Rheumatology Flashcards
(85 cards)
1
Q
Major divisions of arthritis
A
non-inflammatory (OA)
Inflammatory
2
Q
Inflammatory Arthridities
A
–Rheumatoid Arthritis
–Juvenile Idiopathic Arthritis
–Systemic Lupus Erythematosus
–Crystal induced Arthritis
–Spondyloarthropathies
- Ankylosing Spondylitis
- Psoriatic Arthritis
- Reactive Arthritis
3
Q
Most common form of arthritis
A
osteoarthritis (non-inflammatory)
4
Q
Common locations of OA
A
–Knees
–Hips
–Spine (cervical and lumbar)
–Hands (interphalangeal joints: DIP, PIP, thumb CMC)
–Feet (first metatarsophalangeal)
5
Q
Progressive loss of articular cartilage
A
OA
6
Q
Osteoarthritis is __________ disorder
A
age-related
7
Q
Clinical Presentation OA:
- ________ onset
- ______ and ___ -limited: initially
- ___-related Pain:
–Knees & Hips: Worse with _______
–Hands: worse with ______
- Relieved by ______
- Morning stiffness ______________
A
- Gradual onset
- Intermittent and self -limited: initially
- Use-related Pain:
–Knees & Hips: Worse with weight-bearing
–Hands: worse with overuse
- Relieved by rest
- Morning stiffness less than 30 minutes
8
Q
Risk factors OA
A
Increasing Age
Major joint trauma
Obesity (knees)
Repetitive activities
Genetic Predisposition
Congenital/Developmental defects
Females
9
Q
OA: PE
______ pain - Pain at joint line
Limitation in _________
Bony enlargement (_______)
Soft tissue _______
_______ (grinding w/ movement)
______ / ________
Source of pain:
–Tendinitis
–Periarticular muscle spasm
–Periostitis
–Joint capsule irritation
A
•Localized pain
–Pain at joint line
- Limitation in range of motion
- Bony enlargement (osteophytes)
- Soft tissue swelling
- Crepitus (grinding w/ movement)
- Instability / deformity
- Source of pain:
–Tendinitis
–Periarticular muscle spasm
–Periostitis
–Joint capsule irritation
10
Q
X-ray findings OA
A
–Sclerosis
New bone formation in the subchondral trabeculae
–Osteophytes
Formation of new bone at the joint margins
–Loss of cartilage
11
Q
Nonpharmologic therapy for OA
A
Patient Education: self-management
Weight Reduction (Knee OA)
Exercise
Physical Therapy
Muscle strengthening exercises
Range of Motion exercise
Braces
Assistive devices
Cane, walker
Joint Replacement
12
Q
Pharmologic tx for OA
A
–Acetaminophen
–NSAID’s
–Analgesics
–Topical agents
- Capsaicin
- Methyl salicylate, Diclofenac gel
–Intra-articular steroid injections
–Hyaluronic acid derivatives
13
Q
RA RF
A
Smoking, periodontal disease
14
Q
RA more prevalent in ______ , ______
A
women, native populations
15
Q
RA
A
Systemic Inflammatory arthritis (chronic, progressive, disabling disease)
16
Q
Lab Markers RA
A
Positive Rheumatoid factor, positive anti-CCP antibody (ACPAs)
17
Q
Systemic disease sxs of RA
A
–Fatigue, fever, weight loss
–Extra-articular manifestations (Subcutaneous nodules, Pericarditis, Pulmonary nodules/ Interstitial fibrosis, Inflammatory Eye Disease - Episcleritis / Scleritis, Vasculitis)
18
Q
Therapeutic modalities RA
A
- Recognize & Treat early
- Patient Education
- PT / OT
–Joint Protection Protocols
–Splints
–Adaptive Devices
- Exercise / Rest
- Medications
–NSAID’s, Steroids, DMARD’s (slow RA), Biologic DMARD’s (new)
–“Treat to Target” - goal of low disease activity or remission
19
Q
DMARDs for RA
A
Disease Modifying Anti-Rheum Drugs
–Hydroxychloroquine
–Minocycline
–Gold
–Sulfasalazine
–Methotrexate
–Leflunomide / Arava
–Azathioprine / Imuran
–Cyclosporine
20
Q
Biologic DMARDs
A
–TNF Blockers (Enbrel / Etanercept, Remicade / Infliximab, Humira / Adalimumab, Simponi / Golimumab, Cimzia / Certolizumab pegol)
