Rheumatology (Week 2--Weinreb) Flashcards
(91 cards)
1
Q
Autoimmunity
A
Tolerance (normal mechanisms that prevent immune activity against self-antigens) is lost
Abnormal response by immune system against individuals own tissues resulting in tissue damage
Due to genetic, environmental and immune/cellular factors
2
Q
Innate immune system produces which key inflammatory cytokines?
A
TNF
IFN (interferon)
IL-1beta
Does this by neutrophils and APCs recognizing PAMPs
3
Q
Pathologic complement activation
A
Mechanism for autoimmunity
Antigen-antibody (immune) complexes deposited on tissues then bound to complement and Fc receptors –> immune dysregulation and complement activation
Results in localized tissue injury
4
Q
Antigen presenting cells (APCs)
A
Process foreign antigens for presentation to immune cells as part of adaptive immune system
Present self-antigens during development to generate immune tolerance
5
Q
MHC/HLA
A
HLA antigens expressed on cell surface (MHC I on all cells and MHC II on immune cells) and function to present antigens to immune system as peptides that were processed intracellularly
T and B cell receptors recognize these and activate an immune response
6
Q
HLA genes
A
Highly polymorphic (many alleles for each gene encoding different HLA chain)
Lots of genetic diversity in HLA at the population level
7
Q
Peptide, MHC, type of T cell
A
CD4 helper T cell = MHC II = intracellular organisms and cellular proteins
CD8 cytotoxic T cell = MHC I = extracellular organisms and antigens
8
Q
T helper cells
A
Activate specific B cells through specific T cell receptor and MHC II/peptide antigen binding
9
Q
B cells
A
Produce antibody
Contribute to T cell activation via specific MHC II/peptide antigen and T cell receptor interaction
10
Q
Cytokines
A
Dysregulation of cytokines can contribute to autoimmunity
TNF-alpha
IL-1alpha
IL-1beta
IL-17A
IL-17F
Remember these because we have drugs to interfere with them!
11
Q
Tolerance
A
To prevent a response to self antigens (prevent autoimmunity)
Double signaling/costimulation, regulatory T cells, regulatory B cells, clearance of self-antigens (apoptosis)
Also, see “mechanisms of tolerance”
12
Q
Two signal immune cell activation
A
Two signals required for B cell and T cell activation to ensure only activation when threat by foreign antigen
Foreign antigen activates innate immune system to produce cytokines which cause increased costimulatory B7 family (CD80/86) ligand expression and likelihood of second signal (costimulatory) binding
13
Q
Regulatory T cells
A
5-10% of CD4 T cells
Downregulate effector T cells with similar specificity
Downregulate autoreactive lymphocytes
14
Q
Regulatory B cells
A
Population of B cells found in mice, suggested in humans
Suppresses intestinal inflammation, may be defective in lupus
15
Q
Apoptosis
A
Controlled, regulated cell death
Cell and nuclear condensation, membrane bleb, DNA fragmentation, activated capsase, nuclear condensation, crescents, fragmentation
No inflammatory cytokines produced, anti-inflammatory
16
Q
Mechanisms of tolerance
A
1) Clonal deletion
2) Anergy (if no second signal)
3) Inhibition/suppression
17
Q
Factors contributing to tolerance failure
A
1) Genetic susceptibility genes (innate and adaptive immune systems) can cause: altered cytokine production/response, immune cell function/interactions, apoptosis (leading to secondary necrosis with autoantigen exposure/inflammation)
2) Environmental triggers that affect immune responses: toxins, UV light, infection, alterations in microbiome (dysbiosis)
18
Q
How does necrosis cause autoimmunity?
