Approach to Polyarticular Arthritis Flashcards
active vs passive range of motion
- active = patient moves their limb, engaging their own joints and muscles and tendons
passive = dr moves their limb, engaging only their joint.
- if it hurts when active, but doesn’t hurt when passive,e the pain is outside the joint and is most likely not arthritis.
if it hurts both passively and actively, the joint is most likely affected and might be arthritic
general scheme
outline inflammation vs non-inflammation pain in joint based on stiffness, systemic symptoms, joint pattern and extra-articular manifestations
inflammation would also have lab findings like CRP, ferritin, etc.
3 routes of spread that results in septic arthritis
1 .hematogenous route
- dissemination from osteomyelitis
- spread from an adjacent soft tissue infection
- diagnostic or therapeutic measures
- penetrating damage by puncture or trauma.
underlying medical conditions that predispose to MSK infections
common organisms that cuase septic arthritis in neonates
- staphylococcus aureus
- streptococci
- coliform
common organisms that cuase septic arthritis in children
staphylococcus aureus
common organisms that cuase septic arthritis in young adults
staph a
- neisseia gonorrhoeae
common organisms that cuase septic arthritis in adults
staph a
common organisms that cuase septic arthritis in those who are immunocompromised
gram negatives
if you think someone has septic arthritis, you must aspirate the joint and send for:
- cell count and differential
- crystal analysis (gout)
- culture and sensitivity including gram stain.
how does normal, osteoarthritis, RA, and septic arthritis compare in terms of synovial fluid appearance, volume, viscosity, white count and polymorphonuclear cell presence?
- if you can get fluid of of the knee, there’s too much to begin with
- if it’s generally cloudy, it’s inflammed.
- the higher the white count, and the higher the number of PMN, the higher the change of septic arthritis
which sex is more afflicted by gout?
males– up to 28/1000, vs 6/1000 in females/
- most common cause of inflammatory arthritis in med over 40
- does NOT occur in premenopausal females.
risk factors and associations with crystal arthopathies (meds used, other illnesses etc)
- metabolic syndromes, obesity, HTN, dyslipidemia, diabetes
- alcohol
- medication use: ASA, diuretics
- renal insufficiency resulting in uric acid accumulation
- past kidney stones
- fam history of gout
- myeloproliferative disorders (they over produce purines, which have to be broken down into excess uric acid, causing build up and inflammation.)
clinical picture and spread of gout
Clinical picture of gout:
– Usually starts as monoarthritis (often big toe).
– Episodic acute monoarthritis, starting in 30’s.
– Intercritical gout, Normal between attacks, spreads to other joints, usually lower limb first.
– Chronic arthritis +/- tophi, starting average of 12 years after first attack, and occurs 7 years later in women. Not all patients progress to chronic arthritis or tophi
pseudogout vs true gout
pseudogout is often caused by excess calcium in the cartilage and articular regions (ex/ majority of the senior population has chondrocalcinosis)– light spectroscopy on aspirate will reveal CPPD crystals
true gout is caused by the oversaturation of uric acid in the blood, resulting in deposition and inflammation.
clinical picture and diagnosis of pseudogout
pseudogout is caused by calcium pyrophosphate dihydrate crystals that shed from cartilage and set off an inflammatory response (often precipitated by truama)
- clinically, reuslts in episodic mono-arthritis, OFTEN SELF LIMITING AND MOST COMMONLY OCCURING IN THE KNEE (rather than the big toe in true gout)
- diagnosis involves synovial fluid aspirate showing BIREFRINGENCE, RHOMBOID SHAPED CRYSTALS, and Xrays will show chondrocalcinosis.
clinical presentation of ankylosing spondylitis
- alternating buttock pain
- inflammatory back pain lasting for at least 3 months with more morning stiffness. Usually gets worse with rest, disturbs the sleep and improves with exercise.
patient is often <40 years old. 1/3 get peripheral joint disease (usually hip, shoulders and knees)
limited vs diffuse scleroderma
limited: CREST symptoms but thickening and calcinosis does not go above elbows or knees
diffuse: further exacerbated, topoisomerase Scl-70 type +
a person presents with progressive symmetrical proximal muscle weakness, pulmonary interstitial lung disease, aspiration pneumonia, weakness of respiratory muscles, difficulty swallowing, Gottron’s rash on PIPs, heliotrope rash on eyelids and shawl sign. What do you expect this person to have? What labs would reflect this diagnosis?
Inflammatory Muscle Disease
- Run lab investigations CK, a muscle enzyme, is VERY HIGH
- Chest X ray would show infiltrates if interstitial lung disease if lungs involved/
- muscle biopsy– look for muscle damage and inflammation
associated symptoms of fibromyalgida
