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127 Cards in this Set

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CRYSTALS FOUND IN SYNOVIAL FLUID:
Monosodium Urate
- monohydrate

Calcium
- pyrophosphate
- dihydrate
Acute Gout
Tophaceous Gout
Asymptomatic

Acute Pseudogout
Destructive Arthropathy
Asx
Basic Calcium
- Phosphate

Calcium Oxalate

Lipid

Cholesterol
Acute Calcific Periarthritis
Acute Arthritis
Destructive Arthropathy
(Milwaukee Shoulder/Knee)

Acute, Subacute Arthritis
Asx

Acute Arthritis

Asx
Joint morning stiffness >1 hour
Simultaneous involvement (swelling) of >3 joints observed by a physician (PIP, MCP, wrist, knee, elbow, ankle, MTP)
Hand involvement
Symmetrical involvement
Rheumatoid nodules
+ Rheumatoid factor
X-ray changes (erosions or juxtaarticular osteopenia)
Criteria for Classification of RA

must have 4 persisting for >6 wks
RA Epidemiology:
US frequency 1% but up to 2-3% in older person
Female to male 2:1
Increased frequency in ____________(5-7%)
Onset from _______
70 to 80% +___
1.5 to 2 fold increase in frequency if there is a _____________ afflicted
Native Americans

30-50

RF

first degree relative
High specificity autoantibodies have been described in the sera of RA patients

proven 98% specific to RA
Anti-CCP antibodies

always treat if + because w/in 5 yrs will have gross deformities
Less specific than RF and CCP
Useful in distinguishing RA from noninflammatory conditions e.g. OA/FMS
Can be used to monitor disease activity.
Acute phase reactants (ESR & CRP)
Key features:
Painful inflammation with tenderness on applied pressure to joint, or by moving joint.
Swelling due to synovial hypertrophy or effusion
RA
RA Hand Findings:
MCP and PIP involvement is typical
____ and ____ MCP present 1st
PIP ROM less than ____ degrees.
MCP rom less than ___ degrees.
Thickening of the _________
Nodulosis along tendon sheaths
Decreased ______ strength
Ulnar drift, boutenniere changes, swan neck changes
2nd and 3rd

120

90

tendon sheaths

grip
RA Upper Limb findings
_______ is most commonly involved. (loss of extension/flexion), radial drift causes ____________ prominence
________ - loss of extension (fixed flexion). Most common site of nodules
_________ disease is a late finding with rare effusions occuring.
Wrist

ulnar styloid

Elbow

Shoulder
RA Lower Limb Findings:
Tenderness of ____
Erosive damage causes _________ drift of toes
Ankle RA causes swelling at the __________ joint (usually wrongly diagnsoed as edema or cellulitis). Also impinges p. tibial n causing _________
MTP

lateral

tibiotalar

paresthesia
RA Knee & Hip involvement:
__________ of the knee is most common.
__________ of the knee is usually limited
__________ formation common, always assess for rupture (_________ sign at l. malleolus).
Erosions can occur at femoral condyles, tibial plateau causing varus or valgus changes.
______ - Pain in groin, thigh, low back, or referred to knee is common with effusion/involvement
Effusion

Flexion

Bakers cyst

crescent

Hips
RA Atlanto-Axial Subluxation:
Potentially a neurosurgical emergency
Occurs in patients with _________ at onset of RA, more active _________ and rapidly progressive erosive peripheral disease
Approximately 50-60% of RA patients referred for ____ or ____ will have radiographic evidence of subluxation
Inquire about neck pain and neurological symptoms (painless sensory loss in extremities, “drop attacks,” unexplained weakness)
Pre-op C-spine XR (flexion-extension views) in general anesthesia
Look for > ____ separation between the odontoid process and the C1 arch in flexion
5-year mortality rate for patients with cervical subluxation with or without neurologic symptoms is 17%
older age

synovitis

TKR or THR

3mm
RA Cricoarytenoid Joint:
Common in 30% of RA patients
Presents as ___________ and _____________ stridor
hoarseness

inspiratory
RA DDx:
______________: rubella, Parvo, hep B can cause polyarthritis from weeks to months.

Other CT diseases & ___________: usually hard to differentiate early on, but long standing RA will stand out with the am stiffness persisting, symmetry, nodules, and deformities. Also, SLE arthritis is reducible deformities

Hypermobility and ___________: absence of serologies, ESR/CRP

____________: always high on differential with monoarthritis presentation. Must have other features e.g. urethritis, enteric infection, heel pain, sacroilitis on xray, + HLaB27. ReA is assymetrical, rare a.m. stiffness, rare RF or CCP positivitiy. characteristic ‘sausage’ dactylitis.
Acute viral polyarthritis

Sarcoidosis

Fibromyalgia Sx

Reactive Arthritis
RA DDx (cont):
____ - DIP predominance with hard bony heberdeen and bouchard changes.

