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Year 2: LCRS > Muskuloskeletal > Flashcards

Muskuloskeletal Flashcards

1
Q

What is metabolic bone disease?

A

A group of diseases that cause a decrease in bone density and bone strength by:

1) Increasing bone resorption
2) Decreasing bone formation
- May be associated with disturbances in mineral metabolism

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2
Q

Give examples of metabolic bone diseases?

A
  • Primary hyperparathyroidism
  • Rickets/Osteomalacia
  • Osteoporosis
  • Paget’s disease
  • Renal osteodystrophy
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3
Q

What are the symptoms of metabolic bone diseases?

A 
Metabolic: 
Hypocalcaemia, hypercalcaemia, hypo/hyperphosphataemia
Bone: 
Deformity, 
Fractures
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4
Q

How is calcium stored in the bone?

A
  • Inorganic hydroxyapatite
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5
Q

What are the factors that contribute to bone strength?

A 
Quantity: 
- Cortical thickness
- Mineral density 
- Size 
Quality 
- Architecture 
- Bone turnover 
- Cortical porosity 
- Trabecular connectivity
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6
Q

How can bone structure and function be assessed?

A
  • Bone histology
  • Biochemical tests
  • Bone mineral densitometry e.g. osteoporosis
  • Radiology e.g. osteomalacia, Paget’s disease
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7
Q

What are the serum features investigated in metabolic bone disease?

A

Calcium, corrected calcium, albumin, phosphate, parathyroid hormone, 25-hydroxy vitamin D

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8
Q

What are the urine features investigated in metabolic bone disease?

A

NTX
Calcium
Phosphate

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9
Q

Where does absorption of calcium occur?

A

Jejunum and ileum

Passive or active (vit D controlled)

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10
Q

What is the total serum calcium?

A

2.15-2.56 mmol/L

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11
Q

What is the role of PTH in plasma calcium regulation?

A
  • Predominant role in minute by minute regulation
  • Afferent-limb sensing
  • If calcium drops, within seconds there is secretion of PTH from pre-formed stores
  • Acts on bone and kidney
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12
Q

What is the affect of PTH on the bone?

A
  • Increased resorption

- Release of Ca++ and phoshphate

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13
Q

What is the affect of PTH on the kidney?

A
  • Increased phosphate excretion
  • Increased calcium reabsorption
  • Increased calcitorol formation leading to increased intestinal CaH04 absorption
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14
Q

What does serum calcium consist of?

A

46% protein-bound
47% ionised
7% complexes

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15
Q

What is the calcium sensing receptor?

A

Links serum calcium to the PTH gland

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16
Q

How does PTH release calcium from the bone?

A
  • Activates the RANK system

- Osteoblast has rank ligand on its membrane, interacts with macrophages which stimulate osteoclasts

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17
Q

Where does PTH activate vitamin D in the kidney?

A

In the proximal tubule of the kidney

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18
Q

Where does PTH increase calcium re-absorption in the kidney?

A

Distal tubule of the kidney

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19
Q

Where does PTH decrease phosphate re-absorption in the kidney??

A

Proximal tubule

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20
Q

What are the causes of primary hyperparathyroidism?

A
  • Parathyroid adenoma
  • Parathyroid hyperplasia
  • Parathyroid CA
  • Familial syndroms (MEN 1, MEN 2A)
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21
Q

What is the biochemistry of primary hyperparathyroidism?

A
  • Increased serum calcium by absorption from bone/gut/kidney
  • Decreased serum P04, increased absorption is overcome by marked renal excretion
  • Increased urine calcium excretion as increased renal resorption is overcome by the hugely increased filtered load
  • Increased markers of bone resorption
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22
Q

What are the clinical features of primary hyperparathyroidism?

A
  • Mainly due to high calcium: thirst, polyuria, tiredness, fatigue, muscle weakness
    ‘Stones, abdominal moans and psychic groans’
  • Renal colic, nephrocalcinosis, CRF
  • Dyspepsia, pancreatitis
  • Constipation, nausea, anorexia
  • Depression, impaired concentration
  • Drowsy, coma
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23
Q

How is primary hyperparathyroidism managed?

A
  • Depends on age and severity
  • Very young or high calcium patients have a huge risk of developing complications such as osteoporosis, renal stone and renal failure therefore surgery is necessary
  • Other management is conservative, focuses on preventing complications using bisphospnoates and calcimemetics
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24
Q

What is osteomalacia?

A

Inadequate vitamin D activity which leads to defective mineralisation of the cartilaginous growth plate (before a low calcium)

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25
Q

What are the symptoms of osteomalacia?

A
  • Bone pain and tenderness (axial)
  • Muscle weakness (proximal)
  • Lack of play
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26
Q

What are the signs of osteomalacia?

