Pathology Flashcards

1
Q

define osteoarthritis

A

degenerative change in articular cartilage due to ageing and stress

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2
Q

two types of osteoarthritis

A
primary= age related, presents over 50
secondary= predisposing condition e.g. excessive weight bearing, systemic conditions, etc.
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3
Q

what joints does OA affect?

A

hips
knees
lumbar and cervical vertebrae
PIP and DIP joints

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4
Q

pathogenesis of OA

A

early= chondrocyte injury, proliferation and inflammatory mediators, proteases, collagen and proteoglycans lead to remodelling- fissures and fibrillation

late= chronic inflammation leads to loss of cartilage and change in subchdonral bone and joint. this causes worn away cartilage, subchdonral cysts, eburnation and osteophytes

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5
Q

radiological features of OA

A
LOSS
loss of joint space (cartilage loss)
osteophytes (disorganised bone remodelling, can irritate nerves)
subchondral sclerosis (eburnation)
subchondrial cysts (synovial fluid accumulation)
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6
Q

define RA

A

chronic AI inflammatory disorder

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7
Q

presentation of RA

A

joint pain (small joints before large ones)
malaise
fever

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8
Q

progression of RA

A

ankylosis
herniation (Baker’s cyst)
involvement of tendons and ligaments

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9
Q

what can patients have periods of in RA

A

remission

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10
Q

extra-articular manifestations of RA

A

rheumatoid nodules
small vessel vasculitis
pleural and pericardial effusions
pyoderma gangrenosum

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11
Q

cause of RA

A

genetics (HLA DRB1 alleles)

environmental triggers lead to cytokine production

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12
Q

acute phase of RA

A

pannus formation (granulation tissue) and destroyed cartilage

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13
Q

chronic phase of RA

A

fibrosis and deformity

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14
Q

what are seronegative spondyloarthritides associated with?

A

HLA B27

affect ligamentous attachments

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15
Q

types of seronegative spondylarthritides

A
  1. ankylosing spondylitis
  2. reactive arthritis
  3. enteritis arthritis
  4. psoriatic arthritis
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16
Q

describe reactive arthritis

A

reaction to infection e.g. chlamydia, shigella, salmonella, etc.

17
Q

describe enteritis arthritis

A

organisms with high LPS in cell wall trigger immune reaction

18
Q

infectious arthritis

A

suppurative: haematogenous spread of organisms, usually affecting a single joint
mycobacterial, Lyme disease and viral

19
Q

cause of crystal arthropathy

A

hyperuricaemia either by increased production (enzyme defect HGPRT) or reduced excretion by kidney (chronic renal disease or side effect of thiazide diuretics)

20
Q

gout crystals

A

urate needle shaped crystals

21
Q

pseudo gout crystals

A

calcium pyrophosphate rhomboid crystals

22
Q

five examples of non-neoplastic bone disease

A
  1. osteoporosis
  2. osteomalacia
  3. hyperparathyroidism
  4. avascular necrosis
  5. Paget’s disease
23
Q

when does peak bone mass occur

A

young adulthood (varies due to diet, activity, genetics, etc.)

24
Q

describe osteomalacia

A

vitamin D deficiency from diet or lack of sunlight

25
Q

role of vitamin D in bone

A

vitamin D stimulates absorption of calcium and osteoblasts to release osteocalcin. Deficiency elevates PTH which causes calcium absorption and release form bone, increased osteoclastic activity and loss of phosphate impairs bone mineralisation, leads to thick osteoid seams and weakened bone

26
Q

describe hyperparathyroidism

A

PTH activates osteoclasts (increased resorption, released Ca2+ and increased phosphate excretion)

27
Q

progression of hyperparathyroidism

A

Brown tumours and osteitis fibrosa cystica

28
Q

describe avascular necrosis

A

loss of vascular supply

29
Q

causes of avascular necrosis

A

predisposing condition e.g. alcohol, drugs

fractures

30
Q

describe Paget’s disease

A

abnormality of bone turnover

31
Q

causes of Paget’s disease

A
genetics= p62
viral infection (paramyxovirus, measles and RSV)
32
Q

presentation of Paget’s

A

pain (nerve compression and fracture)
enlargement
increased metabolism
secondary malignancy