Joints Flashcards
(37 cards)
What other risk factors for osteoarthritis
Obesity
Age
Trauma
What is degenerative joint disease/osteoarthritis ?
Progressive degeneration of articular cartilage Due to mechanical wear and tear
How does an osteoarthritis patients present?
Go to sleep – > joint gets rest – >
Wake up Joint stiffness @ morning – >
use joints = increase wear+tear (cartilage loss start medially = bowlegged) ->
Increase pain during day
What are the pathologic features of osteoarthritis
Destruction of cartilage lining the articular surface –>
Joint mice – cartilage fragments fall into joint space
Eburnation of subchondral bone – bone rubbing against bone = polish
SUbchondral cysts
Sclerosis+Synovitis
Heberden’s nodes (DIP)
Osteophytes
Bouchard nodes (PIP)
Treatment of osteoarthritis?
Paracetamol NSAIDs intra-articular glucocorticoids
What is rheumatoid arthritis?
Autoimmune inflammatory destruction
of synovial joints
mediated by cytokines & HSR 3 + 4
What is the aetiology + risk factors for rheumatoid arthritis ?
HLA-DR4 Autoimmune = middle-aged woman Rheumatoid factor positive = anti-IgG Anti-cyclic citrullinated peptide AB = more specific Mediated by cytokines + HSR3+4
What joints are involved in osteoarthritis is
Lower lumbar
Knee
Elbow
Distal + proximal interphalangeal joint
What is the hallmark of rheumatoid arthritis?
Synovitis inflammation of the Synovium
Explain how synovitis can lead to clinical features
Synovitis – >produce thick pannus granulation tissue = BV, fibroblasts, myofibroblasts = contract – >
– ankylosis = fusion of joint -> joint space narrowing
– Deviation of joints diff direction eg. ulnar deviation
– Destroy articular cartilage due to pannus taking over
Synovitis – >
inflammatory process wear away @bone – > osteopenia
What is the clinical hallmark Of rheumatoid arthritis
Morning stiffness improves with activity
Patient sleep – >joints rest – >
inflammatory process occurs @joints – >
damage joints – > wake-up + move joints – >
squeeze joints free of him inflammatory debris – > improvement
Which joints are involved in rheumatoid arthritis?
SYMMETRIC
Proximal interphalangeal joint
Elbow + Wrists (metacarpophalangeal joint )
Knee + ankle
Patient presents with
- fever weight loss myalgia
- Rheumatoid nodules, vasculitis, Baker’s cyst,
- lymphadenopathy, interstitial fibrosis, pleural effusion, pleuritis
Explain the fever weight loss and myalgia
Explain rheumatoid nodules and Baker’s cyst
Fever weight loss and myalgia due to inflammatory process i.e. systemic autoimmune disease
Rheumatoid nodules @skin + visceral organs with central area of necrosis surrounded by epithelioid histiocytes
Baker’s cyst = swelling of bursa behind knee
What would you find in the labs with rheumatoid arthritis?
Auto IgM against FC portion of IgG Ie rheumatoid factor
What would we find inside the synovial fluid in rheumatoid arthritis
Neutrophils + high-protein
What are the complications of rheumatoid arthritis
Chronic inflammatory state – >produce acute-phase reactant e.g.
HEPCIDIN– >Block ability to use Fe2+ stored in macrophages – > ANEMIA OF CHRONIC DISEASE
SAA – > Converted to AA – > deposit in tissues = SECONDARY AMYLOIDOSIS
What is gout
Depositions/precipitation of mono sodium urate crystals in tissues e.g. joints leading to acute inflammatory monoarthritis
What is the most common form of gout
What causes primary gout
Primary gout – 90% = under excretion of uric acid
Exacerbated by thiazides
Idiopathic
What are the two main reasons of hyperuricaemia
Push too much uric acid into blood
Not filter enough from blood
What are the three reasons of secondary gout
Leukaemia + myeloproliferative disorders e.g. tumour lysis syndrome:
increased cell turnover – > increased nuclei turnover – > increased breakdown of purines + pyrimidines –> increased uric acid @ joints
Lesch Nyhan syndrome = X-linked
Decreased HGPRT – >
Hyperuricaemia
Gout
Pissed off {Self-mutilation (bite lips + fingers)} Retardation
dysTonia
Renal insufficiency = can’t excreta uric acid
How does a patient with acute gout present
Deposition of uric acid (MSU) + joints
Eat meat = XS DNA + RNA +
Alcohol = compete with uric acid to be excreted ->
XS uric acid MSU crystals – >
Acute inflammation - crystals activate neutrophils – >
Painful arthritis of great toe = PODAGRA @metatarsophalangeal (MTP) joint
How does a patient with chronic gout present
Long-standing acute gout – >
1.developed TOPHI =
white chalky aggregates of URIC acid crystals
+ Fibrosis + giant cell rxn
@Soft tissue + joints
E.g. Achilles tendon, external ear, olecranon bursa
2.renal failure
Uric acid deposit @tubules of kidney -> damage
What do we see in the labs for gout
Hyperuricaemia
Needle shaped crystals with
Negative birefringent under polarised light
yeLLow under paraLLel light / lay LOW = yelLOW
Blue under perpendicular
What is pseudogout
Deposition of calcium pyrophosphate