_____: extremely similar, usually only distinguishing feature is fam hx, skin psoriasis, nail changes, dactylitis.

____________ arthropathy: gout, oxylate, uric acid

_____________: ruled out with aspiration of the joint, culture
A.M. stiffness generally less than 10 minutes
Narrowing of joint spaces on xray vs. erosion
No associated RF, CCP ab, ESR, CRP
OA

PsA

Crystalline

Infectious arthritis
RA Non Disease Modifiers

Analgesics:
1. OTC ________, Pain meds: tramadol, topical steroid creams, hydrocodone.
2. _______: provide analgesia and anti-inflammatory response. Ex. Celebrex, Mobic.
3. ____________: Provide the most rapid response with pain relief and antiinflammatory response
Tylenol

NSAIDS

Glucocorticoids
________: Have the potential to reduce or prevent joint damage, preserve joint integrity and function, reduce health costs, and maintain economic productivity

Types used today:
Early DMARDS, AntiCytokine Therapies, Biologics
DMARDS
Early Use DMARDS
1. _________/___________– more European than US. (100 mg bid)
2. ___________(hydroxychloroquine) 200mg bid
3. __________ (sulfasalazine) 500 mg 1-2 bid
4. _______(lefluonomide) 10-20mg qd as tolerated
5. ____________ 5-20mg once weekly
6. _________ (azathioprine) 50mg 1-2 po bid
Doxycycline/Minocycline

Plaquenil

Azulfidine

Arava

*Methotrexate*

Imuran
There is little conclusive evidence that there is sustained benefit from step-up, step-down, or parallel use of traditional small molecule DMARDs in combinations, unless ___________ is included in the regimen

A combination of methotrexate with an _____________ is often effective in reducing disease activity and reducing the rate of radiographic progression of joint disease
methotrexate

anti-TNF agent
Anti-Tumor Necrosis Factor Alpha
________(etanercept) 50mg sq once weekly.
________ (adalimumab) 40 mg sq q o week
________ (anakinra) 100mg sq daily
________ (infliximab) 3 mg/kg, max 1000mg q 8 weeks IV
*Enbrel*

Humira

Kineret (not used anymore)

Remicade
Biologics: Most recently approved by FDA, usually require failure of all or most DMARD, and all or most Anti Cytokine Therapies.

_________(abatacept) dose dependent on weight, generally 750mg once monthly

________ (rituximab) B cell depleting agent given twice yearly by IV
Orencia

Rituxan
More than 20 persistently inflamed joints
A rapidly declining functional capacity
Elevated levels of ESR or C-reactive protein
Anemia of chronic disease
Hypoalbuminemia
Positive rheumatoid factor tests (often in high titer) or presence in serum of anti-cyclic citrullinated peptide (anti-CCP) antibodies
Extraarticular disease
Evidence of inflammation on plain film radiography such as findings of osteopenia and periarticular swelling; erosions may be present.

Treatment: Depends on prior failed meds.
EARLY, SEVERELY ACTIVE RA
Between 6 and 20 inflamed joints
Absence of extraarticular disease (most commonly)

Elevated erythrocyte sedimentation rate (ESR) or serum C-reactive protein (CPR) concentration

Positive rheumatoid factor or presence in serum of anti-cyclic citrullinated peptide (anti-CCP) antibodies

Evidence of inflammation on plain film radiography such as findings of osteopenia and periarticular swelling; no erosions are observed. However, a more sensitive modality, such as ultrasonography or magnetic resonance imaging (MRI), may detect erosions of bone or cartilage destruction.

This constellation of findings places a patient at greater risk of developing joint damage and disability . Patients presenting with moderately active, previously untreated (or only administered NSAID) disease should receive DMARD therapy in addition to an NSAID

Treatment: One or more DMARD with start, then taper down of steroid. Move to anti-TNF if doesn’t respond within 6 months. Watch ESR, Xrays closely
EARLY, MODERATELY ACTIVE RA
Arthralgias and morning stiffness
Elevation in the erythrocyte sedimentation rate (ESR) or serum C-reactive protein (CRP) concentration
At least three simultaneously inflamed joints
No extraarticular disease
No evidence of erosions or cartilage loss on plain radiographs
No significant impairment of physical function
Absence of rheumatoid factor or antibodies to cyclic citrullinated peptides is a favorable prognostic factor but a patient need not be "seronegative" to be categorized as having mild disease.
Usually responds well with NSAID, and 1 DMARD (preferably MTX)
TX: Watch Xrays and ESR to follow progression
EARLY, MILDLY ACTIVE RA
Other Considerations When Starting a DMARD and treating RA

Risk of _________: Make sure patient is PPD negative, Hep B negative, HIV negative. Educate patient that DMARD lower immunity. Flu and Pnumovax performed as appropriate
Monitor _____ on MTX, ARAVA
Monitor _____ on plaquenil and all anti-TNF
Watch ____ and exam for SOB, MTX can cause ____________ as can RA.
_________ can fall on chronic steroids, DM can be caused by steroids, etc.
infection

LFT’s

WBC

CXR

Pulmonary fibrosis

Bone Density
abrupt onset of severe joint inflammation, often at night

subsides in ______days
75% in ______ joint

urate crystals in synovial fluid

may have hyperuricemia

usually monoarticular
acute gouty arthritis

3-10 days

first MTP
Patients with UA ___ have incidence of acute gout of 5% per year
Overproduction associated with hyperuricosuria and therefore increase in _______
>9

renal stones
Epidemiology of Gout
Affects ___ of all men
Two-fold increase in incidence from 1977-78 to 1995-96 in Rochester, MN (Arromdee E, et al. 2002)
Earlier onset: with first attack in _________(Yu KH, et al. 2003)
>1%

