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Skin MS: Week 6 > Rheumatology > Flashcards

Flashcards in Rheumatology Deck (85):
1

Major divisions of arthritis

non-inflammatory (OA)

Inflammatory

2

Inflammatory Arthridities

–Rheumatoid Arthritis

–Juvenile Idiopathic Arthritis

–Systemic Lupus Erythematosus

–Crystal induced Arthritis

–Spondyloarthropathies

•Ankylosing Spondylitis

•Psoriatic Arthritis

•Reactive Arthritis

3

Most common form of arthritis

osteoarthritis (non-inflammatory)

4

Common locations of OA

–Knees

–Hips

–Spine (cervical and lumbar)

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

–Feet (first metatarsophalangeal)

5

Progressive loss of articular cartilage

OA

6

Osteoarthritis is __________ disorder

age-related 

7

Clinical Presentation OA:

•________ onset

•______ and ___ -limited: initially

•___-related Pain:

–Knees & Hips: Worse with _______

–Hands: worse with ______

•Relieved by ______

•Morning stiffness ______________

•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

Risk factors OA

Increasing Age
Major joint trauma
Obesity (knees)
Repetitive activities
Genetic Predisposition
Congenital/Developmental defects
Females                   

9

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

•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

X-ray findings OA

–Sclerosis
 New bone formation in the subchondral trabeculae
–Osteophytes
 Formation of new bone at the joint margins
–Loss of cartilage

11

Nonpharmologic therapy for OA

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

Pharmologic tx for OA

–Acetaminophen

–NSAID’s

–Analgesics

–Topical agents

•Capsaicin

•Methyl salicylate, Diclofenac gel

–Intra-articular steroid injections

–Hyaluronic acid derivatives

13

RA RF

Smoking, periodontal disease

14

RA more prevalent in ______ , ______

women, native populations

15

RA  

Systemic Inflammatory arthritis (chronic, progressive, disabling disease)

16

Lab Markers RA

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

17

Systemic disease sxs of RA

–Fatigue, fever, weight loss

–Extra-articular manifestations (Subcutaneous nodules, Pericarditis, Pulmonary nodules/ Interstitial fibrosis, Inflammatory Eye Disease - Episcleritis / Scleritis, Vasculitis)

18

Therapeutic modalities RA

•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

DMARDs for RA

Disease Modifying Anti-Rheum Drugs 
–Hydroxychloroquine
–Minocycline
–Gold
–Sulfasalazine
–Methotrexate
–Leflunomide / Arava 
–Azathioprine / Imuran
–Cyclosporine

20

Biologic DMARDs

–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

Iridocyclitis associated with

oligoarticular/pauciarticular onset of juvenile idiopathic arthritis

22

JIA treatment

•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

Crystal induced arthritis

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

24

Clincal presentation of Gout (in different locations)

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

–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

•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

•Not uncommon to have a ______ serum Uric acid level at time of gouty attack
•Hyperuricemia frequently results from _____ ______
•Allopurinol is/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