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CP3 > MSK System and MDD Attachment > Flashcards

MSK System and MDD Attachment Flashcards

1
Q

REHABILITATION MEDICINE:

  1. Describe the terminology of the International Classification of functioning, disability and health (ICF) and relate this to REPAIR
  2. Identify and assess disability and handicap/disadvantage using the REPAIR screen (Review of pathology & impairment; Environment; Activities; Important other people; Risk and prevention).
  3. Describe the main phases of gait and characterise an abnormal gait in terms of phase of gait and abnormal locomotor characteristics.
  4. State some of the measurement scales used to assess disabilty
  5. Understand pressure ulcer aetiology, risk, prevention and management
  6. Describe how to manage neurogenic bladder and bowel
A
  1. ‘Provides a framework for a ‘hollisitic’ approach to illness. ICF examines effect on body functions & structures, activity and participation by the health condition. Whilst also taking environmental factors and personal factors.
  2. (Review of pathology & impairment; Environment; Activities; Important other people; Risk and prevention).
  3. Gait has 2 distinct phases, stance and swing. With stance describing movement from heel strike to toe off.
    • ​​Hemiplegic gait: Upper limb flexors stronger than extensors
    • Parkinsonian (Festinant) gait: Shuffling, reduced arm swing, pill rolling tremor at rest, increased turning circle
    • Ataxic gait: Broad-based, unsteady
    • Neuropathic (e.g. high stepping) gait
    • Myopathic gait (Trendelenburg)
    • Antalgic gait
    • ASIA: A framework for neurological impairment in patients with spinal cord injury
    • Barthel Index: Used to measure performance in activities of daily living, measuring the degree of assistance required
  5. Pressure Ulcers
    • Ateiology: Shear forces, pressure, moisture, prolonged periods in bed
    • Risk factors: Dermatological (dry skin, moist skin, preexisting lesions); iatrogenic (steroids); elderly; low BMI (pressure points); bed bound
    • Prevention: Regular repositioning, cushioning, skin care
    • Management: Regular repositioning, specialised equipment to help relieve pressure, dressings
    • Neurogenic bladder: Antimuscarinic medications (parasympathetic), intermittent catheterisation, prophylactic abx
    • Neurogenic bowel: Chronic laxatives, bowel irrigation may be required
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2
Q

REGIONAL PERI-ARTICULAR PAIN

  1. Describe the typical presentation, risk factors and outcome of a patient with a common peri-articular over usage/strain injury (enthesopathy, tendinitis, tenosynovitis, muscle strain, bursitis)
A

Suprasinatus injury findings on examination:

  • Arms abducted to sides, then brought 30 degrees forward. Apply resistance
  • Empty can test (same position as above but point thumbs down)
  • Pain or weakness, especially unilateral, is indicative of supraspinatus injury

Infraspinatus and Teres Minor injury findings o examination:

  • Pain and/or weakness on external rotation

Findings in adhesive capsulitis (pain then freezing then thaw stages)

  • Reduced ROM in both active and passive movement
  • External rotation is the first motion to be affected
  • There may also be pain upon palpation of the trapezius

Findings in acromioclavicular joint disease

  • Painful arc between 150 and 180 degrees
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3
Q

NECK AND BACK PAIN

  1. Describe the symptoms that may result from spondylolisthesis, spondylolysis and canal stenosis.
  2. Outline an appropriate management plan for chronic back pain and for patients with root entrapment.
A
    • Spondylolysis: Describes a defect or stress fracture in the pars interacrticularis of the intervertebral arch. If left untreated, spondylolysis can weaken the vertebral to such as entent that patients may develop…
    • Spondylolisthesis: Describes displacement of the vertebrae following fracture of the pars interarticularis
    • Canal stenosis: Describes narrowing of the spinal canal, causing compression of the spinal cord. Signs are dependent at which the compression occurs
    • Analgesia: NSAIDs PLUS gastric protection
    • Consider analgesia for neuropathic pain: Amitriptyline, gabapentin and duloxetine
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4
Q