3rd to 5th decade, previously 4th to 6th decade
Why is gout more frequent?
-Higher survival from _______
-Increase in longevity (loss of estrogen in women as age…estrogen is uricosuric)
-Dietary patterns
-Increase in obesity
-Increase use of diuretics and low-dose aspirin
-Increase in CRI/dialysis and organ transplant (cyclosporine use)
-Limitation of ________(especially in renal insufficient)
Increase prevalence of _____(decrease in uric acid secretion)
CHF and CAD

allopurinol

HTN
Gout in the Elder
Equal gender distribution
More _________tophi (eg. DIPs)
Polyarticular presentation
Harder to treat:
--Increase GI toxicity from NSAIDs
--Lower _____
upper extremity

GFR
Definitive dx Made only by _______________on microscopy

__________also allows quick ruling out of infection if WBC count in joint fluid is less than 40 wbc/hpf.
arthrocentesis and crystal isolation

Aspiration
Indications for Allopurinol
Greater than 2 attacks a year
Chronic ___________
Urate overproducer
Purine enzyme defects
Hyperexcretion of urate (800mg/24 hours)
___________
With cytolytic therapy for hematologic malignancies
tophaceous gout

Nephrolithiasis
Diet and Gout
-_____________products lowered the risk of 1st gout attack (casein and lactalbumin uricosuric)
-Seafood, red meat, anchovies, aged and smoked cheese and meats and sweetbread increase risk of attack
-Beer is high in ______and leads to increase risk of attack
Low-fat dairy

purine
pseudogout
pseudo - RA
pseudo - OA
pseudo - neurotrophic Joints
Asx Chondrocalcinosis
CPPD Crystal Deposition Dz.
Presentations
-hyperparathyroidism, fam. hypocalciuric hypercalcemia, hemochromatosis, hemosiderosis, hypophosphatasia, hypomagnesemia, hypothyroidism, gout, neuropathic joints, aging, amyloidosis, trauma
CPPD Crystal Deposition Dz.
Associations
Wilson’s disease
Hemachromatosis/
Hypothyroidism
Idiopathic
Parathyroid (hyper)/
Phosphatemia (hypo)
Acromegaly/amyloidosis
DJD
Ocranosis
Gout
Associations: Chondrocalcinosis
(WHIP A DOG)
Therapy for CPPD
Treat underlying association
__________
NSAIDs
__________
IA corticosteroids
Colchicine

Prednisone
basic calcium phosphate
milwaukee shoulder
Take-Home Points
Gout … not just in men
___________presentation in elders
Consider ____________even when history of crystalline arthropathy is present
Know the indications for allopurinol
Counsel your patients on appropriate diet and weight loss
Remember, ___________should not be started in acute setting
Know disease associations with chondrocalcinosis
Know what CPPD and sodium monourate crystals should look like and the 2 can be seen concurrently
Remember that colchicine causes ________in patients with decrease GFR
Polyarticular

septic arthritis

allopurinol

myopathy
Previously thought to be a consequence of aging
hence “DJD”
Now thought to be caused by joint integrity, _________, local inflammation,
mechanical forces, cellular/biochemical processes
Osteoarthritis

genetics
OA:
General Clinical Presentation
Generally in population over age __.
Symptoms: PAIN!, progressive decreased activity, as it worsens pain occurs at rest, ___________less than 30 minutes.

Remember: How long is the am stiffness of RA?
40

stiffness
OA
Exam findings:
Tenderness to palpation
No warmth, no erythema generally.
Joint effusion: noninflammatory, normal viscosity, modestly elevated protein ct.
__________!! (loss of smooth articulating surface).
__________(Bone spurs) at the periphery of the joints
CREPITUS

Osteophytes
OA generally affects _______________BUT Usually spares elbow, wrist, ankles.
Hands:
Dip: ________
PIP: ________
First CMC (squared)
fingers (PIP/DIP more than MCP), knees, hips, spine.

Heberdens
Bouchard
Feet - 1st MTP. ________.
Knees – Minimally bone spurs, effusion, crepitus, decreased ROM.
Xrays: varus (medial loss) “_________”
valgus (lateral loss) “__________”
Bakers Cyst: popliteal fossa
____________usually first site of cartilage loss.
Bunions

bow legged

knock knees

Medial compartment
Hips:
Determine if in the true hip or referred from the _________.
Pain in the ______ can be referred to the hip.
Trochanteric bursa vs. the true hip. (pain in the groin is the key generally – no limited motion.)

Limited internal/external rotation, limited flexion/extension.
ALWAYS think about ____in someone with risk factors and hip pain.
spine

knee

AVN
OA
Spine: most common at _________ Why? Sites of most flexibility along spine.

