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Hamzah's MSK pathology > Hamzah's MSK pathology > Flashcards

Hamzah's MSK pathology Flashcards

1
Q

What is osteoarthritis?

A

A group of diseases characterised by joint degradation

  • usually primary - no clear underlying disorder
  • can be secondary to joint disease - gout, rheumatoid arthritis
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2
Q

Epidemiology of OA

A
  • most common joint condition
  • F:M = 3:1
  • onset = >50 years
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3
Q

Pathophysiology of OA

A
  • progressive destruction and loss of articular cartilage with accompanying periarticular bone response
  • low-grade inflammation –> IL1 and TNFalpha leads to the release of metalloproteinases from chondrocytes which degrades the cartilage matrix
  • underlying bone is exposed and responds by becoming thickened –> cyst formation
  • osteophytes –> cartilaginous growths at margins of the joint which become calcified
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4
Q

Clinical presentation of OA

A
  • symptoms typically worsen during the day with activity
  • localised - knee and hip
  • pain on movement and crepitus
  • background pain at rest
  • joint gelling –> stiffness after 30 mins of rest
  • joint instability
  • bony nodules - Heberden’s nodules=PIP, Bouchard’s nodules=PIP
  • mild synovitis
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5
Q

Differential diagnosis of OA

A

Rheumatoid arthritis

  • pattern of joint movement
  • absence of systemic features
  • RA has marked early morning stiffness
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6
Q

Diagnostic tests in OA

A
  • Radiography shows LOSS
  • Loss of joint space
  • osteophytes
  • subarticular sclerosis
  • subchondral cysts
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7
Q

Treatment of OA

A
  • non-pharmacological = weight loss, exercise, physical therapy
  • pharmacological - analgesia (paracetamol, NSAIDs (+PPI))
  • hyaluronic acid injections
  • surgery - joint replacement
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8
Q

What is rheumatoid arthritis?

A

= A chronic systemic inflammatory disease with a symmetrical, deforming, peripheral polyarthritis

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9
Q

Epidemiology of RA

A
  • prevalence = 1%
  • F:M = 2:1
  • peak onset = 40-50 years
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10
Q

Aetiology of RA

A
  • pre-menopausal women are significantly more affected than men/post-menopausal women
  • FH
  • Genetic features - HLA DR4 and HLA DR1
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11
Q

Pathophysiology of RA

A
  • activated T cells, macrophages, mast cells and fibroblasts contribute to inflammation
  • local production of rheumatoid factor (autoantibodies against Fc portion of IgG) leads to immune complex formation and complement activation
  • infiltration of synovium occurs by immune cells –> synovitis
  • angiogenesis of synovium occurs
  • synovium proliferates
  • pannus formation
  • pannus erodes into the articular cartilage and destroys the joint, producing bony erosions
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12
Q

Clinical presentation of RA

A
  • symmetrical, swollen and painful joints - worse in morning
  • extra-articular symptoms = fever, fatigue, weight loss, pericarditis
  • ulnar deviation of fingers
  • Boutonniere and swan-neck deformities
  • vasculitis, carpal tunnel syndrome, lymphadenopathy, rheumatoid nodules in elbows and lungs
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13
Q

Differential diagnosis of RA

A

SLE, OA, psoriatic arthritis, spondyloarthropathies

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14
Q

Diagnostic tests in RA

A
  • Rheumatoid factor (not very specific)
  • Anti-cyclic citrullinated peptide antibodies (anti CCP) - highly specific
  • XR - soft tissue swelling, loss of joint space, juxta-articular osteopenia
  • US/MRI - synovitis
  • anaemia of chronic disease
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15
Q

Treatment of RA

A
  • DMARDs - methotrexate
  • Biological agents - Infliximab
  • NSAIDs for symptom relief
  • Physiotherapy and occupational therapy
  • Surgery
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16
Q

What is gout?

A

deposition of monosodium urate crystals in joints

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17
Q

Aetiology of gout

A
  • increased consumption of purines = shellfish, anchovies, red meat
  • decreased clearance of uric acid - kidney failure
  • DM, CVD, hypertension
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18
Q

Pathogenesis of gout

A

purines –> uric acid –> urate ion and sodium ion = monosodium urate crystals

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19
Q

Clinical presentation of gout

A
  • acute monoarthropathy with severe joint inflammation
  • > 50% occur at metatarsophalangeal joint
  • can also affect ankle, foot, hand, wrist, elbow, knee
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20
Q

What are permanent deposits called in chronic gout?

