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Skin MS: Week 6 > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

Major divisions of arthritis

A

non-inflammatory (OA)

Inflammatory

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2
Q

Inflammatory Arthridities

A

–Rheumatoid Arthritis

–Juvenile Idiopathic Arthritis

–Systemic Lupus Erythematosus

–Crystal induced Arthritis

–Spondyloarthropathies

  • Ankylosing Spondylitis
  • Psoriatic Arthritis
  • Reactive Arthritis
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3
Q

Most common form of arthritis

A

osteoarthritis (non-inflammatory)

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4
Q

Common locations of OA

A

–Knees

–Hips

–Spine (cervical and lumbar)

–Hands (interphalangeal joints: DIP, PIP, thumb CMC)

–Feet (first metatarsophalangeal)

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5
Q

Progressive loss of articular cartilage

A

OA

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6
Q

Osteoarthritis is __________ disorder

A

age-related

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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
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8
Q

Risk factors OA

A

Increasing Age

Major joint trauma

Obesity (knees)

Repetitive activities

Genetic Predisposition

Congenital/Developmental defects

Females

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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

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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

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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

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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

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13
Q

RA RF

A

Smoking, periodontal disease

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14
Q

RA more prevalent in ______ , ______

A

women, native populations

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15
Q

RA

A

Systemic Inflammatory arthritis (chronic, progressive, disabling disease)

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16
Q

Lab Markers RA

A

Positive Rheumatoid factor, positive anti-CCP antibody (ACPAs)

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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)

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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

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19
Q

DMARDs for RA

A

Disease Modifying Anti-Rheum Drugs

–Hydroxychloroquine

–Minocycline

–Gold

–Sulfasalazine

–Methotrexate

–Leflunomide / Arava

–Azathioprine / Imuran

–Cyclosporine

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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

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21
Q

Iridocyclitis associated with

A

oligoarticular/pauciarticular onset of juvenile idiopathic arthritis

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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

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23
Q

Crystal induced arthritis

A
  • Gout (Uric Acid)
  • Pseudogout (Calcium Pyrophosphate Deposition Disease / CPPD)
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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

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25
Q

Stages of Gout

A

–Asymptomatic Hyperuricemia

–Acute Intermittent Gout

–Chronic Tophaceous Gout

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26
Q

Acute Intermittent Gout (ages, males vs. females, prevalence, when happens in women)

A
  • 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

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27
Q

Acute Gouty Arthritis: Clinical Presentation

A

•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)

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28
Q

Acute Gouty Arthritis usually _______ extremities initially (usually _______ #joints but may be ________)

A

Lower extremity (podagra = first MTP)

Usually monoarticular, may be polyarticular

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29
Q

Other joints involved w/ acute gouty arthritis

A

–MTPs, Mid-foot, Ankles, Heels, Knees, Wrists, Fingers, Elbows

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30
Q

How to tell between gout and septic arthritis?

A

Joint aspiration (bloody, red infection vs white is likely tophi = gout)

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31
Q

Diagnosing Gout

A

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

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32
Q

Gout Triggers

A
  • 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

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33
Q

Advanced Gout

A

Uncontrolled Hyperuricemia

Chronic arthritis

–Constant pain in joints - Increased intensity during a flare, Flares: Longer duration

–Destructive arthritis

Polyarticular

–upper and lower extremities

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34
Q

Chronic/Advanced Gout =

A

Tophaceous Gout

–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
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35
Q

Risk factors for advanced gout

A

•Long duration of uncontrolled hyperuricemia

36
Q

Location of Tophi

A

–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
Q

Tophi are hard/soft

A

hard to touch

38
Q

Seeing increased prevalence of gout why?

A
  • 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
Q

Gout tx

A
  • 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
Q

Pseudogout

Resembles?

Males vs females

Associated with

A

May resemble gout, OA, RA

Males = females

Aging

41
Q

Causes of pseudogout

A

Idiopathic: most common / aging

Familial

Associated with metabolic disease

–Hyperparathyroidism (15%)

–Hemochromatosis

–Hypothyroidism

Prior Trauma

–Surgery

–Hemophilia

–Neuropathic joints

42
Q

Gout vs pseudogout

age, male vs female, marker? tophi? crystals, common location, renal involvement, Xray

A

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
Q

Multisystem inflammatory disorder

A

Spondyloarthropathies

44
Q

Spondyloarthropathies affect

A

–Spine

–Sacroiliitis

–Peripheral joints

–Periarticular structures (enthesopathy)

45
Q

Spondyloarthropathies, lab negatve and lab positive

A

seronegative, postive HLA B27

46
Q

Spondyloarthropathies nonvertebral sxs

A

–Plantar Fasciitis

–Inflammatory Eye Disease (IED) / Iritis

–Mucocutaneous Lesions

–Asymmetric peripheral arthritis

–Sausage digits / dactylitis

–Achilles tenosynovitis

47
Q

Spondyloarthropathies (diseases and genetic correlation)

A
  • 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
Q

Ankylosing spondylitis clinical presentation

A

•Inflammatory Back Pain

–Onset before age 40

–Insidious

–Duration > 3 months

–Morning stiffness

–Pain Decreases with exercise

49
Q

Ankylosing spondylitis causes _______, and incidence associated w/

A
  • Axial arthritis, sacroiliitis
  • Peripheral arthritis
  • M > F
  • IED: Uveitis
  • Aortitis, Cardiac arrhythmias
50
Q

Psoriatic arthritis clinical presentation

A

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
Q

Genetics of Psoriatic Arthritis

A

–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
Q

If see plantar fasciitis and inflammatory eye disease w/ arthritis, think

A

spondyloarthropathy

53
Q

Reactive Arthritis

Develops after _________

A

Develops after an infection

–Bowel (food poisoning)

Campylobacter, Salmonella, Shigella, Yersinia

–or Genital

Chlamydia

54
Q

Genetic predisposition to Reactive arthritis

A

presence of HLA B27

55
Q

Reactive arthritis typically seen in

A

males between 20-50

56
Q

Reactive arthritis infection?