Two important syndromes associated with OA of the apophyseal joints
___________– bone spurs from the margin of the vertebral body that compromises the spinal canal.
____________– can compromise the neural foramen and impinge exiting nerve roots
C5, T8, L3

Cervical spondylosis

Uncovertebral spurs
____________can cause spinal stenosis, low back pain with radicular type radiation, and pseudo claudication type symptoms that respond more quickly to rest than true claudication.

___________: slipping of one vertebral body on another.
Lumbar apophyseal osteophytes

Spondylolisthesis
OA Shoulders:
__________: anterior pain that worsens with time and with movement.
__________: usually vague tenderness on the joint itsself.
Bone spurs on the underside of the AC joint can cause rotator tendonitis/ or rotator tears.
__________: aggressive/rapid deterioration of the shoulder joint secondary to calcium crystal disease.
Glenohumeral

AC joint

Milwaukee shoulder
What will you find on an OA xray?
Joint space narrowing
Subchondral sclerosis
Osteophytes
Subchondral cysts
Laboratory?
Generally labs are _______with OA
Acute phase reactants elevated:
-When OA is associated with a crystal
-Maybe at the initial onset that generally is more inflammatory than chronic disease.
-When acute phase reactants remain elevated, and xrays show erosions, think ___________….treated like RA with ________,________,____

Joint fluid analysis: wbc, crystals, viscosity
negative

inflammatory OA

plaquenil, doxy, or MTX
OA Differential Diagnosis
____: hook osteophytes on xray at the PIPs. Aspiration of joint needed to view the crystal.
__: MCP, PIP. Swelling is soft, warm, and tender. Stiffness greater than 30 min. Erosions on xray. Elevated CRP, ESR, RF, CCP Ab.
_____________: Highly inflammatory fluid, one joint involved, +/- febrile, culture +.
CPPD

RA

Infectious Monoarticular arthritis
OA Treatment
Pain: OTC NSAIDS, Tylenol, etc.
NSAIDS: ________200mg po qd (assess risk factors for stroke/MI before starting).
_______7.5-15 mg po qd
_______250 – 500 mg bid
_______10-20mg qd
Celebrex
Mobic
Naprosyn
Feldene (piroxicam)
Treatment
Pain – Narcotic : Darvocet, Tramadol, Lortab.
Stiffness: ______1000 mg bid, paraffin baths, Physical therapy
Stiffness/Pain/preventative: ________1500mg/Chondroitin 1200mg po qd
Last resort or if uncontrolled superimposed crystal disease: low dose __________5-10 mg qd.
Flaxseed Oil

Glucosamine

prednisone
SLE Epidemiology
Prevalence: 40-50 per 100,000
1 in 2000 in the U.S.
Peak incidence age ______
Female to male ratio ____:1
15-40

6-10
Higher prevalence in:
Urban __ rural areas
Asians, Asian Indians in England
African-americans, afro-Caribbeans
Hispanics
Lower prevalence in:
Blacks in ________
>

Africa
__________ have a poorer prognosis
Psychosis
Proteinuria
Serositis
+Sm (Smith), RNP
Discoid lupus

______:
Higher one-year mortality
More serositis
Less photosensitivity
African-americans

Men
________:
More severe symptoms
Increase incidence of malar rash, nephritis, pericarditis, hepatosplenomegaly and hematologic abnormalities

________:
Decrease incidence of malar rash, +SSA/SSB, renal or CNS involvement
Increased incidence of sicca, serositis and musculoskeletal manifestations
Children

Elderly
Etiology- Still unknown

Multifactorial:
________ factors
Familial aggregation especially amongst 1st degree relatives
Concordance in monozygotic twins 25-50% and dizygotic twins 5%
_________factors
_________ abnormalities
Environmental factors
Genetic

Hormonal

Immune
Pathogenesis of Clinical Manifestations:
Autoantibodies are ___________
Immune complex deposition
Complement fixation
___________ cascade triggered
Th2 predominant process
Complements fall and dsDNA rises with ___________

Autoantibodies Precede Clinical Onset
pathogenic

Inflammatory

disease activity
Not all +____ is Lupus
Found in 5% of the normal population and presence increases with _____
Found in other autoimmune disease and viral infections:
Hypothyroidism
Neoplasm
Hepatitis B and C
Other CTD (RA, SSc, inflammatory myopathy)
Interstitial lung disease
ANA

age
Manifestation of which autoantibody:

______ - Corresponds well with disease activity
Present in GN

______ - Sicca, Photosensitivity, SCLE, Vasculitis, Late onset of dz

______ - Raynaud’s, Myositis, Sclerodactyly

______ - Thrombosis, Livedo, Valvular heart disease

______ - Psychosis, Hepatitis
ds DNA

SSA, SSB

RNP

aPLA (causes miscarraiges)


Ribosomal P protein
discoid rash
arthritis
malar rash
photosensitivity
antinuclear antibody
serositis
renal disorder
hematologic disorder
immunologic disorder
neurologic disorder
oral ulcers
SLE Classification criteria

must have 4 criteria simultaneously or serially
________: fixed erythema, flat or raised, sparing the nasolabial folds

