pathology Flashcards

1
Q

what is osteoarthritis

A

Most common form of joint disease. Results from damage to articular cartilage induced by an interaction of genetic, metabolic and biochemical factor, leading to an inflammatory response affecting cartilage, subchondral bone, ligaments, menisci, synovium and capsules

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2
Q

what is the pathogenesis of osteoarthritis

A
  • ageing and biochemical stress
  • primary = insidious, no overt cause, age related
  • secondary = predisposing condition, excess/inappropriate weight bearing, deformity, injury, systemic conditions
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3
Q

what is cartilage made of

A

water, organic extracellular matrix components, mainly type 2 collagen and aggrecan or other proteoglycans

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4
Q

what is the pathogenesis of osteoarthritis

A

structural changes include surface fibrillation and ulceration with loss of cartilage that exposes underlying bone to stress, producing microfractures and cysts leading to abnormal sclerotic subchondral bone and overgrowths at joint margins, called osteophytes

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5
Q

what mechanisms can cause osteoarthritis

A
  • abnormal stress and loading
  • obesity
  • matrix degradation
  • tissue inhibitors metalloproteinases
  • osteoprotegerin, RANK and RANK ligand
  • aggrecanase
  • inflammatory mediator release
  • growth factors
  • cell derived and/or cartilage breakdown products
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6
Q

what are clinical features of oesteoarthritis

A

Causes mechanical pain with movement and/or loss of function

Early OA is rarely symptomatic unless accompanied by a joint effusion while advanced radiological and pathological OA is not always symptomatic

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7
Q

what are symptoms of osteoarthritis

A
  • joint pain with movement and/or weight bearing
  • short lived morning joint stiffness
  • functional limitations
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8
Q

pathogenically what are the features of osteoarthritis

A

early

  • damage to cartilage
  • clusters of chondrocytes
  • small fissures in cartilage
  • fibrillation

late

  • cartilage is completely worn away- bone on bone
  • subchondral cysts
  • surface becomes “polished” - eburnation
  • remodelling to cope with stress
  • formation of osteocytes
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9
Q

what are signs of osteoarthritis

A
crepitus 
restricted movement 
bony enlargement 
joint effusion and variable levels of inflammation 
bony instability and muscle wasting
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10
Q

what characterises inflammatory arthritis

A

synovial inflammation

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11
Q

what are the 3 main subgroups of inflammatory arthritis

A

rheumatoid arthritis
spondyloarthritis
crystal arthritis

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12
Q

what are tests for osteoarthritis

A

Plain radiographs show: Loss of joint space, Osteophytes, Subarticular and subchonral cysts

CRP might be slightly elevated

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13
Q

what is rheumatoid arthritis

A

A chronic systemic inflammatory disease, characterised by symmetrical, deforming, peripheral polyarthritis

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14
Q

what does rheumatoid arthritis present with

A
  • symmetrical swollen, painful, stiff small joints of hands and feet worse in the morning
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15
Q

what are early signs of rheumatoid arthritis

A
  • inflammation, symmetrical
  • look for tenosynovitis or bursitis
  • no joint damage
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16
Q

what are later signs of rheumatoid arthritis

A
  • joint damage
  • deformity
  • ulnar deviation and flexion of the wrists and fingers
  • boutonnieres and swan neck deformities of fingers or z deformity of thumbs
17
Q

what are clinical correlations of rheumatic arthritis

A
  • vague systemic features: malaise, fever
  • generalised musculoskeletal pain
  • symmetrical: swollen, warm, painful, limited movement in the morning and after inactivity
  • small joint involvement before big joint involvement
18
Q

what is the progression of rheumatic arthritis

A
  • Joint swelling. Decreased range of movement. Joint fusion (ankylosis)
  • Associated involvement of tendons and ligaments
  • Unstable, very limited ROM
  • Synovial herniation - cysts
  • Joint effusion
19
Q

what is the immunology of rheumatoid arthritis

A
  • Autoimmune inflammation triggered
  • CD4+T helper cells may be critical
  • Cytokine production results from initiation of inflammation:

IFNg activates macrophages and synovial cells
IL-17 recruits neutrophils
TNF and IL-1 stimulate production of proteases from synoviam
RANKL expressed on activated T cells stimulates bone reabsorption

20
Q

what is panes formation

A

type of extra growth in your joints that can cause pain, swelling, and damage to your bones, cartilage, and other tissue

21
Q

what are some extra-articular manifestations of rheumatic arthritis

A
  • nodules: elbows, lungs, cardiac…
  • small vessel vasculitis
  • ocular: keratoconjunctivitis
  • lungs: pleural disease, interstitial fibrosis, bronchiolitis
  • cardiac: pericarditis
22
Q

what is crystal arthropathies: gout

A

typically presents with monoarthropathy with severe joint inflammation. >50% occur in the metatarsophalangeal joint of the big toe

23
Q

how is hyperurucaemia synthesised

A

From purine catabolism

Reflects abnormal purine metabolism

24
Q

how is hyperurucaemia excreted

A

Renal filtration
Reabsorbed in proximal tubule
Limited excretion from distil tubule

25
Q

what can cause hyperuraeceamia

A
  • usually idiopathic
  • known enzyme defect - HGPRT deficiency
  • increased cell turnover
26
Q

what are clinical manifestations of gout

A
  • unclear how crystals end up in joint

- causes secondary degenerative changes in joint