A

tophi

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21
Q

Differential diagnosis of gout

A

pseudogout, septic arthritis

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22
Q

Diagnostic tests in gout

A
  • polarised light microscopy of synovial fluid shows white crystals
  • serum urate is raised or normal
  • radiography - soft tissue swelling, punched out erosions in juxta-articular bone
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23
Q

Treatment of gout

A
  • symptoms subside in 3-5 days
  • colchicine - inhibits leukocyte migration
  • NSAIDs or etoricoxib (selective COX2 inhibitor)
  • Hydrocortisone
  • allopurinol - xanthine oxidase inhibotor
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24
Q

What does xanthine oxidase do?

A

catalyses the conversion of purine to uric acid

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25
Q

How do you prevent gout?

A
  • prophylaxis = allopurinol
  • lose weight
  • avoid prolonged fasts, alcohol, red meat and low-dose aspirin
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26
Q

What crystals are present in pseudogout?

A

calcium pyrophosphate

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27
Q

Risk factors for pseudogout

A

old age, hyperparathyroidism, haemochromatosis, hypophosphatemia

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28
Q

Pathogenesis of pseudogout

A
  • caused by the deposition of calcium pyrophosphate in a joint
  • pyrophosphate is a by-product of the hydrolysis of nucleotide triphosphates within chondrocytes
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29
Q

Typical patient with pseudogout…

A

pseudogout is typically seen in elderly women and usually affects the knee or wrist

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30
Q

Diagnostic tests for pseudogout

A
  • polarised light microscopy of synovial fluid shows calcium pyrophosphate crystals
  • XR - soft tissue calcium deposition
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31
Q

Treatment of pseudogout

A
  • acute attacks = cool packs, rest, aspiration, intra-articular steroids
  • NSAIDs and colchicine may prevent acute attacks
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32
Q

What is osteoporosis?

A

reduced bone mass –> increased fracture risk

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33
Q

Epidemiology of osteoporosis

A
  • > 50 women=18%, men=6%
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34
Q

Aetiology of osteoporosis

A
  • inadequate peak bone mass or ongoing bone loss

- glucocorticoids

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35
Q

What is peak bone mass dependant on?

A

genetics, nutrition, sex hormones, physical activity

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36
Q

How do glucocorticoids cause osteoporosis?

A
  • decrease osteoblast activity and lifespan
  • reduce calcium absorption from the gut and increase renal clearance of calcium
  • suppress sex hormone production –> increases bone turnover and loss
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37
Q

Risk factors for osteoporosis

A

SHATTERED

  • Steroid use (>5mg/day prednisolone)
  • Hyperparathyroidism, hyperthyroidism, hypercalciuria
  • Alcohol and tobacco
  • Thin (<22BMI)
  • Testosterone low
  • Early menopause
  • Renal or liver failure
  • Erosive/inflammatory bone disease - myeloma, RA
  • Dietary calcium low, T1DM
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38
Q

Clinical presentation of osteoporosis

A

Only symptoms tend to be fractures

  • thoracic and lumbar vertebrae
  • proximal femur
  • distal radius (Collie’s fracture)
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39
Q

Diagnostic tests in osteoporosis

A
  • XR
  • bone densitometry - DEXA scan - T score less than -2.5=osteoporosis
  • bloods - calcium, phosphate and alkaline phosphatase all normal
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40
Q

What is used to guide treatment in osteoporosis?

A

FRAX tool - gives ten year probability of fracture

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41
Q

Lifestyle measures in osteoporosis

A
  • quit smoking, reduce alcohol consumption
  • weight-bearing and balance exercises - reduces fall risks
  • calcium and vitamin D supplements
  • Home-based falls prevention programme
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42
Q

Pharmacological management of osteoporosis

A
  • Bisphosphonates = first line treatment = alendronate
  • Calcium and vitamin D supplements
  • HRT - prevents osteoporosis but does not treat
  • Denosumab - monoclonal antibody to RANK-L (twice yearly)
43
Q

What is osteomalacia?

