Joint Pain & Low Back Pain Flashcards
periarticular pain definition
pain from soft tissue surrounding the joint
referred pain definition
pain from proximal or distal structures to the joint or neurogenic
monoarticular vs oligoarticular vs polyarticular
monoarticular - involves a single joint
oligoarticular - involves 2-4 joints
poluarticular - involves 5 or more joints
inflammatory arthritis definition
a combination of redness, swelling, warmth, and/or tenderness
septic joint definition
generally refers to a bacterial infection of the joint
symmetrical arthritis vs asymmetrical arthritis
symmetrical - affecting both sides of the body
asymmetrical - spotty distribution of affected joints
migratory arthritis definition
development of new joint symptoms with improvement of previously affected joints
inflammatory vs non-inflammatory joint pain distinguishing features
- both may or may not present with swelling and tenderness, but only inflammatory joint pain has warmth or redness present
- inflammatory joint pain may worsen with inactivity and have joint stiffness or gelling in the morning vs non-inflammatory joint pain typically worsens with activity
what are some examples of inflammatory joint pain causes
infection
gout
calcium pyrophosphate deposition disease
RA, juvenile RA
SLE
polymyalgia rheumatica
sarcidosis
spondyloarthritides - reactive arthritis, psoriatic arthritis, anklyosing spondylitis, enteropathic arthritis
what are some examples of non-inflammatory joint pain causes
osteoarthritis
trauma
what conditions are commonly monoarticular or oligoarticular
septic arthritis
spondyloarthritides - reactive arthritis, psoriatic arthritis, ankylosing spondylitis, enteriopathic arthritis
gout
pseudogout - calcium pytophosphate deposition disease
osteoarthritis
trauma
hemochromatosis
what conditions are commonly polyarticular
rheumatoid arthritis
SLE
vasculides - polymyalgia rheumatica, polyarteritis nodosa
viral infections - ex. Parovirus B19
disseminated gonococcal infection
sjorgren syndrome
acute rheumatic fever
sarcoidosis
pls take this time to review the questions that should be asked as part of the history for a patient presenting with joint pain
yay, you did it! good job!
what is reactive arthritis
what question would we ask to screen for this?
comes on as an inflammatory response to antibodies that are created in response to a GI infection or STI and the antibodies attack the patient’s own cells, especially in the joints
comes on 2-6 weeks after the GI infection or STI
would ask if they have previously had any gastrointestinal or sexually transmitted disease
what are signs of a true intraarticular disorder?
effusion, redness, swelling
restricted AROM and PROM
maximum pain at end range
pain with motion in multiple directions
what is a sign of periarticular problem?
restriction of only AROM
what symptom is suggestive of tendonitis or bursitis?
pain on RROM
what should we assess when checking for extraarticular manifestations?
examine eyes, skin, oral cavity, lungs, heart
what tests should we consider if the workup of a case of joint pain? why?
synovial fluid analysis - differentiates between inflammatory vs non-inflammatory causes
blood tests: WBC elevated in infection
ESR and CRP - inflammatory markers
serum uric acid - elevated in gout
blood cultures and serology - important in cases of infection
rheumatoid factor - rheumatoid arthritis
anticitrullinated peptide antibodies - RA
ANA - lupus
ultrasound, x-ray, CT, MRI - show inflammation or trauma in intraarticular or periarticular areas
what happens in septic arthritis
what population is it most prevalent in
duration of condition
sudden onset
infection in a joint
commonly observed in children and persons >55 yo
increased risk with increasing age, immunosuppression, lower SES
duration: lasts until 6 weeks after effective antimicrobial treatment
what organisms are responsible for causing septic arthritis? which is most common?
caused by nongonococcal bacterial in more than 80% of cases
staphylococcus aureus is the most common causative pathogen, followed by staphylococcus species
can involve bacteria, viruses, fungi, mycobacterium
if gonococcal (20% of cases), most commonly caused by Niesseria gonorrheae
risk factors for septic arthritis
skin infection, cutaneous ulcers, osteomyelitis, septic bursitis, abscess
previous intraarticular injection, arthrocentesis, arthroscopy, prosthetic joint, recent joint surgery, trauma
diabetes mellitus, HIV infection, immunosuppressive mediations, IV drug abuse, other causes of sepsis, sexual activity (specifically for gonococcal arhtritis)
clinical presentation of septic arthritis
acute joint swelling, pain, erythema, warmth, joint immobility
usually monoarticular
knee most commonly affected, followed by hip, shoulder, ankle, elbow, wrist (ie larger joints more commonly affected)
constitutional symptoms such as fever, chills, rigors may be present
in septic arthritis, what joints are commonly affected in patients with history of IV drug abuse?