A
  • Age dependent deformity
  • Myopathy
  • Hypotonia
  • Short stature
  • Tenderness of percussion
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27
Q

What are the causes of osteomalacia?

A
  • Vitamin D related which may be dietary
  • Gastrointestinal: Small bowel malabsorption, bypass, Pancreatic insufficiency, Liver/biliary disturbance,
    Drugs: phenytoin, phenobarbitone
  • Renal: chronic renal failure, vitamin D dependent rickets type I, autosomal recessive, no 1a hydroxylation
  • Resistance: vitamin D dependent rickets type II, autosome recessive
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28
Q

What is the biochemistry of osteomalacia?

A 
Calcium= N/low 
Phosphate= N/low 
Alkaline phosphate= High 
PTH= High
Urine phosphate= high 
-Glycosuria, aminoaciduria, high pH and proteinuria
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29
Q

How does osteomalacia relate to phosphate?

A

Can get osteomalacia with renal phosphate loss, when calcium and Vitamin D levels are usually normal

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30
Q

How does oestrogen deficiency affect bone?

A

1) Increases the activation frequency of remodelling units (number of osteoblasts and blasts)
2) Causes remodelling imbalance
- Decreases osteoclast apoptosis apoptosis, increases osteoblast apoptosis
- Deeper and more resorption pits
- Increased bone resorption compared to bone formation
3) Remodelling errors
- Trabecular perforation
- Cortical excess Haversian excavation
4) Decreased osteocyte sensing

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31
Q

What are the causes of osteoporosis due to high turnover?

A

Increased bone resorption greater than bone formation

  • Oestrogen deficiency- primarily in postmenopausal women
  • Hyperparathyoidism
  • Hyperthyroidism
  • Hypogonadism in young women and in men
  • Heparin
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32
Q

What are the causes of osteoporosis due to low turnover?

A

Decrease bone formation more pronounced than decreased bone resorption

  • Liver disease- primarily primary biliary cirrhosis
  • Heparin
  • Age above 50
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33
Q

What are the causes of osteoporosis due to increased bone resorption and decrease bone formation?

A

Glucocorticoids

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34
Q

What is the biochemistry of osteoporosis?

A

Should be normal but check for vit D deficiency and secondary endocrine causes
- Exclude multiple myeloma

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35
Q

Why should bone density be measured?

A

Single best predictor of fracture risk BMD represents 70% of total risk

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36
Q

What is DXA?

A

Dual energy X-ray absorptiometry

  • Measureres transmission through the body of X-rays of two different photon energies
  • Enables densities of two different tissues to be inferred i.e. bone mineral, soft tissue
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37
Q

How is osteoporosis defined by T-score?

A

Measured BMD- young adult mean BMD

/young adult standard deviation

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38
Q

What situations interfere with vertebral measurement interpretations?

A
  • Degenerative change, osteoarthritis
  • Vertebral fractures
  • Metal artefacts
  • Osteomalacia
  • Vascular calcification
  • Scoliosis
  • Paget’s disease
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39
Q

How is collagen synthesised for bone formation?

A

Alpha 1 and 2 chains of type I collagen produced by osteoblast

  • Proline and lysine residues hydroxylated
  • 3 hydroxylysine molecules on adjacent tropocollagen fibrils condense to form a pyridinum ring linkage
  • Collagen breakdown products are good markers of bone resorption as they are directly linked to the amount of bone resorbed
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40
Q

How is osteoclast activity measures?

A

By measuring urine hydroxyproline or urine-collagen cross-links

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41
Q

What are markers of bon resorption?

A

Serum CTX
NTX
Tartrate resistant acid phosphatase

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42
Q

What is bone specific alkaline phosphate? (BSAP_

A
  • Tissue specific form: liver vs bone, intestine, germ cell, placental forms
  • Essential for mineralisation, regulates concentrations of phosphocompounds
  • Increased in Paget’s disease osteomalacia, bone metastases, hyperparathyroidism, hyperthyroidism
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43
Q

What is tertiary hyperparathyroidism?

A
  • Due to chronic renal impairment
  • Nephron loss> reduce production of active calcitrol
  • Reduced vit d levels leads to osteomalacia
  • Deceased calcitrol leads to hypoacalcaemia, secondary PTH increase, increased bone resportion
  • Nephron loss leads to phosphate retendtion causing hyperphosphataemia, leading to metastatic calcification
  • Nephron loss causes acidosis which causes demineralisation contributing to osteoporosis
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44
Q

What is the function of bone?

A
  • Mechanical: support and site for muscle attachment
  • Protective: vital organs and bone marrow
  • Metabolic: reserve of calcium
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45
Q

What is the composition of bone?