A

Inadequate bone mineralisation –> soft bones

  • children = rickets
  • adults = osteomalacia
44
Q

Causes of osteomalacia

A
  • impaired metabolism of vitamin D, phosphate or calcium
  • Vit D deficiency: intestinal malabsorption (coeliac, crohn’s), not enough UV exposure, phenytoin, liver and kidney diseaese
45
Q

Osteoblasts secrete

A

osteoid - made of type 1 collagen

- this provides the framework and calcium and phosphate crystals are then deposited

46
Q

What enzyme is involved in bone mineralisation?

A

alkaline phosphatase - increases in response to osteoblast activity

47
Q

How does vitamin D regulate calcium and phosphate?

A
  • inactive vitamin D –> 25-hydroxyvitamin D (liver, 25-hydroxylase)
  • 25-hydroxyvitamin D –> 1,25-dihydroxyvitamin D (calcitriol) - (kidneys, 1-alpha hydroxylase)

Calcitriol =

  • increases renal absorption of calcium
  • increases intestinal absorption of calcium and phosphate
48
Q

Parathyroid hormone

A
  • secreted in response to low calcium levels
  • stimulates calcium and phosphate resorption from bone
  • boosts 1,alpha hydroxylase activity –> more vit D absorbed from gut
  • increases calcium reabsorption and potassium secretion from the kidneys
49
Q

Inadequate mineralisation in children

A

leads to soft bones, impaired growth and malformations

50
Q

Inadequate mineralisation in adults

A

weakening and softening of bones –> easier to fracture

51
Q

Clinical presentation of osteomalacia

A
  • diffuse bone and joint pain
  • proximal bone weakness
  • bone fragility
  • increases risk of fractures
  • muscle spasms and numbness
  • rickets = delayed closure of fontanelles, bowlegs, prominent frontal bone
52
Q

Diagnosis of osteomalacia

A
  • Bloods - low vitamin D, calcium, elevated alkaline phosphatase and high PTH
  • XR = decreases bone mineral density, loss of cortical bone
  • bone biopsy - incomplete bone mineralisation
53
Q

Treatment of osteomalacia

A
  • oral vitamin D supplementation
  • treat underlying cause
  • prevention = vit D supplements during pregnancy and to neonates/infants
54
Q

What are spondyloarthropathies?

A
  • arthritis affecting the spinal column and peripheral joints and enthesitis
  • ankylosing spondylitis
  • reactive arthritis
  • psoriatic arthritis
55
Q

What is the gene associated with spondyloarthropathies?

A

HLA B27

56
Q

What is ankylosing spondylitis?

A
  • chronic inflammatory disease of the spine and sacroiliac joints
  • men present earlier
57
Q

Clinical presentation of ankylosing spondylitis

A
  • male <30 with gradual lower back pain
  • spinal morning stiffness relieved by exercise
  • pain improves towards the end of the day
  • pain radiates from sacroiliac joints to hip/buttock
  • enthesitis, iritis, fatigue
  • associated with osteoporosis, aortitis, pulmonary fibrosis
58
Q

Diagnostic tests in ankylosing spondylitis

A
  • XR - bamboo spine, sacroiliitis
  • MRI
  • vertebral syndesmophytes
  • FBC - normocytic anaemia
  • raised ESR/CRP
  • HLA B27 positive
59
Q

Treatment of ankylosing spondylitis

A
  • exercise
  • NSAIDs
  • Infliximab - TNF alpha blocker
  • local steroid injections
  • bisphosphonates - alendronate
  • hip replacement
60
Q

Psoriatic arthritis

A

occurs in 10-40% of psoriasis patients

  • mostly affects DIP joint
  • symmetrical polyarthritis
61
Q

Presentation of psoriatic arthritis

A
  • nail changes, synovitis, acneiform rashes, palmoplantar pustulosis
  • radiology - erosive changes, ‘pencil in cup’ deformity
62
Q

Treatment of psoriatic arthritis

A
  • NSAIDs
  • infliximab
  • methotrexate
63
Q

What is reactive arthritis?

