Musculoskeletal Flashcards

1
Q

Describe the organic and inorganic structure of bone.

A

Inorganic (65%) mainly calcium hydroxyapatite. Contains 99% of the body’s calcium, 85% of its phosphorus, 65% of its sodium.
Organic (35%) is made up of cells and protein matrix (type 1 collagen).

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2
Q

Describe osteocytes

A

Osteocytes lie within lacunae and form a mechanosensory network (osteocyte canaliculi network) embedded in mature bone through cytoplasmic extensions which allow metabolic exchange. They never divide.
Osteocytes maintain the bone matrix and are involved in repair.
If a bone is damaged, osteocytes are freed from their lacunae and differentiate into osteoblasts or osteoprogenitor cells.

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3
Q

What are the 5 different classes of anatomical bones?

A

Flat, long, short/cuboid, irregular, sesamoid.

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4
Q

Contrast compact (cortical) and cancellous bones.

A

Cortical is 80-90% calcified and functions mainly as structural, mechanical and protective bone. Basic unit is the osteon. Osteocytes arranged in layers around a central Haversian canal. Each canal carries a blood and nerve supply to the osteon. The canals run parallel to the bone surface. Osteons arranged into lamellae - mostly concentric.

Cancellous is 15-25% calcified and has mainly metabolic functions. Lamellae not arranged into osteons. Matrix develops into an interlacing network of rods called trabeculae. Less heavy.

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5
Q

Briefly describe the process of remodelling.

A

Osteocytes sense new stress which requires remodelling - apoptose to release RANK-L. Binds to RANK-R on osteoclasts, resulting in resoprtion. Bone subsequently laid down by osteoblasts.
Remodelling 5% of skeleton at any given time, total skeleton replaced over 7 years.

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6
Q

What is woven bone?

A

Immature bone founding in the growing skeleton or after a fracture.
It is more random than lamellar bone, and is weaker or more flexible than lamellar bone.

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7
Q

What is lamellar bone?

A

Mature bone found in the normal skeleton. 2 types: cortical and cancellous bone.

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8
Q

What properties are afforded to bone by collagen and hydroxyapatite?

A

Collagen gives bone cable-like flexibility and resistance to tension.
Hydroxyapatite confers pillar-like stiffness and resistance to compression.

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9
Q

Describe osteoblasts

A

Osteoblasts produce osteoid, which is calcified to form bone matrix. Ultimately, the osteoblasts become osteocytes.

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10
Q

Describe osteoprogenitor cells

A

Stem cells which differentiate into osteoblasts. Only a small number present, actively involved in bone fracture repair.
Mostly located in periosteum, endosteum and the vascular canals in the bone matrix.

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11
Q

Describe osteoclasts

A

Also called giant cells, remove bone matrix (resorb bone). They are derived from monocytes and are of a different lineage from other bone cells.

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12
Q

What is the periosteum and what is the endosteum?

A
Periosteum = fibrous outer layer and cellular inner layer surrounding the superifical layer of compact bone.
Endosteum = incomplete cellular layer lining the marrow cavity.
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13
Q

Describe intramembranous ossification.

A

Mesenchymal models of bones from embryonic development directly ossify into bone. Bones directly below skin ossify this way (skull, mandible, clavicle).
Mesenchymal cells produce the matrix (osteoid), which becomes calcified. Mesenchymal cells differentiate into osteoblasts to form an ossification centre. As ossification progresses, some osteoblasts are trapped in bony pockets (lacunae) and transform into osteocytes. Blood vessels grow into the area to maintain the metabolism of the bone. Initially cancellous bone, can subsequently be remodelled into compact bone. Periosteum forms around the bone and “traps” a surface layer of osteoblasts.

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14
Q

Describe endochondral ossification.

