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MSK Flashcards

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
Q

Natural history of ankylosing spondylitis

A

Spinal enthesitis
->
Bridging syndesmophytes
(new bone growth between adjacent vertebra)
->
Spinal fusion

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26
Q

Management of Ankylosing spondylitis

A

Physiotherapy and a lifelong exercise program
Pharmacological - NSAIDS
Biologics - Therapeutic monoclonal antibodies : Anti TNF- alpha, ANti IL17
e.g adalimumab
MAB

27
Q

How can you categorise inflammatory arthritis?

A
  1. Primary or Secondary Inflammation
  2. Sterile or Non-sterile
28
Q

What 5 broad categories can we used to distinguish between different arthritis before imaging?

A
  1. Inflammation
  2. Speed of onset
  3. Synovial flluid analysis
  4. CRP
  5. WCC
29
Q

Osteoarthritis
1. Inflammation
2. Speed of onset
3. Synovial flluid analysis
4. CRP
5. WCC

A
  1. Non or little
  2. Slow
  3. No inflammatory cells, Sterile
  4. Normal
  5. Normal
30
Q

Immune mediated arthritis
1. Inflammation
2. Speed of onset
3. Synovial flluid analysis
4. CRP
5. WCC

A
  1. Yes
  2. Subacute
  3. Inflammatory cells, sterile
  4. Slightly high
  5. Normal ( usually)
31
Q

Crystal arthritis
1. Inflammation
2. Speed of onset
3. Synovial flluid analysis
4. CRP
5. WCC

A
  1. Yes
  2. Rapid
  3. Inflammatory cells, Sterile, Crystals
  4. High or very high
  5. Normal ( usually)
32
Q

Septic arthritis
1. Inflammation
2. Speed of onset
3. Synovial flluid analysis
4. CRP
5. WCC

A
  1. Yes
  2. Rapid
  3. Inflammatory cells, bacteria
  4. Very high
  5. High
33
Q

Rheumatoid arthritis overview
1. What synovium are involved?
2. What is the sex bias shown?
3. Usual age of onset
4. Key features

A
  1. PIP, Extensor tenosynovitis, olecranon bursa
  2. Female
  3. 30 -50s
  4. Prolonged morning stiffness, polyarthritis, symmetrical, pain, swelling, —-> joint erosions
34
Q

What environmental factors influence onset of RA?

A

Smoking, Microbiome, Porphyromonas gingivalis, poor oral health

35
Q

What is the strongest genetic factor in RA?

A

HLA - DR

36
Q

What is the implication of HLA genetic association?

A

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
Q

What joints are involved in RA?

A

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
Q

RA extra articular features

A

Fatigue, Fever, Weight Loss, Lung disease, Vasculitis, Amyloidosis, Episcleritis

39
Q

What is felty’s syndrome?

A

Triad of splenomegaly, leukopenia and rheumatoid arthritis

40
Q

What histiopathological changes occur in rheumatoid arthritis?

A
  1. Neovascularisation
  2. Lymphangiogenesis
  3. Inflammatory cells:
    activated B and T cells
    plasma cells
    mast cells
    activated macrophages
41
Q

What is pannus

A

A proliferated mass of tissue - RA

42
Q

What cellular players are involved in RA ?

A

Auto reactive B ( rituximab) & T cells (Abatacept)
TNF - alpha & IL6
(anti-TNKa, anti-IL6r)

43
Q

What influence does TNFa have in RA pathologenesis?

A

Inflammatoy cell recruitment , Angiogenesis, Lymphanogiogenesis –> Pannus formation

Matric metalloproteases –> Cartillage loss

Osteoclast activation –> Bone loss , erosions and osteopenia

44
Q

Rheumatoid arthritis investigations

A

Bloods - Increased ESR, Increased CRP
Sometimes normocytic anaemia, increased platelet count

Autoantibodies - Rheumatoid factor
Anti CCP autoantibodies (associated with more aggresive disease)

45
Q

Rheumatoid arthritis imaging

A

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
Q

Rheumatoid arthritis management

A

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
Q

How is ‘treat to manage’ implemented in RA?

A

DAS28 = composite of

no. of tender joints,

no. of swollen joints,

patient visual analogue score (VAS),

ESR (or CRP)

48
Q

Biological therapies involved in RA management

A

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
Q

What is a-ccp and which arthritis is it involved in>?

A

anti-cyclic citrullinated peptide (anti-CCP)

RA

50
Q

Psoriatic arthritis:
Presentation
RF featured or not?
Predominent ILs

Skin

A

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
Q

Reactive arthritis:
Description

Common infections

Extra articular manifestations

A

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
Q

Key features of autoimmune connective tissue disorders

A

Arthralgia and arthritis is typically non-erosive (unlike rheumatoid)

Serum autoantibodies are characteristic

Raynaud’s phenomenon

53
Q

SLE clinical features

A

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
Q

Autoantibodies and testing in SLE

A

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
Q

Main autoantivodies in SLE and what it correlates to

A

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
Q

SLE - immunopathogenesis

A

Overactivity of type 1 interferon pathway
Complement pathway abnormalities
Autoreactive B and T cells

57
Q

SLE – the ‘waste disposal hypothesis’

A

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
Q

SLE investigations

A

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
Q

SLE – measuring disease activity

A

Unwell Patient with active lupus typically has:

Low complement C3 and C4 levels

High anti-dsDNA antibodies

60
Q

SLE - management: Steroids risks

A

Infection

Osteoporosis

Avascular necrosis (AVN) - often affects hips: higher incidence in lupus, especially in presence of APL Abs

61
Q

SLE - management

A

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
Q

Drug considerations SLE Pregnancy

A

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
Q

What are the names of the nodes present in OA?

A

Heberden’s nodes (at the DIPJs) and Bouchard’s nodes (at the PIPJs)

BRS missed out (10 decks)

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