FIBROMYALGIA

  1. Describe the symptoms, signs and diagnostic criteria for diagnosis of fibromyalgia
  2. Outline screening investigations for co-morbid treatable conditions
  3. Outline the abnormalities of sleep and pain physiology associated with fibromyalgia
  4. Discuss an appropriate management and rehabilitation plan for a pt with fibromyalgia
A
    • Symptoms: Widespread chronic body pain (>3/12), fatigue unrelieved by rest, cognitive changes (memory), disturbance to mood and/or sleep
    • Signs: Diffuse tenderness on examination
    • Diagnostic criteria:
      • ​Severe pain in 3-6 different areas of the body, OR milder pain in 7 or > different areas
      • Continuous symptoms for at least 3 months
      • No other explanation for symptoms found
    • ​Ddx includes RA, anxiety, depression, polymyalgia rheumatica, CFS, SLE, IBS
    • ?anxiety ?depression - GAD,
    • ?Vit D deficiency - Serum Vitamin D
    • ?IDA - serum iron, transferrin saturation
    • ?RA - RF, antiCCP, ESR or CRP
    • ?SLE - ANA
    • ?Hypothyroidism
    • ?Chronic liver disease - HCV serology
  3. Sleep abnormalities - increased alpha sleep when delta would be expected (?not as ‘deep’)
  4. Management:
    • Conservative:
      • ONCE some improvement in symptoms with pharmacological therapies - Education, exercise and CBT approaches can be suggested
      • Education: Emphasise that there is no cure but that a reasonable level of function id very achievable
    • Medical:
      • ​Analgesia: TCAs, SNRIs and gabapentoids have been shown to have the greatest efficacy
      • MDT involvement e.g. psychotherapist
    • Surgical: -
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5
Q

JOINT PAIN

  1. Describe the typical presenting symptoms and signs of a patient presenting with joint inflammation and/or joint damage and construct an appropriate differential diagnosis and plan of investigation for a patient presenting with:
    • Acute monoarthritis
    • Chronic monoarthritis
    • Acute or chronic oligoarthritis
    • Inflammatory polyarthritis
A
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6
Q

OSTEOARTHRITIS: Describe symptoms and signs of OA and specify relative prevalence of knee, hip and hand osteoarthritis

A

Symptoms

  • Progressive joint pain: Initially activity related then finally constant rest pain
  • Joint stiffness
  • Reduced ROM and functional difficulties
  • Pain/stiffness improved following mobilisation (< 30 mins)

Signs

  • LOOK:
    • Joint deformity: Heberden’s and Bouchard’s nodes at DIPs and PIPs respectively
    • Muscle wasting in late stages (due to reduced use)
  • FEEL:
    • Tenderness over the joint line​
  • MOVE:
    • Weakness in affected joints
    • Reduced ROM on active and passive movement
    • Crepitus detected on movement

Relative prevalence:

  • Knee > Hip > Hand
  • Note that hand OA spares the MCP, helping distinguish the condition from RA
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7
Q

OSTEOARTHRITIS: Describe the main risk factors for development and progression of knee, hip and hand osteoarthritis and classify osteoarthritis according to presence of nodes, number of sites involved and presence of associated calcium crystal deposition.

A

Risk Factors for OA:

  • Reduced oestrogen: Post-menopausal, late menarche, early menopause
  • Female gender
  • Age > 50 years
  • FHx
  • Smoking
  • Low peak bone density
  • Low BMI
  • Trauma to joint

Classification of OA:

????

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8
Q

OSTEOARTHRITIS: Discuss the correlation between symptoms, disability and structural change of osteoarthritis and specify the major associations of pain.

A
  • Early OA is rarely symptomatic, unless accompanied by effusion
  • Advanced radiological/pathological OA is not always symptomatic - poor correlation between disability, symptoms and structural change
  • Quadriceps strength and low mood are much better predictors of pain, than radiological severity
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9
Q

OSTEOARTHRITIS: Describe the pathology and the associated radiographic features of osteoarthritis.

A

Pathology: A disease of synovial joints in which the degradation and synthesis of bone is disrupted.

Radiographic features:

Loss of joint space

Osteophytes

Subchondral cysts

Subchondral sclerosis

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10
Q

OSTEOARTHRITIS: Outline an appropriate management (medical, surgical, rehabilitation) plan for a patient with knee, hip or hand osteoarthritis.

A

Management of Osteoarthritis

  • Conservative management
    • Pt education
    • Exercise programmes: resistance training, tai chi, yoga, swimming
    • Physiotherapy
    • OT
  • Medical management
    • Analgesia:

1st line: Topical analgesia

2nd line: Paracetamol + topical analgesia

3rd line: NSAID + paracetamol + topical analgesia. Gastroprotection should also be provided

4th line: Opioid + NSAID + paracetamol + topical analgesia

  • ​Intra-articular corticos
  • teroid injections: For acute exacerbations or when NSAIDs are contraindicated/not tolerated
  • Surgical management
    • ​Indicated if pain is not controlled or requiring regular opioids or causing severe disability
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11
Q

OSTEOARTHRITIS: Specify the indications for large joint replacement surgery, outline the procedure for hip and knee total joint replacement and list the complications (and approximate incidence) of hip and knee joint replacement.

