Joint Disorders Flashcards
Synovial fluid
Cartilage is most commonly the problem in a presenting patient. It does not have any blood supply and wears and tear with time and increased body mass. Synovium secretes nutrients (synovial fliuids) provides nutrients to cartilage and lubrication
Ligaments
connect bone to bone. Issue = lack of stability. Main purpose of ligament is stability.
Tendon
Tendons connect bone to the muscle. This main purpose is mobility. Tendon tear = lack of mobility, weakness.
Nerve (referred pain)
active and passive is normal, Poorly localized, “ burning”, parasthesia, numb, loss of sensation
Tendon, bursa
active is limited, passive is normal, localized pain
Muscle
active limited, passive is normal, Bilateral and proximal, Myalgia muscle pain is usually bilateral and proximal (shoulders, thighs) never localized
Joint
active and passive are limited, localized
Diagnostic approach to joint pain
History and physical: Distribution? Timing (acute vs. chronic)? Inflammatory pain? Distribution? Extra-articular manifestation?
Arthragia
pain
Arthritis
true joint inflammation
RA and Lupus
Same joints inflammed on both sides. Symmetrical small joints (wrists, hands) These are both chronic. > 6 weeks. Polyarticular
Viral (Hepatitis B&C, Epstein Barr, HIV, Parvovirus B19)–
symmetric, smaller joints more common Polyarticular
Polyarticular
> 4 joints. RA. Lupus. Viral.
Mono/ Olygoarticular
1-3 joints
Osteoarthritis
weight bearing joints (hips, knees, low spine)
Septic arthritis
monoarticular
Crystal arthritis (Gout/ pseudo-gout)
monoarticular, most common 1st metatarsophalangeal
Ankylosing spondylitis
(severe back pain in young patients < 40, more common in men)- spine joints
Other monoarticular causes
Lyme arthritis
Psoriatic arthritis (<10% of patients w/ psoriasis)
Arthritis w/ IBD ( in 20-30% )
Reactive arthritis ass with immune response to bacterial infections (usually 3 weeks after GI or GU infections)
Inflammation
Erythema
Warmth
Swelling
Stiffness (“gelling”) during period of inactivity > 1 h (better with exercise, hot shower, movement)
Examples of inflammation
RA, SLE, Ankylosing spondylitis, Gout, septic
No inflammation in this condition
OA
History of inflammation
Prolonged morning stiffness (> 1 hour), stiffness/ pain improves with activity
OA symptoms
No or minimal morning stiffness (< 30 min), pain worse with activity, Bony crepitus , mild tenderness, hard bony joint enlargement
NO redness, NO warmth, NO soft effusion, ESR, CRP normal
RA, SLE, Ankylosing spondylitis, Gout, septic inflammation s/s
Joint effusion (soft joint swelling, “bogginess”), tenderness, redness, warmth, ESR , CRP elevated
SLE extra articular symptoms
SLE – multiple extra-articular symptoms (arthritis is one of the manifestations). Skin lesions are common. Renal involvement is common
RA extra articular symptoms
few extra-articular symptoms (predominantly arthritis). Skin lesions are unusual and limited to subcutaneous nodules
OA extra articular symptoms
none
Psoriatic arthritis
skin (plaques), nails (pitting)
HIV, Hepatitis extra articular symptoms
asymptomatic or multiple systemic symptoms
A 67 y/o presents with a red and swollen Rt. knee for one day. He is unable to bear weight today. There is a limited passive and active ROM. Right knee joint appears swollen, red and tender
Both passive and active = joint
Acute = 1 day
Red, tender joint
Septic arthritis
Gout
Presents similarly
A 67 y/o obese female presents with Rt. knee pain for one year. She denies morning stiffness but reports that pain is worsen when a day goes by.