A

Mesenchyme differentiates into cartilage bone models. Most bones ossify this way.
Mesenchymal cells differentiate into chrondroblasts which form cartilage models of the bones. Cartilage bone model grows by expansion (interstitial growth) and new growth of cartilage at outer surface (appositional growth). In the middle of the bone, the cartilage calcifies and the chondroctyes die. Becomes primary ossification centre: grows in both directions replacing cartilage to form the diaphysis. Secondary ossification centres from in the epiphyses. The epiphyseal plate is the cartilagenous area between the diaphysis and epiphysis. The bone continues to grow until the epiphysis fuses with the diaphysis.

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15
Q

In endochondral ossification, how do short bones ossify and at what age do primary and secondary ossification centres tend to appear?

A

Short bones ossify via only one primary ossification centre.

Primary centres appear at around 2 months in utero; secondary centres appear about 2 years after birth.

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16
Q

Describe fracture repair.

A

Torn blood vessels bleed to produce a fracture haematoma. Osteoprogenitor cells and relatively inactive osteoblasts from the periosteum and endosteum differentiate into active osteoblasts and migrates towards the fracture. They form a provisional type of bone and cartilage called external callus, which bridges the end of the bones. Cartilage replaced by bone (initially woven bone) - then restructures to cancellous bone. Osteoblasts and osteoclasts remodel the cancellous bone to cortical bone.

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17
Q

What are the 2 types of bone biopsy?

A

Closed core biopsy - Jamshidi needle.

Open biopsy - for sclerotic/ inaccessible lesions.

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18
Q

If the reason for a bone biopsy is general, what biopsy would you perform?

A

A transiliac bone biopsy, since all types of bone can be seen in the one core.

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19
Q

What stains are used to look at bone?

A

H&E staining for decalcified samples
Masson-Goldner Trichrome staining looks at degree of mineralisation.
Tetracycline staining gives a fluorescent line at the frontier of osteoblasts to look at whether turnover is fast or slow.

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20
Q

What are metabolic bone diseases?

A

A group of diseases which cause reduced bone mass and strength due to imbalance of various chemicals in the body, causing altered bone activity.

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21
Q

What is osteoporosis?

A

Defined as a bone mineral density T-score of -2.5 or lower.
Primary causes include age and menopause.
Secondary causes include drugs and systemic disease.
Can be high turnover or low turnover osteoporosis (resorption > formation in both cases).
Thin trabeculae. Loss of cortical bone (thinning of cortex). Structurally normal, just reduced mass.

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22
Q

What is osteomalacia?

A

Defect of mineralisation of normally synthesised bone matrix. Leads to rickets in children. Use Masson-Goldner Trichrome stain.
2 types: deficiency of vitamin D, deficiency of PO43-
Pain/tenderness/ fractures/ proximal weakness.
Horizontal fractures in Looser’s zone (areas of high tensile stress). 90 degrees to bone.

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23
Q

What causes osteitis fibrosa cystica?

A

Hyperparathyroidism.
Characteristic “brown tumours” on X-ray. Fibrous tissue replaces bone. Also, chondrocalcinosis seen (calcification of articular cartilage).

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24
Q

Describe renal osteodystrophy.

A

Comprises all skeletal changes arising from renal deficiency. Increases resorption, osteomalacia, osteosclerosis, osteoporosis, growth retardation.

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25
Q

What is Paget’s disease?

A

A disorder of bone turnover. 3 stages: osteolytic, osteolytic-osteosclerotic, quiescent-osteosclerotic.
Onset >40yrs. M>F. Mono-ostotic 15%.
Thickened cortices (sclerosis) with irregular trabeculae.

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26
Q

Why might a bone biopsy be performed?

A

To confirm diagnosis, find cause, investigate abnormality on X-ray, diagnose bone tumour (benign vs malignant), determine cause of unexplained infection, evaluate therapy performance.

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27
Q

What is a radiological sign?

A

A change in imaging appearance, whether functional or structural, that may point towards a pathology.

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28
Q

What types of imaging are useful for investigating bones and what do they look at?