A
  • INORGANIC - 65%
    – calcium hydroxyapatite (10Ca 6PO4 OH2) – is storehouse for 99% of Ca in the body
    – 85% of the phosphorous, 65% Na & Mg
  • ORGANIC - 35%
    – bone cells and protein matrix
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46
Q

How is bone classified?

A 
Cortical:
Long bones, 80% of skeleton, appendicular, 80-90% calcified, mainly mechanical and protective 
Cancellous:
- Vertebrae & pelvis, 20% of skeleton 
- Axial 
- 15-25% calcified 
- Mainly metabolic 
- Large surface
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47
Q

What are the indications for use of bone biopsy?

A
  • Investigating an abnormality seen on an x-ray
  • Evaluate bone pain or tenderness
  • Bone tumour diagnosis (benign vs malignant)
  • Determining the cause of unexplained infection
  • Evaluating the progress of therapy
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48
Q

What are the types of bone biopsies?

A
  • Close: used most commonly as poses smallest risk

- Open: for sclerotic or inaccessible lesions

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49
Q

What are the different bone cells?

A
  • Osteoblasts: build bone by laying down osteoid
  • Osteoclasts: multinucleate cells of macrophage family resorb or chew bone
  • Osteocytes: osteoblast like cells which sit in the lacunae in bone
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50
Q

What is RANK?

A

Receptor activator for nuclear factor kB

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51
Q

What is OPG?

A

Osteoprotegerin-

Inhibits RANK/RANKL binding therefore inhibiting osteoclastogenesis

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52
Q

How are types of bone classified anatomically?

A

1) Anatomically- flat/long/cuboid bones
- Intramembranous ossification (flat) and endochrondral ossification (long)
2) Trabecular bone (cancellous)
3) Compact bone (cortical)
4) Women bone (immature)
5) Lamellar bone (mature)

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53
Q

What is metabolic bone disease?

A
  • Disordered bone turnover due to imbalance of various chemicals in the body (vitamins, hormones, mienrals)
  • Overall effect is reduced bone mass (osteopaenia) which often results in fracture with little or no trauma
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54
Q

What are the 3 main categories of metabolic bone disease?

A

1) Related to endocrine abnormality (Vit D; Parathyroid hormone)
2) Non-endocrine (e.g. related osteoporosis)
3) Disuse osteopaenia

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55
Q

What is osteomalacia?

A

Defective bone mineralisation
Types:
1) Deficiency of vitamin D
2) Deficiency of P04

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56
Q

What is the mechanism of osteomalacia?

A
  • Vitamin D plays integral role in calcium metabolism
  • Vit D deficiency results in increased PTH and subsequent increase bone resorption
  • Vit D deficiency also cause hypocalcaemia
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57
Q

What are the effects of osteomalacia?

A
  • Bone pain/tenderness
  • Fracture
  • Proximal weakness
  • Bone deformity
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58
Q

What is hyperparathyroidism?

A

Excess PTH

  • Increased Ca + P04 excretion in urine
  • Hypophosphataemia
  • Skeletal changes of osteitis fibrosa cystica
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59
Q

Which 4 organs are directly or indirectly affected by PTH and between them control Ca metabolism?

A
  • Parathyroid glands
  • Bones
  • Kidneys
  • Proximal small intestine
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60
Q

What are the difference between primary and secondary hyperparathyroidism?

A 
Primary:
- Parathyroid adenoma 
- Chief cell hyperplasia 
Secondary:
- Chronic renal deficiency 
- Vit D deficiency
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61
Q

What is renal osteodystrophy?

A

Results from from chronic renal disease. Comprises all skeletal change of chronic renal disease:

  1. Increased bone resorption (osteitis fibrosa cystica)
  2. Osteomalacia
  3. Osteosclerosis
  4. Growth retardation
  5. Osteoporosis
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62
Q

What are the symptoms of osteodystrophy?

A
  • PO4 retention – hyperphosphataemia
  • Hypocalcaemia as a result of ↓vit D
  • Secondary hyperparathyroidism
  • Metabolic acidosis
  • Aluminium deposition
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63
Q

What is Paget’s disease?

A 
- Disorder of bone turnover
Divided into 3 stages 
1) Osteolytic 
2) Osteolytic-osteosclerotic 
3) Quiescent osteosclerotic
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64
Q

What are the clinical symptoms of Paget’s disease?

A
  • Pain
  • Microfractures
  • Nerve compression
  • Skull changes may put medulla at risk
  • Deafness
  • +/- haemodynamic changes, cardiac failure
  • Hypercalcaemia
  • Development of sarcoma in area of involvement
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65
Q

What is a Haversian canal?

A

Channel that the blood vessels run in the bone

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66
Q

What are Canaliculae?