A

Indications:

  • Pain and stiffness leading to loss of function
  • Pain requiring regular opioids

Complications of total hip replacement:

  • Leg length discrepancy (15%)
  • Dislocation (3%)
  • Infection (0.5-1%)
  • Periprosthetic fracture
  • Persistent pain (1%)
  • Neurovascular injury
  • Infection - rare but devastating. If suspected then aspiration should be performed. Management involves removal of the prosthesis and length course of abx prior to insertion of the new prosthesis

(General - infection, bleeding, injury to adjacent structures, failure)

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12
Q

CRYSTAL ASSOCIATED ARTHRITIS: Specify the risk factors and target sites for development of gout, calcium pyrophosphate crystal deposition, and calcific periarthritis.

A

Risk factors:

  • Purine rich diet (monosodium urate monohydrate crystals) - meat, seafood and alcohol
  • Older age
  • Male sex
  • Medications: Thiazide diuretics, aspirin, cyclosporin, tacrolimus or pyrazinamide
  • Inherited isolated defect in uric acid excretion
  • Excess food/alcohol consumption or dehydration → acute attack

Target sites for…

Gout:

  • 1st MTP joint

Calcium pyrophosphate crystal deposition:

  • Generally, larger joints.
  • Most commonly occurs at the knee, followed by the wrists and pelvis.

Calcific periarthritis: Juxta-articular deposition of calcium hydroxyapatite crystals causing local inflammation of adjacent soft tissues. Deposition may occur in tendons, hyaline cartilage and subcutaneous muscle

  • Pain and swelling around one joint, usually of the finger or toe
  • Calcium deposits may be seen on X-ray imaging of the joint
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13
Q

CRYSTAL ASSOCIATED ARTHRITIS: Describe the symptoms, signs, differential diagnosis and appropriate investigation of a patient with: acute crystal synovitis (gout, acute calcium pyrophosphate crystal arthritis); chronic (tophaceous) gout and acute calcific periarthritis. Appropriate management plan

A

Associated imaging changes of crystal-associated disease:

  • Chronic gout - ‘punched out’/’rat bite’ erosions
  • Calcific periarthritis - calcium deposits in extra-articular soft tissues
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14
Q

CRYSTAL ASSOCIATED ARTHRITIS: Specify the indications, mechanism of action and side-effects of urate lowering therapy and specify the objectives and monitoring of such treatment.

A

Examples: Allopurinol, febuxostat

Indications:

  • Offered to all with a Dx of gout
  • There are specific pt groups in which it is particularly important to offer urate lowering therapy (2 or > gout attacks in 12 months, tophi, joint damage, renal impairment, hx of urinary stones, diuretic use)

MoA: Xanthine oxidase inhibitor, preventing the production of uric acid (through breakdown of purine catabolism)

Objectives of treatment:

  • Titration of dose, every 4 weeks, until serum urate acid (SUA) level is < 300 micromol/L
  • Prophylactic NSAID or colchicine should be continued for at least 1/12 after uric levels are corrected to avoid precipitating an acute attack

Side-effects

  • Rash (?Stevens-Johnson Syndrome: Flu-like symptoms, red/purple rash with blistering)
  • Nausea and vomiting
  • Agranulocytosis
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15
Q

RHEUMATOID ARTHRITIS: Describe the symptoms, signs and pattern of joint involvement in rheumatoid arthritis and outline appropriate investigations for diagnosis and assessment of rheumatoid arthritis.

A
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16
Q

RHEUMATOID ARTHRITIS: Describe the clinical features relating to extra-articular rheumatoid disease including vasculitis, Sjogren’s syndrome, scleritis, nodulosis, fibrosing alveolitis, pericarditis, peripheral neuropathy, entrapment neuropathy and amyloidosis.

A
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17
Q

SERONEGATIVE SPONDYLOARTHRITIS: Discuss the overlapping clinical, pathological and genetic features of the seronegative spondyloarthritides (ankylosing spondylitis, reactive arthritis, psoriatic arthritis and arthropathy associated with inflammatory bowel disease).

A
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18
Q

RHEUMATOID ARTHRITIS: Describe the clinical presentation and assessment of a patient with atlantoaxial subluxation due to rheumatoid arthritis.

A

Pathology: Synovitis and damage to the ligaments and bursae around the odontoid peg of axis (C2) can allow for axis to shift within the atlas (C1).