SC or SI joint infection more common in patients with history of IV drug abuse
should we rely on constitutional symptoms for diagnosis for septic arthritis? why or why not?
no, they aren’t as reliable. instead use a combination of other signs and symptoms
what provides the best evidence, if present, for septic arthritis?
what findings do not present good evidence for septic arthritis?
recent joint surgery
prosthetic implant and skin infection
arthrocentesis findings with increased WBCs showing better LR+
not as good: fever; serum lab values have limited usefulness
are elevated WBCs in a CBC enough evidence to rule in septic arthritis diagnosis?
if ESR and CRP are elevated, does this confirm that a patient has septic arthritis? what are these markers used for
no, they WBCs are not enough to rule in - need synovial fluid analysis with gram staining
ESR and CRP can be normal in septic arthritis - when elevated, these markers are used to monitor therapeutic response
what is the diagnostic criteria for ruling in septic arthritis?
WBCs >50,000 WBC/m^3
arthrocentesis for synovial fluid analysis showing >90% polymorphonuclear cells
gram stain of bacterial culture gives definitive diagnosis
if you are suspecting Lyme arthritis, what testing will not be helpful in ruling in?
synovial fluid analysis won’t be helpful because Borrelia burgdorferi cannot be cultured from synovial fluid
need to do PCR testing
how is septic arthritis managed? why?
this is a medical emergency and needs immediate diagnosis and urgent referral to treatment
failure to initiate appropriate antibiotic treatment within 24-48 hours of onset can lead to subchondral bone loss and permanent joint dysfunction
what happens in gout
most affected population
onset type?
duration of condition
middle aged men (increased prevalence with advancing age) and post-menopausal women
onset: sudden
duration: not constant; acute attacks last 3-14 days
morning pain or stiffness usually present but intermittent
in gout, is there a connection to hormones? what are the implications of this?
hormonal component to developing gout in women - later onset and comorbidities like chronic kidney disease and hypertension
demographic risk factors for developing gout
indigenous Taiwanese, Pacific Islander, New Zealand Maori
living in high-income countries like North America and Western Europe
male sex (2-6x higher incidence than females)
dietary risk factors for developing gout
high alcohol intake
diet rich in meat and seafood = high purine diet
high fructose consumption
what conditions can be comorbid with gout
hyperuricemia
metabolic syndrome
type 2 diabetes mellitus
cardiovascular disease
hypertension
hyperlipidemia
obesity
chronic kidney disease
diuretic use
obstructive sleep apnea
menopause
conditions with rapid cell turnover - psoriasis, hemolytic anemia, certain cancers
Lesch-Nyhan syndrome
Kelley-Seegmiller syndrome
what is metabolic syndrome?
combination of:
hypertension
high blood sugar
high cholesterol
central obesity
elevated waist circumference: >88cm for women, >102cm for men
why are conditions with rapid cell turnover often comorbid with gout
gout is an issue due to purine turnover which is due to increased protein breakdown
therefore, increased purines in the blood will contribute to elevated uric acid crystals in the bloodstream
what is Lesch-Nyhan syndrome?
a rare hereditary condition of purine metabolism
X-linked recessive pattern - only males affected
mutation of HPRT1 gene leading to deficiency or absence of HPRT enzyme causing elevated purine levels in these patients - they aren’t recycled
people have lower levels of dopamine and can see self injury behaviours like biting and head-banging specific to this syndrome
what is Kelley-Seegmiller syndrome?
