MSK Flashcards
cardinal signs of inflammation
rubor = redness callor = hot dolor = pain tumour = swelling
what deformities do you see in RA
boutonniere
swan neck
ulnar deviation
which cells can act as APCs
macrophages
dendritic cells
b cells
give some examples of extra-articular symptoms/involvement in RA
eyes - scleritis and sicca (esp secondary to sjogrens)
skin - nodules and vasculitis
soft tissue - bursitis, tenosynovitis and muscle wasting
kidneys - amyloidosis
lungs - pleural effusions
CVS - pericarditis, pericardial rub
neuro - polyneuropathy
haematological - anaemia and splenomegaly
difference in morning stiffness in OA and RA
OA 60 mins
difference in joint involvement in OA and RA
OA - weight bearing joints, CMCJ and DIPJ
RA - NEVER DIPJ
–> symmetrical involvement of small joints of hands and feet, common in wrists, MCP and PIPs
examples of TNF-a inhibitors used in RA and explain mechanism of action
etanercept, infiliximab, adalimumab
- -> bind to TNF and prevent its interaction with receptors (remove it from inflam sites and prevent it reaching its receptors)
- -> prevents its effects of mediating/stimulating release of other cytokines
what is tocilizumab and how does it work
= DMARD - IL-6 inhibitor
- -> binds to IL receptor therefore prevents IL-6 from binding and inhibiting cell communication
- -> inhibits production of more T and B cells and therefore reduces inflam at joints
what is anakinra
IL-1 inhibitor
what is rituximab and how does it work
= B cell inhibitor
targets CD20 and prevents the release of cytokines and inflam mediators
also prevents B cells acting as APCs
what is abatacept and what is its mechanism of action
= t cell inhibitor
decreases t cell activation and prolif
decreases release of pro-inflam cytokines
upstream modulation (preventing downstream changes)
decreases autoAb production
regulates function of CD4+ cells
what triad of features do you see in Felty’s syndrome
seropositive RA
splenomegaly
neutropenia
why are women at higher risk of osteoporosis post-menopause
because bone turnover occurs more rapidly in the absence of oestrogen –> more bone resorbed than reformed –> bone loss
how does cortisol lead to osteoporosis
it increases bone resorption and induces osteoblast apoptosis (–> decreased bone formation)
composition of bone
70% mineral cortex - mostly HYDROXYAPATITE = ca and phosphate
30% organic cortex - mostly type 1 collagen fibres