A

X-rays, CT, DEXA - look at density.
MRI - biochemical composition
Radionuclide bone studies - bone turnover.

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29
Q

What are insufficiency fractures?

A

Stress fractures due to normal stresses on bone, typically seen in osteoporosis.

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30
Q

How is the result of a DEXA scan interpreted?

A

Compare to normal population at peak (25 year olds).

T score

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31
Q

What does Paget’s disease look like on imaging.

A

Cortical thickening, bone expansion, coarsening of trabeculae, osteolytic, osteoslcerotic and mixed lesions.
Doesn’t cross joint.

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32
Q

What are codfish vertebrae?

A

Biconcave vertebrae seen on x-rays - a sign of osteoporosis and osteomalacia.

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33
Q

Give radiological signs of rickets

A

Indistinct/ frayed metaphyseal margin.
Widened growth plate without calcification
Osteopenia
Enlarged anterior ribs
Cupping/ splaying of metaphyses due to weight bearing.

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34
Q

What are looser zone fractures a radiological sign of?

A

Looser zone fractures = short fractures associated with sclerotic margin (which is whiter) - 90 degrees to bone.
Seen in osteomalacia.

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35
Q

What symptoms are associated with metabolic bone disease?

A

Metabolic symptoms - hyper/hypocalcaemia, hyper/hypophosphatemia.
Symptoms specific to bone - fractures and deformity.

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36
Q

How is primary hyperparathyroidism diagnosed?

A

Elevated total/ ionised calcium with PTH levels frankly elevated or in the upper half of the normal range.
Subjects with hypercalcemia and PTH in the upper half of the normal range are physiologically not normal.

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37
Q

What is the problem with CHRONICALLY elevated PTH?

A

Chronic PTH = catabolic (increased cortical bone resorption).
Pulsatile/ acute PTH = anabolic.

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38
Q

Give an overview of systemic lupus erythematosus (SLE).

A

One of a family of chronic overlapping autoimmune diseases.
M:F 1:9 (female preponderance)
Presentation 15-40 years old
Multiple genes implicated: complement deficiency
Principally affects joints and skin, lungs, kidney, bone marrow. Clinical features depend on organ affected.

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39
Q

Describe the presentation of systemic lupus erythematosus (SLE).

A

Malaise, fatigue, fever, weight loss.
Specific features: butterfly rash, alopecia, arthralgia, Raynaud’s phenomenon.
Other features: inflammation of kidney, CNS, heart, lungs, accelerated atherosclerosis, vasculitis.

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40
Q

Describe the aetiology of SLE (systemic lupus erythematosus).

A

Complex cause, involving genetic and environmental factors.
Abnormal clearance of apoptotic cell material.
Dendritic cell uptake of autoantigens - activation of B-cells.
IgG autoantibody production
Immune complexes
Complement activation, cytokine generation etc.

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41
Q

What is interesting about ESR and CRP in SLE?

A

ESR increases, but CRP remains the same.

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42
Q

How is systemic lupus erythematosus classified?

A
Mild = skin +/- joint involvement
Moderate = inflammation of other organs
Severe = severe inflammation of vital organs.
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43
Q

How do we treat mild SLE?

A

Paracetamol +/- NSAID.

Hydroxychloroquine (rash), topical corticosteroids (rash, not face).

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44
Q

How do we treat moderate SLE?

A

Indication: failure of hydroxychloroquine/ NSAID.

Use high initial dose of corticosteroids, then reduce the dose.

45
Q

How do we treat severe SLE?

A

Azathioprine - effective steroid-sparing agent,

Cyclophosphamide - severe organ involvement - has severe side effects (BMR suppression, infertility, cystitis).

46
Q

Give the 15 year survival of SLE and its bimodal mortality pattern.

A

15 year survival = 85% no nephritis, 60% with nephritis.
Bimodal mortality pattern:
Early = active lupus (renal failure, CNS disease)
Late = MI.

