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Musculoskeletal > Musculoskeletal Pathology > Flashcards

Musculoskeletal Pathology Flashcards

1
Q

What kind of condition are connective tissue diseases?

A

Autoimmune conditions = inflammatory conditions characterised by the presence of autoantibodies

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2
Q

What are some specific autoantibodies that have strong links with specific diseases?

A

Rheumatoid factor = rheumatoid arthritis
Structural parts of DNA = SLE
Anticentromere, antitelomere = Scleroderma
Anti Jo = Dermatomyositis

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3
Q

What occurs in rheumatoid arthritis?

A

Inflammation of joints = cartilage is destroyed by inflammatory process causing loss of joint space

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4
Q

What is rheumatoid factor?

A

Autoantibody against Fc IgG

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5
Q

What occurs in the acute and chronic phases of rheumatoid arthritis?

A 
Acute = Pannus formation (inflammatory granulation tissue), hyperplastic/reactive synovium
Chronic = fibrosis, deformity
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6
Q

What occurs in SLE?

A

Prototypic autoimmune disease where autoantibodies are directed at the structural parts of DNA

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7
Q

What are some autoantibodies involved in SLE?

A

ANA (>95%), Anti double stranded DNA (40-60%), Anti-Sm, RNP, SS-A and B

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8
Q

What occurs in inflammatory arthritis usually?

A

Chronic inflammation = lymphocytes and plasma cells

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9
Q

What are some acute features of inflammatory arthritis?

A

Oedema, fibrin, reactive features in synovial cells

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10
Q

When should a biopsy be taken in inflammatory arthritis?

A

To exclude other conditions

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11
Q

What are some examples of metabolic diseases that affect the joints?

A

Crystal arthropathies, Paget’s disease, osteomalacia

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12
Q

How can gout arise?

A

Urate formed in DNA replications as adenine and guanine are purine based, uric acid is the end product of purine synthesis, leads to needle shaped crystal formation

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13
Q

What are the two ways hyperuricaemia can arise?

A

Increased production

Reduced excretion = under-excretion most common cause, drug side effect (thiazide diuretics reduce urate excretion)

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14
Q

What are some causes of increased uric acid production?

A 
Usually idiopathic (unknown enzyme defect in 90%)
HGPRT deficiency = Lyoch Nyhan syndrome (rare)
Increased cell turnover (e.g cancer, psoriasis)
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15
Q

Where do urate crystals tend to form?

A

In joints (lower temperatures)

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16
Q

What is the name for the deposition of urate crystals in soft tissue?

A

Gouty tophus

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17
Q

What are some clinical manifestations of crystal arthropathies?

A

Precipitation of crystals (reduced solubility)
Acute inflammatory reaction
Gouty tophus
Secondary degenerative changes in joint
Renal disease (stones and direct deposition in tubules and interstitium)

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18
Q

How is cytology performed of crystal arthropathies?

A

Joint fluid examined under cross-polarised light to detect needle shaped crystals

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19
Q

What does histology of crystal arthropathies show?

A

Amorphous eosinophilic debris and inflammation (giant cells), crystals lost during tissue processing, pyrophosphate arthropathy

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20
Q

What crystal arthropathies can calcium pyrophosphate cause?

A

Pseudogout or chondrocalanosis, usually older patients in large joints, idiopathic

21
Q

What are some causes of calcium pyrophosphate crystal arthropathies?

A

Hypercalcaemia (e.g hyperparathyroidism), haemachromatosis, hypomagnesaemia, ochronsis, hypothyroidism

22
Q

How does calcium pyrophosphate appear on x-rays?

A

Dense deposits

23
Q

What are some features of pseudogout?

A

Usually asymptomatic, incidental finding, range of joint pain, crystals aren’t distinct histologically, weak positive birefringence on fresh microscopy

24
Q

How are pseudogout crystals different from the crystals of regular gout?

