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MSK Flashcards

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1
Q

In what ways do child bones differ from adult bones and how?

A

Elasticity - increased haversion canals
Physis
Length/ Speed of healing
remodelling

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2
Q

how is hip dysplasia examined?

A

Rotation : Hip abductiont ends to be limited
Orientol and Bowlow’s test (Non specicific > 3 months)
Leg length (Galeazzi)

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3
Q

How is hip dysplasia investigated?

A

US < 4 months - measures level of acetabular dysplasia and position of hip
X ray > 4 months

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4
Q

How is Congenital Talipes Equinovarus caused?

A

PITX1 gene

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5
Q

What does CAVE in Congenital Talipes Equinovarus represent?

A

Caveous - arch of foot
Adduct - adduction of foot
Verous - plantar (tendoachilles tight)
Equinous- base of foot towards midline (tendoachilles tight)

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6
Q

How do you treat Clubs foot?

A

Series of casts
Foot orthosis brace
Surgery if needed for final reformation

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7
Q

What causes achondroplasia?

A

Dominant disorder
G380 - FGFR

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8
Q

What is decreased in osteogenesis imperfecta and in what way?

A

Decreased Type I collagen due to either:

  • Decreased secretion (quantity of collagen)
  • Production of abnormal collagen (quality of collagen)
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9
Q

What is mechanical back pain vs neurological back pain?

A

Mechanical - Back pain as a result of abnormal stress on the vertebral column
Neurological - Back pain radiating down to the lower limbs +/- neuroplegic symptoms

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10
Q

Which parts of the spine shows kyphosis and which shows lordosis?

A

Kyphosis - Cervical and Thoracic
Lordosis - Lumbar

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11
Q

Mechanical back pain:
1. Does movement make it better or worse?
2. Does rest make it better or worse?
3. What are the common causes?
4. What neurological issue could it happen with?

A
  1. Worse
  2. Better / No issue at all
  3. Degenerative disc disease
    Osteoarthritis of the facet joints
    Muscle sprain
    Muscular tension
  4. Sciatica
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12
Q

Sciatica:
1. Features
2. Most common cause
3. How to predict location of pain

A
  1. Unilateral lower limb pain that is worse than lower back pain, may be accompanied by parasthesisa
  2. Slipped disc ( disk herniation)
  3. Dermatomes
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13
Q

Back pain more serious causes

A

Infection
Inflammatory spondyloarthropathy
Fracture
Large disc prolapse
Tumour

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14
Q

What is associated with inflammatory spondyloarthropathy

A

ankylosing spondylitis, psoriatic arthritis, inflammatory bowel disease (IBD)-associated

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15
Q

Red flag symptoms of back pain

A

Fever/ Night Sweats
Pain at night or increased pain when supine
Parasthesia or leg weakness
Constant or progressive pain
Thoracic pain
Immunosuppressed
Age <20 or >55 yrs
Weight loss
Previous malignancy
Bowel incontinence
Urinary incontinence

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16
Q

Cauda Equina Syndrome:
1.Symptoms
2.Investigation
3.Causes
4.Treatment

A
  1. Bowel/Bladder incontinence
    Saddle paraesthesia
    Back pain
    Radicular leg pain
    Weak Anal tone PR
    Absent ankle jerk reflex
  2. Urgent MRI L spine
  3. Myeloma, Large disc herniation, bony mets, TB, Abscess
  4. Depending on cause, may require surgery
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17
Q

Examination of Spine

A

Look

Feel

Move

Straight leg raise (SLR) - recreates pain for patients with sciatica

Lower limb neurological exam

General exam (signs of malignancy, AAA)

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18
Q

Treatment for non red flag leg pain

A

Time
NSAIDS
Keep moving
Physiotherapy - Soft tissue work, corrective exercise

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19
Q

What blood test results would you expect for the following conditions:
1. Myeloma
2. Chronic inflammation
3. TB
4. Chronic disease
5. Infection
6. Bony Metasteses

A
  1. Increased LDH, Anaemia, raised ESR, raised calcium
  2. Raised CRP, Anaemia, Raised ESR
  3. Raised ESR
    4.Anaemia
  4. Raised WCC, Raised CRP
  5. increased ALP, raised calcium, raised PSA
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20
Q

MRI findings TB

A

L4/5 endplate destruction. Soft tissue mass encroaching spinal canal
altered signal in sacral segments

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21
Q

Management of Herniated disc

A

. Conservative as for LBP without sciatica

-Analgesia especially NSAIDs
-Physiotherapy to improve core strength and treat associated muscle spasm
2. Nerve root injection (local anaesthetic and glucocorticoid)
3. Surgery if neurological compromise or symptoms persist

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22
Q

Ankylosing Spondylitis:
1. Primary inflammation of which joints?
2. extra articular manifestations

A
  1. spine, sacroiliac joints
  2. Anterior uveitis (iritis) – ocular inflammation
    Apical lung fibrosis
    Aortitis/aortic regurgitation
    Amyloidosis – due to chronically serum amyloid A (SAA) depositing in organs
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23
Q