A

Provide routes for cell communication

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67
Q

What is Howship’s lacunae?

A

Pits in the bone surface in which osteoclasts are found, often called resorption bays

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68
Q

What is ‘Codfish vertebra’?

A

In osteomalacia

  • Biconcave loss of height
  • Osteopenic
  • Pencilled-in margin
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69
Q

What are the radiological features of osteomalacia?

A
  • Less mineral
  • Osteopenia
  • Bend and bow be
    fore break
  • Codfish vertebrae
  • Changes in mature bone
  • Looser’s zon’s
70
Q

What are the radiological features of osteoporosis?

A
  • Osteopenia
  • Break
  • Anterior wedging
71
Q

What are the radiological features of Ricket’s?

A
  • Indistinct frayed metaphyseal margin?
  • Widened growth plate (no calcification)
  • Cupping/splaying
  • Rickety rosary - splayed and cupped anterior ends of ribs
  • Osteopenia
72
Q

What is rheumatoid arthritis?

A
  • Chronic joint inflammation that can result in joint damage
  • Site of inflammation is in the synovium
  • Associated with antibodies: rheumatoid factor, anti-cyclic citrullinated peptide (CCP) antibodies
73
Q

What is ankylosing spondylitis?

A
  • Chronic spinal inflammation that can result in spinal fusion and deformity
  • Site of inflammation is the enthesis
  • No antibodies ‘seronegative’
74
Q

Give examples of seronegative spondyloarthropathies

A
  • Ankylosing spondylitis
  • Reiters syndrom and reactive arthritis
  • Arthritis associated with psoriasis (psoriatic arthritis)
  • Arthritis associated with gastrointestinal inflammation (enteropathic synovitis)
75
Q

What is systemic lupus erythematosus (SLE)?

A
  • Chronic tissue inflammation in the presence of antibodies directed against self-antigens
  • Multi site inflammation but particularly the joints, skin and kidney
  • Associate with autoantibodies: Antinuclear antibodies, anti-double stranded DNA antibodies
76
Q

Give examples of connective tissue diseases

A
  • Systemic lupus erythematous
  • Inflammatory muscle disease: polmyositis, dermatomyositis
  • Systemic sclerosis
  • Sjogren’s syndrome
  • A mixture of the above: ‘Overlap syndromes’
77
Q

What HLA subtype is rheumatoid arthritis linked to?

A

HLA-DR4

- HLA-DR4 triggers CD4+ T cell responses

78
Q

What HLA subtype is Systemic Lupus Erythematosus linked to?

79
Q

What HLA subtype is Ankylosing Spondylitis linked to?

A

HLA- B27

- HLA-B27 triggers CD8+ T cell responses

80
Q

What are the levels of complements and anti-ds-DNA antibodies in SLE?

A

Low complement levels

High serum lvels of anti-ds-DNA antibodies

81
Q

What is the pathogenesis of SLE?

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
82
Q

What is the role of cytokines in rheumatology?

A
  • TNFalpha is the dominant pro-inflammatory cytokine in rheumatoid synovium and its actions are detrimental in this setting
  • We can target:
    IL-2 antibodies in organ transplants
    IL-6 in rheumatoid arthritis
    TNF-alpha
83
Q

What is the importance of RANKL in rheumatology?

A

RANKL is important in bone destruction in rheumatoid arthritis

  • Acts to stimulate osteoclast formation
  • Upregulated by: IL-1, TNFalpha, IL-17, PTH-related peptide
  • Binds to ligand on osteoclast precursors- osteoprotegerin (OPG)
84
Q

What is Denosumab?

A

Monoclonal antibody against RANKL

- Indicated for treatment of osteoporosis, bone metastases, multiple myeloma and Giant cell tumours

85
Q

What is the role of B cells in SLE?

A

B cell hyperreactivity is a key feature.

- To treat SLE, biological therapies have been used with target B cells

86
Q

Which drugs act against B cells to treat SLE?

A

Rituximab- chimeric anti-CD20 antibody used to deplete B cells
Belimumab- monoclonal antibody against a B cell survival factor called BLYS. Inhibits activity of BLYS resulting in impaired B cell survival and reduced B cell numbers

87
Q

What are the key features of rheumatoid arthritis?

A

1) Chronic arthritis:
- Polyarthritis, swelling of the small joints of the hand and wrists
- Symmetrical
- Early morning stiffness in and around joints
- May lead to joint damage and destruction- ‘joint’ erosions on radiographs
2) Extra-articular disease
- Rheumatoid nodules
3) Rheumatoid ‘factor’ may be detected in blood
- IgM auoantibody against IgG

88
Q

What environmental factor contributes to rheumatoid arthritis?

89
Q

What are the commonly affected joints in rheumatoid arthritis?

