MR Angiography
    • Managed with Prednisolone for all patients, and further immunosuppression (e.g. methotrexate) in some
  • Giant Cell (Temporal) Arteritis
    • Presents with scalp tenderness, jaw claudication, fatigue and headache
    • Diagnosed by high ESR or biopsy
    • Managed with PO Prednisolone
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9
Q

Describe the presentation, diagnosis and management of medium vessel vasculitis

A
  • Polyarteritis Nodosa
    • Severe systemic manifestations with fibrinoid necrosis of the vessel wall with microaneurysm formation, thrombosis and infarction
    • Systemic features include fever, weight loss, malaise, myalgia and arthralgia
    • Associated with infarction and ischaemia of organs including the gut, brain, heart, liver, skin, PNS, limbs and kidneys
    • Investigated with CRP/ESR and CT/MR angiography and biopsy
    • Treated with PO/IV Prednisolone with or without DMARD
  • Kawasaki Disease
    • Vasculitis of young children characterised by aneurysm formation in medium to large sized arteries, including the coronary, axillary, iliac and popliteal arteries
    • Early features include high fever, mucositis and conjunctivitis
    • Late features include (fatal) aneurysms
    • Investigated with bloods, USS of testes and gallbladder and lumbar puncture
    • Managed with IV immunoglobulin or methylprednisolone plus aspirin
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10
Q

Describe Henoch-Schonlein Purpura

A

An immune complex mediated small vessel vasculitis

Most common vasculitis in childhood

Characterised by deposition of IgA

Diagnostic triad of palpable purpura, abdominal pain and arthritis

Investigations include urinalysis, IgA levels, U&Es

Treated with analgesics only if simple

If renal involvement, add corticosteroids and/or immunosuppressants

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11
Q

Describe ANCA associated small vessel vasculitis

A

cANCA or pANCA

Granulomatous Polyangiitis (classically involves the upper and lower respiratory tracts and kidneys)

Eosinophilic Granulomatous Polyangiitis - Churg-Strauss (Associated with eosinophilia, asthma, eosinophil-rich granulomata, peripheral neuropathy, pulmonary infiltrates)

Microscopic Polyangiitis (common manifestations are glomerulonephritis, weight loss, skin lesions, peripheral neuropathy, fever)

Investigations include ANCA, CT Chest, biopsy, bloods and urinalysis

Corticosteroid and Cyclophosphamide/Methotrexate

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12
Q

Describe the presentation and investigations of secondary bone tumours

A

Found in up to 60% of patients dying from cancer

Most often from the bronchus, breast, prostate, kidney and thyroid

Bones with a good blood supply are most often affected, including the long bones and vertebrae

Effects include bone pain, destruction and hypercalcaemia

May result in pathological fractures in the long bones

In the vertebrae there may be vertebral collapse, spinal cord/nerve root compression and back pain

Investigated with MRI and/or PET-CT

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13
Q

Describe the difference between lytic and sclerotic metastatic bone lesions

A
  • Lytic
    • Most common
    • Tumour replaces bone marrow
    • Tumour cells produce cytokines which activate bone resorbing osteoclasts
    • These patients are therefore more prone to pathological fracture
    • Bisphosphonates inhibit bone resorption so can be used to treat this
  • Sclerotic
    • Thickening of the bone
    • Most common cause is Prostate CA but also seen in breast carcinoma
    • Tumour cells promote deposition of immature woven bone by osteoblasts
    • Appears sclerotic (thickened and white) on x-ray
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14
Q

Describe myeloma, its presentation and management

A

Most common malignant primary bone tumours

Monoclonal proliferation of plasma cells

Effects include:

Bone Lesions (generalised osteopenia and punched out lytic foci)

Marrow Replacement (anaemia, leukopenia, thrombocytopenia and pancytopenia)

Diagnosed by Immunoglobulin Excess (ESR >100, Serum Electrophoresis and Urine Bence Jones Protein), Biopsy and Pepper Pot Skull on X-Ray

High dose chemotherapy with a bortezomib regimen and autologous SCT

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15
Q

Describe benign tumours of the bone

A

Osteoid Osteoma

Small, benign osteoblastic proliferation

Common in any age, especially adolescents

Can affect any bone, including long bones and spine

C/F include pain (worse at night, relieved by aspirin) and may cause scoliosis

Managed with analgesia and surgical resection

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16
Q

Describe malignant tumours of the bone

A

Osteosarcoma; a malignant tumour with cells arising from osteoid or bone and a peak age of 10-25yrs. Highly malignant with early lung metastases

Chondrosarcoma; central, within the medullary canal or peripheral on the bone surface. Predominantly affects middle-aged and elderly, more commonly men