–T-Cell costimulator (Orencia / Abatacept)
–B Cell (Rituxan / Rituximab)
–IL-6 (Actemra / Tocilizumab)
–IL-1 (Kineret / Anakinra)
–JAK (Xeljanz / Tofacitinib)
**Usually start w/ TNF (most respond to this), otherwise trial and error
21
Q
Iridocyclitis associated with
A
oligoarticular/pauciarticular onset of juvenile idiopathic arthritis
22
Q
JIA treatment
A
- Patient / Parent Education
- Physical / Occupational Therapy
- NSAID’s
- Steroids: Intra-articular / oral
- DMARD’s:
–Methotrexate
–Sulfasalazine
–Leflunomide
•Biologic DMARD’s: Anti TNF, Anti IL-1
23
Q
Crystal induced arthritis
A
- Gout (Uric Acid)
- Pseudogout (Calcium Pyrophosphate Deposition Disease / CPPD)
24
Q
Clincal presentation of Gout (in different locations)
A
Deposition of monosodium urate
–Joints: Acute inflammatory arthritis
–Skin: Accumulation of crystals (tophi)
–Kidney: Uric acid urolithiasis, nephropathy
25
Stages of Gout
–Asymptomatic Hyperuricemia
–Acute Intermittent Gout
–Chronic Tophaceous Gout
26
Acute Intermittent Gout (ages, males vs. females, prevalence, when happens in women)
* First attacks occur between the fourth and sixth decades of life.
* Males \> females 4:1
* Prevalence 3.1% in the US
* In women: later onset (menopause)
–Diuretic use
–Hypertension
–Renal Insufficiency
27
Acute Gouty Arthritis: Clinical Presentation
•Abrupt onset of inflammatory arthritis
–Local release of inflammatory mediators
–Often occurring at night
–Pain escalates over a 8 to 10 hour
–May subside within 3 to 10 days
–In severe cases: Fever, chills, malaise
•Involvement of
–Joints
–Periarticular structures (resembling cellulitis) (Bursa, Tendon)
28
Acute Gouty Arthritis usually _______ extremities initially (usually _______ #joints but may be \_\_\_\_\_\_\_\_)
Lower extremity (podagra = first MTP)
Usually monoarticular, may be polyarticular
29
Other joints involved w/ acute gouty arthritis
–MTPs, Mid-foot, Ankles, Heels, Knees, Wrists, Fingers, Elbows
30
How to tell between gout and septic arthritis?
Joint aspiration (bloody, red infection vs white is likely tophi = gout)
31
Diagnosing Gout
**Serum uric acid levels**
–not sensitive nor specific, May be normal, high or low at the time of an acute attack, Helpful in long term management (trend, keep \< 6)
**H & P: clinical manifestations**
**Gold standard: Synovial fluid analysis**
–Crystals may not be observed all the time, Infection CAN coexist
32
Gout Triggers
* Alcohol Ingestion (Beer & liquor)
* Trauma
* Severe illness (Surgery / MI / Stroke / Infection)
* IV Hydration
–Hyperalimentation
•Medications:
–Thiazide diuretics
–Low dose aspirin (\< 2 gm/day)
–Cyclosporine
•Dietary excess
–High purine foods
•Contrast dye
33
Advanced Gout
Uncontrolled Hyperuricemia
Chronic arthritis
–Constant pain in joints - Increased intensity during a flare, Flares: Longer duration
–Destructive arthritis
Polyarticular
–upper and lower extremities
34
Chronic/Advanced Gout =
Tophaceous Gout
## Footnote
–Solid uric acid deposits (white chalky material)
–Will need urate lowering therapy
•Xanthine Oxidase Inhibitors
–Generally painless
* but cause stiffness, deformity
* can drain and become infected
35
Risk factors for advanced gout
•Long duration of uncontrolled hyperuricemia
36
Location of Tophi
–Helix of the ear
–Periarticular regions:
•Fingers (Heberden’s nodes), Wrists, Olecranon bursa
–Can also occur in unusual areas:
•Knee, Spine, Symphysis pubis, Subserosa of transverse colon
37
Tophi are hard/soft
hard to touch
38
Seeing increased prevalence of gout why?
