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ISCM > PATHOLOGY > Flashcards

PATHOLOGY Flashcards

1
Q

what is rickets

A

defective mineralization of growth plates in children (open growth plates )

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2
Q

what does rickets result in

A
  • reduced apoptosis of hypertonic chondrocytes in the growth plate
  • reduced mineralization of primary spongiosa in the metaphysis
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3
Q

what are symptoms of rickets

A
  • bone pain
  • growth retardation
  • delayed achievement of motor milestones
  • bony deformities e.g. bowlegs
  • muscle weakness due to hypocalcemia or hypophosphataemia
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4
Q

what is osteomalacia

A

defective mineralization of existing bone during remodeling process

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5
Q

what happens in osteomalacia

A

bone softening

occurs everywhere in bones of adults (closed growth plates)

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6
Q

what are symptoms of osteomalacia

A
  • proximal muscle weakening and wasting
  • myalgias and arthralgias
  • muscle spasms
  • altered or waddling gait
  • spinal,limb or pelvic deformities
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7
Q

what causes rickets and osteomalacia

A

low dietary ca2+ or inability to absorb it

low vitamin D

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8
Q

what are sources of vitamin D

A
  • made in human skin (D3) after exposure to UV light

- ingested in food (D2) found in plants and D3 in animal products

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9
Q

which organs convert vitamin D and to what

A

liver to calcidiol (25-hydroxyvitamin D)

kidney to calcitriol (active hormone 1,25 dihydroxyvitamin D)

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10
Q

what is the function of calcitriol in low ca2+ conditions

A
  • increased absorption of dietary calcium
  • increased reabsorption of calcium from kidney
  • releasing calcium from bone store
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11
Q

how is ca2+ absorbed from the diet

A
  • in the jejunum

- when the conc is low active transport takes place

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12
Q

how is ca2+ reabsorbed in the kidney

A

-distal tubular calcium re-absorption involves a transcellular mechanism

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13
Q

how is ca2+ conc increased by bone resorption

A
  • at low ca2+ levels the bone is broken down

- calcitriol appears to increase expression of RANKL in osteoblasts resulting in increased osteoclast formation

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14
Q

what are the risk groups of rickets and osteomalacia

A
  • significant poverty
  • low food availability
  • diets low in calcium
  • seasonal lack of sunlight
  • older age reduced bone formation and less ca absorption from diet
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15
Q

what is rheumatoid arthritis

A

a chronic autoimmune disease that causes inflammation of affected joints resulting in cartilage destruction and bone erosion

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16
Q

what are the early signs of rheumatoid arthritis

A
  • fatigue
  • flu like feeling
  • swollen tender joints
  • morning stiffness
17
Q

what are the more advanced symptoms of rheumatoid arthritis

A
  • pleural effusions
  • lung nodules and interstitial lung disease
  • lymphomas
  • atheroscelrosis
  • joint malalignment
  • loss of range of motion
18
Q

what are the clinical manifestations of RA

A
  • octular
  • pulmonary
  • skin
  • gastrointestinal
  • neurological
  • vascular
  • cardiac
  • renal
  • muscular skeletal
  • haematological
19
Q

what causes RA

A
  • genetic predisposition of the respective patient resulting in generation of auto reactive T and B cells
  • a triggering event e.g. a viral or bacterial infection
20
Q

what is autoimmune tissue destruction presented as

A

synovitis which is inflammation of the joint capsule i.e. synovial membrane and synovial fluid

21
Q

what is the joint inflammation maintained by

A
  • dendritic cells
  • T cells
  • macrophages
  • neutrophils
  • fibroblasts
  • osteoclasts
22
Q

what does the chronic inflammation lead to

A

expansion of the synovial membrane which invades the periarticular bone at the cartilage bone junction and this results in bone erosion and cartilage degradation

23
Q

which cells start the process of RA

A

auto reactive Th1 or Th17 primed in the lymph nodes

24
Q

what do the activated auto reactive T cells do

A

activate the macrophages and fibroblasts

25
Q

what do activated macrophages do

A

secrete large quantities of strongly pro inflammatory cytokines and this matins an inflammatory environment in the synovium

26
Q

what do the activated fibroblasts do

A

produce RANK-L promote the differentiation of osteoclasts from macrophages and leads to cartilage destruction and erosion

27
Q

what are the treatments for RA

A

-NSAIDs, immunosuppressive glucocorticoids and disease modifying anti-rheumatic drugs (DMARDs)

ISCM (19 decks)

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