47
Q

What is rheumatoid arthritis?

A

A chronic autoimmune disease characterised by pain, stiffness and symmetrical synovitis (inflammation of the synovial membrane).

48
Q

What are key features of rheumatoid arthritis?

A

Polyarthritis (5 or more joints affected), usually swelling of small joints in the hands and wrists.
Symmetrical, early morning stiffness, may lead to joint damage - “joint erosions” on radiograph.
Extra-articular disease can occur - such as subcutaneous rheumatoid nodules.
1% of population affected, F:M 3:1, genetic component.

49
Q

What is rheumatoid factor?

A

An IgM autoantibody which recognises the Fc region of an IgG.
Seropositive rheumatoid arthritis = rheumatoid factor positive.
70% of sufferers seropositive at disease onset: a further 10-15% become positive over first 2 years of diagnosis.

50
Q

What are the commonest joints affected in rheumatoid arthritis?

A

MCPs, PIPs, wrists, knees, ankles, MTPs.

Sparing of DIP joints.

51
Q

What is swan-neck deformity?

A

Hyperextension at PIP and hyperflexion at DIP.

52
Q

What is Boutonniere (button-like) deformity?

A

Hyperflexion at PIP, hyperextension at DIP.

Associated with rheumatoid arthritis.

53
Q

What are rheumatoid nodules?

A

Central areas of fibrinoid necrosis surrounded by histiocytes (stationary phagocytic cells present in connective tissue) and peripheral layer of connective tissue.
Occur in 30% of patients.
Associated with severe disease.

54
Q

What is Felty’s syndrome?

A

A triad of splenomegaly, leukopenia and lung disease.

55
Q

On radiographs, how does rheumatoid arthritis present?

A

Early: juxta-articular osteopenia
Later: joint erosions at margins of the joint
Later still: joint deformity and destruction.

56
Q

Describe the physiological structure of a synovial joint.

A

Articular cartilage - type II collagen and proteoglycans (mainly aggrecan).
Synovium - 1-3 cells deep lining containing macrophage-like phagocytic cells (type A synoviocyte) and fibroblast-cells that produce hyaluronic acid (type B synoviocyte).
Synovial fluid - hyaluronic acid-rich viscous fluid.

57
Q

Describe the rheumatoid synovium.

A

A proliferated mass of tissue due to neurovascularisation, lymphangiogesis, inflammatory cells. Cytokine tumour necrosis factor A (TNF-A) is the dominant pro-inflammatory cytokine.

58
Q

How is rheumatoid arthritis treated?

A

Treat early and aggressively - goal is to prevent joint damage (destruction = inflammation*time).

DMARDs (disease modifying anti-rheumatic drugs) are steroid-sparing agents - safer as long-term treatment.
Steroids useful as short-term treatment to control flare of disease or control single joint inflammation.
These induce remission, not curative.

TNF-A inhibition through parenteral (e.g. S.C.) administration of antibodies (e.g. infliximab).
IL-6 and IL-1 blockade now also available.
Can deplete B-cells by i.v. administration of an Ig against CD20. However, Ab therapy expensive and immunosuppression puts patients at risk of infection.
E.g. B-cell depletion associated with hep B reactivation - must screen all patients for hep B before treatment.

59
Q

What is reactive arthritis?

A

Sterile inflammation in joints following infection - especially urogenital and GI infections.
Important extra-articular manifestations - skin and eye inflammation.
May be first manifestation of HIV or hepatitis C infection.
Commonly in young adults with a genetic predisposition and environmental trigger.
Distinct from septic arthritis (which requires antibiotics)

60
Q

Give common presentations of reactive arthritis.

A

Asymmetrical, oligoarthritis, large joints affected, often of the lower limbs.
M > F. 20-40 years old.
No rheumatoid factor, no subcutaneous nodules.
Most common cutaneous presentation is circinate balanitis (dermatitis of glans penis), enthesitis, spondylitis, sterile conjunctivitis, sterile urethritis.