On exam- Rt. Knee- no swelling, or redness
Chronic, monoarticular
No morning stiffness = no inflammation
Pain worsens as the day goes by = degenerative bone problem
Joint problem = both active and passive are limited
A 36 y/o presents w/ symmetric wrist joints pain and swelling for 6 months. She reports 2 hours morning stiffness and improvement in symptoms when the day goes by. She is chronically tired. On exam – wrist joints are “boggy”, tender and warm
Symmetrical = polyaricular Wrist – small joint Chronic Morning stiffness = inflammation Boggy, tender, warm Lupus, Rhematoid Limited acitve and passive == joint pain
A 36 y/o presents w/ symmetric wrist joints pain and swelling for 3 weeks. She reports 2 hours morning stiffness and improvement in symptoms when the day goes by. She is chronically tired. There is no rashes reported. On exam – wrist joints are “boggy”, tender and warm
3 weeks
Multiple joints
Morning stiffness = inflammation
Need 6 weeks until you can dx lupus
describe RA
Chronic autoimmune inflammatory disorder that predominantly affects joints
PROGRESSIVE disease (progress to joint destruction) if untreated
More common in women
Peak age of onset 25-50
Chronic PROLIFERATIVE SYNOVYTIS (inflammation of synovium) Joint EROSION joint deformities (advanced stage)
Clinical presentation of RA
SYMMETRIC SMALL joint involvement (wrists , hands, but NOT DIP) for at least 6 WEEKS Morning stiffness (> 1 h), IMPROVES w/ ACTIVITY On PE joints are swollen ( “bogginess”), tender, sometimes warm and erythematous, limited active and passive ROM. Deformities (advanced disease)
Extra-articular manifestations: rheumatoid nodules on exterior surfaces (20%), anemia of chronic disease, fatigue, osteoporosis. Pleural effusion and pericarditis are rare
RA is associated with an increased CV risk !!!
Diagnosis of RA
Diagnosis is CLINICAL (polyarticular arthritis > 6 week duration not attributed to viral arthritis or SLE). Tests to support clinical diagnosis (should never be used as the sole criteria for diagnosis) :
Tests to support clinical diagnosis of RA
Elevated ESR or CRP
(+) Rheumatoid factor in 70-80% (fairly sensitive) and poor specificity. High titers in patient with classic symptoms predict RA
(+) Anti-CCP (antibodies to cyclic citrulinated peptide) is more specific (95%) and slightly more sensitive (80-85%)
-Presence of both RA and anti-CCP makes a diagnosis is more likely
(+) abnormalities on x-rays
Anti CCP +
Severe RA
Abnormalities on x-ray in RA
Soft tissue swelling, bone erosions, joint narrowing
RA treatment goals
Stop progression of the disease !!! (RA is not curable) Improve symptoms (minimize pain, improve mobility)
Medications that improve symptoms of RA
NSAIDS, +/- steroids
Symptomatic control (breakthrough pain)
Work fast
Disease modifying antirheumatic drugs (DMARD)
Methotrexate, TNF inhibitors
Methotrexate
initial oral , weekly dosage, well tolerated, inexpensive. Supplement daily folate
TNF inhibitors
(Adalimubab- Humira®, Infliximab- Ramicade® )- IV or SubQ injections, well tolerated, expensive. Can be used in combination with MTX (more effective than alone)
70% achieve clinical remission
Do not work immediately (6 weeks)
Should start EARLY rather than later ( EARLY aggressive approach) Check for TB.
Major s/e methotrexate
liver dysfunction and suppression of bone marrow. Monitor CBC and liver enzymes. Excreted in the kidneys. If renal dysfunction toxicity. Also given in ectopic pregnancy, will stop DNA synthesis.
Systemic lupus erythematous (SLE)
Autoimmune disease with multi-organ involvement
More common in women ( 90%)
The disease is more common and more severe among women of African American and Hispanic backgrounds
Relapsing and remitting course (unpredictable flares)
Clinical presentation of SLE Skin manifestations
in 70% of patients:
acute malar rash (butterfly rash), alopecia, painless oral ulcers
chronic discoid rash (raised edges, leaves scars)
subacute photosensitivity rash (sun exposed areas,” sunburn” that lasts months)
Arthritis in SLE
in 40% (small joints, non-erosive deformities unusual)
Lupus nephritis
in 70%: glomerulonephritis of varies degrees of histologic and pathologic abnormalities
Cardiac and pulmonary in SLE
in 30-50% of patients :pericarditis, pericardial effusion, pulmonary effusion
SLE CNS abnormalities
in 70%: headaches, cognitive/behavioral dysfunction, depression, seizures
Hematologic SLE
anemia, thrombocytopenia, leukopenia
Constitutional SLE
fatigue, weight loss, low grade fever, myalgia
Discoid rash
This is chronic skin infection. Annular, raised, scaly borders. Tinea is itchy because it is fungal. This is not itchy. Is chronic.