* Increased longevity
* Increased prevalence of Hypertension (diuretics and decreased kidney function)
* Dietary trends (high protein diets)
* Increased incidence of obesity
* Improved survival form CHF & CAD
* Increased prevalence of diuretic use and low dose aspirin
39
Gout tx
* Aspiration of Joint / Analysis of fluid
* Dietary counseling
–Alcohol
–Obesity / weight reduction
–Hyperlipidemia / Diabetes / Hypertension
* NSAID's
* Colchicine
* Allopurinol / Febuxostat / Probenecid
* Pegloticase IV
* Glucocorticoids: oral or intra-articular
* Analgesics
40
Pseudogout
Resembles?
Males vs females
Associated with
May resemble gout, OA, RA
Males = females
Aging
41
Causes of pseudogout
![]()Idiopathic: most common / aging
![]()Familial
![]()Associated with metabolic disease
–Hyperparathyroidism (15%)
–Hemochromatosis
–Hypothyroidism
![]()Prior Trauma
–Surgery
–Hemophilia
–Neuropathic joints
42
Gout vs pseudogout
age, male vs female, marker? tophi? crystals, common location, renal involvement, Xray
Gout
30-60 year olds, Males \>\> Females, High Uric Acid, Tophi, Monosodium urate crystals (needle shaped), -- Ist MTP, instep, ankles, knees-- , Kidney involvement / stones, X-ray: soft tissue swelling / erosions
Pseudogout / CPPD
Older \>50, M = F, No marker, No tophi, Calcium pyrophosphate (rhomboid shaped), --wrist, knee, MCP, elbow, shoulder --, No renal complications, X-ray: chondrocalcinosis osteoarthritis
43
Multisystem inflammatory disorder
Spondyloarthropathies
44
Spondyloarthropathies affect
–Spine
–Sacroiliitis
–Peripheral joints
–Periarticular structures (enthesopathy)
45
Spondyloarthropathies, lab negatve and lab positive
seronegative, postive HLA B27
46
Spondyloarthropathies nonvertebral sxs
–Plantar Fasciitis
–Inflammatory Eye Disease (IED) / Iritis
–Mucocutaneous Lesions
–Asymmetric peripheral arthritis
–Sausage digits / dactylitis
–Achilles tenosynovitis
47
Spondyloarthropathies (diseases and genetic correlation)
* Ankylosing Spondylitis
* Psoriatic Arthritis
* Reactive Arthritis
–Reiter’s Syndrome
•Arthritis associated with Inflammatory Bowel Disease
–UC, Crohn’s disease
\*\*HLA B27 strongly associated with all of these diseases
48
Ankylosing spondylitis clinical presentation
•Inflammatory Back Pain
–Onset before age 40
–Insidious
–Duration \> 3 months
–Morning stiffness
–Pain Decreases with exercise
49
Ankylosing spondylitis causes \_\_\_\_\_\_\_, and incidence associated w/
* Axial arthritis, sacroiliitis
* Peripheral arthritis
* M \> F
* IED: Uveitis
* Aortitis, Cardiac arrhythmias
50
Psoriatic arthritis clinical presentation
Approx 7- 30 % of pts with psoriasis
Skin and nail lesions (pits)
Inflammatory Eye disease
Peripheral arthritis DIP joints
Dactylitis / sausage toe
Enthesopathy –Achilles Tendinitis, Plantar Fasciitis
Sacroiliitis
Arthritis mutilans
51
Genetics of Psoriatic Arthritis
–Higher rate in twins
–Familial cluster
–Ongoing studies:
* HLA B7,B27: destined for development of arthritis
* HLA DR7a: found in high frequency among patients with psoriasis and psoriatic arthritis
52
If see plantar fasciitis and inflammatory eye disease w/ arthritis, think
spondyloarthropathy
53
Reactive Arthritis
Develops after \_\_\_\_\_\_\_\_\_
![]()Develops after an infection
–Bowel (food poisoning)
![]()Campylobacter, Salmonella, Shigella, Yersinia
–or Genital
![]()Chlamydia
54
Genetic predisposition to Reactive arthritis
presence of HLA B27
55
Reactive arthritis typically seen in
males between 20-50
56
Reactive arthritis infection?