61
Q

How would you go about diagnosing reactive arthritis?

A

Investigate to exclude other causes:
Microbiology - check for septic arthritis (cultures, serology), examine synovial fluid (especially if one joint affected).
Immunology - check for rheumatoid factor.

62
Q

Describe the treatment of reactive arthritis.

A

In most patients, there is complete resolution within 2-6 months.
No role for antibiotics.
Articular - NSAIDS, intraarticular corticosteroid therapy.
Extra-articular - typically self-limiting, hence symptomatic therapy.

63
Q

What is osteoarthritis?

A

A chronic, slowly-progressing disorder due to failure of articular cartilage that typically involves the joints of the hand, spine and weight-bearing bones (hips, knees).
Affects older people.
Their articular cartilage is defective and causes damage to underlying bone.

64
Q

What joints are typically involved in osteoarthritis?

A

PIPs, DIPs (MCPs spared), first carpometatarsal joint (CMC) and first metatarsophalangeal joint (MTP).

65
Q

What are Heberden’s and Bouchard’s nodes?

A

Heberden’s nodes = swelling at DIPs
Bouchard’s nodes = swelling at PIPs.
Found in osteoarthritis.

66
Q

What symptoms are commonly associated with osteoarthritis?

A
Joint pain (worse with activity)
Joint crepitus (creaking, cracking, grinding sound made when moving affected joint)
Joint instability
Joint enlargement (e.g. Heberden's nodes)
Joint stiffness after immobility
Limitation of motion.
67
Q

Describe radiological changes in osteoarthritis.

A

Joint space narrowing (loss of cartilage), subchondral bony sclerosis, osteophytes (bony spurs), subchondral cysts.

68
Q

Describe changes in articular cartilage in osteoarthritis.

A

Cartilage is avascular and aneural (no pain). Loads of proteoglycans (e.g. aggrecans), reduced collagen, chondrocyte changes e.g. apoptosis and proliferation of osteoblasts.
New bone formation at joint margins.

69
Q

How do we manage osteoarthritis?

A

Education, physical therapy (keep muscles strong to stabilise joint), occupational therapy, weight loss where appropriate, exercise, analgesia (paracetamol / NSAIDs)
joint replacement.
Unlike rheumatoid arthritis, no disease modifying osteoarthritis drug (DMOAD).

70
Q

What is enthesitis?

A

Enthesitis is inflammation of the entheses, the sites where tendons or ligaments insert into the bone.
Common in reactive arthritis - heel pain (achilles tendonitis), swollen fingers (dactylitis), painful feet.

71
Q

What is spondylitis?

A

Inflammation of the vertebra.
Common in reactive arthritis.
Sacroiliitis (inflammation of sacroiliac joint).

72
Q

Compare rheumatoid arthritis and reactive arthritis.

A

Rheumatoid arthritis:
F > M, all ages, symmetrical, polyarticular, small and large joints, subcutaneous nodules, rheumatoid factor.

Reactive arthritis:
M> F, 20-40 years, asymmetrical, oligoarticular, large joints, enthesitis, spondylitis, sterile urethritis.

73
Q

Briefly describe rheumatoid arthritis.

A

Chronic joint inflammation that can result in joint damage, the site of inflammation being the synovium. Associated with autoantibodies - rheumatoid factor and CCP antibodies.

74
Q

Describe ankylosing spondylitis.

A

Chronic spinal inflammation that can result in spinal fusion and deformity. Site of inflammation is the enthesis. No autoantibodies (seronegative). Increased thoracic kyphosis and loss of normal lumbar lordosis.

75
Q

Briefly define SLE.

A

Chronic tissue inflammation in the presence of antibodies directed against self-antigens.
Multi-site inflammation, particularly the joints, skin and kidneys. Associated with antinuclear and anti-dsDNA antibodies.

