Rheum Flashcards
two specific circumstances where methotrexate is commonly used
RA, its usualyl a first line drug
SLE when there is significant arthritis
Systemic lupus erythematosus description
an inflammatory autoimmune disease typically affecting women caused by antinuclear antibodies that leads to trapped antigen complexes in blood vessels
SLE therapy
NSAID
depends on symptms
NSAIDs for joint pain
hydroxychloroquine for joint pain, rash, fatigue
steroids for arthritis, serositis, major organ involvement
methotrextate for arthritis
leflunomide arthritis, rash, major organ involvement
angiogram findings with polyarteriris
multiple anuerysms with tapered narrow and skip areas
diagnosis of psoriatic arthritis
Elevated ESR
normochromic, normocytic anemia
hyperuricemia with significant skin involvement
normal rheumatoid factor
pencil cup deformitity at the PIP on xray
SLE therapy
steroids
steroids for arthritis, serositis, major organ involvement
fibrocartiliaginous joints
synarthrosis with limited movement
ankylosing spondylitis clinical presentation
limited ROM in the lumbar spine, hips, shoulder
synovitis in the knees, achilles, plantar fascia
up to 25% will have anterior uveitis
pain and stiffness that lasts for hours and is made better with activity
uveitis
what is this and what causes it
chondrocalcinosis
gout or arthritis
Dx of fibromyalgia
clinical presentation
exclusion of other factors (hypothyroid, hep c, vitamind D deficiency)
PE findgs for psoriatic arthritis
dactlyitis
enthesitis
skin lesions
nail dystrophy/pitting
sacroilitis
why are eye or pulmonary involvement or vasculitis common in RA
b ecause RA is an inflammatory systemic disease
top three treatment for myositis
steroids
methotrexate
azathioprine
management of OA
medication, rest, exercise, diet, surgery, aids
biologics defined for RA
genetically engineered molecules that work on specific targets
splinter hemorrhages
cause
vertical hemorrhages under the nails
can be caused by vasculitis or bacterial endocarditis
GI protective strategies for NSAIDs
cox 2 nsaid
nsaid with PPI
nsaid with misprostol
nsaid with H2 blocker
radiographic findings associated with OA
narrowed joint space, osteophytes, subarticular cysts
proteoglycans
glucosamine and chondriotin
Dx of giant cell arteritis
elevated ESR and CRP
most patients will have normochromic normocytic anemia with thrombocytosis
temporal artery biopsy that shows thickening
patient presents with a gout flare up and they are curently not on allopurinol
should you start it?
what if they are in a flare up and on allopurinol
no, don’t start it during an acute flaire
no, don’t stop it during a flare if you are already on it
Rhabdomyolysis
a syndrome of acute necrosis of skeletal muscle indicated by myoglobinuria and elevated creatine kinase
T/F the risk of CVD in patients with RA is the same as with diabetes
treu
Takayasu’s arteritis clinical presentation
fatigue, fever, weight loos
vascular damage
GI involvement with PSS
esophagitis
distal motor function
small bowel and colon hypomobility with malabsorption and psuedo obstruction
saddlenose deformity
two distinctive features of Lupus rash
usually involves face and hands and gets worse with sun exposure
Osteoarthritis defined
a degenerative disorder of the joints that produces minimal articular inflammation and no systemic symptoms
skin changes assocaited with limited sclerodactyl
early diffuse fingers welling
slow progression
involves hands below wrists and mouth
telangectasias common
subcutaneous calcium present see a the sights of trauma
renal conditions associated with PSS
major cause of death if untreated
more likly to be in patients with friction rubs, rapid progression, no raynauds
requires BP monitoring and poss treatment with ACE inhibitors
what is the age and gender bias of systemic lupus
female to male 8:1
usually between 20-50 but can be any age and usuallly more mild in elderly
pathogenesis of SLE
excessive helper T activity with low suppressor T leading to prolferation of B cellls and autoantibody production
ankylosing spondylitis treatment
exercise and physical activty
NSAIDs
TNF inhibitors
why is acute gout not treated with allopurinol
it can precipitate episodes by blocking urate pathways
only used for chronic gout
four types of spondyloparhtopathies
ankylosing spondylitis
psoriatic arthetis
reactive arthritis
arthritis from IBD
septic arthritis (gonococcal) signs and symptoms
prodromal migratory poly arthraligias
tenosynovitis
purulent monoarthritis
skin lesion
why is rapid treatment of Granulomatosis with polyangiitis important
because one renal involvement starts it progresses quickly
renal involvement owith polyerarteritis
segmental necrotizing glomerulonephritis
osteoarthritits clinical presentation
decreased ROM
crepitus
pain in the morning that goes away in 15 minutes then come back
tends to effect load bearing joints
safety issues associated with TNF vlockers
adminstration reactions
opportunistic infections
malignancy
demyelination
hematologic abnormalities
congestive heart failure
lupus like symptoms
what will hapen to compliment during active lupus