Malar rash
This is an acute manifestation, comes and goes. NOT CHRONIC. Strep skin infection is well demarcated and on one side and raised. Impetigo is honey colored crusting.
Diagnosis of SLE
Clinical dx.
Decreased complement level in SLE flare ( indicates disease activity and flare)
X-ray- negative ( non-erosive arthritis)
ANA
ANA ( anti-nuclear antibody): very sensitive ( 99%). Almost all SLE patients have ANA. Negative ANA – probably not SLE. Positive ANA – not just SLE. INITIAL test
Anti-dsDNA
(antibodies against double stranded DNA) : very specific to SLE (90%). Used to CONFIRM the diagnosis if ANA is positive
Lupus nephritis
Deposition of immune complexes in glomerular capillary membrane damage to the membrane
Histological changes and symptoms are variable
Symptoms from asymptomatic to renal failure
Diagnosis of lupus nephritis Initial diagnosis ( and monitoring )
Serum for creatinine/GFR
Urinalysis for protein and RBC (dysmorphic)
24-h urine collection for urine protein or spot urine protein-to-creatinine ratio (more accurate to determine proteinuria)
Definitive diagnosis of lupus nephritis
Renal biopsy (to determine histopathology) to determine therapy
Treatment of SLE For acute exacerbations
Corticosteroids (IV or PO high dose)
For maintenance (prevent exacerbations, treat symptoms)
Sun screen: exposure to UV light can exacerbate a flare
Hydroxycholoroquine (Plaquenil ®) for skin rashes, arthritis, prevent flares
Cytotoxic drugs (Cyclophosphamide IV) for severe cases of lupus nephritis
MTX s/e
GI upset, liver toxicity , marrow suppression (anemia, leukopenia, thrombocytopenia)
MTX monitoring
CBC, liver function, renal function. Screen for viral hepatitis prior. Contra-indicated pregnancy
TNF-inhibitors s/e
Reactivation of latent TB, fungal and bacterial inf
TNF monitoring
Screen for latent TB, HIV, viral hepatitis prior and during the therapy
Repeat TB screening annually . continue in pregnancy
Hydroxy-choloroquine side effects
Retinal damage (irreversible ) – RARE
Hydroxy-choloroquine monitoring
Fundoscopic exam by a specialist prior and annually, ok in pregnanacy
Osteoarthritis (OA)
Degenerative disorder affecting cartilage (“ wear and tear”)
PROGRESSIVE
Incidence increases w/ age
Weight-bearing joint is most commonly affected ( knees, hips, lumbar spine). Can affect both DIP and PIP
Risk factor- obesity
Clinical manifestations of OA
Monoarticular/ Olygoarticular joint involvement. Pain relieved by rest, worsen w/ activity. May be joint stiffness in AM (not prolonged, < 30 min) .On physical exam: bony enlargement and bony crepitus, no warmth, no redness. Limited active and passive ROM due to bony enlargement of joints (osteophytes) and pain. No systemic symptoms
Diagnosis of OA
Diagnosis is CLINICAL. Tests to support the diagnosis:
Normal CRP, ESR
Abnormalities on x-ray: Joint space narrowing, osteophytes ( bone overgrowth), subchondral bone damage (sclerosis). NO bone erosions
Treatment of OA
Dx clinical + xray
Treatment weight loss and exercise
Start w tylenol
Move to NSAID
tx OA
Weight loss
Regular exercise activity to improve ROM, muscle strength (strong muscles joint protection ).