76
Q

Which MHCs are associated with rheumatoid arthritis, ankylosing spondylitis and SLE?

A

SLE = HLA-DR3
Rheumatoid arthritis = HLA-DR4
Ankylosing spondylitis = HLA-B27

77
Q

What is MHC restriction?

A

The concept of T-cells only being able to “see” antigen presented on MHC molecules.

78
Q

Which autoimmune musculoskeletal diseases are seronegative and which are seropositive?

A

Seropositive: SLE and rheumatoid arthritis.
Seronegative: osteoarthritis, ankylosing spondylitis, gout, reactive arthritis.

79
Q

Describe how you identify SLE in a lab. How do you identify when an SLE patient is relapsing?

A

Antinuclear antibodies (ANA) seen in all SLE cases. Not specific for SLE. If ANA+, the lab will perform further tests to determine which types of ANA are present.
Anti-dsDNA antibodies - SPECIFIC for SLE. Correlates with disease activity.
Sick lupus patients commonly have low complement and high serum levels of anti-dsDNA antibodies.

80
Q

What is the link between abnormal apoptosis and autoimmune diseases?

A

Apoptosis leads to translocation of nuclear antigens to membrane surfaces. Impaired clearance of apoptotic cells results in enhanced presentation of nuclear antigens. Leads to B-cell autoimmunity. Tissue damage by antibody effector mechanisms (e.g. complement activation & Fc receptor engagement).

81
Q

What is the main pro-inflammatory cytokine in SLE?

A

TNF-A

82
Q

Describe the role of denosumab in treatment of rheumatoid arthritis.

A

In rheumatoid arthritis, RANKL is produced by T-cells and synovial fibroblasts, stimulating osteoclast formation (upregulated by IL-1 and TNF-A). Denosumab is a monoclonal antibody against RANKL.

83
Q

Why is B-cell biological therapy useful in SLE?

A

Since B-cell hypersensitivity is a key feature of SLE.
Rituximab is a chimeric anti-CD20 antibody used to deplete B-cells.
Belimumab is a monoclonal antibody against a B-cell survival factor (BYLS).

84
Q

Explain the analgesic, anti-pyretic and anti-inflammatory responses of glucocorticoids and NSAIDS.

A

Prostaglandins are lipid mediators of inflammation which act on platelets, endothelium and uterine tubes and mast cells.
Glucocorticoids inhibit phospholipase A2 (which converts phospholipids to arachidonic acid).
NSAIDS inhibit COX enzymes (which convert arachidonic acid to prostaglandins).

85
Q

What is the GALS screen?

A

An assessment to rapidly determine whether any joints are abnormal.
GALS = gait, arms, legs, spine.

86
Q

Give 3 key intro questions when performing a GALS screen.

A

Have you had any pain or stiffness in your muscles, joints or back?
Can you dress yourself completely without any difficulty?
Can you walk up and down stairs without any difficulty.

87
Q

How is gait assessed in the GALS screen?

A

Observe the patient walking, turning and walking back.

Look for normal stride length, ability to turn quickly, smoothness and symmetry in the legs, pelvis and arms.

88
Q

How is the spine assessed in the GALS screen?

A

Are parasternal and shoulder muscles symmetrical? Is the spine straight? Are the iliac crests level? Are curvatures normal? Is the C-spine normal? etc…

89
Q

How are the arms assessed in the GALS screen?

A

Full extension at elbows? Shoulder joints normal? Observe supination, pronation, grip and finger movements. Test for synovitis at MCP joints (squeeze across 2-5 MCP joints - discomfort suggests synovitis). Etc…

90
Q

How the legs assessed in the GALS screen?

A

Look for knee or foot deformity. Assess flexion of the hip and knee. Look for knee swelling. Test for synovitis at MTP joints. Inspect the soles of the feet. Etc…

91
Q

When investigating the nature of any abnormal joints identified when performing a GALS screen, what are the signs of inflammation?