A
  • Metacapophalangeal joints (MCP)
  • Proximal interphalangeal joints (PIP)
  • Wrists
  • Knees
  • Ankles
  • Metatarsophalangeal joints (MTP)
90
Q

What is the primary site of pathology in rheumatoid arthritis?

A 
Synovium 
This includes 
- Synovial joints 
- Tenosynovium surrounding tendons 
- Bursa
91
Q

What are sub-cutaneous nodules?

A 
Central area of fibrinoid necrosis surrounded by histiocytes and peripheral layer of connective tissue 
 Associated with:
- Severe disease 
- Extra-articular manifestations 
- Rheumatoid factor
92
Q

What is Rheumatoid factor?

A
  • Antibodies that recognise the Fc portion of IgG as their target antigen
  • Typically IgM antibodies
93
Q

Why do antibodies to citrullinated protein antigens develop in rheumatoid arthritis?

A
  • PADs present in high concs in neutrophils and monocytes, there is increased citullination of autogolous peptides in the inflamed synovium
  • ACPA associated with smoking and HLA ‘shared epitope’
  • Shared epitope binds non-polar amino acids like citrulline but not positively charged ones like arginine.
94
Q

What is citrullation of peptides mediated by?

A

Peptidul arginine deiminases (PADs)

- Convert arginine to citrulline

95
Q

What are the extra-articular features of rheumatoid arthritis?

A

Common: Fever, weight loss, subcutaneous nodules
Uncommon: vasculitis ocular inflammation, neuropathies, amyloidosis

96
Q

What are the radiographic abnormalities of rheumatoid arthritis?

A

Early: Juxta-artciular osteopenia
Later: Joint erosions at margins of the joint
Later still: Joint deformity and destruction

97
Q

What is the pathogenesis of rheumatoid arthritis?

A

Synovial membrane is abnormal in rheumatoid arthritis
Synovium becomes proliferated mass of tissue due to:
Neovascularisation
Lymphangiogenesis
Inflammatory cells (activated B and T cells, plasma cells, mast cells, activated macrophages
- Recruitment, activation and effector functions of these cells is controlled by a cytokine network

98
Q

What are DMARDs

A

Disease Modifying Anti-Rheumatic Drugs
- Drugs that may induce remission (not cure) and prevent joint damage
Work by
- Reducing the amount of inflammation in the synovium
- Slow or prevent structural joint damage e.g. bone erosions

99
Q

Give examples of DMARDs

A 
Methotrexate 
Sulphasalazine 
Hydroxychloroquine 
Leflunomide 
Gold 
Penicillamine
100
Q

What are the problems with biological therapies for rheumatoid arthritis?

A
  • TNFalpha inhibition is associated with increased susceptibility to mycobacterial infection
  • B cell depletion therapy can be associated with hepatitis B reactivation
  • B cell depletion therapy can be associated with JC virus infection and progressive multifocal leukoencephalopathy
101
Q

What is reactive arthritis?

A

Sterile inflammation in joints following infection, especially urogenital and gastrointestinal infections

  • May be first manifestation of HIV or heptatitis C infection
  • Distinct from infection in joints (septic arthritis)
102
Q

What are the extra-articular manifestations of arthritis?

A
  • Enthesopathy
  • Skin inflammation
  • Eye inflammation
103
Q

What are the arthritis symptoms of reactive arthirits?

A
  • Joint inflammation and morning joint stiffness
  • Patterns of joints involved can help distinguish from rheumatoid arthritis
  • Asymmetrical oligoarthritis (
104
Q

What are the enthesitis symptoms of reactive arthritis?

A
  • Inflammation where a ligament, tendon, fascia or capsule insert the bone
  • Heal pain (Achilles tendon), swollen fingers (dactylitis), Painful feet (metatarsalgia due to plantar fascilitis)
105
Q

What are the spondylitis symptoms of reactive arthritis?

A
  • Inflammation of the spine
  • Patient may suffer sacroilitis- sacroiliac joint inflammation
  • Spondylitis allows for exclusion of rheumatoid arthritis without any need for investigations
106
Q

What are the extra-articular features of reactive arthritis?

A
  • Ocular: Sterile conjuctivitis
  • Genito-urinary: sterile urethritis
    Skin- circinate balanitis, psoariasis-like rash on hands and feet
107
Q

How does rheumatoid arthritis compare to reactive arthritis with regards to sex and age?

A 
Rheumatoid arthritis:
F>M 
All ages 
Reactive arthritis:
M>F
20-40 years
108
Q

What are the differences between the features of arthritis in rheumatoid and reactive arthritis?

A

Rheumatoid:
- Symmetrical, polyarticular, small & large joints
Reactive:
- Asymmetrical, Oligoarticular, Large joints

109
Q

Is the enthesopathy, spongylitis and urethritis in rheumatoid arthritis and reactive arthritis?