________: raised patches, adherent keratotic scaling, follicular plugging, older lesion may cause scarring

____________: skin rash from sunlight

____________: nonerosive, inflammatory in 2 or more peripheral joints

__________: pleuritis or pericarditis
malar rash

discoid rash

photosensitivity

arthritis

serositis
____________: persistent proteinuria or celluar casts, >0.5gm

____________: seizures or psychosis

____________: hemoylytic anemia, leukopenia or lymphopenia on 2 occasions, thrombocytopenia

____________: LE cells or Abs to ds-DNA or Sm or false positive serologic test for syphilis for at least 6 months

_______________: positive
renal disorder

neurologic disorder

hematologic disorder

immunologic disorder

antinuclear Ab test
Malar
Discoid
SCLE
Photosensitivity
Oral ulcers
Scarring alopecia
Mucocutaneous Manifestations
90% non-erosive
Deformities are reducible (Jaccoaud deformity/arthritis)
Joint Manifestations
Found in ~50% of SLE patients
Poor prognostic factors:
African american
Elevated Cr
Increased proteinuria
Anemia
Renal biopsy with findings consistent with severe or chronic activity and crescent formation/tubulointerstitial fibrosis
Renal*** Manifestations
WHO Classification of Lupus Nephritis

Class 1: _____________

Class 2: ___________ disease
Mild renal disease
Minimally active urinary sediment
+/-Active SLE serology
Non-nephrotic range proteinuria
Normal glomeruli

Mesangial
WHO Classification of Lupus Nephritis

Class 3: ______________ Glomerulonephritis
More active urinary sediment
More likely active SLE serology
25% have NRP
HTN
May evolve into DPGN
Focal Proliferative
WHO Classification of Lupus Nephritis

Class 4: _______
Most severe of renal involvement with active urinary sediment
HTN
Frequent NRP
Reduced GFR
SLE serology very active

Usually on dialysis
DPGN (diffuse proliferative glomerulonephritis)
WHO Classification of Lupus Nephritis

Class 5: ___________
Significant NRP
Less active SLE serology
Bland sediment

Always on dialysis
Membranous
Estimated to be present in 50% of patients
MRI brain may demonstrate cortical and subcortical areas of increased T2 signal enhancement
Arteriogram usually normal with no true vasculitis seen at autopsy
*psychosis*
seizures
headaches/migraines
myopathy
Neurologic Manifestations
Pericarditis, myocarditis, endocarditis
Premature atherosclerotic disease
Vasculitis
Raynaud’s phenomenon
Cardiovascular Manifestations
Lupus pneumonitis and interstitial lung disease
Lymphocytic interstitial pneumonia
Vanishing lung syndrome
Pulmonary hemorrhage
Pulmonary hypertension
Pulmonary embolism
Pleuritis
Diaphragmatic weakness
Pulmonary Manifestations
May occur in up to 25% patients
Occurs in overlap syndrome in the presence of RNP, Raynaud’s, GERD
Strictures may form induced by
Esophageal candidiasis secondary to steroids
Medication-induced ulcerations
May present as dysmotility or dysphagia


60 to 90% SLE patients develop peritonitis during their lifetime
Esophageal Involvement

SLE Peritonitis***
Estimated to occur in 4-21% SLE patients
Secondary to NSAIDS and steroids
Dyspepsia/PUD
Increase risk in patients with peripheral vasculitis or CNS lupus
If perforation suspected or irreversible ischemia:
NPO
BC, antibiotics
__________ 1-2mg/kg qd or IV _______________1-1.5gm qd x 3 days + CTX 1 gm IV or 750 mg/meter square
Mesenteric Vasculitis and Infarct

Prednisolone

methylprednisolone
May be from vasculitis or thrombosis in association with antiphospholipid syndrome
_________ 1mg/kg per day
Lupus Pancreatitis

Prednisolone
Cirrhosis
Cholestatic picture
Chronic active or persistent hepatitis
Granulomatous hepatitis
Centrilobular necrosis
PBC (associated with +Ro/SSA)
Steatosis/fatty liver
Liver toxicity secondary to medications
Hepatic Involvement
Occurs in young lupus female patients
Edema and hypoalbuminemia
Presents with diarrhea in 50% cases
Diagnosis made by assaying increase amount of indium-labeled plasma in a 4 day stool collection and confirmed by increased 24 hour stool alpha 1 antitrypsin excretion
Protein Losing Enteropathy
Drug-induced lupus
Two types: systemic symptoms vs. drug-induced SCLE

Thought to occur in slow acetylators of aromatic amine and hydrazine compounds
____________, ____________, _____, _________ are the most frequently associated drugs with drug-induced lupus with systemic sxs (serositis, arthritis, antihistone antibodies in 90-100% and P ANCA with INH)

_____ and _____ are the most frequently associated drugs triggering SCLE (no systemic sxs)
Hydralazine, minocycline, INH, procainimide

HCTZ and CCB
Treatment
_______ disease: antimalarial agents, thalidomide, prednisone, intralesion CS, MMF, dapsone, azathioprine, MTX
______ disease: antimalarial agents, MTX, Arava, azathioprine, prednisone
______ disease: corticosteroids, CTX IV, MMF, azathioprine
__________: CTX IV, corticosteroids
____________(autoimmune): CTX IV, corticosteroids, plasmapheresis
_______ disease: CTX IV, corticosteroids
Skin