A
Extracellular exposure of autoantigens and a release of DAMPs (danger associated molecular patterns) that can promote an inflammatory response
19
Q
Working hypothesis for loss of tolerance to self-antigens
A
Autoimmune predisposing alleles and environmental factors (cross-reactive infectious antigens or exposure of hidden self-antigens) contribute to abnormal apoptosis and altered immune function; this leads to exposure of self intracellular antigens and release of inflammatory cytokines that generate pathologic cellular and autoantibody responses
20
Q
Subchondral bone
A
Bone right beneath cartilage and there may be changes there that will help you diagnose different conditions
21
Q
Pannus
A
Proliferative synovium which may cause erosions to bone
(inflamed synovium, hypertrophy, kind of like aggressive benign tumor)
22
Q
Joint space narrowing
A
Decrease in distance between articulating bones due to loss of cartilage
23
Q
Erosions
A
Areas of bone loss within or around a joint
(can be caused by crystals)
24
Q
Subluxation
A
Partial dislocation of a joint
25
Arthritis vs. arthralgia
**Arthritis**: symptoms due to **abnormalities** in **structure** and/or **inflammation** directly involving the **structures within the joint capsule**
**Arthralgia**: pain involving a joint **not associated** with any obvious joint abnormality
26
Periarthritis
Symptoms due to abnormalities in structure and/or function of the **structures around a joint** (**tendons, bursae, nerves**)
27
Synovitis
Inflammation and proliferation of the tissue layer **lining the inside of a joint** (consists of synovial lining cells and underlying connective tissue)
28
Tenosynovitis
Inflammation and proliferation of the tissue layer lining the **inside of a tendon sheath**
(**joints won't be painful** but around tendon will be)
29
Enthesitis
Inflammation of the **sites of tendon or ligament insertion** (entheses) **into bone**
30
Arthroscopy
Imaging used to look in a joint
31
What can you see on an X-ray regarding arthritis?
**Periarticular osteopenia** (bone loss around joint)
**Subluxation**
**Joint space narrowing**
**Erosion**
32
Additive sequence of involvement
Involvement of a joint or joints followed by an **increasing number** of affected joints
More typical of **chronic polyarticular types of arthritis** (**rheumatoid arthritis**)
33
Migratory sequence of involvement
Involvement of one joint, followed by resolution then shortly after get involvement of another joint (arthritis **"jumps" from joint to joint** over **hours** or a few **days**)
Less common presentation
34
Intermittent sequence of involvement
Involvement of a joint or joints, followed by resolution then recurrence in **same or different joint** usually time between is **weeks** to **months**
Typical of **crystal arthropathies**
35
Extraarticular involvement in arthritis
**Eye** symptoms: pain, redness, dryness
**Mucocutaneous**: oral ulcers, rashes, photosensitivity, skin ulcers, skin thickening
**Respiratory**: cough, shortness of breath, dyspnea on exertion, hemoptysis, pleuritic chest pain
**Gastrointestinal**: dysphagia, GERD, post-prandial pain, GI bleeding
Lab abnormalities suggesting organ involvement: **hematuria, proteinuria, renal failure, hematologic abnormalities, liver function abnormalities**, etc
36
Exam findings suggesting inflammatory articular source of symptoms
Joint **swelling**
Increased **warmth** and/or **erythema**
Joint tenderness to palpation
Joint **effusion**
**Pain on passive range of motion**
37
Monoarticular arthritis
**Septic arthritis**
**Crystal arthropathy**
Other monoarthritis
38
2 classes of polyarticular arthritis
**Inflammatory** (symmetric/small joint or asymmetric/large joint)
**Noninflammatory** (degenerative/**osteoarthritis**)
39
Inflammatory symmetric/small joint arthritis
**Rheumatoid arthritis**
**SLE**
**Systemic sclerosis/scleroderma**
**Sjogren's syndrome**
Other collagen-vascular diseases
40
Inflammatory asymmetric/large joint arthritis
**Seronegative spondyloarthropathy** (oligoarticular, 2-4 joints)
**Ankylosing spondylitis**
**Reactive arthritis/Reiter's syndrome**
**Psoriasis**
**Inflammatory bowel disease**
41
Indications for arthrocentesis (joint aspiration)
To rule out a **septic joint**
To evaluate for **crystal arthropathy**
To determine whether an effusion is **inflammatory or noninflammatory**
**Therapeutic** drainage (to remove joint damaging enzymes; pain relief)
42
Tests for synovial fluid analysis
**Appearance**: clear (noninflammatory) vs. cloudy (inflammatory or hemorrhagic)
**Cell count** and differential: WBC, neutrophil %, RBC
**Gram stain**: gram positive vs. gram negative organism
**Culture** and sensitivities: aerobic organisms, special cultures and/or testing for fungi or mycobacteria when suspected
**Polarizing microscopy for crystals**: negatively vs. positively birefringent crystals
43
Types of joint effusions
**Normal**: clear, colorless, viscous; \<200 WBC
**Noninflammatory**: clear, yellow, viscous; 200-2000 WBC, \<25% PMNs
**Inflammatory**: cloudy, yellow, decreased viscosity; 2,000-100,000 WBC, \<50% PMNs
**Pyarthrosis** (**subset** of **inflammatory**): purulent, markedly decreased viscosity; usually \>50,000 WBC, \>95% PMNs