A

Rhomboid shaped crystals (rather than needle shaped), thicker and bigger than urate crystals

25
Q

What is Paget’s disease?

A

Abnormality of bone turn-over, increased osteoclastic activity, more bone but not structured normally

26
Q

What are some suggested mechanisms of Paget’s disease?

A

Genetic elements = SQSTM1/p62
RANKL = osteoclast receptor activator Nf kb ligand
Viral infection = paramyxovirus, RSV ,measles (virus capsule protein MVNP stimulates osteoclast activity)

27
Q

What are the three stages of Paget’s disease?

A

Osteolytic, mixed, burnt out

28
Q

What is the net result of Paget’s disease?

A

Thick excess bone with abnormal reversal lines (mosaic patterns)

29
Q

How can pain arise in Paget’s disease?

A

From microfracture or nerve compression

30
Q

What are some features of the abnormal growth and enlargement that occurs in Paget’s disease?

A

Leontiasis ossea (new hates), platybasia (skull base abnormality), sabre tibia

31
Q

Which bones are less affected by Paget’s disease?

A

Axial or small bones

32
Q

What are some results of the high metabolism caused by Paget’s disease?

A

Heat, warm skin, AV shunt, high output cardiac failure

33
Q

What secondary malignancy can arise from Paget’s disease?

A

Osteosarcoma

34
Q

What is osteomalacia, and how does it manifest?

A

Abnormal vitamin D metabolism related to sun-exposure; manifests as Rickets in young = bowed legs, square heads, pigeon chests, rickety rosary

35
Q

What occurs when a fracture initially happens?

A

Trauma, bone breaks causing pain (from periosteum), haemorrhage

36
Q

What occurs in the initial phase of fracture healing?

A

Haematoma (fibrin mesh), influx of inflammatory cells, cytokine release to recruit osteoprogenitor cells form periosteum and medullary cavity

37
Q

What should have occurred one week after a fracture occurs?

A

Callus formed, organised haematoma, early recruitment and remodelling at ends of bone

38
Q

What is present between two and three weeks after a fracture has occurred?

A

Maximum girth of callus, woven bone deposits perpendicular to cortical bone, some cartilage deposition at fracture site (undergoes endochondral ossification), bridging with bony callus

39
Q

What occurs in remodelling of a bone?

A

Woven bone in callus constantly remodelled, areas under less stress are resorbed and eventually bone returns to normal shape

40
Q

What are some features of pathological fractures?

A

Most common cause for hips to come to pathology, bone isn’t normal prior to break, bone breaks with low level of injury

41
Q

What are some causes of pathological fractures?

A

Osteoporosis, tumours = benign (children, primary tumours) or malignant (adults, metastatic disease)

42
Q

What cancers tend to cause bony metastases?

A

Lung, kidney, breast and prostate

43
Q

What are the three kinds of metastatic bone disease?

A 
Osteolytic = most common, bone is resorbed, appear as radiolucent
Osteosclerotic = prostate cancer, appear as opacity
Myeloma/plasmacytoma = malignant proliferation of plasma cells causes bony lesions
44
Q

What is the first thing that occurs when a joint is changing?

A

Small cracks in cartilage, followed by fibrillation

45
Q

What occurs once cartilage has been completely worn away at a joint?

A

The surface become polished (eburnation) and the cortical bone thickens greatly to cope with the load

46
Q

What do fractures cause to happen in a changing joint?

A

Leakage of synovial fluid through bone, forming small cysts

47
Q

What occurs as a result of rapid remodelling to cope with stress at a changing joint?

A

Remodelling is disorganised and produced abnormal outgrowths (osteophytes)

48
Q

What are some radiological appearances of joint changes?

A

Loss of joint space = cartilage loss
Subchondral sclerosis = eburnation
Subchondral cysts = synovial fluid accumulation
Osteophytes = disorganised bone remodelling

Musculoskeletal (57 decks)

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