A

arthritis that occurs within 1 month of an infection elsewhere in the body
- usually related to a GU infection with chlamydia or GI infection with shigella, salmonella or campylobacter

64
Q

Clinical presentation of reactive arthritis

A
  • stiffness and pain in lower limb, asymmetric pattern with urethritis
  • Reiter’s triad = urethritis, arthritis, conjunctivitis
65
Q

Diagnostic tests in psoriatic arthritis

A
  • Raised ESR/CRP
  • culture stool if diarrhoea
  • XR - enthesitis with periosteal reduction
66
Q

Treatment of psoriatic arthritis

A
  • NSAIDs/steroid injections

- methotrexate

67
Q

What is septic arthritis?

A

joint inflammation caused by a microbe
- all joints get infected

CAN COMPLETELY DESTROY A JOINT WITHIN DAYS

68
Q

How can bacteria enter a joint?

A
  • pre-existing infection
  • haematogenous spread
  • contiguous spread = infection spreads from one area to another
69
Q

Pathophysiology of septic arthritis

A
  • Bacteria have PAMPs and these initiate an immune response
  • inflammatory response occurs - joint becomes red, swollen and warm
  • fluids accumulate in joint space - increased intra-articular pressure –> compressed blood vessels –> necrosis of affected bones and cartilage
70
Q

Clinical presentation of septic arthritis

A
  • differ according to underlying pathogen
  • joint pain
  • impaired range of movement
  • fever
  • Neisseria gonorrhoeae = haematological spread –> affects multiple joints and tenosynovitis
71
Q

Aetiology of septic arthritis

A
  • majority = non-gonococcal arthritis - staph aureus

- minority = gonococcal arthritis - Neisseria gonorrhoeae

72
Q

Diagnosis of septic arthritis

A
  • joint aspiration - MC&S of synovial fluid, high WCC, positive gram stain
  • XR, US, CT, MRI - bone erosion and joint effusion
73
Q

Treatment of septic arthritis

A
  • antibiotics
  • analgesics
  • joint aspiration - arthrocentesis
  • surgical operation - arthrotomy
74
Q

What is osteomyelitis?

A

inflammation of the bone or bone marrow due to an infection

75
Q

Cortical bone structure

A

contains osteons which have an empty centre - Haversian canals - contain blood vessels and nerves

76
Q

Aetiology of osteomyelitis

A
  • staph aureus

- salmonella - particularly affects individuals with sickle cell disease

77
Q

Pathophysiology of osteomyelitis

A
  • bacteria proliferates at bone
  • immune response
  • acute myelitis can be resolved –> osteoblasts and osteoclasts can repair the damage if the lesion is not extensive
  • chronic –> affected bone becomes necrotic and separates from healthy bone = SEQUESTRUM –> osteoblasts may form new bone which wraps around the sequestrum = INVOLUCRUM
  • inflammation may involve periosteum - can separate and allow abscess to form between
  • infection can spread to a nearby joint
78
Q

Clinical presentation of osteomyelitis

A

Acute osteomyelitis

  • pain at site of infection
  • fever
  • may affect use of bone

Chronic osteomyelitis

  • prolonged fever
  • weight loss
79
Q

Diagnosis of osteomyelitis

A
  • FBC - high WCC, ESR, CRP
  • XR - thickening of cortical bone and periosteum, elevation of periosteum, loss of trabeculae architecture, osteopenia
  • MRI - identifies abscess
  • bone biopsy - find pathogen responsible and confirm diagnosis
80
Q

Treatment of osteomyelitis

A
  • antibiotics
  • abscess - surgery
  • surgery to remove any necrotic bone (sequestrum)
81
Q

What is SLE?