Clinical presentation

  • Symptoms: Neck pain
  • Neurological deficits as impingement of the spinal cord progresses:
    • Signs of UMN lesion: Hyperreflexia, muscle weakness
    • Broad based gait
    • Reduced hand dexterity
    • Bladder problems
  • Spinal cord compression

Assessment

  • X-ray imaging:
    • Open mouth odontoid allows for displacement to be assessed
  • MRI scan - particularly important to assess in pts with RA prior to anaesthetic/intubation as subluxation may occur during neck movements
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19
Q

SERONEGATIVE SPONDYLOARTHRITIS: Describe the pathology and associated radiographic changes of seronegative spondyloarthritis.

A

Associated radiographic changes

AS - SIJ involvement (inflammation and eventual fusion); squaring of the vertebrae with progression to a ‘bamboo spine’ appearance in later stages of the disease

ReA - May have SIJ involvement (asymmetrical sacroiliitis)

PA - Bony erosions and a small degree of osteopenia; ‘pencil in a cut’ appearance to digits in later stages; sacroillitis may be present

IBD associated arthropathy -

20
Q

SERONEGATIVE SPONDYLOARTHRITIS: Outline an appropriate management plan for a patient with seronegative spondarthritis

A

General approach:

`1st line - NSAIDs +/- articular corticosteroids, physio

2nd line - Use of DMARDs e.g. methotrexate

21
Q

SERONEGATIVE SPONDYLOARTHRITIS: Describe the clinical features relating to associated extra-articular disease in this group

A
  • Dermatologial:
    • Psoriasis in psoriatic arthritis
  • Ophthalmic:
    • Anterior uveitis in AS and psoriatic arthritis (HLA-B27). Presents as acute pain, photophobia, aniscoria, circumcorneal erythema and hypopyon. Caution as anterior uveitis is also associated with IBD
    • Scleritis and episcleritis in RA. Pain → scleritis, painless → episcleritis. Conjunctival inflammation seen on examination
22
Q

INFECTION OF LOCOMOTOR TISSUES: Specify risk factors, common sites and common organisms for infections of joints or bones

A

Risk factors

  • Extremes of age
  • DM - foot ulcers
  • IVDU
  • Trauma or recent surgery
  • Immunosuppression (including DM)

Common sites

  • Metaphyseal plates of long bones in young children
  • Spine in immunosuppressed adults

Common organisms

  • Staph aureus
  • Strept pyogenes
  • *** Consider disseminated gonococcal in young adults (consider genitourinary symptoms e.g. dysuria, urethral discharge, gram negative dipolococcus on gram staining)

*Usually via haematological spread from the skin or respiratory tract

23
Q

INFECTION OF LOCOMOTOR TISSUES: Describe the symptoms, signs and appropriate differential diagnosis of a patient with acute or chronic joint or bone sepsis.

A

Signs and symptoms

  • Erythematous, painful, swollen and warm joint
  • Reduced ROM
  • Extreme pain, even with passive movement
  • Evidence of effusion
  • Knee held in flexion
  • Evidence of infective route e.g. recent surgery, trauma

Ddx

  • Gout
  • Pseudogout
  • Soft tissue injury
  • Reactive arthritis (can’t see, pee or climb a tree)
  • Osteomyelitis
  • Monoarticular RA
24
Q

INFECTION OF LOCOMOTOR TISSUES: Specify the immediate investigation and management of a patient with acute septic arthritis.

A

Immediate investigation of septic arthritis:

  • Joint aspiration
    • ​3 C and 1 G (Cells, culture, crystals and gram stain)
  • Imaging (X-ray)

Management

  • Empirical abx until sensitivities back
  • Analgesia with NSAID +/- PPI
25
Q

INFECTION OF LOCOMOTOR TISSUES: Describe the pathology and associated imaging radiographic changes of locomotor sepsis.

