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Home , Reactive arthritis

INTENSIVE UPDATE AUGUST 24 - 26, 2018 & BOARD REVIEW Loews Chicago O’Hare Hotel Rosemont, IL

INNOVATIVE • COMPREHENSIVE • HANDS-ON

The Road to Rheumatologic Readiness in Primary Care

Carl Kinzel, DO

The American College of Osteopathic Family Physicians is accredited by the American Osteopathic Association Council to sponsor continuing medical education for osteopathic physicians.

The American College of Osteopathic Family Physicians designates the lectures and workshops for Category 1-A credits on an hour-for-hour basis, pending approval by the AOA CCME, ACOFP is not responsible for the content.

8/13/2018

INTENSIVE BOARD REVIEW UPDATE 2018

Carl J. Kinzel, D.O. ACOFP member

Disclosure

I HAVE NO FINANCIAL RELATIONSHIPS WITH PHARMACEUTICAL COMPANIES. ANY USE OF NAME BRAND MEDICATIONS IS FOR EDUCATIONAL PURPOSES ONLY.

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OBJECTIVES Rheumatoid Juvenile Arthritis

Gout

Reactive Arthritis

Granulomatosis with Polyangitis (Wegners’)

Polyarteritis Nodosa /

Systemic Erythematosus

Scleroderma

Sjogrens

Fibromyalgia

RHEUMATOID ARTHRITIS (RA)

Chronic, systemic inflammatory disorder

unknown ecology, primarily affects joint

MOST COMMON FORM of

symmetrical

leads to destruction of joint due to erosion of the cartilage and bone

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RHEUMATOID ARTHRITIS (RA) extra-articular manifestations may be present (such as nodules, neuropathy, scleritis, , and splenomegaly)

Incidence:

Female>Male 3:1 mean age 50-55 typical age of onset 20-40 years

RHEUMATOID ARTHRITIS (RA)

DIAGNOSTIC CRITERIA; needs 5 of 7 diagnosed, first 4 must be continuous > 6 weeks

1.) morning stiffness over 1 hour

2.) arthritis of three or more joint groups with soft tissue swelling

3.) swelling involving one or more joint groups: wrist, ankles, , PIP, MCP, MTP joint

4.) active symmetric joint swelling

5.) hand x-ray diagnosis (can be normal in first 2 years)

6.) subcutaneous nodules

7.) Positive Rheumatoid factor

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RHEUMATOID ARTHRITIS (RA) VS.

RHEUMATOID OSTEOARTHRITIS ARTHRITIS

Age of Onset 20-40 old age

Speed of Onset RAPID:weeks - months over years

Joint Affected small and large joints often begins SYMMETRICAL UNILATERAL

improves with worse as day goes Morning Stiffness movement on

RHEUMATOID ARTHRITIS (RA) TREATMENT

DMARDS are divided into two categories (biological and non biological)

BIOLOGICAL- target specific cytokines or their receptors, such as tumor necrosis factor. Others include B-cell depleting agents and T-cell co- stimulatory blockers. This class is referred to as “TARGETED THERAPY.”

NON-BIOLOGICAL- Methotrexate, , Lefunomide are all PRIMARY OPTIONS. Hydroxychloroquine is normally used as adjunct with other DMARDS

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RHEUMATOID ARTHRITIS

FELTY SYNDROME-

RA, SPLEENOMEGALY, AND NEUTROPENIA

JUVENILE IDIOPATHIC ARTHRITIS (JIA/JRA)

most common form of arthritis affecting children

onset is before 16 years old

Presents with painful joints, swelling, decreased ROM for over 6 weeks

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JUVENILE IDIOPATHIC ARTHRITIS (JIA/JRA)

3 SUBTYPES

systemic: 10-20 % fever and evanescent (fading) rash

polyarticular: 30-40%, involves >4 joints (large and small)

pauciarticular: 40-50%, involves < 4 joints. Risk for chronic uveitis in females, axial skeletal problems in males

JRA

ANA positive 40% (baseline test)

RA factor positive (2 positive tests needed for diagnosis for JRA)

ESR (may be normal or elevated, non specific)

Radiology-soft tissue swelling, periosteal reaction, junta-articular demineralization

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JRA TREATMENT

First line is PT/OT with lifestyle modification

NSAIDs in conjunction (effective in 50%)

DMARDS if not responsive

GOUT

Inflammatory reaction to URATE crystals formed within a joint, bones, and subcutaneous structures

Crystals found in joint aspirate is diagnostic

Birefringent needle shaped crystals

Most common joint involved is great toe (podagra)

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GOUT

Acute onset, typically nocturnal and usually mono-articular

Post inflammatory desquamation and pruritis (not always present)

Hyperuricemia in most

Dramatic therapeutic response to NSAIDs or colchicine

Repetitive attacks can lead to urate deposits in subcutaneous tissues, bone, joints, and other tissues.