A

Rheumatoid: None of the 3
Reactive: All 3

110
Q

How is skin involved in rheumatoid and reactive arthritis?

A

Rheumatoid: Subcutaneous nodules
Reactive: K.blennorhagicum, Circinate balantis

111
Q

What is the HLA association in rheumatoid and reactive arthritis?

A

Rheumatoid: HLA-DR4
Reactive: HLA-B27

112
Q

How is diagnosis of reactive arthritis established?

A
  • Clinical diagnosis
  • Investigations to exclude other causes of arthritis e.g. septic arthritis
    Investigations:
    Microbiology: cultures, serology
    Immunology: rheumatoid factor
    Synovial fluid examination
113
Q

What are the differences between septic and reactive arthritis?

A 
- Septic arthritis:
Synovial fluid culture- positive 
Antibiotic therapy- yes 
Joint lavage- yes for large joints 
- Reactive arthritis: 
Synovial fluid culture- sterile 
Antibiotic therapy- No 
Joint lavage- no
114
Q

How is reactive arthritis treated?

A
  • Articular: NSAIDs, intra-articular corticosteroid therapy
  • Extra-articular: Typically self limiting, hence symptomatic therapy e.g. topical steroids
  • Refractory disease: oral glucocorticoids, steroid-sparing agents
115
Q

What is osteoarthritis?

A

Chronic slowly progressive disorder due to failure of articular cartilage that typically affects joints of the hand, spine and weight-bearing joints

116
Q

What is affected in osteoarthritis?

A
  • Joints of the hand- distal interphalangeal joints (DIP), Proximal interphalangeal joints (PIP), First carpometacarpal joint (CMC)
  • Spine
  • Weight-bearing joints of lower limbs: esp. knees and hips, first metatarsophalageal joint (MTP)
117
Q

What are osteophytes at DIP joints called?

A

Heberden’s nodes

118
Q

What are osteophytes at the PIP joints called?

A

Bouchard’s nodes

119
Q

What can osteoarthritis be associated with?

A
  • Joint pain
  • Joint crepitus (creaking, cracking grinding sound on moving affected joint)
  • Joint instability
  • Joint enlargement (e.g. Heberden’s nodes)
  • Joint stiffness after immobility
  • Limitation of motion
120
Q

What are the radiographical features of osteoarthritis?

A
  • Joint space narrowing
  • Subchondral bony sclerosis
  • Osteophytes
  • Subchondral cysts
121
Q

How do radiographic changes in rheumatoid arthritis differ from Osteoarthritis?

A 
Rheumatoid arthritis:
Joint space narrowing- YES 
Subchondral sclerosis- NO 
Osteophytes- NO 
Osteopenia- YES
Bony erosions- YES
Osteoarthritis:
Joint space narrowing- YES 
Subchondral sclerosis- YES 
Osteophytes- YES 
Osteopenia- NO 
Bony erosions- NO
122
Q

What causes the problems in osteoarthritis?

A

There is defective and irreversible articular cartilage and damage to the underlying bone
- Develops because of excessive loading on joints and/or abnormal joint components

123
Q

What do the properties of articular cartilage depend on?

A

Weight bearing properties depend on intact collagen scaffold and high aggrecan content

124
Q

What are the cartilage changes in osteoarthritis?

A
  • Reduced proteoglycan
  • Reduced collagen
  • Chondrocyte changes e.g. apoptosis
125
Q

What are the bone changes in osteoarthritis?

A

Changes in denuded sub-articular bone:
- Proliferation of superficial osteoblasts results in production of sclerotic bone e.g. subchondral sclerosis
- Focal stress on sclerotic bone can result in focal superficial necrosis
New bone formation at the joint margins (osteophytes):

126
Q

How is osteoarthritis managed?

A
  • Education
  • Physical therapy
  • OT
  • Weight loss where appropriate
  • Exercise
  • Analgesia (paracetamol, NSAID, intra-articular corticosteroid inject)
  • Joint replacement
127
Q

How does SLE present?

A
  • Malaise
  • Fatigue
  • Fever
  • Weight loss
  • Lymphadenopathy
128
Q

What are the features of SLE?

A 
Specific: 
- Butterfly rash, alopecia 
- Arthralgia 
- Raynaud's phenomenon
Other:
- Inflammation of kidney, CNS, heart, lungs 
- Accelerated atherosclerosis 
- Vasculitis
129
Q

What is the ACR criteria?

A

4 or more indicative of SLE

  • Malar rash
  • Discoid rash
  • Photosensitivity
  • Oral ulcers
  • Arthritis
  • Serositis
  • Renal disorder
  • Neurological disorder
  • Haematological disorder
  • Immunological disorder
  • Anitnuclear antibody in raised titre
130
Q

What is the pathogenesis of SLE?