A

Imaging does not help diagnosis but there are associated characteristic changes

First 2/52:

  • Soft tissue swelling
  • Widening of the joint space due to effusion

Later imaging:

  • Narrowed joint space due to cartilage destruction
  • Bone destruction and ankylosis (stiffening anf fusion) if severe
26
Q

INFECTION OF LOCOMOTOR TISSUES: Describe the symptoms, signs and investigations of a patient with viral arthropathy

A

Signs and symptoms

  • Tends to occur during the prodromal phase, with accompanying rash
  • Symmetrical distribution

Investigations

  • Can be caused by any viral infection
  • Viral titres/antigens
  • RhF
27
Q

BONE DISEASE: Define osteoporosis, describe its clinical consequences and specific the risk factors for its development

A

Osteoporosis: A pathological reduction in bone density and microarchitectural degradation of bone

Clinical consequences:

  • Fragility #
  • Vertebral wedge #

Risk factors

  • Increasing age
  • Female gender
  • Late menarche or early menopause
  • Low BMI
  • Low peak bone density
  • Smoking
  • FHx
  • Disuse
  • Low calcium content in diet/vitamin D deficiency
  • Secondary causes:
    • Primary hyperparathroidism
    • Thyrotoxicosis
    • Steroid induced (including Cushing’s disease)
    • Chronic inflammatory conditions
28
Q

BONE DISEASE: Describe appropriate investigations to confirm and assess osteoporosis

A

Investigations

  • FRAX score to calculate 10 year risk of fracture. Can be calculated +/- DEXA results.
    • ​Can be calculated to allow need for DEXA scan to be assessed
  • DEXA scan
    • T score < -2.5 allows dx
  • Serum calcium and phosphate levels
  • Endocrine screen: PTH, Ca, TFTs, cortisol, sex hormones
  • Consider iatrogenic causes:
    • ​Long term steroid use
    • Long term use of SSRIs, PPIs, anti-epileptics and anti-oestrogens
29
Q

BONE DISEASE: Outline an appropriate management plan for a person who (1) is at risk of developing osteoporosis, or (2) has established osteoporosis, taking into account the different options according to sex and age

A
  1. At risk of osteoporosis
    • Lifestyle interventions:
      • Exercise, smoking cessation, reduce alcohol intake, maintain a healthy weight
    • Ensure adequate vitamin D and calcium intake
    • Avoid falls
    • Follow up in 5 years for repeat assessment
  2. Established osteoporosis
    • Bisphosphonates1
      • Second line treatment includes denoxumab, raloxifene and HRT
    • Calcium and vitamin D supplementation
    • Repeat DEXA at 3-5 years and ‘treatment holiday’ (18 months - 3 years) considered if their bone mass density has improved and they have not suffered any fragility #

1: Bisphosphonates counselling points - take 30 minutes before food, sit upright and with a whole glass of water. Normally taken once a week. Can be associated with atypical femoral fractures and osteonecrosis of the jaw (consult medical professional if experiencing jaw pain)

30
Q

BONE DISEASE: Define osteomalacia and specify the risk factors for its development

A

Osteomalacia: Inadeqeuate bone mineralisation a.k.a. ‘Soft bones’, usually caused by vitamin D deficiency. When occuring in children prior to growth plate fusion this is known as Ricket’s.

Risk factors

  • Low levels of sun exposure (especially in darker skin tones)
  • Malabsorptive conditions (CF1, IBD)
  • Chronic kidney disease (required for activation of vitamin D)

​1: As vitamin D is a fat soluble vitamin without pancreatic lipase absorption is interrupted. Hence, when pancreatic dysfunction is seen supplementation is required

31
Q

BONE DISEASE: Outline the clinical presentation, investigation and treatment of a patient presenting with osteomalacia.

A

Clinical presentation:

  • May be asymptomatic
  • Fatigue
  • Bone pain
  • Muscle weakness and aches
  • Pathological1 or abnormal #
  • Risk factors for low vitamin D present: darker skin tone, low exposure to sunlight, majority of time spent indoors

Investigation:

  • Vitamin D (serum 25-hydroxyvitamin D, < 25nmol/L is deficiency)
  • Bone profile: Ca2+, phosphate, ALP
    • ​↓ calcium and phosphate
    • ↑ PTH and ALP
  • PTH
  • Imaging - osteopenia
  • DEXA - low bone density

Treatment:

Supplementary vitamin D: Correct deficiency and then provide a maintenance dose

1: Pathological fracture describes fractures occuring in abnormal bone that occur spontaneously or following minor trauma that would not otherwise fracture normal/healthy bone

32
Q

BONE DISEASE: Outline the histology and pathogenesis of Paget’s disease of bone and list its clinical consequences.

A

Paget’s disease: Excessive bone turnover, due to increased activity of osteoblasts and osteoclasts, leads to patchy areas of high and low bone density. This condition particularly affects the axial skeleton (cranium and spine).

Clinical consequences:

  • Osteogenic sarcoma: Paget’s disease increases the risk of developing this bone cancer
  • Spinal stenosis and subsequent spinal cord compression
  • Pathological #
  • Enlarged and misshapen bones
  • Bone pain
  • Hearing loss if the auditory ossicles are affected
33
Q

BONE DISEASE: Outline the investigation and treatment of a patient presenting with Paget’s disease.