Joint

Renal

Vasculitis

Thrombocytopenia

CNS
SLE Morbidity (3)
AVN
osteoporosis
cognitive dysfunction
Diffuse proliferative glomerulonephritis
Hypertension
Male
Young
African-american
Poor socioeconomic status
Positive antiphospholipid antibodies
Overall high disease activity
Factors Heralding a Poor Prognosis
SLE Mortality
Early death (3)

Late death (3)
Active dz: CNS, renal, CV

Active dz, tx complications (infections), premature CAD
**stiff in am but gets better in late afternoon**
Exclusively affects patients over age __
Incidence varies geographically (north Europe 113/100,000, southern Italy 13/100,000
Characterized by subacute or chronic onset of aching and am stiffness in the shoulders/hip girdles, neck and torso.
Usually _________
Synovitis/bursitis causes discomfort/stiffness.
Polymyalgia Rheumatica

50

symmetric
DDX for PMR:
RA: Considerable overlap between PMR and RA. Usually patients present with PMR then RA secondarily.
_________: slow DTR, low T4, elevated TSH
___________: Persistent fever, heart murmur, + blood cultures, vegetation on the heart valves on echo
__________: usually younger than age 50. Widespread musculoskeletal pain, no constitutional symptoms, normal ESR, normal exam.
___________: symmetric proximal muscle weakness, no prominent shoulder/hip pain. Elevated CPK, elevated LFT.
Hypothyroidism

Infective endocarditis

Fibromyalgia

Polymyositis
PMR
Physical Exam Findings
Decreased ROM of the _____________.
Muscle tenderness is NOT a prominent feature on exam, despite the name.
________normal

________ usually between 40-100 mm/hr.
Other labs are nonspecific: __________
Imaging: not beneficial
shoulders, neck and hips

Strength

Elevated ESR

normocytic anemia
When to think about PMR?
Age over __
Bilateral aching and morning stiffness lasting _________or more, persisting at least one month, and involving at least two of the three areas: neck, shoulders, hip girdle
ESR elevated to _______or more
50

30 minutes

40 mm/hr
Treatment of PMR:
Generally rapidly resolves with _____________.
Patient usually reports complete loss of symptoms within 2-3 days of starting ____________orally.
25-50% of patients usually relapse. Low dose steroids chronically may be needed.
low dose steroids

10mg of prednisone
spondylarthropathy
Collection of diseases that share the following clinical features:
________ inflammation (spinal/SI joints)
asymmetric _________
enthesitis
______ and _____ lesions
eye and bowel inflammation
association with or ongoing infectious disease
likely positive _______
axial

arthritis

genital and skin

HLA B27
Undifferentiated spondylarthropathy
Ankylosing spondylitis
Psoriatic arthritis
Reactive arthritis
Reiters syndrome
Spondylarthropathy associated with Chrons/ulcerative colitis
Juvenile spondylarthropathy
dz included in spondylarthropathies
Clinical Manifestations of SpA

____________: acute onset, predominantly lower extremities (knees/ankles/feet), asymmetric and occurring in 2-3 joints.
Sensitivity and specificity for asymmetric oligoarthritis (1-3 joints) for spondylarthropathy is 44 and 95%.

___________: inflammation around the tendon/ligament/joint capsule/fascia insertion sites on bones. New bone forms at site causing immobility.

__________: inflammation of the soft tissues between the joints.

Common enthesopathy site: ____________
Peripheral arthritis

Enthesopathy

Dactylitis

achilles tendon
Clinical Manifestations of SpA

_______________: insidious onset in the neck/back, occurring at least 3 months, morning stiffness, improved with exercise

_______________: genital characteristic of Reiters. Painless.

Skin lesions (_______________) start as clear vesicular lesion that progress to maculopapular.

Nonspecific ____________ with negative cultures.

Inflammatory eye disease: ____________ common in Reiters.
________: more severe, acute, unilateral, redness, pain, photophobia. Can cause visual impairment.

_______________: Strong link between active peripheral arthritis and histologic gut inflammation
Inflammatory spine pain

Genital/skin/mucosal lesiions

keratoderma blennorrhagica

urethritis

conjunctivitis

Iritis

Inflammatory bowel mucosal lesions
Evidence of preceeding infection: ReA onset of sx occurs following GU infection or diarrhea (within one month of episode.
________: chlamydia
________: shigella, salmonella, campylobacter, Yersinia
GU infection

Diarrhea
Common Labs in SpA:
________ helpful, but not always +, if a patient has 3 of the criteria including xray evidence of sacroilitis then HLA B27 positivity/negativity doesn’t affect dx.
Test for bacterial infections
____ test, ongoing link between positivity and SpA
HLA B27