A

Regulation of B cell function is lose. Hyperactive B cells with a failure to clear apoptotic cells allow for the production of autoantibodies

131
Q

How are autoantibodies formed?

A
  • Abnormal clearance of apoptotic cell material
  • Dendritic cell uptake of autantigens and activation of B cells
  • B cell Ig class switching and affinity mutation
  • IgG autoantibodies
  • Immune complexes
  • Complement activation, cytokine generation
132
Q

What laboratory tests are available for SLE?

A

1) Antinuclear antibodies
2) Anti-dsDNA and Sm
3) Anti-Ro and/or La
4) Haematology
- Lymphopaenia
- Leukopaenia
5) Renal
- Proteinuria
- Active urinary sediment

133
Q

How is the severity of SLE distinguished?

A 
Mild: Joint and/or skin involvement 
Moderate: Inflammation of other organs, pleuritis, pericarditis, mild nephritis
Severe: Severe inflammation in vital organs 
- Severe nephritis 
- CNS disease 
- Pulmonary disease 
- Cardiac involvement 
- AIHA, Thrombocytopaenia, TTP
134
Q

How is mild SLE treated?

A

1) Paracetamol and/or NSAID
- Monitor renal function
2) Hydroxychloroquine
- Arthropathy
- Cutaneous manifestations
- Mild disease activity
3) Topical corticosteroids

135
Q

How is moderate SLE treated?

A

Indicated by failure of hydroxychloroquine/NSAID with presentation of organ/life threatening disease
Corticosteroids:
- High initial dose to suppress activity
- IV methylprednisolone

136
Q

How is severe SLE treated?

A

1) Azathioprine:
- Effective steroid-sparing agent
2) Clycophosphamide:
Used in nephritis
- Can cause BM suppression, infertility, cystitis

137
Q

What is the bimodal mortality pattern of SLE?

A

In early disease of active lupus there is renal failure and CNS disease, as well as infection
- In later less active disease, these patients are at risk of myocardial infarction

138
Q

What is the GALS examination?

A

The purpose is to see if any of the joints are abnormal

Gait, Arms, Legs, Spine

139
Q

How is gait observed in the GALS examination?

A

Observe the patient waking, turning and walking back. Look for:

  • Smoothness and symmetry of leg, pelvis and arm movements
  • Normal stride length
  • Ability to turn quickly
140
Q

How is the spine observed in the GALS examination?

A
  • Is the paraspinal and shoulder girdle muscle bulk symmetrical
  • Is the spine straight?
  • Are the iliac crests level?
  • Is the gluteals muscle bulk normal?
  • Are there popliteal swellings?
  • Are the Achilles tendons normal?
  • Are the spinal curvatures normal?
  • Is lumbar spine and hip flexion normal
  • Is the cervical spine normal?
141
Q

How are the arms observed in the GALS examination?

A
  • Look for normal girdle muscle bulk and symmetry
  • Look to see if there is full extension at the elbows
  • Are shoulder joints normal
  • Examine hands palms down with fingers straight
  • Observe supination, pronation, grip and finger movements
  • Test for synovitis at the metacarpo-phalangeal joints (MCP)
142
Q

How are the legs observed in the GALS examination?

A
  • Look for knee or foot deformity
  • Assess flexion of hip and knee
  • Look for knee swellings
  • Test for synovitis at the metatarso-phalangeal joints
  • Inspect soles of the feet
143
Q

What does a detailed examination of any abnormal joints identified in the GALS screening include?

A
  • Inspection: swelling, redness, deformity
  • Palpitation: warmth, crepitus, tenderness
  • Movement: active, passive, against resistance
  • Function: loss of function
144
Q

What are signs of inflammation?

A
  • Swelling
  • Warmth
  • Eryhthma
  • Tenderness
  • Loss of function
145
Q

What is arthritis?

A

Refers to definite inflammation of joints i.e. swelling, tenderness and warmth of affected joints

146
Q

What is arthralgia?

A

Refers to pain within joints without demonstrable inflammation by physical examination

147
Q

What is dislocation?

A

Articulating surfaces are displaces and no longer in contact

148
Q

What is subluxation?

A

Partial dislocation

149
Q

What is varus deformity?

A

Lower limb deformity whereby the distal part is directed towards the midline
e.g. varus knee with medial compartment osteoarthritis

150
Q

What is valgus deformity?

A

Lower limb deformity whereby the distal part is directed away from the midline
e.g. hallux valgus

151
Q

What is gout?

