Flashcards in Clinical Approach to Patient with Joint Pain I and II Deck (38):
1. What is the most common location of arthritis?
2. What % of adults have some form of self-reported MD diagnosed arthritis?
1. back and spine
1. What are some general clinical characteristics of arthritis?
2. What is it called if its inflammatory?
3. How is the disease defined?
4. What are findings are important?
1. Pain and stiffness in a joint
3. distribution and chronology
4. presence of extra-articular findings are important
Acute Monoarticular Arthritis
1. Time course
2. Etiologies (6)
1. about 7 days or fewer in duration; can go out to 14
2. Septic (most urgent to diagnose)
3. Crystal induced (most common, not urgent)
5. Hemorrhage- may not be obvious; check for anticoagulants
6. Mechanical (occupation/weight)
7. Atypical polyarticular
Acute Monoarticular Arthritis
Extra-artciular clues in Sepsis (4)
5. What can also cause inflammation?
1. fever and shaking chills
2. Cutaneous clues
4. Mucosal involvement
Synovial Fluid analysis in acute monoarticular arthritis
1. How important is it?
2. What does it mean if there are 200 WBCs?
3. What does it mean if there are 2000 WBCs and 25% or fewer are PMNs?
4, What does it mean if there are 2000 WBCs and 50% or greater PMNs?
5. Other tests that can be done
1. VERY, single most important test for making correct diagnosis
2. fluid is normal
4. may be inflammatory
5. Gram stain, culture, crystals
What kind of crystals can cause gout? What does each look like under microscope (2)
1. Sodium Urate crystals: needle shaped that may be w/in neutrophil; changes from blue --> yellow on polarized microscopy
2. Calcium pyrophosphate: blunt ended crystal with weak positive birefringence
What tests are not that helpful?
1. Radiology- can show demineralization, both gout and sepsis do this
2. Bloodwork (NEVER a substitute for SF);
Uric acid- doesn't correlate with presence of gout
Leukocytosis- can be in gout and sepsis
Blood cultures- can show sepsis
1. Which gender tends to have more gout?
2. When does the other gender catch up?
2. females approach male incidence after menopause,
3. estrogen promotes urate excretion in the urine
Gout Mechanism/ Pathogenesis
1. How is IL-1 upregulated?
2. What does IL-1 do?
1. uric acid crystals are ingested by macrophages, which release IL-1
2. recruits neutrophils
1. Why isn't Colchicine used?
2. Natural course of disease
3. NSAIDs aren't used much. why?
4. Short term
5. Long term treatment & mechanism
1. Side effect is diarrhea, which is bad with gout
3. decrease renal function, so you excrete less uric acid
4. large dose corticosteroids
5. Allopurinol- inhibits Xanthine Oxidase
Chronic Monoarticular Arthritis
1. Time duration
2. Differential Diagnosis
1. about 2 months
2. Degenerative Joint Disease (Osteoarthritis)
3. Mechanical Internal Derangement (like a meniscus tear)
4. Chronic infection
5. Joint Neoplasm (rare)
6. Pigmented Villonodular synovitis
7. Rheumatoid arthritis (rare)
Synovial Biopsy in Chronic Monoarticular Arthritis
1. How does it compare to Synovial Fluid?
2. What does it help ID/rule out? (4)
1. usually not better than it, good for some things
Infection (especially fungal)
Pigmented Villonodular synovitis
1. How many joints?
2. How long?
3. Differential Diagnosis
1. more than 4
2. less than 8 weeks duration
3. Acute Rheumatic Fever
Post-viral arthritis (common)
Immune complex arthritis
1. Which adult population is at risk?
2. What causes arthritis?
3. Disease course
1. People exposed to little kids (elementary school teachers)
2. Ab cross-reactivity (?)
3. usually self-limited
How can you differentiate between these 3 causes of acute polyarthritis?
1. Rheumatic fever
1. true migratory arthritis, unique skin lesion (only present in 10%)
2. Geography, season, and unique skin lesion (erythema migrans; 90-95% will have it)
3. skin lesions
Diagnosis of Acute Polyarthritis
1. Acute Rheumatic Fever
1. ASO- strep Ag; DNAase- other serum Ag;
2. culture appropriate sites (oral, ano-rectal, cervix, urethra); can appear near period or 1st trimester
3. Elisa for screening (+ test doesn't make dx); PCR for confimation
4. IgM titer (shows pt having acute parvo)
Pathogenesis of GC arthritis
1. Which joints are affected initially?
2. What happens next?
3. What kind of lesions are common?
4. When does it occur? why?
5. What predisposes people to repeated bouts of the syndrome?
1. knees, ankles, wrists, fingers; multiple, bilateral, symmetrical
2. culminates in 1 or 2 joints as disease progresses
3. skin lesions
4. perimenstraul time frame or during pregnancy; driven by progesterone?