HIV
Imaging in SpA
Peripheral joints: _________ at hind foot with fluffy erosions can be seen.
SI joints: ___________, usually unilateral in early disease
_____________ of the spine: bony outgrowths induced by an enthesopathy on the spine. Comma shaped, lower three thoracic/upper three lumbar are common sites
enthesitis

sacroiliitis

Syndesmophytes
Reactive Arthritis
No generally accepted criteria
__________ following infection of Chlamydia, Yersinia, Shigella, Salmonella , Campylobacter.
No more than ____ weeks between infection and synovitis.
Asymmetric ___________
Confirmation of infection with culture/serology or + ______
Synovitis

6

oligoarthritis

HLA B 27
Reiters Syndrome

Patient had triad: ________, ____________, __________
Term ‘incomplete Reiters” when not all criteria or met, now ‘undifferentiated SpA.’
usually in males
uveitis, urethritis, arthritis
Patients with criteria to be diagnosed SpA but don’t fit in any specific group
Undifferentiated SpA
Dx: H&P, labs, imaging.
______________: insidious onset neck/back pain, morning stiffness in spine improved with exercise, onset _______ age 40.
___ more features other than spine pain must be present: alternating buttock pain, enthesitis, arthritis, dactylitis, iritis, inflammatory bowel disease, psoriasis, elevated esr/crp, HLA B27, imaging evident of spondylitis/sacroiliitis, family h/o SpA
inflammatory spine pain

before

2
Differential
___ – small joint involvment
_______________- associated with untreated urethritis in the past
______________- sausage digits present
RA

Gonococcal Arthritis

Psoriatic Arthritis
self limiting that never recurs
remits but recurs intermittently
never subsides but waxes and wanes
Course of Reiters, ReA, and undifferentiated SpA
Treatments
Acute inflammation: ______(celebrex, mobic, indomethacin, etc)
Local intraarticular injections
__________ may be of benefit if no bacterial infection is active
Antibiotics for active GU infection generally __________ 100mg qd.
Self limited enteric infection, no Abx needed.
Non self limited enteric infection: generally use one of the __________
___________ (sulfasalazine) used for chronic arthritis forms. Given 500 – 1000 mg po qd to bid.
____________ and/or ____: joint/spine involvement
NSAID

Steroids

doxycycline

quinolones

Azulfidine

Anti TNF alpha agents and/or *MTX*
Chronic inflammation of the axial skeleton
Young adult onset age 20-30.
Name refers to a fibrous or bony bridging of joints
Ankylosing Spondylitis (AS)
Clinical Features
__________: improves with exercise, before age 40. “wakes me up in the middle of the night.”
_________: SI joint involvement
Limited __________: decreased flexion forward (+Schober), increased flexion of the neck (head to wall), increased thoracic kyphosis, loss of lumbar curves.
Hip pain
_______ pain: inflammation of the suprspinatus tendon into greater tuberosity of humerus limits mobility.
____________: generally acute, nonerosive, nondeforming. One joint to 2-4 joints (oligo)
___________ of heel
______________: fatigue/malaise secondary to poor sleep secondary to back pain at night
Low back pain

Buttock pain

spinal mobility

Shoulder

Peripheral arthritis

Enthesitis

Constitutional Symptoms
Imaging:
___ joint involvement
__________/osteitis at ischial tuberosities, iliac crest, pubic symphysis, femoral trochanter.
*________ of vertebral bodies*
Bridging ___________
Calcification of __________________
___________ of facet joints
SI

Erosions

Squaring

syndesmophytes

anterior longitudinal ligament

Ankylosis
Extra articular involvement:
_________/________– needs to be treated by opthalmologist
___________ symptoms: result of cord/spinal nerve compression caused by: fracture of ankylosed spine, atlanto-axial subluxation, cauda equina syndrome
_____ disease:usually aortic regurg. Caused by scarring of the aortic valve cusps and aorta.
_________ disease: restrictive chest expansion. Some with pulmonary fibrosis.
________ disease: analgesic abuse nephropathy the most common occurrence.
__________ ulcerations
Osteopenia
Uveitis/Iritis

Neurologic

CV

Pulmonary

Renal

Bowel mucosa
Goals of Therapy:
______________— To eliminate, or reduce to the minimum level possible, symptoms such as pain and stiffness.
____________— To return the patient to the best possible functional capacity.
_____________— For those patients with hip or shoulder and/or peripheral joint involvement, to prevent joint destruction or bony ankylosis.
_____________— To prevent progressive bony erosions and ankylosis of the spine to maintain spinal mobility, and prevent development of spinal deformities.
Minimize __________ and __________ manifestations — To reduce the impact of AS-associated disorders such as uveitis and aortic valve insufficiency
Prevent complications of ___________— To prevent spinal fractures, flexion contractures especially of the cervical spine
Symptomatic relief

Restore function

Prevent joint damage

Prevent spinal fusion

extraspinal and extraarticular

spinal disease
Treatments
Acute inflammation: _____(celebrex, mobic, indomethacin, etc)
Local intraarticular injections
_________ (sulfasalazine) used for chronic arthritis forms. Given 500 – 1000 mg po qd to bid.
_________ and _____: joint/spine involvement now indicated for spine involvement
NSAID

Azulfidine

anti TNF and MTX
Psoriatic Arthritis
Several clinical patterns of joint involvement have been identified:

Distal arthritis, characterized by involvement of the _____ joints
Asymmetric oligoarthritis in which less than ___ small and/or large joints are affected in an asymmetric distribution
Symmetric polyarthritis, similar and at times indistinguishable from ____
___________, characterized by deforming and destructive arthritis
Spondyloarthropathy, including both ___________ and ____________
DIP

5

RA

Arthritis mutilans

sacroiliitis and spondylitis
Other Rheumatic Features of PsA
___________
___________ of the flexor tendons of the hands, the extensor carpi ulnaris, or at other sites
___________
______ lesions — pits and onycholysis
Enthesitis

Tenosynovitis

Dactylitis

Nail
Imaging:
coexistence of erosive changes and new bone formation in the ______ joints
lysis of the terminal _________
fluffy periostitis and new bone formation at the site of _________
gross destruction of isolated joints
"__________" appearance
occurrence of both joint lysis and ankylosis in the same patient
distal

phalanges

enthesitis

**pencil-in-cup **(classic)
NSAIDS
Steroids
IA steroids
MTX, ARAVA, Azulfidine
Anti TNF (Enbrel, Humira, Remicade) all now indicated for skin disease as well
Treatment of PsA:
Chronic Vasculitis of large and medium vessels.
Occurs in people over age 50 (200 per 100,000)
Usually involves the cranial branches of the arteries that originate from the aortic arch
Giant Cell (temporal) Arterits
GCA S/S:
Onset is generally _________.
Systemic Symptoms: _________
Symptoms associated with narrowing/inflammation, and/or occlusion of the characteristic arteries e.g. Head Pain, Jaw claudication, visual loss, arm claudication, polymyalgias, tenosynovitis, upper respiratory symptoms, aneurysm, aortic dissection, Risk of Cancer, etc
gradual

fever, fatigue, weight loss
GCA:
Head Pain: New onset headache occurs in at least 2/3 of patients. Localized over ___________. May become progressive worse, or start to remit for treatment is sought. Tender temporal/occipital arteries usually found in ____ of patients.
Jaw claudication: fatigue with chewing.
Tongue claudication: Tongue pain/fatigue with chewing/talking.
Visual Loss: Permanent or partial loss of vision can occur. GCA is an ocular emergency!! Usually complain of __________
Arm claudication: ___________arteries become narrowed. Patient complains of numbness/paresthesia to the affected side.
temporal arteries
1/3

abrupt partial field defect

subclavian/axillary
GCA
-Polymyalgia: aching and am stiffness in the shoulder, hip girdle, neck. *ESR over 40*. Not usually associated with ________. 40-50 % of patients with GCA have __________.

-Tenosynovitis

-Upper respiratory: 10% complain of __________, sore throat.

-Aneurysms: __________is a late, serious finding that requires q 3-6 month monitoring dependent on size.

-Aortic dissection: Can occur with or without anuerysmal dilation.
fever
secondary PMR

cough, non productive

aortic aneurysm
GCA Exam Findings
Usually patient presents __________.
Tender or thickened ____________, maybe visually swollen and/or erythematous.
Bruits heard on auscultation of the ____________areas, brachial/axillary arteries
chronically ill

cranial arteries

carotid or supraclavicular
GCA Laboratory
High ESR often ______
_____________anemia
Microscopic hematuria (glomerular origin)
Increased liver enzymes
Increased factor __________ related to vascular inflammation
>100 mm/hr

Normochromic

VIII/von Willebrand factor
When to consider GCA?
Age over ___.
Headache
Abrupt loss of _______.
Symptoms of PMR
Unexplained __________
High ESR >100 mm/hr
High CRP
50

vision

fever or anemia
How to Confirm the Diagnosis?
____________ by a skilled vascular surgeon.
Biopsy timing: ideal to perform before treatment, however, if visual symptoms are occurring treatment may be needed before biopsy to prevent visual loss.
Arterial Biopsy
Treatment OF GCA
_________: Start at 60mg/day oral.
Once ESR starts to normalize and symptoms remit, start decreasing prednisone slowly.
____________ agent may be needed, e.g. MTX.
Corticosteroids

Steroid Sparing
calcifications along tendon insertions
fibromyalgia
FM:
women __ men
presents w/ ________
_______ sleep & exercisors
anxiety/depression
---------------------
these pts research dz on internet and think this is a debilitating chronic dz.
>

pain all over

poor
FM dx must have 5/8:
1. ________epicondyle
2. Ant. _______ chain
3. Ant. _______ wall
4. Supraspinatus
5. Trapezius
6. Post _________
7. _________Bursa
8. _________Bursa
1. lat
2. cerrvical
3. chest

6. Iliac Spine
7. Trochanteric
8. Anserine
FM tx:
-encourage good health
-___________: elavil(amitriptyline) 10-50 mg, Ambien 10 mg, Ambien CR 6.25-12mg, Lunesta 2-3 mg, Rozerum 8mg

- 30 min cardio 3x/wk
- ___________: cymbalta 20-60mg, effexor , lexapro 10-20mg
- ________: coQ10, Provigil

**AVOID PAIN MEDS & HANDICAP TAGS**
sleep meds

Anxiety/Depression

fatigue