Ewing’s Sarcoma; Peaks at 5-15yrs, usually in the diaphysis/metaphysis of the long bones or flat bones of the limb girdles. Early metastases to lung, bone marrow and bone

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17
Q

Describe septic arthritis, its presentation, investigation and management

A

‘inflammation of the synovium due to pathogenic inflammation of the joint’

Common organisms include Staph. Aureus, Neisseria Gonorrhoea and Haemophilus Influenzae

Presents with a hot, red, swollen and painful joint

Investigations include joint aspirate, blood cultures and FBC

Manage with IV antibiotics for 1-2 weeks (Flucloxacillin or Erythromycin)

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18
Q

Describe reactive arthritis, its presentation and management

A

‘sterile inflammatory synovitis occurring following an infection’

Trigger organisms include salmonella, shigella, yersinia and chlamydia trachomatis

Preceding illnesses include gastroenteritis, urethritis and chlamydia infection

Presents with acute, asymmetrical lower limb arthritis, days to weeks after the initial infection

Also associated with enthesitis, sacroiliitis, spondylitis, anterior uveitis, conjunctivitis, keratoderma blemorrhagica

Managed with analgesia (NSAIDs or intra-articular steroids)

Usually self-limiting with occasional chronic progression or cardiac complications

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19
Q

Describe gout, its presentation and management

A

Excess levels of uric acid leads to deposition of urate crystals in joints or soft tissue

Commonly affects the big toe

Risk factors include obesity, diabetes, high alcohol consumption and high protein diet

Severely painful, red, hot, swollen joint

Investigate with aspirate or serum urate levels

Manage with NSAIDs, colchicine, corticosteroids or allopurinol

20
Q

State indications for allopurinol in the prophylaxis of gout

A

Urate-lowering drug

Recommended for gout prophylaxis after one attack

Usually lifelong treatment

NSAID/Colchicine may need to be taken in conjunction for the first 4-6 weeks

21
Q

Describe the investigation of a patient presenting with acute joint pain and swelling, as per BSR guidelines

A

All patients presenting with a hot, red, swollen, tender and restricted joint should be regarded as having septic arthritis until proven otherwise (even in the absence of fever)

Synovial fluid should be aspirated, gram-stained and cultured prior to antibiotics

Infected prosthetic joints should be referred to an orthopaedic surgeon

Blood cultures should be taken

ESR, WCC and CRP should all be measured

X-Ray should be conducted as a baseline

22
Q

Describe the pathophysiology of osteoporosis

A
  • Osteoporosis results from a cellular process imbalance, i.e. an increase in bone resorption by osteoclasts and decrease in bone formation by osteoblasts
    • In younger patients, it is usually a decrease in bone formation, while in post-menopausal women, it is usually increased bone resorption
  • Oestrogen Deficiency
    • Oestrogen levels decrease greatly in females during the menopause
    • This can cause increased osteoclast recruitment, differentiation and prolonged osteoclast survival
      • This is achieved by increased activity of Interleukin-1 (increases production of osteoclasts) and Interleukin-6 (normally inhibited by oestrogen and secreted by osteoblasts to induce osteoclast formation)
    • The RANK receptor is normally expressed on pre-osteoclasts, where binding of the RANK-Ligand causes differentiation to mature osteoclasts, while Osteoprotegerin (OPG) inhibits the RANK receptor
      • Oestrogen deficiency causes increased RANK expression and decreased OPG secretion, resulting in increased osteoclast formation (i.e. increased bone resorption)
  • Age Related
    • The efficiency of calcium absorption in the intestines diminishes with age, meaning many elderly people are at risk of hypocalcaemia
      • This can be worsened by a vitamin D deficiency, which reduces the amount of calcium that can be absorbed
  • The above factors cause low bone density and quality, leading to an increased fracture risk
23
Q

State the role of DEXA scanning in osteoporosis and indications for its use

A

Measurement of bone mineral density

DXA scan should be offered to patients over the age of 50 with a history of fragility fracture, or to those under 50 with a major risk factor for fragility fracture

Major risk factors include frequent oral corticosteroid use, low BMI, premature menopause, hypogonadism, COPD, CKD, excess alcohol intake

T-Score (number of standard deviations below average BMD for a young female):

≥ -1 = Normal

-1 to -2.4 = Osteopenia

≤ -2.5 = Osteoporosis

24
Q

Describe the mechanism of action of bisphosphonates

A

PO - Alendronate, Risedronate

IV - Zalendronate (Zoledronic Acid)

Bisphosphonates are absorbed into hydroxyapatite crystals on bone, thereby slowing their rate of growth and dissolution to reduce the rate of bone turnover