GOUT TREATMENT

NSAIDs- indomethacin is most frequently used medication

Colchicine- less favored sine 80% of patients report ABD cramping, diarrhea, nausea or vomiting

Corticosteroids - effective. Best reserved for patients who are intolerant to NSAIDs

Analgesics- opioids are used at times. Avoid aspirin as it can aggravated hyperuricemia

Bed rest

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GOUT

90% of patients with primary gout are men

Usually over 30 years of age

Women are affected in postmenopausal age

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BE MINDFUL OF THE LITTLE THINGS

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REACTIVE ARTHRITIS

Formerly known as “Reiter’s Syndrome.”

Triad of symptoms:

Arthritis

Conjunctivitis

Urethritis of

4th symptom may be buccal ulceration or

REACTIVE ARTHRITIS

2 FORMS:

Sexually transmitted. usual organism. Symptoms present 7-14 days after exposure

Postdysenteric (Shigella, , Yersina, Campylobacter). More common in young men.

80% of white patients, and 50-60% of blacks

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REACTIVE ARTHRITIS

Sterile joint with starting at non-articular site.

NSAIDs are mainstay of treatment

Antibiotics given at time of a non- gonococcal STI may reduce chance of developing Reactive Arthritis

REACTIVE ARTHRITIS

20-40 years old, M>F

Ankylosing spondylitis develops in 30-50% in patients positive for HLA-B27

Asymptomatic arthritis (knees, ankles, MTP)

Enthsopathy (disorder involving the attachment of a tendon or ligament to a bone)

Urogenital tract- //cervicitis

Eye- /scleritis/keratitis

Skin- mucocutaneous ulcers

Constitutional- fever/malaise/weight loss

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REACTIVE ARTHRITIS

Can’t See

Can’t pee

Can’t climb a tree

GRANULOMATOSIS WITH POLYANGITIS (FORMERLY WEGENERS’)

Originally defined by triad of:

1.) upper respiratory tract disease

2.) lower respiratory disease

3.) glomerulonephritis

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WEGENER’S

Suspect if mild respiratory symptoms (nasal congestion, sinusitis) are refractory to regular treatment

Pathology defined by triad of small vessel vasculitis, granulomatous inflammation, and necrosis

WEGENER’S

Renal disease often rapidly progressive without treatment

Is a rare disorder (3:100,000)

Occurs in 4th and 5th decade of life

Affects men and women equally

Without treatment it can be fatal, most surviving less than 1 year after diagnosis

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WEGENER’S

Labs show slight anemia, mild leukocytosis, and elevated ESR

Chest CT is more sensitive than CXR,

CT shows lesions including infiltrates, nodules, masses and cavities

often radiograph results prompt concern for lung CA

Hilar adenopathy is UNCOMMON in Wegener’s, if present consider , tumor or infection

WEGENER’S TREATMENT

Remission has been induced in up to 75% of patients with cyclophosphamide and prednisone

Early treatment is crucial in preventing the devastating end organ complications

Wegener’s may involve sinuses or lungs for months, once proteinuria or hematuria develops renal failure can occur in weeks

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POLYARTERITIS NODOSA / GIANT CELL ARTERITIS

Ongoing segmental inflammatory, systemic necrotizing vasculitis

Occurs within the tunica media of medium sized muscular arteries

Labs: non-specific. May have RF, endothelial cell AB, elevated neutrophils, anemia, elevated ESR and CRP,

Biopsy of involved organs shows NECROTIZING VASCULITIS

POLYARTERITIS NODOSA

Treatment-

Prednisone is associated with good outcomes

Prednisone and DMARDS are associated with poor outcomes

Severe disease is treated with cyclophosphamide

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DIAGNOSIS OF POLYARTERITIS NODOSA

Must have 3 of the following 10 criteria present

weight loss (4kg since disease onset, not from other reasons)

livido reticularis

testicular or tenderness

myalgia, weakness or leg tenderness

mononeuropathy or polyneuropathy

Diastolic BP > 90mmHg

Elevated BUN (>40mg/dl) / creatinine (>1.5mg/dl)

Hep B virus surface Ag or Ab in serum

Arteriographic abnormalities

Biopsy of small or medium vessels with changes

POLYARTERITIS NODOSA

Livedo reticularis is a common skin finding consisting of a mottled reticulated vascular pattern

lace like purplish discoloration of skin caused by swelling of the venules

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GIANT CELL ARTERITIS

Gradual onset of constitutional symptoms: fatigue, malaise, fever, weight loss, polymyalgia rheumatica (PMR)

Followed by development of jaw claudication, new HA, scalp tenderness +/- diplopia and vision loss due to retinal ischemia

+/- change in taste or hearing

Always consider giant cell arteritis in pt over 50y/o with new onset HA, elevated ESR, abrupt loss of vision, prolonged fever, and PMR

Treat vision loss emergently with prednisone

GIANT CELL ARTERITIS

Diagnosis:

Age >50y/o

New/localized HA

Tenderness / decreased pulse of temporal artery

ERS >50mm/hr

Temporal artery biopsy

TREATMENT- 2-4 weeks of prednisone.