A

Investigation:

  • Bone profile: Ca2+, PO4-, ALP, PTH
    • ↑ ALP
  • Imaging
    • Bone enlargement and deformity
    • Osteoporosis circumscripta
    • Cotton wool appearance of the skull
    • V-shaped defects in long bones

Treatment:

  • Bisphosphonates
  • NSAIDs for bone pain
  • Calcium and vitamin D supplementation
  • Monitor ALP - should normalise and symptoms eliminated
34
Q

BONE DISEASE: Describe the pathogenesis of (primary) osteonecrosis and specify the risk factors and target sites for its development.

A

Primary osteonecrosis: Bone breakdown (necrosis) due to ischaemia

Risk factors:

  • Fracture → interruption of arterial supply
  • Interrupted venous drainage and retrograde arterial stoppage
  • Idiopathic
  • Bone marrow infiltration (malignancy)
  • Alcohol abuse
  • Exogenous sterouds/Cushing’s
  • Infection e.g. septic arthritis
  • Bisphosphonates increase the risk of secondary osteonecrosis, particularly of the jaw and the external auditory canal

Target sites:

  • Femoral head
  • Scaphoid
  • Lunate
  • Body of the talus
35
Q

BONE DISEASE: Describe the typical clinical presentation, differential diagnosis and appropriate investigation of a patient with osteonecrosis, and outline a management plan.

A

Typical clinical presentation:

  • Bony tenderness
  • Stiffness and swelling the the joint/over the bone

Differential diagnosis:

  • Simple fracture
  • Septic arthritis

Appropriate investigation:

  • Imaging: Approximately 6/12 after the injury an area of increased bone density will be seen, as new bone formation occurs
  • MRI/radionucleotide scans show earlier changes

Management plan:

  • Eliminate the cause
  • Prevent complications, such as fracture (through reducing weight bearing)
36
Q

FRACTURES: Specify classification systems of fractures based on causation, site, frature pattern and involvement of adjacent tissues

A

of the lateral malleolus- Weber’s classification according to whether below, involving or above the syndesmosis

Intracapsular NOF - Garden’s classification

in skeletally immature - Salter-Harris classification of physeal # according to whether the growth plate is involved

Elbow supracondylar # - Gartland classification (non-displaced, intact posterior cortex, completely displaced humerus)

Forearm #

  • Colles: Dorsal displacement of the distal fragment of the radius
  • Smiths: Ventral displacement of the distal fragment of the radius
  • Galleazzi: Fracture of the distal radius with dislocation of the radioulnar joint
  • Monteggia: Fracture of the proximal ulnar with dislocation of the radial head
    • A is proximal, Z is distal
37
Q

FRACTURES: Specify the risk factors for fracture and outline the mechanisms of primary and secondary fracture repair.

A
  • Osteoporosis
  • Pathological factures - malignancy, congenital disease
  • Bone cysts
38
Q

FRACTURES: Describe the relative prevalence, clinical features, classification, associations and complications, investigation, management, rehabilitation and outcome of common adult fractures including: Distal Radius fracture, Scaphoid fracture, Femoral neck fracture, Vertebral fracture, Tibial fracture, Ankle fracture

A
39
Q

MULTISYSTEM CONNECTIVE TISSUE DISEASE: Outline the clinical features, underlying pathology and outcomes of systemic lupus erythematosus (SLE) with respect to skin, MSK, renal, heart, lung and CNS involvement.

A

SLE: Autoimmune disease in which there is defective clearance of apoptotic cells, leading to antibodies against the material

Most common clinical features:

  • Relapsing-remitting symptoms
  • Malar rash
  • Arthralgia and myalgia - predominantly morning stiffness, swelling is unusual
  • Non-specific symptoms: Severe fatigue, malaise, fever, splenomegaly, weight loss, dry eyes and mouth, hair loss

Underlying pathology:

  • Autoantibodies: ANA, anti-dsDNA,
  • Possible precipitants include:
    • Viral infection (EBV)
    • Medications (chlorpromazine, methyldopa, hydralazine, isoniazid)
    • UV light
    • DR3 and DR2 HLA

Systemic effects:

Skin: Photosensitivity, malar rash, discoid lupus erythematous, livedo reticularis, alopecia, mouth ulcers, keratoconjunctivitis sicca (dry eyes)

MSK: Myalgia, arthralgia, Raynaud’s

Renal: Nephritis

Heart: Pericarditis, HTN, increased risk of CAD

Lungs: Pleurisy, fibrosing alveolitis, increased risk of PE (if have 2º APLS)

CNS: Stroke (if have 2º APLS)

40
Q

MULTISYSTEM CONNECTIVE TISSUE DISEASE: Outline the investigation and management of a patient presenting with SLE.