Not an infection in the joint but rather an inflammation triggered by the bacteria.
57
Reactive arthritis in _____ joints
Arthritis of large joints
–Lower extremities (knees, ankles)
–Usually within 1 month of infection
Spine often involved
58
enthesopathy
Ligament involvement
59
Extra articular manifestations of reactive arthritis
–Conjunctivitis
–Urethritis or cervicitis
–Genital Ulcers
–Rash in palms or soles (keratoderma blenorrhagica)
60
Spondyloarthropathies therapy
* Physical Therapy / ROM / Posture
* Medications:
–NSAID’s
–Peripheral arthritis
* Sulfasalazine
* Methotrexate
–Axial arthritis
•Biologics: Anti TNF blockers
–Antibiotic Rx for Chlamydia
61
Juvenile Idiopathic Arthritis
Cause? Age? Girls vs boys
* Chronic synovial inflammation
* Unknown cause
* Prevalence: between 57 and 220/100,000 children
* Age \< 16
* girls \> boys
62
Criteria for Diagnosing Early Inflammatory Disease
Swollen Joints
–Large vs. Small
Small Joints:
–Wrists, MCP, PIP, MTP
Large Joints:
–Ankles, knees, elbows, shoulders
Serologies:
–Positive RF (sensitivity 70%, specificity 82%)
–Positive CCP Antibody (sensitivity 80%, specificity 95%)
Inflammatory markers:
–Elevated CRP and ESR
63
RA genetics
–1% general population
–2-5 % fraternal twins
–30-50% identical twins
–HLA DR 4
* HLA DRB1 alleles are over represented among RA patients
* Ongoing studies:
–Severity of RA
–Response to therapy
–“Pre-RA”
64
Lab tests for JIA
None
65
Different subsets of JIA
–Systemic onset (very sick)
–Polyarticular onset
–Pauciarticular onset
66
JIA Systemic Onset Clinical presentation
Prevalence, Boys vs. girls, age, main sxs, systemic features, lab testing, resolution?
2-17% of children with JIA
Boys = girls
Any age during childhood (peak 1-6 years old)
Daily Spiking fevers accompanied by an evanescent, salmon colored rash
Systemic Features:
–Lymphadenopathy
–Hepatosplenomegaly
–Pericardial / pleural effusions
–Fatigue, muscle atrophy, weight loss
–Leukocytosis, Anemia
RF and ANA generally negative
About 20-50% patients ultimately have severe, chronic arthritis
67
JIA Polyarticular Onset Clinical Presentation
Joints, Girls vs Boys, Sxs, Subdivisions
Arthritis in 5 or more joints
Girls \> Boys (3:1)
Malaise, weight loss, low grade fever, lymphadenopathy, anemia
Subdivided by RF:
–RF positive: in 2-10% children
Girls, later onset age 8, HLA DR 4+, greater risk of erosions, nodules, poor functional outcome
Resembles adult RA
–RF negative: in 10-28% children
68
JIA Oligoarticular/Pauciarticular Onset Clinical PResentation
Prevalence, # joints, age, girls vs boys, joints, lab
* Occurs in 24-58% of all JIA
* Arthritis affecting 4 or fewer joints
* Early onset (1-5 years old at onset)
* Girls \> boys 4:1
* Joints: knees, ankles, wrists, elbows
* Positive ANA
–Iridocyclitis develops in 30-50% \*
69
Enthesitis
inflammation of the entheses, the sites where tendons or ligaments insert into the bone. It is also called enthesopathy, or any pathologic condition involving the entheses.