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SYSTEMIC LUPUS ERYTHOMATOSIS (SLE)

Can have multiple clinical presentations and is known as the “GREAT IMITATOR.”

Female to male ratio is 9:1, with onset often in 20’s-30’s.

Three times more common in African Americans.

Nearly 90% of patients have joint symptoms

SLE MANAGEMENT

Topical are first line therapy for cutaneous lupus.

Sun and stress avoidance and skin protection.

Treatment depends on severity of disease and degree of organ involvement. NSAIDs for SLE myositis, serositis, and arthritis; topical and systemic steroids; antimalarials for persistent cutaneous lesions; methotrexate and IVIG

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DRUG INDUCED LUPUS

Equal prevalence between men and women (drug induced)

Most commonly associated drugs: hydralazine, procainamide, isoniazid, quinidine, methyldopa, and chlorpromazine.

SYSTEMIC LUPUS ERYTHROMATOSUS (SLE)

diagnostic criteria can be summarized with mnemonic DOPAMINE RASH.

DISCOID RASH, ORAL ULCERS, PHOTOSENSITIVE RASH, ARTHRITIS, MALAR RASH (butterfly), IMMUNOLOGIC CRITERIA (positive anti-dsDNA or positive anti-Smith), NEUROLOGIC or PSYCHIATRIC SYMPTOMS, RENAL DISEASE, ANA +, SEROSITIS (pleural, peritoneal, or pericardial), HEMATOLOGICAL DISORDERS (thrombocytopenia, anemia, or leukopenia)

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SJOGRENS

Autoimmune disorder, T-cell mediated exocrine gland destruction.

Dry eyes (keratoconjunctivitis sicca) dry mouth (xerostomia) may be associated with fatigue and general malaise.

Symptoms and clinical signs of ocular dryness, dry mouth, and serum findings of (elevated RF >1:320 or elevated ANA <1:320, or anti-SS-A(Ro) or anti-SS-B(La) antibodies).

SJOGRENS

Systemic treatment with humidifiers, artificial tears, frequents sips of water, gum or mints.

Systemic treatment with NSAIDs and antimalarials

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FIBROMYALGIA

Is a poorly understood non-inflammatory soft tissue pain disorder

Onset is typically between 30-60 years old

Affects 2-8% of population

Risk factors: female, low socioeconomic status, poor functional status, stressful life events

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FIBROMYALGIA

Diagnosis is NO LONGER based on tenderness at trigger points.

It is based on structured symptom history

IBS has overlap with fibromyalgia

70% of patients with fibromyalgia has IBS symptoms

FIBROMYALGIA

Diagnosis is based on presence of widespread pain and muscle tenderness, severe fatigue, non restorative sleep, and cognitive symptoms.

Duration of symptoms greater than 3 months

Regular labs are done to rule out other causes of chronic fatigue, NOT to diagnose fibromyalgia

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FIBROMYALGIA TREATMENT

Non pharmacological:

Aerobic exercise/physical activity

Sleep hygiene

Self management support

Cognitive behavior therapy

Complementary and alternative therapy

FIBROMYALGIA TREATMENT

Pharmacologic treatment:

Antidepressants:

Limited evidence for TCA or SSRI

Duloxetine (Cymbalta) and Milnacipran (Savella) are FDA approved for treatment of fibromyalgia

Limited evidence for Pregabalin (Lyrica) FDA approved

AVOID opiates- 2015 Cochrane review showed no evidence of benefit

Limited evidence of benefit with NSAIDs

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REFERENCES

Tao Le, Michael Mendoza, Diana Coffa, Lamercie Saint-Hilaire; First Aid for the Family Medicine Boards, 3rd edition, 2018, McGraw Hill Education

https://www.rheumatology.org/I-Am-A/Patient-Caregiver/Diseases-Conditions

Braunwald, Fauci, Kasper, Hauser, Longo, Jameson; Harrison’s Internal Medicine, 15th edition, 2001

Lawrence Tierney, Stephen McPhee, Maxine Papadakis,Clinical Medical Diagnosis and Treatment, 44th edition, 2005, Lange

William Bennett, Jeffrey Callen, Thomas Duffy, David Ettinger, Mark Feldman, Gene Hunder, Stanley Korenman, Phillip Lieberman, Willis Maddrey, Gerald mandell, Keith Payne, Roger Rosenberg, Atlas of Internal Medicine, second edition, 2002, McGraw Hill

Frank Domino, The 5-Minute Clinical Consult, 16th edition, 2008

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