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MSK Flashcards

Don't you wanna come with me? Don't you wanna feel my boneson your bones? It's only natural

1
Q

What are the X-ray changes in OA?

A

LOSS

Loss of joint space
Osteophytes
Subarticular sclerosis
Subchondral cysts

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2
Q

What are some hand signs of OA?

A

Heberden’s nodes (DIP)
Bouchard’s nodes (PIP)
Squaring at the base of the thumb (CMC)
Weak grip
Reduced range of motion

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3
Q

How can OA be diagnosed clinically according to NICE guidelines?

A

The NICE guidelines (2022) suggest that a diagnosis can be made without any investigations if the patient is over 45, has typical pain associated with activity and has no morning stiffness (or stiffness lasting under 30 minutes).

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4
Q

Management for OA

A
  1. Non-pharm: exercise, weight loss, OT
  2. Pharm: topical NSAIDs, then oral NSAIDs
    :::::::::::::weak opiates and paracetamol only for short-term, strong opiates not recommended::::::::::::::
  3. Intra-articular steroid injections may temporarily improve symptoms
  4. Joint replacement
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5
Q

What is the most common associated gene with RA?

A

HLA DR4

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6
Q

What antibodies are associated with RA? What are the sensitivities?

A

RF and anti-CCP (anti-cyclic citrullinated peptide)

RF present in 70% of RA pts
anti-CCP present in 80% of RA pts, more sensitive and specific

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7
Q

What are the hand signs in RA?

A

Z-shaped deformity to the thumb
Swan neck deformity (hyperextended PIP and flexed DIP)
Boutonniere deformity (hyperextended DIP and flexed PIP)
Ulnar deviation of the fingers at the MCP joints

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8
Q

How can RA affect the cervical spine?

A

Atlantoaxial subluxation => SCC (emergency)
risk of this during GA and intubation

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9
Q

What are some extra-articular manifestations of RA?

A

Pulmonary fibrosis
Felty’s syndrome (a triad of rheumatoid arthritis, neutropenia and splenomegaly)
Sjögren’s syndrome (with dry eyes and dry mouth)
Anaemia of chronic disease
Cardiovascular disease
Eye manifestations:
:::::::::Dry eye syndrome (keratoconjunctivitis sicca)
Episcleritis
Scleritis
Keratitis
Cataracts (secondary to steroids)
Retinopathy (secondary to hydroxychloroquine):::::::::::::::
Rheumatoid nodules (firm, painless lumps under the skin, typically on the elbows and fingers)
Lymphadenopathy
Carpel tunnel syndrome
Amyloidosis
Bronchiolitis obliterans (small airway destruction and airflow obstruction in the lungs)
Caplan syndrome (pulmonary nodules in patients with rheumatoid arthritis exposed to coal, silica or asbestos dust)

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10
Q

How is RA diagnosed?

A

urgent rheum referral (within 3w) for persistent synovitis
Bloods:
- RF
- anti-CCP Ab’s
- inflam markers: CRP, ESR
- X-rays of hands and feet
- USS/MRI to detect synovitis

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11
Q

What are the X-ray findings in RA?

A

LESS
Loss of joint space
Erosions
Soft tissue swellings
Soft bones (periarticular osteopenia)

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12
Q

What are some scoring systems for RA?

A

Health Assessment Questionnaire (HAQ) - functional ability

Disease Activity Score 28 Joints (DAS28) - monitor disease activity and response to treatment

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13
Q

What is the management of RA and how do you monitor response to treatment?

A

Short-term steroids while initiating treatment and during flares

conventional disease-modifying anti-rheumatic drugs (cDMARDs) and biologic DMARDs e.g.
1. monotherapy: methotrexate, leflunomide or sulfasalazine
2. combination treatment with multiple cDMARDs
3. biologic therapies alongside methotrexate

hydroxychloroquine - in mild disease, mildest DMARD, safe in pregnancy

cDMARDs - azathioprine, ciclosporin, cyclophosphamide, mycophenolate

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14
Q

What DMARDs are safe in pregnancy?

A

Hydroxychloroquine - mildest DMARD

Sulfasalazine - needs extra folic acid

Methotrexate and leflunomides are VERY BAD AND TERATOGENIC!!!

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15
Q

What are some different biologic therapies for RA?

A

Tumour necrosis factor (TNF) inhibitors (e.g., adalimumab, infliximab, etanercept, golimumab and certolizumab)

Anti-CD20 on B cells (e.g., rituximab)

Anti-interleukin-6 inhibitors (e.g., sarilumab and tocilizumab)

JAK inhibitors (e.g., upadacitinib, tofacitinib and baricitinib)

T-cell co-stimulation inhibitors (e.g., abatacept)

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16
Q

Which autoantibody is most associated with SLE? How do they function?