Ankylosing spondylitis pathophysiology

A
  1. Characterised by enthesitis
  2. HLA-B27 is the strongest genetic risk factor
  3. Cytokines play important roles in pathogenesis

tumour necrosis factor alpha (TNF-alpha)

interleukin-17 (IL-17)

interleukin-23 (IL23)

  1. Aberrant peptide processing pathways
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24
Q

Imaging of ankylosing spondylitis

A

early MRI - shiny corners on spine
X- rays normally used

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25
Natural history of ankylosing spondylitis
Spinal enthesitis -> Bridging syndesmophytes (new bone growth between adjacent vertebra) -> Spinal fusion
26
Management of Ankylosing spondylitis
Physiotherapy and a lifelong exercise program Pharmacological - NSAIDS Biologics - Therapeutic monoclonal antibodies : Anti TNF- alpha, ANti IL17 e.g adalimumab *MAB*
27
How can you categorise inflammatory arthritis?
1. Primary or Secondary Inflammation 2. Sterile or Non-sterile
28
What 5 broad categories can we used to distinguish between different arthritis before imaging?
1. Inflammation 2. Speed of onset 3. Synovial flluid analysis 4. CRP 5. WCC
29
Osteoarthritis 1. Inflammation 2. Speed of onset 3. Synovial flluid analysis 4. CRP 5. WCC
1. Non or little 2. Slow 3. No inflammatory cells, Sterile 4. Normal 5. Normal
30
Immune mediated arthritis 1. Inflammation 2. Speed of onset 3. Synovial flluid analysis 4. CRP 5. WCC
1. Yes 2. Subacute 3. Inflammatory cells, sterile 4. Slightly high 5. Normal ( usually)
31
Crystal arthritis 1. Inflammation 2. Speed of onset 3. Synovial flluid analysis 4. CRP 5. WCC
1. Yes 2. Rapid 3. Inflammatory cells, Sterile, Crystals 4. High or very high 5. Normal ( usually)
32
Septic arthritis 1. Inflammation 2. Speed of onset 3. Synovial flluid analysis 4. CRP 5. WCC
1. Yes 2. Rapid 3. Inflammatory cells, bacteria 4. Very high 5. High
33
Rheumatoid arthritis overview 1. What synovium are involved? 2. What is the sex bias shown? 3. Usual age of onset 4. Key features
1. PIP, Extensor tenosynovitis, olecranon bursa 2. Female 3. 30 -50s 4. Prolonged morning stiffness, polyarthritis, symmetrical, pain, swelling, ----> joint erosions
34
What environmental factors influence onset of RA?
Smoking, Microbiome, Porphyromonas gingivalis, poor oral health
35
What is the strongest genetic factor in RA?
HLA - DR
36
What is the implication of HLA genetic association?
HLA class 1= A, B, C Present on all cells Present to CD8 T cells HLA class 2 = D Only expressed on APCs Present to CD4 T cells Therefore B cells Therefore autoantibodies
37
What joints are involved in RA?
MCP PIP Wrists Knees Ankles MTP Make sure you check for rheumatoid nodule at the ulnar border of forearm - invariably associated with rheumatoid factor Swan neck deformity - hyperextension of PIPJ, hyperflexion of DIPJ
38
RA extra articular features
Fatigue, Fever, Weight Loss, Lung disease, Vasculitis, Amyloidosis, Episcleritis
39
What is felty's syndrome?
Triad of splenomegaly, leukopenia and rheumatoid arthritis
40
What histiopathological changes occur in rheumatoid arthritis?
1. Neovascularisation 2. Lymphangiogenesis 3. Inflammatory cells: activated B and T cells plasma cells mast cells activated macrophages
41
What is pannus
A proliferated mass of tissue - RA
42
What cellular players are involved in RA ?
Auto reactive B ( rituximab) & T cells (Abatacept) TNF - alpha & IL6 (anti-TNKa, anti-IL6r)
43
What influence does TNFa have in RA pathologenesis?
Inflammatoy cell recruitment , Angiogenesis, Lymphanogiogenesis --> Pannus formation Matric metalloproteases --> Cartillage loss Osteoclast activation --> Bone loss , erosions and osteopenia
44
Rheumatoid arthritis investigations
Bloods - Increased ESR, Increased CRP Sometimes normocytic anaemia, increased platelet count Autoantibodies - Rheumatoid factor Anti CCP autoantibodies (associated with more aggresive disease)
45
Rheumatoid arthritis imaging
X rays: Soft tissue swelling, peri- articular osteopenia, bony erosions Ultrasound: Synovial thickening, increased blood flow, may detect micro erosions MRI but expensive and time consuming
46
Rheumatoid arthritis management
First line: DMARD therapy ( disease modifying anti rheymatic drugs) Methotrexate + Hydroxychloroquine +/- Sulfasalazine PLUS IM or short course oral steroids Second line: Biological therapies; anti TNF alpha blockade
47
How is 'treat to manage' implemented in RA?
DAS28 = composite of no. of tender joints, no. of swollen joints, patient visual analogue score (VAS), ESR (or CRP)