5. late complement deficiencies; some GC subtypes have an increased propensity to cause the syndrome
1. How many joints?
2. For how long?
3. What is usually the diagnosis?
1. more than 4
2. at least 2 months
3. Rheumatoid arthritis
Features of Rheumatoid Arthritis (4)
5. What drives the disease?
1. AM stiffness
2. soft tissue swelling
3. Systemic manifestations (fatigue)
4. Symmetrical Joint Involvement (bilateral; small, medium, large joints)
Epidemiology of RA
1. What countries get it?
2. Racial groups?
3. Which gender gets it more often?
5. What does it do to life expectancy?
6. What is happening to risk of getting it?
2. slightly increased in Europeans and Asians, but all get it
4. 1 %
5. cuts it by 3-5 years
1. How does RA destroy hand function?
2. Which joints are affected in the hand?
3. Which other joints in the body are affected?
4. Which area is notably not affected?
1. erodes ligaments
2. PIP and MCP; NEVER affects Distal interphalangeal joints; if DIP is involved; it's not RA
3. cervical, shoulder, elbow, wrist, knee, ankle, foot joints
4. lumosacral spine/area NEVER involved
Extra-articular manifestations of RA (6)
1. Nodules- becoming rare
2. anemia- chronic inflammation shuts down Fe utilization
4. Neuropathy- distal, peripheral
5. Serositis- pleural, common
6. Vasculitis- lower extremity
1. What kind of dx?
2. What is usually not diagnostic?
3. What new tech is very helpful
4. What is seen in synovial fluid
2. routine blood work (ESR, CRP, RF, CBC); if all are negative, pt usually won't have RA, but they don't narrow it down
3. ACPA- citrullinated peptide antibodies- shows inflammation and auto-antigenicity; 80-85% specificity
4. inflammatory, low glucose, nonspecific
What are some Genetic (2) and Environmental Factors (4) that contribute to RA?
1. monozygotic concordance: 15-30%; many genes involved
2. having HLA DRB1 and +RF and ACPA; DRB1 is the "shared epitope"
3. smoking- synergistic with DRB1 --> poor prognosis
4. adverse life events precipitate it, suggesting like w/ pit-adrenal axis
5. Gut microbiome
6. Peridontal disease
1. Overall Pathogenesis of RA
2. What cytokine may also play a major role?
1. B cells create Ab to some self Ag; activates neutrophils and macrophages --> destruction
2. IL-17 (which suggests IL-23 is present too)
1. What is recommended but not realistic?
1. rest for long time
2. too many side effects, esp in older pts
3. excellent for bridging until Disease Modifying Anti-Rheumatic Drugs take effect; acute suppression
1. 2 types
2. Causes of the second type
1. Primary and Secondary
prior inflammatory disease
avascular necrosis (common when pt takes many steroids)
1. Which joints are commonly affected?
2. When are unusual joints involved?
3. What happens?
1. weight bearing joints: 1st MTP, Knee, Hip, Lumbosacral spine, Cervical vertebrae;
2. when a person has an unusual occupation
3. bone on bone -->reactive bone formation
Epidemiology of DJD
1. Linear relationship to what 2 things?
3. How does it vary with race?
1. age and weight; 90% have some evidence of it at 65
3. gene mutation in black families in the South --> higher incidence of debilitating knee disease
Pathogenesis of DJD: what 3 things lead to it?
1. What are the functions of cartilage (2)
3. Main cartilage cell
4. 4 Main components of Cartilage
1. smooth, low resistance surface for movement
2. compressibility for diffusion of mechanical forces; anything that disturbs weight bearing --> loss of cartilage
4. Water, proteoglycans (compressibility), collagen (tensile strength), chondrocytes (maintain and synthesize cartilage)
1. what are they
2. What happens when their mechanoreceptor activity is activated?
3. What other cells do they communicate with?
1. sole cell component of cartilage
2. release growth factors, metalloproteinases (degrade cartilage's ability to function normally), and innate inflammatory cytokines
Pathogenesis of DJD
1. What is increased?
2. What is decreased?
3. What is altered?
4. What properties of proteoglycan are altered?
5. What do released metalloproteinases do?
2. functional proteoglycan
3. collagen structure
4. aggregation and biomechanical properties
5. break down matrix and activate innate inflammatory responses
1. If obesity/weight is so important in OA, why are NON-weight bearing joints sometimes affected?
1. visceral fat adipocytes secrete adipokines (leptin) that are found in the synovial fluid in OA; these fat cytokines appear to trigger cartilage destruction by activating metalloproteinases, aggrecanases (alter compressibility) and collagenases --> DAMPS(?)
Clinical Presentation of DJD
1. When is pain worse?
2. When is pain better?
3. How much morning stiffness?
4. Physical Exam finding
5. Which joints are affected?
1. with weight bearing
2. with rest
3. very little AM stiffness
4. Joint crepitus
5. Cervical, Lumbar Spine, weight bearing joints including 1-MTP and CMC joint of thumb
DJD: 1. What lab tests are useful?
2. What imaging tests are useful?
2. can be misleading; very bad looking knee may not be very painful at all
Management of OA (DJD) (6)
2. Weight alleviation (won't get better until weight is lost)
3. Physical Therapy (helpful in OA, not very helpful in other diseases)
4. Restrained use of NSAIDs
6. Alternative therapy- generally not very helpful;