**Hemarthrosis**: grossly bloody (trauma vs. coagulopathy); similar to CBC (?)
44
Polarizing microscopy for detection of birefringent crystals
Put crystal between two filters that are perpendicular to each other
Plane of polarized light is rotated by a birefringent crystal
Orientation of second filter is the plane of polarized light and is used to orient long axis of crystals
45
Gout crystals on polarizing microscopy
**Yellow parallel** and blue perpendicular crystals = **negatively** birefringent = **urate** **crystals** (**gout**)
**Intracellular** crystals are highly indicative of an **acute** gouty flare (usually not seen between attacks)
46
Calcium pyrophosphate (pseudogout) crystals on polarizing microscopy
**Blue parallel** and yellow perpendicular crystals = **positively** birefringent = **calcium pyrophosphate (pseudogout) crystals**
47
Noninflammatory effusion could mean which diseases?
**Osteoarthritis**
Internal derangements (**tendon/ligament/meniscal injuries**)
48
Inflammatory effusion could mean which diseases
Infection
Crystal disease
Rheymatoid arthritis
Seronegative spondyloarthropathy
SLE
49
Pyarthrosis effusion could mean which dieseases?
**Infection**
Intense inflammation: **crystal disease, psoriatic arthritis**
50
Hemarthrosis effusion could mean which diseases?
**Trauma** (intraarticular fracture)
**Coagulopathy** (hemophilia, anticoagulant related)
51
Acute phase response
Increase in **liver-synthesized proteins** and **immunoglobulins** that occurs in response to trauma/tissue injury or a variety of inflammatory/immunologic stimuli
Acute phase proteins: **fibrinogen** (major contributor), C-reactive protein, haptoglobin, ceruloplasmin, alpha-1-antitrypsin, complement C3 and C4, serum amyloid A protein, immunoglobulins
52
Testing for systemic inflammation
Use **ESR** and **CRP**
**Sensitive** for inflammation, but **not specific** enough to be used to make diagnosis of specific disease
53
Erythrocyte sedimentation rate (ESR)
Measures **distance in mm that RBCs fall** over 1h
Normal range: 0-20mm/h
Age adjustment (\>50yrs) for upper limit of normal: Males = age/2; females = age+10/2
Indirect measure of **acute phase proteins** because acute phase proteins are **anionic** (fibrinogen) so allow **RBCs to pack together** more closely, decrease surface area and **sediment more rapidly**
**High sensitivity** for many **inflammatory** conditions
**Not very specific**: many diseases and non-disease states can result in increased ESR
Slow decay time (weeks) so **can't follow changes over short periods of time**
54
C-reactive protein (CRP)
Increased specificity because is a **directly measured protein level** so less affected by non-disease factors than the ESR
Increases within 24h of inflammatory stimulus, peaks within 24-48h and rapidly normalizes with resolution of stimulus
More useful measure for changes over shorter periods of time (days) than ESR
55
Why shouldn't you measure ESR every day?
ESR won't change every day because is affected by anionic acute phase proteins, which stick around for weeks!
Ex: **fibrinogen stays around for 2 weeks** after initial inflammatory stimulus
56
Points about using ESR and CRP
**Nonspecific**: these tests should **NOT be used as general screening test** for any disease; limited role in diagnosis and prognosis; most useful for **monitoring disease activity** and response to therapy
**False-positives**: most are of short duration and spontaneously normalize
**False-negatives**: ESR and CRP can be **normal with many conditions,** so a normal result alone cannot rule out a specific disease
57
Rheumatoid factor
Rheumatoid factor (RF) is an **IgM, IgG, or IgA antibody** which binds to **Fc portion of an IgG immunoglobulin**
IgM RFs are clinically measured
Not specific for any given condition: reflects a state of **chronic immune activation**
Increased RF occurs normally in older individuals with chronic infections and other autoimmune diseases
Helps to make diagnosis of RA, but is NOT diagnostic of RA (could mean many other things)
58
Antinuclear antibody (ANA)
ANA test detects **antibodies** directed against different **nuclear antigens**
Antinuclear antibody in plasma caused LE cells (PMN) to phagocytose nuclei, which happened a lot in people with SLE (not specific for SLE though)
ANA titer is highest dilution giving positive signal (immunofluorescence); abnormal result is titer \>1:40
59
Approach to diagnosing arthritis
1) Determine if complaints due to true **arthritis** or periarticular
2) Monoarticular or **polyarticular** arthritis?