A

Autoimmune disease that affects a wide variety of organs and causes red lesions on the skin

Lupus is characterised by periods of flare ups and remittance

82
Q

Pathogenesis of SLE

A
  • environmental trigger (e.g. UV) damages cells and causes apoptosis
  • genetic component means that susceptible individuals have certain genes that mean that cell debris is not effectively cleared –> lots of nuclear antigens
  • immune response against nuclear antigens
  • antigen-antibody complexes are deposited in numerous tissues (T3 hypersensitivity) –> this leads to an inflammatory response
  • antibodies can also be made against erythrocytes and leukocytes (T2 hypersensitivity)
83
Q

Clinical presentation of SLE

A

Classic presentation = fever, rash, joint pain in women of child-bearing age

  • weight loss
  • specific = depends on affected organs/tissues
84
Q

Diagnosis of SLE

A

4 or more of 11 criteria

  • malar rash - butterfly rash
  • discoid rash
  • ulcers in mouth and nose
  • serositis - pericarditis, pleuritis
  • arthritis - >2 joints
  • renal disorders
  • neurological disorders - seizures
  • haematological disorders - cytopenia
  • anti-nuclear antibodies (not specific as seen in other autoimmune conditions)
85
Q

Treatment of SLE

A
  • prevent flare ups and limit the severity of flare ups
  • avoid sunlight exposure
  • corticosteroids - limits immune response
  • immunosuppressants
86
Q

What is the difference between primary bone tumours and secondary bone tumours?

A
  • primary = arise from bone cells

- secondary = metastasise from somewhere else and spread to bone (source = breast, prostate, thyroid, lung, kidneys)

87
Q

Parts of bone (top to bottom)

A
  • Epiphysis
  • Metaphysis (contains growth plates)
  • Diaphysis (bone shaft)
88
Q

What do proto-oncogenes do?

A

promote normal cell growth

89
Q

What do oncogenes do?

A

overstimulate cell growth

90
Q

What do tumour suppressor genes do?

A

promote apoptosis

91
Q

Give examples of benign bone tumours

A
  • osteochondroma
  • giant cell tumour of bone
  • osteoblastoma (large nidus)
  • osteoid osteoma (small nidus)
92
Q

Give examples of malignant bone tumours

A
  • osteosarcoma

- chondrosarcoma

93
Q

Clinical presentation of bone tumours

A
  • bone pain, fractures, swelling
  • can cause numbness due to pressure on nerve
  • malignant tumours –> chronic inflammatory response = fever, night sweats, weight loss, pulmonary symptoms (can metastasize to lungs)
94
Q

Diagnosis of bone tumours

A
  • Imaging = XR, CT, MRI - osteochondroma=exostosis, giant cell tumour=soap bubbles (multicystic bone lesions), osteosarcoma=lytic bone lesions-sunburst appearance
  • testing for serum markers
95
Q

Treatment of bone tumours

A
  • depends on whether they are benign or malignant
  • benign = surgically removed
  • malignant = radiotherapy, chemotherapy, surgery
96
Q

What is Paget’s disease

A

disorder where there is a lot of bone remodelling - excessive bone resorption and growth –> skeletal deformities and potential fractures

97
Q

What do osteoblasts secrete?

A
  • osteoid
  • RANK-L
  • OPG - osteoprotegerin (binds to RANKL and stops it binding)
98
Q

Etiology of Paget’s diseaes

A
  • unknown
  • infection - measles virus
  • genetic mutations - SQSTM1
99
Q

Phases of disease in Paget’s

A
  • lytic phase = osteoclasts aggressively demineralise bone
  • mixed phase = lytic and blastic phase - rapid proliferation of new bone tissue by osteoblasts - collagen deposited in a haphazard way
  • sclerotic phase = new bone formation exceeds bone resorption - disorganised and weaker bone
100
Q

Clinical presentation of Paget’s disease

A
  • typically no symptoms early on
  • misshapen bones can impinge nerves and cause pain
  • overgrowth of skull –> leontasis (lion-face), hearing and vision loss
  • Kyphosis
  • lower limb muscle weakness
  • Pelvic asymmetry
  • Bowlegs
  • arthritis
  • osteosarcoma –> Paget’s sarcoma
101
Q

Diagnosis of Paget’s disease

A
  • high alkaline phosphatase, calcium and phosphate normal
  • XR - lytic lesions - thickened bone cortices
  • Bone biopsy - excludes malignancy
102
Q

Treatment of Paget’s disease

A
  • pain relief
  • antiresorptive medications = bisphosphonates
  • surgery - correct bone deformities, decompress impinged nerves, reduce fractures
103
Q

What is Sjogren’s syndrome?

A

autoimmune destruction of exocrine glands

Hamzah's MSK pathology (1 decks)

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