A

Investigation of suspected SLE

  • Bloods:
    • ESR
    • Autoantibodies: ANA, anti-dsDNA, anti-phospholipid
    • Complement levels
  • Urinalysis
  • Imaging to check for complications of SLE: CXR, renal USS, CT CAP, ECHO

Management of SLE

  • Conservative: Minimise sun exposure, wear sun protection, smoking cessation
  • Medical
    • Hydroxychloroquine
    • Adjuncts: NSAIDs, corticosteroids (+ methotrexate and folic acid)
41
Q

MULTISYSTEM CONNECTIVE TISSUE DISEASE: Define the antiphospholipid syndrome, describe its main presentations, and outline the investigation and management of this disorder

A

Antiphospholipid syndrome: A prothrombotic condition of venous and arterial vessels. Mechanism is not well known, speculation of activating of clotting by autoantibodies.

May be primary or may follow other connective tissue diseases, such as SLE, RA, systemic sclerosis, Behcet disease, GCA, Sjogren’s syndrome

Main presentation:

  • Recurrent miscarriage
    • 1 or more foetal death at > 10 weeks
    • Premature birth due to severe pre-eclampsia
  • VTE and arterial thrombosis
  • Chronic headaches
  • CRAO
  • Dementia (?vascular)
  • Seizures

Investigation:

  • Autoantibodies: Lupus anticoagulant and anticardiolipin (aCL) on 2 tests taken > 12/52 apart, anti-b2-glycoprotein
  • Bloods - thrombocytopenia, haemolytic anaemia
  • Clotting screen
  • CT scan or MRI (cerebrovascular accident, PE, Budd-Chiari syndrome)
  • Doppler for DVT
  • ESR ~, APTT increased, positive Coombs’ test

Management:

  • Conservative
    • ​Avoid smoking, regular exercise, avoid excessive alcohol intake
    • Management of CVD factors
  • Medical
    • ​Prophylactic treatment following VTE - warfarin or antiplatelet therapy
    • Aspirin in pregnancy and LMWH (to replace warfarin)
    • Monitor end organ damage
42
Q

MULTISYSTEM CONNECTIVE TISSUE DISEASE: Describe the clinical features, underlying pathology, and prognosis of diffuse systemic and limited systemic sclerosis.

A

Systemic sclerosis: An autoimmune inflammatory disease where perivascular fibrosis leads to ischaemic damage in tissues. Results in widespread fibrosis and vascular abnormalities. Skin sclerosis and Raynaud’s are the predominant features.

Limited (70%): Previously referred to as CREST (calcinosis, Raynaud phenomenon, oesophageal dysmotility, sclerodactyly, telangiectases)

Diffuse: Sclerodactyly (skin thickening of the fingers and toes), abnormal nail fold capillaries, internal organ fibrosis and/or vascular damage

Clinical features:

Limited:

  • Anti-centromere antibodies
  • Raynaud’s then skin tightening at extremities
  • Early symptoms: Constitutional symptoms, GORD, ulcers on digital tips secondary to Raynaud’s
  • Later symptoms: Oesophageal strictures, small bowel malabsorption, pulmonary fibrosis
  • CREST

Diffuse:

  • Anti-Scl-70 antibodies, RNA polymerase antibodies
  • Greater systemic symptoms (lethargy, weight loss, anorexia)
  • Short Hx of Raynaud’s amd skin sclerosis
  • Complications occuring within first 3 years: Myocardial, pulmonary and renal fibrosis

Underlying pathology:

  • Pro-thrombotic state

Prognosis:

  • Systemic sclerosis has the highest mortality of any of the autoimmune rheumatic diseases
43
Q

MULTISYSTEM CONNECTIVE TISSUE DISEASE: Describe the clinical features, underlying pathology and prognosis of Sjogren’s Syndrome and outline its investigation and management.

A

Sjogren’s syndrome: An autoimmune condition in which there is lymphocytic infiltration of exocrine glands (lactimal glands, salivary glands).

May be primary or secondary to other autoimmune conditions, such as RA, SLE and systemic sclerosis

Mx involves artificial tears and saliva.