3) Inflammatory or **non-inflammatory**?
4) Symmetric of asymmetric?
5) Is there axial joint involvement?
Now in the right diagnostic "neighborhood"
6) Modify hypotheses based on mode of onset, duration, sequence of involvement, presence of extraarticular findings
7) Rule out or confirm diagnoses with appropriate lab, radiologic and other testing
60
Monoarticular arthritis
Most common types are acute **septic arthritis** and **crystal arthritis**...and they **present identically**!
61
Septic arthritis
Inflammatory arthritis caused by an **infectious** process involving the synovium and joint space
Most commonly a **single joint**, but polyarticular presentation 10-20% of the time
Infections can be acute or chronic
Considered a **medical emergency** because: (1) marker for underlying **systemic** **infection** with increased morbidity and mortality, and (2) can result in **irreversible damage to the joint** in just a few days resulting in impaired joint function and/or chronic pain
Two most common causes of septic joint are **nongonococcal** bacterial arthritis and **gonococcal** bacterial arthritis (disseminated gonococcal infection)
62
Mechanisms of entry of nongonococcal bacterial arthritis into the joint
1) **Hematogenous spread**: most common; **bacteremia** (bacteria in the blood) results in seeding of joint
2) **Direct innoculation**: following **procedures** or **penetrating trauma**
3) **Direct spread** from an **adjacent tissue infection**: cellulitis (skin infection), bursitis, or osteomyelitis (bone infection)
63
Progression and pathology of nongonococcal bacterial arthritis
**Bacterial seeding** results in **acute** **inflammation** with migration of neutrophils into synovium, **synovial** **hyperplasia**, and development of **joint effusion**
Over next **5-7 days**, release of various inflammatory **cytokines**, host **proteolytic** **enzymes** and **bacterial toxins** contribute to **cartilage and bone degradation** (bones look **mushed together** on x-ray: irregular bony margins, joint space narrowing, osteopenia)
64
What is the most common cause of nongonococcal bacterial arthritis?
**Staphylococcus aureus** (gram **positive** coccus)
Gram negative bacterial joint infections are much less common and associated with older age, GI infections, GU infections, and IV drug use
65
Clinical presentation of nongonococcal bacterial arthritis
**Acute onset** of inflamed joint
Typically **monoarthritis** (polyarticular 10-20% and usually with immunosupression or marked bacteremia)
Most commonly **large** (shoulder, hip, knee (50%, most common)) or **intermediate** (wrist, ankle) joints; small or fibrous joints (sacroiliac, sternoclavicular) much less common
Constitutional symptoms: fever, chills, rigors (bacteremia)
Signs of infection in other organ systems
Physical exam: **erythema** and **warmth**, **tenderness** to palpation, **pain** on **passive** range of motion, **swelling** and **effusion**
66
Risk factors for nongonococcal bacterial arthritis
Anything contributing to **increased risk of bacteremia**, **joint seeding, or decreased ability to clear infection from joint**
**Local** factors: prior joint damage, surgery/arthrocentesis, prosthetic joint
**Systemic** factors: younger/older age, immunosuppression, comorbid disease
**Social** factors: IV drug abuse, homelessness, animal exposures
67
Gonococcal bacterial arthritis
***Neisseria gonorrhea*** (gram **negative**) enters into joint via **hematogenous** **spread** from its mucosal site of infection (urethra, cervix, rectum, pharynx)
Develops in only **1-3%** of people infected with *Neisseria gonorrhea*
Most common form of septic arthritis in youg sexually active adults in the US but can occur in older adults too
3x more common in women and more common in homo/bisexual men
68
Two types of clinical presentation of gonococcal bacterial arthritis
1) **Purulent arthritis**: mono or oligoarticular arthritis (wrist, knee, and/or ankles); **purulent joint effusion** present from which **organism can be cultured**; may not be associated with other signs of gonococcal infection
2) **Triad**: macular or vesicopustular **skin lesions**; **tenosynovitis** involving tendon sheaths of wrists, fingers, ankles, toes (important distinguishing feature); **blood and mucosal cultures usually positive** but **synovial fluid cultures negative**