Alendronic Acid is given once weekly PO

Zoledronic Acid is given by a 6-monthly IV infusion

25
Q

State indications for the use of bisphosphonates

A

Treatment of osteoporosis with a T-Score <2.5 and Paget’s Disease

26
Q

Describe other treatments to reduce fracture risk in osteoporosis

A
  • Denosumab
    • A monoclonal antibody that inhibits osteoclast formation, function and survival to deserve bone resorption by binding to RANKL to prevent osteoclast activation
    • Given by 6 monthly subcutaneous injection
    • Major side effects include atypical femoral fractures and osteonecrosis of the jaw
  • Teriparatide
    • Intermittently high levels of PTH, in the form of Teriparatide, stimulates osteoblast activity at the pluripotent stem cell level to increase bone formation
    • Given by daily, self-administered subcutaneous injection
    • Only anabolic treatment
    • Given for a two-year course only
  • Raloxifene
    • Selective Oestrogen Receptor Modulator
    • Binds to oestrogen receptors, exerting both agonistic and antagonist effects
    • In bone, this causes increased osteoblast and decreased osteoclast activity to reduce bone turnover
    • Given by daily tablet
27
Q

Describe the spectrum of autoimmune connective tissue disease

A

Arises from dysfunction of the immune system

SLE, Myositis and Scleroderma

Can be Undifferentiated CTD or Mixed CTD

28
Q

Describe the presentation, diagnosis and management of Systemic Lupus Erythematosus

A

Causes include genetics, EBV exposure, some drugs, UV light and sex hormone status (post-menopausal women)

SLE is characterised by auto-antibody production, complement/neutrophil activation and abnormal cytokine production

Deposition of IgG and complement and influx of neutrophils in the skin and kidneys

Fever, malaise, symmetrical small joint arthralgia, myalgia, butterfly face rash, recurrent pleurisy, pleural effusions, pericarditis, nephritis, psychiatric disturbance (depression), migraine, retinal vasculitis, mouth ulcers

FBC, U&Es, ANA, anti-dsDNA, Urinalysis, PCR, Low Complement, Excess Total Ig

NSAIDs, Topical/Parenteral/Oral Corticosteroids

Immunosuppressant; Cyclophosphamide, Azathioprine, Rituximab

29
Q

Describe the presentation, diagnosis and management of Polymyositis

A

Inflammation of striated muscle, causing proximal muscle weakness

When the skin is also involved, it is known as Dermatomyositis

General malaise, weight loss and fever during the acute phase

Cardinal symptom is proximal muscle weakness (sparing of face and distal limb muscles)

Movements such as squatting and climbing stairs become difficult

As the disease progresses, involvement of pharyngeal, laryngeal and respiratory muscles can lead to dysphonia and respiratory distress

In Dermatomyositis, there is often arthralgia, polyarthritis, Raynaud’s, Gottron’s Papules (purple-red, raised vasculitic patches) over the knuckles

Investigated with serum creatine kinase, raised ESR/CRP, serum autoantibodies, MRI, needle muscle biopsy

Managed with bed rest, exercise programme, prednisolone, steroid-sparing agents and biologics

30
Q

Describe the presentation, investigation and management of Scleroderma

A

Widespread vascular damage in small arteries, arterioles and capillaries with endothelial and intimal damage

Damage produces widespread obliterative arterial lesions and chronic ischaemia

Fibroblasts synthesise increased collagen I and III

Causes fibrosis of the lower dermis and internal organs

Clinical features include Raynaud’s Phenomenon, Limited Cutaneous Scleroderma, Myocardial Fibrosis, Dysmotility/Stricture of Oesophagus

Autoantibodies; LcSSC, DcSSC, ANA, RF

Imaging with CXR, HR-CT, Barium Swallow

Oral Vasodilators (ACEi, CCB) for Raynaud’s

PPIs for Oesophageal Symptoms

Immunosuppression for Pulmonary Fibrosis

ACEi for Renal Involvement

31
Q

Describe the MOA and potential side effects of Methotrexate

A

Folate antagonist with an affinity for many of the enzymes of folate metabolism

Principally inhibits dihydrofolate reductase to inhibit thymidylate synthase and arrest DNA synthesis, stopping the cell cycle at G1

Adverse include nausea, vomiting, diarrhoea, hepatitis, stomatitis, leukopenia, pulmonary fibrosis, frequent infections

32
Q

Describe the MOA and potential side effects of Azathioprine

A

Converted within cells into a nucleoside analogue which is incorporated into DNA and RNA, leading to termination of nucleic acid strands