A

An example of arthritis

  • Disease in which tissue deposition of monosodium urate (MSU) crystals occur as a result of hyperuricaemia and leads to one or more of the following
  • Gouty arthritis
  • Tophi (aggregated deposits of MSU in tissue)
152
Q

What is gouty arthritis?

A

Commonly affects the metatarsophalangeal joint of the big toe (1st MTP joint)

  • Abrupt onset
  • Extremely painful
  • Joint red, warm, swollen and tender
  • Resolves spontaneously over 3-10 days
153
Q

What is enthesopathy?

A

A non-articular soft tissue at the enthesis (the site where ligament or tendon inserts into bone
e.g. plantar fascilities and Achilles tendinitis

154
Q

What is polyarthritis, olgioarthritis and monoarthritis?

A 
Polyarthritis= >4 joints involved
Oligoarthritis= 2-4 joints involved 
Monoarthritis= Single affected joint
155
Q

Why should the symmetry, size of involved joints and axial involvement of arthritis be noted?

A
  • Bilateral and symmetrical involvement of large and small joints is typical of rheumatoid arthritis
  • Lower limb asymmetrical oligoiarthritis and axial involvement would be typical of reactive arthritis
  • Exclusive inflammation of the first metarsophalangeal joints is highly suggestive of gout
156
Q

What joints are commonly involved and spared in rheumatoid arthritis?

A 
Involved= PIP, MCP, wrist, elbow, should, cervical spine, hip, knee, ankle, tarsal, MTP 
Spared= DIP, thoracic spine, lumbar spine
157
Q

What joints are commonly involved and spared in osteoarthritis?

A 
Involved= 1st CMC, DIP, PIP, cervical spine, thoracolumbar spine, hip, knee, 1st MTP, toe IP 
Spared= MCP, wrist, elbow, shoulder, ankle, tarsal joints
158
Q

What joints are commonly involved and spared in polyarticular gout?

A 
Involved= 1st MTP, ankle, knee 
Spared= Axial
159
Q

What is synovial fluid?

A

Viscous fluid present in joint space of synovial joints (diarthroses)

  • Synthesised by synovial lining cells
  • Abnormal increase in synovial fluid volume is termed ‘synovial effusion’
160
Q

What causes non-inflammatory synovial effusions?

A
  • Osteoarthritis

- Mechanical defects

161
Q

What causes inflammatory synovial effusions?

A
  • Gout

- Rheumatoid arthritis

162
Q

When is it useful or important to examine synovial fluid?

A
  • Mandatory when joint infection is suspected

- Useful to confirm diagnosis in suspected crystal arthritis

163
Q

What are characteristics of connective tissue disorders?

A
  • Arthalgia and arthritis is typically non-erosive
  • Serum autoantibodies are characteristics
  • Rayndaud’s phenomenon is common in these conditions
164
Q

What are the clinical manifestations of SLE?

A
  • Malar rash (erythema that spared the nasolabial fold)
  • Photosensitive rash
  • Mouth ulcers
  • Hair loss
  • Raynaud’s phenomenon
  • Athralgia and sometimes arthritis
  • Serositis
  • Renal disease- glomerulonephritis
  • Cerebral disease - ‘cerebral lupus’
165
Q

What is Sjogren’s syndrome?

A
  • Autoimmune exocrinopathy
  • Typically diagnosed in middle ages females
  • Exocrine gland pathology results in dry eyes, dry mouth and parotid gland enlargement
  • Commonest extra-glandular manifestations are non-erosive arthritis and Raynaud’s phenomenon
166
Q

What is inflammatory muscle disease?

A
  • Proximal muscle weakness due to autoimmune-mediated inflammation either with (dermatomyositis) or without (polymyositis) rash
  • Skin changes in dematomyositis: helitrope, Gottron’s papules, subcutaneous calcinosis, mechanic’s hands
  • Associated with autoantibodies
167
Q

What is systemic sclerosis?

A
  • Thickened skin with Raynaud’s phenomenon: dermal fibrosis, cutaneous calcinosis, telangiectasia
  • Skin changes may be limited or diffuse
168
Q

What is overlap syndrome?

A
  • When features of more than 1 connective tissue disorder are present e.g. SLE and inflammatory muscle disease we can use the term overlap syndrome
169
Q

What substance makes synovial fluid viscous?

A

Hyaluronic acid

- A non-sulphated glycosaminoglycan

170
Q

What is a key pathological finding in osteoarthritis?

A

Irreversible loss of articular cartilage

171
Q

What is a proteoglycan?

A

Glycoproteins containing sulphated glycosaminoglycan chains

e.g. Aggrecan

172
Q

What is a glycosaminoglycan?

A

Repeating polymers of disaccharides

e. g.
- Chondroitin sulphate
- Keratan sulphate
- Hyaluronic acid

Year 2: LCRS (8 decks)

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