69
Risk factors for gonococcal bacterial arthritis
**Local** factors: female, previous gonococcal infection (increased risk of asymptomatic infection)
**Systemic** factors: bacterial factors, complement deficiencies that impair the formation of the attack complex (C5-8)
**Social** factors: unprotected sexual activity, IV drug abuse, lower educational status, urban residence
70
Diagnosis of septic arthritis
**Clinical**: monoarthritis is considered a **septic joint** until proven otherwise!
**Lab**: WBC possibly elevated but normal 40% of the time; positive blood cultures indicate **bacteremia**; culture mucosal sites if suspect disseminated gonococcal infection
**Joint aspiration**: inflammatory fluid (**WBCs \> 2,000**mm3, increased **neutrophils**); gram stain of fluid may be positive (but sensitivity only 20-45%); **synovial fluid culture** to confirm infection is gold standard (allow culture to grow for 72 hours)
71
Management of septic arthritis
If you suspect septic joint, start I**V antibiotics** right after **joint aspiration**/sent for culture/**blood culture** taken
Evaluate other organ systems for infection
Joint should be **serially** **drained** to remove damaging inflammatory and toxic mediators and to monitor cell count and if cell count \> 50,000mm3, call orthopedics to perform **washout of joint** (using big tube to wash w/saline)
After clinical improvement, low level rehab starte
Treatment delay increases the risk of chronic joint damage
72
Crystal arthropathy (gout)
**Purines** metabolized to uric acid but uric acid exists in ionic urate form in plasma, which is excreted by the kidney
Physiologic saturation of plasma causes m**onosodium urate crystals (gout crystals)** to form in tissues
Inflammatory response to urate crystals via innate immune system (same as rsponse to septic joint, which is why they present identically!)
73
Causes of hyperuricemia
**Increased production**: increased cell **turnover** (some tumors/chemotherapy, psoriasis), increased intake of purine rich **food** (shellfish, organ meat, beer), increased **alcohol** intake (binging causes increased breakdown of ATP/ADP), **genetic** predisposition (mutations in purine metabolizing genes)
**Decreased excretion**: acute/chronic **renal failure**, **drugs** that interfere w/excretion (thiazide diuretics), **diabetes** (increased insulin interferes with excretion), **genetic** predisposition (polymorphisms in renal urate transporters)
74
Pathophysiology of gout
Not completely known
Not just urate crystal deposition, because extracellular crystals found in non-inflamed joints
**Changes** in serum uric acid concentrations (**increases AND decreases**) associated with flare ups
75
3 phases of gout
1) **Acute** arthritis: acute monoarthritis
2) **Intercritical** gout: asymptomatic period between attacks, but extracellular MSUM crystals may still be present in synovial fluid
3) **Chronic** **tophaceous** gout: increasing frequency and severity of attacks with formation of tophic and erosive polyarticular arthritis
Can cycle through phases 1 and 2 or 2 and 3
76
Clinical presentation of gout
History of **hyperuricemia** or condition associated with hyperuricemia
**Sudden onset** of **monoarthritis**
Inflammation 3-10 days, **spontaneous resolution** 3-7 days
Most common at **1st metarsalphalangeal, ankle, knee, wrist**
**Tenosynovitis** and **bursitis** bc urate crystals in synovium of tendon sheaths and bursae
With longstanding hyperuricemia, chronic gout can develop
Low grade fever, inflamed joint, **tophi** in soft tissues (skin, bursae, tenosynovium)
77
Chronic gout
Develop with **longstanding hyperuricemia**
Flares can become more frequent, more prolonged, polyarticular
Associated with nodular collections of monosodium urate crystals (**tophi**)
Chronic low to moderate **joint inflammation** that **doesn't spontaneously resolve** and is poorly responsive to treatment
Tophi formation can cause **bony erosions**
Can cause renal precipitation of urate crystals and thus **kidney damage**
78
Diagnosis of gout
Should be suspected in acute monoarthritis or tenosynovitis, especially if there are risk factors
Since identical to septic joint on appearance, synovial fluid must be obtained for cell count, gram stain, culture, crystal analysis
Definitive diagnosis of gouty arthritis made by finding **negatively birefringent (yellow parallel)** needle-shaped crystals (and intracellular crystals mean acute gouty flare)
Can sometimes have septic joint at same time
79
Management of gout
First treat **inflammation** (colchicine, steroids, NSAIDs, intraarticular steroid injection)
Avoid anything that would **change** serum uric acid concentration (don't give allopurinol bc that would decrease uric acid concentration and don't want it to change at all!)