a milder form of Lesch-Nyhan syndrome
a rare hereditary condition of purine metabolism
mutation of HPRT1 gene leading to DEFICIENCY of HPRT enzyme causing elevated purine levels in these patients - they aren’t recycled
patients have a higher risk of developing kidney stones and gout
clinical features of gout
acute, rapidly developing, self-limiting monoarthritis - commonly the first MTP joint or midfoot or knee
flares usually resolve within 14 days and are interspersed between asymptomatic and intercritical period
over time, flares become more frequent and severe and can be polyarticular, affecting upper limbs as well
presence of tophi -> tophaceous gout usually develops 10 years after initial gout flare
podagra definition
a gout flare at the first MTP joint (big toe)
what is an intercritical period (re: gout)
the time between flare ups where there is no joint pain
tophi definition
uric acid crystals that form lumps underneath the skin and can cause chronic pain and destroy the bones around the joint
where in the body are tophi most commonly found
first MTP joint
other joints and tendons of the foot and ankle (Achilles tendon)
prepatellar bursae
olecranon bursae
helix of ear
what is the gold standard for gout diagnosis
joint aspiration and microscopy analysis showing presence of monosodium urate crystals
what happens in pseudogout
what is the medical term for pseudogout
onset
duration of the condition
commonly affected population
calcium pyrophosphate dihydrate crystal deposition
common in ages >65yo
onset: sudden
duration: flares lasting days to weeks
usually with morning pain or stiffness
how is pseudogout diagnosed?
calcium pyrophosphate dihydrate crystals are polymorphic and weakly positive under birefringent microscopy
this is different from the MSU crystals that present with regular gout
what are the types of crystal-induced arthritis?
gout
pseudogout - calcium phyrophosphate dihydrate crystal deposition
calcium oxalate
hydroxyapatite
rheumatoid arthritis
overall description
implications
major risk factors
chronic relapsing descrtuctive synovitis - local inflammation, cartilage destruction, bone erosion
genetic disposition: HLA-DR1 and HLA-DR4
higher risk in women (2-3x higher than men)
cytokines drive chronic synovial inflammation
environmental risk factors for RA
smoking - dose response effect
airborne agents related to air pollution
overall microbiome
diet high in red meat, sugar, sodium
blue collar jobs
pesticide exposure
work stress
infectious exposure - parovirus 19, HCV, EBV
host-associated risk factors for RA
allergic and respiratory: rhinitis, atopic dermatitis, asthma, COPD
immune-mediated risk factors - autoimmune conditions (IBD, T1D, MS, autoimmune thyroid conditions)
sleep disorders
schizophrenia
neuroendocrine factors like decreased HPA axis function/relative adrenal insufficiency
clinical features of RA
symmetrical polyarticular pain and stiffness
morning stiffness >1hr
systemic symptoms: fatigue, weight loss, anemia
boggy swelling caused by synovitis and palpable synovial thickening
what joints are most commonly affected in RA
wrists
PIP joints
MCP joints
MTP joints
what is observed in advanced RA
ulnar deviation of MCP joints
MCP joint subluxation
swan neck deformity
Boutonniere deformity
what extra-articular manifestations can be observed in RA?
accelerated atherosclerosis
pericarditis
keratoconjunctivitis sicca
epicerlitis/scleritis
interstitial lung disease
pulmonary nodules
rheumatoid nodules
pleural effusion
vasculitis
what risk factors predispose someone to developing extra-articular manifestations of RA?
male sex
seropositivity for RA, anticitrullinated antibodies, antinuclear antibodies
smoking history - especially for nodules, vasculitis, and interstitial lung disease
anticitrullinated protein antibodies may be present for __ years before onset of ___ disease in RA
may be present for 10 years before onset of clinical disease in RA
serology markers you might test for in RA
rheumatoid factor
anticitrullinated protein antibodies
what does it mean to be seropositive for RA
if someone tests positive for rheumatoid factor and anticitrullinated protein antibodies
does a negative serum anticitrullinated protein antibody result rule out RA diagnosis?
no. but it is a little better than rheumatoid factor in predicting RA
what fraction of patients with RA are seronegative for rheumatoid factor?
1/3 - rheumatoid factor is not diagnostic of RA
how is RA managed? why?
there is a low threshold for referral to a rheumatologist
>12 week delay in treatment is associated with reduced chance of drug-free remission and increased risk for progressive joint damage
complications of RA
osteopenia and osteoporosis leading to fracture
lung manifestations - pleuritis, bronchiolitis, interstitial fibrosis
accelerated atherosclerosis
increased insulin resistance, diabetes mellitus
vasculitis, thromboembolic disease
anemia of chronic disease
depression due to low quality of life
felty syndrome
what implication does the complication of accelerated atherosclerosis have on disease outcomes in RA
increases risk for cardiac events
risk of mortality in RA is 3x that of the general population