C3 and C4 will be decreased because you have a lot of cell death
therpay for polyarteritis
steroids, cyclophosphamide
calcium pyrophosphate dihydrate (CPPD)(pseudogout) clinical presentation
painful inflammation similar to gout (red, swollen, hot, tender)
differentiate between fibromyalgia and RA
FM has trigger points and an absence of articular pathology
polymyalgia rheumatica clinical presentation
stiffness in the shoulder worse after rest and in the AM
usually bilateral, proximal, and symmetrical
systemic symptoms
most often presents in women
heliotrope rash
typical distribution
a rash indicative of dematomyositis
usually in shawl type pattern over the chest and eyes (places exposed to sunlight)
syndesmophytes
calcification of ligaments see in ankylosing spondylitis
what two features do scleroderma and crest have in common
raynauds phenomena and positive ANA
FANA test
fluorescent ANA
what percent of people with SLE have APA
how many have APA syndrome
30-40%
less
Direct Coombs
hemolytic anema
are narcotics generally effective for managing PFS
no, PFS is neuropathic pain that nacrotics don’t work well on
blood work associated with myositis
elvated CPK, serum aldolase, sgot
key indicator of diffuse proliferative glomerular nephritis
sudden jump in BP
T/F antiphospholipid antibody syndrome may exist without SLE
true, 5% of people have low level APA
differentiate between radiographic finds of gout and RA
they will both have bite out lesions but gout will have less joint narrowing and speculed appearance
key for RA treatment
goal
early and aggresive treatment
put patient in remission
reactive arthritis clinical presentation
urethritis, conjuctivitis, oligoarthritis, mucous ulcers in conjuction with an STI or gastroenteritis
often effects large joints of the lower body
causes of OA
physical stress
abnormal healing after injury
biochemical/genetic factors
normal components of a joint
water
cartillage
bone
muscle
ligaments
nerves
vasculature
osteonecrosis
bone death that can be associated with corticosteroid use and SLE, among other things
five clincal presentation of psoriatic arthritis
- symmetrical polyarthritis like RA with usually fewer joints
- oligoarticular form that leads to significant destruction of joints
- assymetric for that affects the DIP and leads to nail deformities (pitting, onycholysis)
- arthriris mutilans
- spondylitc form with sacroiliitis and spondylosis
treatment of sjogrens
salagen/evogen
tear duct ablation
plaquenil
nsaids
raynauds associated with limited scleroderma
always presents, usually years before skin changes
incolves all the fingers
calcium channel blocker can be effective to control vasospasm
dactylitis
swelling “sausage fingers” that are assocaited with recative arthritis, ankylosing spondylitis, and psoriatic arthitis
explain cox 2 and cox 1 in respect to NSAIDs
cox 2 is an inducible enzyme that acts on inflammatory sites, inhibition of this will increase the function of NSAIDs
how is gout DX
negatively birefringent needle shaped crystals
differiate between scleritis and conjuctivitis
scleritis wil go all the way to the iris
diagnosis of sjogrens
positive schirmer test
postive rose bengal stain
abnormal salivary gland or lip biopsy
positve RA or ANA or SSA/SSB
levamisole associated purpura
vasculitis caused by tainted cocaine that presents as retiform purpura and cutaneous necrosis over the ears, extremities, and cheeks
three functionsof disease modifying anti-rheumatic drugs (DMARDs)
reduces symptoms and signs of RA
reduce functional disability
retard radiographc progression
Granulomatosis with polyangiitis treatment
initial induction of remission with rituxumab or cyclophosphamide with corticosteroids
maintenance
juxaarticular erosion
a classic xray sign of RA cuased by the synovium wrapping around the adjacent edges of bone
differentiate between crest and scleroderma
sclereoderma is wide spread especially over the trunk and is much less common
Crest is just the face, neck, and distal extremities and is much more common
pulmonary involvement wth PSS
restrictive pulmonary fibrosis
usually bibasilar in the lungs
if there is an inflammatory component it may response to cyclophosphamide
usually indicated by a gigh SCL 70
treatment for acute gout
colchicine
NSADs (indocin)
steroids
nutrition
septic arthritis (gonococcal) Dx
high leukocyte count in the synovial fluid
positive gonorrhea cultures in the urethral, throat, cervix, or rectum
good response to IV antibiotics
Anti-neutrophil cytoplasmic antibody (ANCA) tests for
wegeners, almost 100% specific
neuro conditions associaed with lupus
headaches
sz
coma
psych
symptoms of RA
morning stiffness greater than 1 hour
diffuse fatigue and aching
subcutaneous nodules
eye involvement
pulmonary involvement
vasculitis
knee problems that commonly effect the knee
anserine bursitis
prepatellar bursitis
baker’s cyst
chondromalacia patella
OA
why can ESR be misleading when diagnosing arthritis
what about rheumatoid factor
ESR will go up with age, up to 1/2 their age
rheum factor will also go up
differentiate between pleural effusion caused by RA and heart failure
RA effusion will have more protein