A

anti-nuclear antibodies (ANA) - positive in 85% of pts
autoantibodies against protein within cell nucleus
generate chronic inflammatory response

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17
Q

Name some associated symptoms/signs of SLE

A

Photosensitive malar rash “butterfly” shape

Arthralgia (joint pain), Non-erosive arthritis
Myalgia (muscle pain)

Fatigue, Weight loss, Fever
Shortness of breath, Pleuritic chest pain

Lymphadenopathy, Splenomegaly

Mouth ulcers
Hair loss
Raynaud’s phenomenon
Oedema (due to nephritis)

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18
Q

What lab findings are seen in SLE?

A

Autoantibodies - ANA in 85% of pts
anti-dsDNA (anti-double stranded DNA) - highly specific to SLE
anti-Sm, anti-centromere, anti-Ro, anti-La, anti-Scl-70, anti-Jo-1

FBC:
::::::::: anaemia of chronic disease, low WCC, low plt

Chem: CRP and ESR may be raised

C3 and C4 (reminder: compliment cascade in immune response, low levels indicate autoimmune disease)

Urinalysis: urine Pr:Cr shows proteinuria and lupus nephritis

Renal biopsy: lupus nephritis

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19
Q

What autoantibodies can be present in SLE?

A

⭐⭐anti-nuclear antibodies (ANA) - positive in 85% of pts

⭐Anti-double stranded DNA (anti-dsDNA) antibodies - highly specific, can be used to monitor disease activity

  • Anti-Sm (highly specific to SLE but not very sensitive)
  • Anti-centromere antibodies (most associated with limited cutaneous systemic sclerosis)
  • Anti-Ro and anti-La (most associated with Sjögren’s syndrome)
  • Anti-Scl-70 (most associated with systemic sclerosis)
  • Anti-Jo-1 (most associated with dermatomyositis)
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20
Q

What can be used as diagnostic criteria for SLE?

A

European League Against Rheumatism (EULAR) / American College of Rheumatology (ACR) criteria (2019)

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21
Q

What are some complications of SLE?

A
  • Cardiovascular disease - leading cause of death
  • Infection
  • Anaemia - anaemia of chronic disease, autoimmune haemolytic anaemia, bone marrow suppression by medications or kidney disease
  • Pericarditis
  • Pleuritis
  • Interstitial lung disease => pulmonary fibrosis
  • Lupus nephritis
  • Neuropsychiatric SLE - optic neuritis, transverse myelitis, psychosis
  • Recurrent miscarriage, IUGR, pre-eclampsia, pre-term labour
  • VTE (assoc w antiphospholipid syndrome)
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22
Q

What is the management of SLE?

A

1st line:
::::::::: hydroxychloroquine ⭐
NSAIDS
steroids e.g. pred

2nd line:
::::::::::::DMARDs e.g. methotrexate, mycophenolate mofetil, cyclophosphamide
:::::::::::::Biologics - rituximab (targets CD20 protein on the surface of B cells), belimumab (targets B-cell activating factor)

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23
Q

What biologics can be used in SLE and what do they target?

A

rituximab (targets CD20 protein on the surface of B cells)

belimumab (targets B-cell activating factor)

24
Q

Which genetic factors are most associated with SLE?

A

major histocompatibility complex (MHC) region, notably HLA-DR2 and HLA-DR

25
Q

What is the pathophysiology of gout?

A

crystal arthropathy
high blood uric acid
urate crystals deposited in joint

26
Q

What is a critical differential for gout?

A

Septic arthritis

27
Q

What investigations and findings are found in gout?

A

Bloods: high serum uric acid

Joint aspiration - monosodium urate crystals, needle-shaped 🪡 negatively birefringent of polarised light 🌈 and NO bacterial growth

X-ray;
- Maintained joint space (no loss of joint space)
- Lytic lesions in the bone
- Punched out erosions
- Erosions can have sclerotic borders with overhanding edges

28
Q

What is the finding on joint aspiration in pseudogout?

A

calcium pyrophosphate crystals of pseudogout are rhomboid-shaped and➕ positively birefringent.

29
Q

What are the X-ray findings in gout?

A

Maintained joint space (no loss of joint space)
Lytic lesions in the bone
Punched out erosions
Erosions can have sclerotic borders with overhanding edges

30
Q

What is the management of gout? Prophylaxis?

A

Acute flares: NSAIDs e.g. naproxen +PPI
2nd line - colchicine (renal impairment or sig heart disease)
3rd line - oral steroids e.g. pred

Prophylaxis - xanthine oxidase inhibitors
::: allopurinol ::: febuxostat :::

31
Q

Which signs may indicate cervical myelopathy in patients with neck pain?