If more than **2 flares per year** then **lower serum uric acid** concentration (hypouricemic therapy): decrease purine intake, decrease meds that would cause hyperuricemia, take hypouricemic meds
80
Calcium pyrophosphate deposition disease (CPPD), or pseudogout
**CPPD** **crystals** can form in cartilage and intraarticular fibrous structures and shedding of crystals can cause **inflammatory** response that occurs through same innate immune pathway as gout
Clinical presentation of joint inflammation, tenosynovitis, bursitis **identical to gout** except **NO tophi**
81
Clinical presentations of CPPD
**Acute arthritis** (pseudogout causes **inflammation**, monoarticular)
**CPPD arthropathy** (**degenerative** changes similar to **osteoarthritis**)
**Tenosynovitis** alone or with inflam arthritis
Radiologically as **chondrocalcinosis** (calcification of cartilage/fibrocartilage)
Common with older age but sometimes associated with **metabolic disease** (parathyroid, thyroid, hemachromatosis)
82
Diagnosis of CPPD
**Positively** birefringent (**parallel blue**) rhomboid-shaped crystals on polarizing microscopy
83
Treatment of CPPD
**Inflammation treated** same way as gout (colchicine, steroids, NSAIDs, intraarticular steroid injection)
No hypouricemic therapy (uric acid isn't a problem!)
Consider metabolic workup
84
Osteoarthritis
Complex group of non-autoimmune **mechanically-induced** conditions due to **altered joint loading** that results in failure and **loss of intraarticular cartilage** and dysfunction of other articular components (synovium, ligaments, neural components, bone) resulting in **chronic joint pain** and **loss of joint function**
Most prevalent type of arthritis
85
Primary vs. Secondary osteoarthritis
**Primary** osteoarthritis: not associated with trauma or other medical condition; joint involved usually **DIP, PIP, 1st CMC, wrists, acromioclavicular, cervical/lumbar spine, hips, knees, MTPs**
**Secondary** osteoarthritis: associated with **trauma** or other **metabolic conditions** (such as **CPPD**); joint involved usually NOT the ones listed above
86
Pathology of osteoarthritis
In the cartilage, get **fibrillations** and **fissures**
**Thinning and loss of cartilage** in response to altered forces which cause **osteophytes**
87
Clinical presentation of osteoarthritis
Mechanical joint pain exacerbated by weight bearing and/or **relieved by rest** (can contribute to inactivity)
**Stiffness** less than **30 min in the morning** or after not moving for a while
**Decreased range of joint motion** secondary to **pain** or severe joint damage
**Muscle weakness/atrophy** secondary to pain and inactivity, can result in altered gait and increased risk for fall
**Non-inflammatory swelling**
Characteristic presentation: bilateral DIP joint space narrowing with osteophytes
Trauma, CPPD and other metabolic conditions suggest secondary osteoarthritis
88
Physical exam findings of osteoarthritis
**Tenderness** to palpation without joint swelling
**Decreased ROM** with **crepitus** (crackling due to loss of cartilage)
**Pain on passive range of motion** (if disease is in advanced stage)
**Osteophytes**, joint malalignment
Altered gait
**Bursitis** and/or **tendonitis** due to altered gait and joint deformities
89
Diagnosis of osteoarthritis
History and associated joint exam findings in **absence of inflammation**
**Secondary** osteoarthritis diagnosed if joints other than those usually seen in primary, if **trauma** or underlying associated condition
Only do lab testing for underlying condition for secondary osteoarthritis
**X-rays** helpful to confirm diagnosis
90
X-rays in diagnosis of osteoarthritis
Only take x-ray to **confirm** the diagnosis
**Asymmetric joint space narrowing**
**Osteophytes**
**Subchondral** bony **sclerosis** (hardening from inflammation)
**Subchondral** bony **cysts** (looks darker)
Note: radiologic severity does not always correlate with given patient's pain or level of joint function
91
Management of osteoarthritis
**No therapy can restore lost cartilage**
Goal of treatment is to **control pain** (meds, PT, weight loss), **restore function** (pain control, PT), **prevent/minimize progression** (PT, weight loss)
If pain/loss of function severe, consider **joint replacement surgery**