Acetaminophen ( most guidelines recommend for initial use, < 3g/d) NSAIDS topical or oral
Intra-articular injection (no more than 3-4/ year)
Surgery for serious disability
Nutritional products ( OTC glucosamine and chondrotin sulfate) – no good evidence of benefit
OA
Mainly weight-bearing joints , non inflammatory. No systemic sx. dx- X-ray ( narrowing, osteophytes) . Tx: Weight loss,
Acetaminophen, Surgery
RA
Small joints hands, wrists, ankles, symmetric ( no DIP), inflammatory ,erosive. Systemic: Minimal, rheumatoid nodules , anemia. Dx: RF, anti-CCP, X-ray ( narrowing, joint erosion, deformities). Tx: Methotrexate+/- TNF inhibitors
SLE
Small joints, symmetric, inflammatory , non-erosive, Systemic - Multiple ( skin, renal, cardiac, pulmonary, blood), dx - ANA initially, anti-DS DNA X-ray (may be normal), tx Hydroxycholoroquine, steroids
Gout
Manifestation of hyperuricemia (increased production or decreased excretion)
Deposition of monosodium urate crystals (MSU) in joints
More prevalent in men, in obese individuals, in patients with chronic renal disease
Peak age 40-60
Gout foods
Precipitated by alcohol ingestion (beer), red meat, seafood
Meds causing gout
niacin, thiazides, ASA
joints affected in gout
1st metatarsophalangeal joint is involved (podagra), knee, ankle
pseudogout is a build up of
calcium
gout patho
Super saturation of uric acid crystals –> goes to distal joints where is grows in lower temperatures. Uric acid breaks down to purines/nucleic acids – produces DNA
formation of uric acid crystals
Food with a lot of cells – increased purines and uric acid – seafood, wine
Cell turover like in cancer – releases dna
Clinical manifestations of gouty arthritis
Sudden onset of exquisite joint pain, often wakes from the sleep
Most often affects big toe
Redness, warm, swelling, tenderness
In recurrent and poorly controlled gout ( chronic) – tophi
Gouty tophi
aggregation of urate crystals under the skin (chronic gout)
Diagnosis of gout
Uric acid – is non diagnostic 25 percent of the time this is negative Need synovial fluid aspiration Septic will destroy a joint very fast Send to the ER if not near an ortho Best diagnosis is the fluid aspiration
Elevated serum uric acid
(may be normal in 25% of gout patients) non-diagnostic
X-ray normal during early stages
(bone erosions in chronic/recurrent) non-diagnostic
Elevated CPR, ESR (non-specific)
non-diagnostic
Aspiration of synovial fluids
(WBC 5,000-50,000 cells, with neutrophils < 75%, needle-shape crystals on polarization microscopic examination) diagnostic
Degenerative (OA) Labs
wbc <5k, PMN <25%, crystals negative
Inflammatory (gout , pseudo-gout ) labs
wbc 5-50k PMN >50% crystals Needle shaped crystals –gout, Rhomboid crystals-pseudo gout
Septic labs
wbc > 50, 000, PMN > 75%, no crystals
Clinical diagnosis of gout
Strongest clinical predictors of gout (the more factors the more confidence in diagnosis):
Acute onset, with maximal symptoms within one day
Joint erythema
History of chronic kidney disease
Male patient
Previous attack of arthritis or joint pain
First metatarsophalangeal joint involved
Serum uric acid >6 mg/dl
f/u gout
If aspiration is deferred, vigilant follow-up is warranted. Tight follow up like a hawk, if septic will ruin the joint
Treatment of acute gout
NSAIDs +/- Colchicine – initial
Steroids – if poor response to initial therapy or for patients with renal insufficiency
Colchicine not good if
kidney disease
Very good at antiinflammatory
Excreted in the urine, biggest side effect is diarrhea
Preventative therapy for gout attacks
Reduce alcohol intake, high-purine food (red meat, organ meat, seafood, alcohol beverages esp. beer)
Urate lowering therapy if more than 2 attacks per year
Urate lowering therapy should be initiated between flares, not during the attack
Start slow and titrate to uric acid level < 6 mg/ dl
Decrease production of uric acid
Allopurinol ( first line)
Febuxostat (Uloric®) – if cannot tolerate Allopurinol. Do not give allopurinol in an acute attack. Given inbetween. If during an attack it is given It will mobilize uric acid and will worsen the attack.
increase excretion of uric acid
Probenecid
Colchicine
Anti-inflammatory, for acute flare. s/e: GI: diarrhea ( 80% of pt) Excreted in urine> lower doses or avoid
Allopurinol
Decrease production of uric acid , for prevention s/e: Mild rash. Severe cutaneous reactions are rare DO NOT USE during acute attack
Febuxostat (Uloric)
Decrease production of uric acid, for prevention s/e: Mild rash and liver function abnormalities. DO NOT USE during acute attack
Probenecid
Increase excretion of uric acid. for prevention Contraindicated in renal insufficiency, nephrolithiasis