A

Paresis, sensory changes, altered muscle tone, clumsy or weak hands, gait disturbance, Babinski’s sign, Hoffman’s sign, Lhermitte’s sign, profound hand weakness, bowel or bladder dysfunction, and severe gait ataxia.

32
Q

What is Babinski’s sign?

A

up-going plantar reflex, hyper-reflexia, clonus, spasticity.

33
Q

What is Hoffman’s sign

A

involuntary flexion and adduction of the thumb and flexion of the index finger when the nail of the middle finger is flicked downwards. (Not reliable in isolation as may be present normally).

34
Q

What is Lhermitte’s sign?

A

flexion of the neck causes an electric shock-type sensation that radiates down the spine and into the limbs.

35
Q

What are the main causes of neck pain?

A

Muscle or ligament strain, torticollis, whiplash, and cervical spondylosis.

36
Q

What are the main causes of sciatica?

A

Herniated disc, spondylolisthesis, and spinal stenosis.

37
Q

What is a red flag for cauda equina syndrome in a patient with sciatica?

A

Bilateral sciatica.

38
Q

What cancers commonly metastasise to the bones, potentially causing back pain?

A

Prostate, Renal, Thyroid, Breast, and Lung (PoRTaBLe mnemonic)

39
Q

What tool is used to stratify the risk of a patient with acute back pain developing chronic back pain?

A

The STarT Back Screening Tool.

40
Q

What medications should be avoided in the treatment of non-specific low back pain according to NICE guidelines?

A

Opioids, antidepressants, amitriptyline, gabapentin, and pregabalin.

41
Q

What medications are NOT recommended for sciatica according to NICE guidelines?

A

Gabapentin, pregabalin, diazepam, oral corticosteroids, and opioids for chronic sciatica.

42
Q

What specialist treatments may be considered for chronic sciatica?

A

Epidural corticosteroid injections, local anaesthetic injections, and radiofrequency denervation.

43
Q

Where does the cauda equina begin in the spinal column?

A

The cauda equina begins after the spinal cord terminates at the conus medullaris around L2/L3.

44
Q

What functions do the nerves of the cauda equina supply?

A
  • Sensation to the lower limbs, perineum, bladder, and rectum
  • Motor innervation to the lower limbs and sphincters
  • Parasympathetic innervation of the bladder and rectum
45
Q

What is the most common cause of cauda equina syndrome? Name three other causes of cauda equina syndrome

A

Herniated disc.

Tumours (especially metastasis)
Spondylolisthesis
Abscesses or infection
Trauma

46
Q

What are the key red flags for cauda equina syndrome?

A

Saddle anaesthesia
Urinary retention or incontinence
Faecal incontinence
Bilateral sciatica
Severe motor weakness in the legs
Reduced anal tone on PR examination

47
Q

What are the sensory and motor symptoms of CES?

A

Sensory: Numbness in the perineum, bladder, or rectum.

Motor: Weakness or paralysis in the legs, loss of control over bladder and bowel function.

48
Q

What is the initial management of suspected cauda equina syndrome?

A

Immediate hospital admission
Emergency MRI scan to confirm diagnosis
Neurosurgical input for potential lumbar decompression surgery

49
Q

What are the possible outcomes even after surgery for cauda equina syndrome?

A

Even with early surgery, patients may have persistent issues like bladder, bowel, or sexual dysfunction, as well as leg weakness and sensory impairment.

50
Q

How does metastatic spinal cord compression (MSCC) differ from cauda equina syndrome?

A

MSCC involves compression of the spinal cord higher up than CES, leading to upper motor neuron signs like increased tone, brisk reflexes, and upgoing plantar responses, while CES causes lower motor neuron signs (reduced tone, reduced reflexes).

51
Q

What are common treatments for metastatic spinal cord compression (MSCC)?

A

High-dose dexamethasone
Analgesia
Surgery, radiotherapy, or chemotherapy depending on individual factors.

52
Q

What is spinal stenosis?

A

The narrowing of part of the spinal canal, leading to compression of the spinal cord or nerve roots, typically affecting the cervical or lumbar spine.

53
Q

What are the possible causes of spinal stenosis?

A

Congenital spinal stenosis
Degenerative changes (facet joint changes, disc disease, bone spurs)
Herniated discs
Thickening of ligamenta flava or posterior longitudinal ligament
Spinal fractures
Spondylolisthesis
Tumours

54
Q

What are the key symptoms of intermittent neurogenic claudication, associated with lumbar spinal stenosis?

A

Lower back pain
Buttock and leg pain
Leg weakness

55
Q
A

MSRA (16 decks)

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