70
JIA Subgroups
* Psoriatic JIA (2-11%)
* Enthesitis-related JIA (3-11%)
* Undifferentiated JIA (2-23%)
71
Enthesitis-related JIA
Male vs female, genetics, labs, other sxs
–Male predominance (\> 6 years old)
–Positive HLA B 27 (lumped w/ spondyloarthropathies)
–Negative RF and ANA
–Enthesopathy
–Sacroiliitis
–Ocular inflammation: up to 25%
72
Psoriatic JIA clinical presentation
Dactylitis, nail pitting, sacroiliitis
73
•Autoimmune disease
–Production of antibodies to components of the cell nucleus
•“Antinuclear antibodies” / ANA
–Present in 95% of patients
Systemic Lupus Erythematosus
74
SLE peak incidence age and male vs females
peak incidence 15-10, female:male 9:1
75
Lupus clinical features
Butterfly or malar rash
Discoid rash
Photosensitivity
Oral ulcers
Arthritis
Serositis
Renal
Neurologic
Hematologic
Immunologic
–Positive ds DNA
–Positive anti SM (Anti Smith)
–False + RPR
–APL +
Positive ANA
76
SLE autoantibodies
* Double stranded DNA (dsDNA) antibody and glomerulonephritis
* Antibodies to Ro (SSA) association
–Neonatal lupus
–Congenital heart block
–Subacute cutaneous lupus
77
SLE genetics
* Most cases are sporadic
* Strong familial aggregation
* SLE occurs concordantly in:
–25-50% monozygotic twins
–5% dyzygotic twins
78
SLE Therapy
•Sunscreen, Patient education, NSAID’s, Corticosteroids, Antimalarials /Hydroxychloroquine, Methotrexate, Leflunomide, Cyclophosphamide,Mycophenolate (Cell Cept),Cyclosporine, Dapsone, Azathioprine / Imuran, Belimumab / Benlysta
\*\*\*Avoid TNF Biologics
79
Drug-Induced Lupus
* Clinical features are less severe
* Most common presentations:
–Fever, malaise
–Arthritis / Arthralgias
–Serositis
–Rashes
* CNS and renal involvement are rare
* Anti histone antibodies present in 90%
* _Therapy_: STOP the medication
80
Causes of Gout (overall)
Uric Acid overproduction (i.e. enzymes, psoriasis, ethanol, warfarin) or Uric Acid underexcretion (i.e. renal failure, hypertension, obesity)
81
Genetics of Gout
Family occurence
## Footnote
* American series: 40% have family history of gout
* X-linked inheritance of HPRT deficiency & PRPP synthetase superactivity
* Autosomal inheritance (G6PD deficiency)
82
Joints of pseudogout (# and most common)
•Monoarticular or Oligoarticular Arthritis
–becoming polyarticular
–Acute or subacute attacks of Inflammatory arthritis:
* Wrists
* Knees (Most common)
* Hips
* Shoulders
* Ankles
82
Pearls: Gout Arthritis
## Footnote
* Not uncommon to have a _\_\_\_\_\_\__ serum Uric acid level at time of gouty attack
* Hyperuricemia frequently results from _____ \_\_\_\_\_\_
* Allopurinol i_s/is not_ appropriate _initial_ therapy during an acute attack of gout
* _Goal:_ Keep uric acid level \_\_\_\_\_
* Not uncommon to have a _NORMAL_ serum Uric acid level at time of gouty attack
* Hyperuricemia frequently results from diuretic therapy
* Allopurinol is _not_ appropriate _initial_ therapy during an acute attack of gout
* _Goal:_ Keep uric acid level \< 6
–“Treat to target”
83
Xrays and Pseudogout --\> show ______ and locations
In about 75% cases, x-rays will show chondrocalcinosis
–Wrists
–Knees
–Symphisis pubis
84
Gout vs Pseudogout tx
Gout -- NSAID’s effective, Colchicine effective, Allopurinol and Febuxostat (Tophi and Stones), Probenecid (Age \< 60, GFR of \> 50 ml/min, No nephrolithiasis), Pegloticase (Large burden of tophi, IV), Intra-articular steroids: effective
Pseudogout -- NSAIDs effective, Colchicine less effective, no preventive drugs, intra-articular steroids effects