Cell growth and metabolism halts, especially in lymphocytes

Adverse effects include nausea, vomiting, diarrhoea, hepatitis, cholestasis, leukopenia, thrombocytopenia, frequent infection, hair loss

33
Q

Describe the MOA and potential side effects of Cyclosporine

A

Small molecule inhibitor of calcineurin

Inhibits signal transduction from the activated TCR complex, resulting in profound inhibition of T-Cell activation

Adverse effects include nephrotoxicity, HTN, hepatotoxicity, anorexia, lethargy, hirsutism, paraesthesia

34
Q

State common indications for immunosuppressants and biologic therapies

A

RA

Psoriasis

UC/Crohn’s

Eczema

Post-Organ Transplant

35
Q

Describe the broad categories of biologic therapies used in auto-immune conditions and risk associated with their use

A

Anti-TNF agents (e.g. Infliximab), monoclonal antibodies that target a soluble cytokine

Anti-CD20 (e.g. Rituximab), monoclonal antibodies that target surface markers

Side effects include hypersensitivity reactions, infusion reactions and mild GI toxicity

Risk of infectious complications (e.g. activation of disseminated TB with Anti-TNF, increased pneumonia/RTI risk with Abatacept and Anti-IL1 therapy)

36
Q

Describe the features of mechanical back pain

A

Onset at any age

Generally worsens with prolonged standing or movement

Better with rest

Morning stiffness lasting less than 30 mins

Causes include lumbar strain/sprain, degenerative discs/facet joints, disc prolapse, spinal stenosis, and compression fractures

Managed with an exercise programme, physiotherapy and simple analgesia

37
Q

State red flags for serious causes of back pain

A

New Onset Age <16 or >50

Following Significant Trauma

Previous Malignancy

Systemic Symptoms (fever, weight loss, malaise, rigours)

Previous Steroid Use

IV Drug Use, HIV or Immunosuppression

Recent Significant Infection

Urinary Retention

Non-Mechanical Pain (e.g. Worse at Night)

Thoracic Spine Pain

Saddle Anaesthesia

Reduced Anal Tone

Hip/Knee Weakness

Generalised Neurological Deficit

Progressive Spinal Deformity

38
Q

Describe the features, natural history and management of acute disc prolapse

A

Acute onset, worse with coughing, typically leg and back pain (sciatica/radiculopathy), straight leg raise test +ve, dermatomal pain distribution, reduced reflexes

Most resolve spontaneously

<10% need surgery (helps leg pain)

39
Q

Describe the features of inflammatory back disease

A

Onset <45 yrs

Early morning stiffness >30mins

Back stiff after rest and improves with movement

May wake in the 2nd half of the night with buttock pain

Insidious onset, less likely to be acute

40
Q

Define spondylolisthesis

A

Slippage of one vertebra over the one below

Increased pain with extension

Pain may radiate to posterior thigh

41
Q

Define spondylosis

A

Degeneration of the spinal column, usually with age but possibly from other causes

Increases with flexion, sitting and sneezing

42
Q

Define spinal stenosis

A

Anatomical narrowing of the spinal canal

May be congenital or degenerative

Often presents with ‘claudication’ in the legs/calves

Worse when walking, rest in the flexed position

43
Q

State the benefits of exercise in the healthy individual

A
  • Regular physical activity can help reduce the risk of:
    • Cardiovascular – Stroke, IHD, PVD, Congenital HD, Heart Failure
    • Respiratory – Asthma, COPD, CF
    • MSK – RA, OA, Hip Fx, Low Back Pain, Fibromyalgia
    • Endocrine – Diabetes
    • Psychiatric & Neurological – Depression, Dementia, Schizophrenia, Parkinson’s
    • Cancer – Breast, Prostate, Colon
    • Other – Obesity, BP, Cholesterol
44
Q

Describe the epidemiology and presentation of Rheumatoid Arthritis

A

Affects 0.5-1% of the European and North American population

F:M - 3:1

Usually presents with symmetrical joint involvement (usually small joints of the hands and feet) with pain, erythema and swelling

Late joint features include swan neck, z-thumb and boutonniere deformities, ulnar deviation of the digits and radial deviation of the wrist

45
Q

State the serological investigations for patients presenting with joint pain and swelling

A

FBC, U&Es, LFTs

ESR and CRP

RF (60% Sens, 80% Spec)

APCA (60% Sens, 80-90% Spec) - prognostic marker; associated with smoking

ANA

46
Q

Describe Juvenile Idiopathic Arthritis

A

Disease of childhood-onset characterised primarily by arthritis persisting for at least 6 weeks and currently having no known cause

Chronic inflammatory arthropathy

Clinical diagnosis

Phase 3 (14 decks)

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