A

Not an infection in the joint but rather an inflammation triggered by the bacteria.

57
Q

Reactive arthritis in _____ joints

A

Arthritis of large joints

–Lower extremities (knees, ankles)

–Usually within 1 month of infection

Spine often involved

58
Q

enthesopathy

A

Ligament involvement

59
Q

Extra articular manifestations of reactive arthritis

A

–Conjunctivitis

–Urethritis or cervicitis

–Genital Ulcers

–Rash in palms or soles (keratoderma blenorrhagica)

60
Q

Spondyloarthropathies therapy

A
  • Physical Therapy / ROM / Posture
  • Medications:

–NSAID’s

–Peripheral arthritis

  • Sulfasalazine
  • Methotrexate

–Axial arthritis

•Biologics: Anti TNF blockers

–Antibiotic Rx for Chlamydia

61
Q

Juvenile Idiopathic Arthritis

Cause? Age? Girls vs boys

A
  • Chronic synovial inflammation
  • Unknown cause
  • Prevalence: between 57 and 220/100,000 children
  • Age < 16
  • girls > boys
62
Q

Criteria for Diagnosing Early Inflammatory Disease

A

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
Q

RA genetics

A

–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
Q

Lab tests for JIA

A

None

65
Q

Different subsets of JIA

A

–Systemic onset (very sick)

–Polyarticular onset

–Pauciarticular onset

66
Q

JIA Systemic Onset Clinical presentation

Prevalence, Boys vs. girls, age, main sxs, systemic features, lab testing, resolution?

A

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
Q

JIA Polyarticular Onset Clinical Presentation

Joints, Girls vs Boys, Sxs, Subdivisions

A

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
Q

JIA Oligoarticular/Pauciarticular Onset Clinical PResentation

Prevalence, # joints, age, girls vs boys, joints, lab

A
  • 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
Q

Enthesitis

A

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
Q

JIA Subgroups

A
  • Psoriatic JIA (2-11%)
  • Enthesitis-related JIA (3-11%)
  • Undifferentiated JIA (2-23%)
71
Q

Enthesitis-related JIA

Male vs female, genetics, labs, other sxs

A

–Male predominance (> 6 years old)

–Positive HLA B 27 (lumped w/ spondyloarthropathies)

–Negative RF and ANA

–Enthesopathy

–Sacroiliitis

–Ocular inflammation: up to 25%

72
Q

Psoriatic JIA clinical presentation

A

Dactylitis, nail pitting, sacroiliitis

73
Q

•Autoimmune disease

–Production of antibodies to components of the cell nucleus

•“Antinuclear antibodies” / ANA

–Present in 95% of patients

A

Systemic Lupus Erythematosus

74
Q

SLE peak incidence age and male vs females

A

peak incidence 15-10, female:male 9:1

75
Q

Lupus clinical features

A

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
Q

SLE autoantibodies

A
  • Double stranded DNA (dsDNA) antibody and glomerulonephritis
  • Antibodies to Ro (SSA) association

–Neonatal lupus

–Congenital heart block

–Subacute cutaneous lupus

77
Q

SLE genetics

A
  • Most cases are sporadic
  • Strong familial aggregation
  • SLE occurs concordantly in:

–25-50% monozygotic twins

–5% dyzygotic twins

78
Q

SLE Therapy

A

•Sunscreen, Patient education, NSAID’s, Corticosteroids, Antimalarials /Hydroxychloroquine, Methotrexate, Leflunomide, Cyclophosphamide,Mycophenolate (Cell Cept),Cyclosporine, Dapsone, Azathioprine / Imuran, Belimumab / Benlysta

***Avoid TNF Biologics

79
Q

Drug-Induced Lupus

A
  • 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
Q

Causes of Gout (overall)

A

Uric Acid overproduction (i.e. enzymes, psoriasis, ethanol, warfarin) or Uric Acid underexcretion (i.e. renal failure, hypertension, obesity)

81
Q

Genetics of Gout

A

Family occurence

  • American series: 40% have family history of gout
  • X-linked inheritance of HPRT deficiency & PRPP synthetase superactivity
  • Autosomal inheritance (G6PD deficiency)
82
Q

Joints of pseudogout (# and most common)

A

•Monoarticular or Oligoarticular Arthritis

–becoming polyarticular

–Acute or subacute attacks of Inflammatory arthritis:

  • Wrists
  • Knees (Most common)
  • Hips
  • Shoulders
  • Ankles
82
Q

Pearls: Gout Arthritis

  • 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 _____
A
  • 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
Q

Xrays and Pseudogout –> show ______ and locations

A

In about 75% cases, x-rays will show chondrocalcinosis

–Wrists

–Knees

–Symphisis pubis

84
Q

Gout vs Pseudogout tx

A

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

Skin MS: Week 6 (12 decks)

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