48
Biological therapies involved in RA management
Inhibition of tumour necrosis factor-alpha (‘anti-TNF’) Inhibition of interleukin-6 (IL-6) signalling B cell depletion Rituximab – antibody against the B cell antigen, CD20 Blocking T cell co-stimulation Abatacept - fusion protein - extracellular domain of CTLA-4 linked to modified Fc portion of human immunoglobulin G1
49
What is a-ccp and which arthritis is it involved in>?
anti-cyclic citrullinated peptide (anti-CCP) RA
50
Psoriatic arthritis: Presentation RF featured or not? Predominent ILs Skin
Scaly red plaques on extensor surfaces, Classically asymmetrical arthritis affecting IPJs -Enthesitis (inflammation of tendon insertions) rheumatoid factors are not present (“seronegative”) pathogenic pathway is interleukin-17/interleukin-23 (IL17-IL23) Psoriasis but may only present as nail pitting
51
Reactive arthritis: Description Common infections Extra articular manifestations
Sterile inflammation in joints following infection elsewhere in the body urogenital (e.g. Chlamydia trachomatis) gastrointestinal (e.g. Salmonella, Shigella, Campylobacter infections) Enthesitis (tendon inflammation) Skin inflammation Eye inflammation Symptoms follow 1-4 weeks after infection genetic predisposition (e.g. HLA-B27)
52
Key features of autoimmune connective tissue disorders
Arthralgia and arthritis is typically non-erosive (unlike rheumatoid) Serum autoantibodies are characteristic Raynaud’s phenomenon
53
SLE clinical features
Arthritis and deformity of fingers, Including swan neck deformity. X-rays showed no bony erosions i.e. deformity due to soft tissue damage Typical onset between 15 – 45 years F:M ~9:1 Prevalence and severity varies by ancestry African > Asian > White European
54
Autoantibodies and testing in SLE
A hallmark of SLE is the presence of ANA Found in all SLE patients Negative ANA effectively rules out SLE Anti-ds-DNA antibodies Anti-Ro Anti-La Anti-Smith (Sm) Anti-RNP antibodies directed to phospholipids on cell membrane APL are associated with ↑ risk of: 1) Thrombosis arterial (e.g. stroke) venous (e.g. deep vein thrombosis, DVT) 2) Pregnancy loss (miscarriage) Persistent presence of APL + a clinical event = “anti-phospholipid antibody syndrome”
55
Main autoantivodies in SLE and what it correlates to
ANA - present in SLE but not diagnostic Anti SM- specific but doesn't show severity Anti ds- DNA specific and shows severity APL - shows increased risk for thrombolitic activity in SLE but also primary disorder Anti Ro, Anti La - Secondary Sjögren’s syndrome Neonatal lupus syndrome (transient rash in neonate, permanent heart block)
56
SLE - immunopathogenesis
Overactivity of type 1 interferon pathway Complement pathway abnormalities Autoreactive B and T cells
57
SLE – the ‘waste disposal hypothesis’
Apoptosis leads to translocation of nuclear antigens to membrane surface Impaired clearance of apoptotic cells results in enhanced presentation of nuclear antigens to immune cells B cell autoimmunity Tissue damage by antibody effector mechanisms e.g. complement activation and Fc receptor engagement
58
SLE investigations
high ESR but usually normal C-reactive protein very important to measure urine protein (urinalysis + quantify with urine protein:creatinine ratio [uPCR]) Creatinine (part of “U&E”, measure of renal function) look at albumin Kidney biopsy if persistent proteinuria Immunological
59
SLE – measuring disease activity
Unwell Patient with active lupus typically has: Low complement C3 and C4 levels High anti-dsDNA antibodies
60
SLE - management: Steroids risks
Infection Osteoporosis Avascular necrosis (AVN) - often affects hips: higher incidence in lupus, especially in presence of APL Abs
61
SLE - management
FLM: Hydroxychloroquine Steroids for acute flare Mycophenolate +/- rituximab usually used for renal disease B cell targeted therapies Rituximab = anti-CD20 monoclonal antibody: depletes B cells Belimumab = anti-BAFF antibody SLE + APL - anticoagulation (warfarin)
62
Drug considerations SLE Pregnancy
Hydroxychloroquine, azathioprine, low molecular weight heparin (LMWH) safe 1) Antiphospholipid antibodies associated with miscarriage. Can reduce risk with aspirin or heparin 2) Pregnancy increases haemodynamic demands – will worsen renal dysfunction 3) Ro antibodies: can cause fetal heartblock
63
What are the names of the nodes present in OA?
Heberden’s nodes (at the DIPJs) and Bouchard’s nodes (at the PIPJs)

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