A

Swelling, warmth, erythema (redness of skin due to hyperemia), tenderness, loss of function.
Inspection (Swelling, redness), palpation (warmth, tenderness), movement, function.

92
Q

What is arthalgia?

A

Pain within a joint without demonstrable arthritis (arthritis = inflammation of a joint).

93
Q

Contrast dislocation and subluxation.

A

Articulating surface displaced and no longer in contact.

Subluxation is partial dislocation.

94
Q

Contrast varus deformity and valgus deformity.

A

Varus deformity is a lower limb deformity where the distal part is directed towards the midline.
Valgus deformity is a lower limb deformity where the distal part is directed away from the midline.

95
Q

What is gout?

A

A disease where deposition of monosodium urate (MSU) crystals occurs as a result of hyperuricemia and leads to gouty arthritis and tophi (aggregates of MSU in tissues) - especially the ears.

96
Q

Describe gouty arthritis.

A

Commonly affects the MTP joint of the hallux. Has an abrupt onset, is extremely painful. The joint is red, warm, swollen and tender. Resolves spontaneously after 3-10 days.

97
Q

What are signs of a joint abnormality being mechanical in nature?

A

Painful restriction of motion in absence of features of inflammation.
Instability.

98
Q

How does the pattern of joint involvement help to differentiate between rheumatoid arthritis, reactive arthritis and gouty arthritis as differentials?

A

Rheumatoid arthritis = bilateral, symmetrical involvement of large and small joints.
Reactive arthritis = lower limb asymmetrical oligoarthritis and axial involvement.
Gouty arthritis = exclusive inflammation of 1st MTP joints.

99
Q

What extra-articular features may help distinguish between SLE, rheumatoid arthritis and gouty arthritis?

A

Rheumatoid = presence of subcutaneous rheumatoid nodules.
SLE = Malar (butterfly) rash.
Tophi (subcutaneous deposits of uric acid) = gout.

100
Q

Describe the differences in synovial effusion (abnormal increase in the pale yellow/ colourless fluid produced by cells lining the synovium) in inflammation, infection and abnormal mechanical stimulation.

A

In infection, the synovial fluid is turbid.
In inflammation, the effusion is inflammatory exudate, which has abnormal composition.
In abnormal mechanical stimulation, hyaluronic acid production is increased by synovial fibroblasts due to mechanical forces. The resulting oncotic pressure draws in more water. Composition the same.

101
Q

What is arthrocentesis?

A

Aseptic needle aspiration to take a synovial fluid sample, e.g. when infection is suspected.

102
Q

What is Raynaud’s phenomenon?

A

A phenomenon common amongst patients with connective tissue disorders.
Intermittent vasospasm of digits on exposure to cold: white –> blue –> red.
Blanching, cyanosis as static venous blood deoxygenates, reactive hyperemia.

103
Q

What is Sjorgren’s syndrome?

A

An autoimmune exocrinopathy.

Dry eyes and mouth, parotid gland enlargement. Associated with ANA and rheumatoid factor.

104
Q

What is overlap syndrome?

A

Where features of 1 or more connective tissue diseases are present, e.g. SLE and inflammatory muscle disease.

105
Q

What is undifferentiated connective tissue disease?

A

Where incomplete features of a connective tissue disorder are present.

106
Q

What is ‘reversal’ in the bone remodelling process?

A

Apoptosis of osteoclasts, replacement by osteoblasts as you transition from resportion to formation.

107
Q

Which types of infections is reactive arthritis most likely to follow?

A

Urogenital and enterogenic infections.

Typically 1-4 weeks later.

108
Q

Explain what the radiological sign of ‘salt and pepper’ skull in osteitis fibrosa cystica is caused by.

A

Trabecular bone resorption of skull = mottling appearance (alternating areas of lucency and sclerosis).