Clinical features:

  • Xerostomia (dry mouth)
  • Xerophthalmia (dry eyes)
  • Enlargement of the parotid glands
  • Vaginal dryness
  • Investigation findings:
    • Schirmer tear test - defective tear production
    • RF raised
    • ANA raised
    • Anti-Ro/SSA positive (70%)
    • Anti-La/SSB positive (30%)

Underlying pathology:

Autoimmune condition directed against exocrine glands.

Investigation

  • Bloods: FBC, CRP/ESR
  • Tear test
  • Autoantibodies: ANA, RF, anti-Ro, anti-La

Management

  • Artificial tears and saliva
  • 1/6 develop Non-Hodgkin’s B cell lymphoma
44
Q

MULTISYSTEM CONNECTIVE TISSUE DISEASE: Describe the clinical features that require consideration of Idiopathic Inflammatory Myopathies (IIM: polymyositis, dermatomyositis, inclusion body myositis) and outline the investigation and management principles for IIM.

A

Idiopathic Inflammatory Myopathies (polymyositis, dermatomyositis, inclusion body myositis)

  • A group of disorders which describe moderate-severe proximal muscle weakness, due to inflammation of skeletal muscles
  • Common develops in adults between 4-50 years of age
  • May be associated with dysphagia, fatigue, difficulties with breathing, and skin lesions.
  • Associated with ILD and myocarditis
  • Gottron’s papules and heliotrope rash on the eyelids

​Investigation

  • Serum muscle derived enzymes
    • ​Elevated CK
    • Aldolase
    • Myoglobin (sensitive for evaluating the integrity of the muscles)
  • Electromyography
  • ​Muscle biopsy
  • ESR (can be normal in ~ 50% of patients)

Management

  • The main objectives of treatment are to improve muscle strength
  • Conservative:
    • ​Physiotherapy and aerobic exercise to reduce muscle wasting
    • Low-sodium, low-carbohydrate, high-protein diet and counselled to prevent excessive weight gain.
  • Medical:
    • ​Oral corticosteroids or IV (if severe weakness or life threatening complications)
    • 2nd line: IV Igs, methotrexate, azathioprine
  • Surgical: -​
45
Q

MULTISYSTEM CONNECTIVE TISSUE DISEASE: Auto antibodies associated with conditions

A
46
Q

MULTISYSTEM CONNECTIVE TISSUE DISEASE: Describe the clinical features, investigation and management of Polymyalgia Rheumatica and Giant Cell Arteritis.

A

Polymyalgia Rheumatica

Clinical Features:

  • Difficulty rising from a seated position
  • Pain and morning stiffnes in the neck, around the shoulder and pelvic girdle
  • +/- oligoarthritis
  • Constitutional symptoms: Fever, malaise, anorexia, weight loss

Investigation:

  • ESR (elevated)
  • CRP (elevated)
  • FBC
  • Ultrasound (trochanteric bursitis)

Management:

  • Steroids (prednisolone, with gradual tapering of dose to lowest possible)
    • ​Most patients should experience resolution within 1 year
    • +/- NSAIDs
  • Calcium, Vitamin D and bisphosphonates should also be provided for bone protection
  • 2nd line: Methotrexate

Giant Cell Arteritis (vasculitis)

Clinical Features

  • Unilateral temporal headache
  • Tenderness over the scalp that is precipitated by combing the hair and mastication
  • Painless loss of vision (amaurix fugax or total)
  • Polymyalgia Rheumatica symptoms (neck/shoulder/pelvic girdle pain, stiffness after inactivity)

Investigation

  • Bloods: ESR, CRP, FBC, LFTs
  • Temporal artery ultrasound (shows narrowing - ‘halo sign’)
  • Temporal artery biopsy
  • Ophthalmology review

Management

  • Prednisolone for 4/52, with tapering over 6-12 months
  • Methylprednisolone if there is optical involvement
47
Q

MULTISYSTEM CONNECTIVE TISSUE DISEASE: Describe the clinical features that require consideration of systemic vasculitis and outline the investigation and management principles for systemic vasculitis.

A

Clinical features of systemic vasculitis:

  • Signs and symptoms of chronic inflammation (autoimmune mediated)
  • Constitutional symptoms: Fatigue, anorexia, fever, myalgia, arthralgia

Investigation

  • CRP
  • ESR
  • ANCA (c = GPA, p = eosinophilic granulomatosis with polyangiitis)
  • Serum urea and creatinine, urinalysis - small vessel vasculitis is associated with renal dysfuction
  • Biopsy

​Management

  • Corticosteroids
  • Bone protective agents (vitamin D, calcium, bisphosphonates)

CP3 (14 decks)

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