swelling of the synovial sack of the knee
three types of crystal arthritis
gout
pseudogout
hydroxyapatite
why is using colchincine and allopurinol in gout treatment a good idea
colchincine is stopping crystal formation why allopurinal decreases uricemia
age and gender bias of scleroderma
3-4x more common in women, typically onset 30-50
Microscopic polyangitis Dx
ANCA positive
microscopic hematuria
proteinuria
red blood cell casts
segemental necrotizing glomerulonephritis
polymyalgia rheumatica Dx
Clinical presentation without any other explanation
ESR markedly elevated
temporal artery biopsy if suspected GCA
acute bacterial arthritis
Dx
is xray useful
aspriation of synovial fluid with a leukocyte count greater than 2000/mcL, usuallyl over 50,000 mcL
it can help exclude gout due to lack of crystals, but joint aspriation is best
ANA Profile (patterns)
DS DNA
antihistone
anticentromere
anti SCL
SLE (homogeneous, Rim)
drug induced SLE (homogeneous, rim)
Crest
PSS (nucleolar)
primary and secondary indications of sjogren’s syndrome
primary: dry eyes, mouth, common in older women
secondary: associated to another connective tissue disease (lupus, scleroderma, etc)
what is needed before a diagnosis for fibromyalgia can be made
other conditions with suggestive history need to be excluded
most patients with lupus present with what three things
less common signs
fatigue, rash, joint pain
renal, neuro, hematological disorders
diarthroidal joints
synovial joint
Antiphospholipid syndrome DX
venous and arterial occlusions
positive ANA with no features of SLE
repeated SAB
Vectra DA
Ra
gottrons papules
discrete red papules found over the knuckles of people with juvenile dermatomyositis
T/F inflammatory joint disease tend to have stiffness in the morning that quickly goes away
false, that is more typically osteoarthritis
what type of drug is Hydroxychloroquine (plaquenil)
conditions it is used to treat
DMARD
RA, cutaneous and systemic lupus, scleroderma and CREST, sjogrens
What makes TNF blockers a risky treatment for people who have been exposed to TB
what can you do to combat this
what is alternative treatment
usually reactive of latent TB
PPD yearly, CXR area with fungal disease
MTX with isoniazid
heberdens nodes
hard bony swellings of the DIP common in osteoartritis
what is a typical cause of early onset OA
abnormal type II collagen
conditions associated with uveitis
granulamatosus
spondyloarthtitis
behcet disease
why is it useful to add control points when looking for trigger points for PFS
to rule out a significant psychological issue
possible enviromental triggers of scleroderma
vinyl chloride
contaminated tryptophan
trichlorethylene
silicone
epoxy resin
lab monitoring for methotrexate
baseline CBC with platelets, liver enzymes, renal function, CXR
maintenance CBC (8-12 weeks), liver enzymes (4-8), renal function every 6 momths
raynauds
first choice drug for RA
what is an important supplement with this
methotrexate
inclusion of folic acid to decrease toxicity rate
Sjogren syndrome is strongly correlated with what
increased incidence of lymphoma
giant cell arterities
describe Granulomatosis with polyangiitis
a type of vasculitis that causes dysfunction in the respiratory tract and glomerulonephritis caused by vasculitis, granulomatous inflammation, and necrosis
aggrivating factors for PFM
cold or humid
poor sleep
physical/mental fatigue
excess physical activity
lack of exercise
stress
ESR tests for
>100 might indicate what
how to get the upper limit lab value
OA vs RA
PMR, GCA, Wgeners
divide age by 2
limb changes associated with Kawasaki disease
edema, desquamtion, erythema of the palms and soles, induration of the hands and feet
fibromyalgia symptoms
point tenderness
fatigue
stiffness
anxiety
headaches
irritable bowel
parethesia
acute bacterial arthritis
defined
acute monoarticular arthritis usually seen in weight bearing joints that have previous joint injuries or injections
Dx of polymyositis
elevated muscle enzymes and aldolase
myopathic inflammation on biopsy
why is plaquenil useful in RA treatment
can be combined with other drugs
minimal side effects other than occasional GI
+5yrs has small risk of retinal toxicity
drug monitoring for NSAID use
annual monitoring for hepatic and renal function
annual monitoring of CBC
clinical presentation of fibromyalgia
nonarticular muscloskeletal pain
fatigue
sleep distrubance
trigger points
for at least three months
indicators of a prognosis in RA
reduced function
early xray changes
more joints
age
high rheumatoid factor
prolonged high ESR
treatment for wegener’s granulomatosus
steroids
cyclophosphamide
methotraxate
rituximab
what causes anemia in RA
hepcidin is elevated preventing iron from being made into HgB leading to anemia
scleritis
inflmmatory condition of the sclera associated with RA, vasculitis, granulomatosus, and henoch schonlein purpura
two specific uses for Hydroxychloroquine (plaquenil)
in RA as mild treatment or combination therapy
SLE to help with joint pain, rash, fatigue, and combination therapy with steroids for flares
other organs affected by polymyositis
joint, lungs, heart, GI
age and gender bias with polyarteritis
usually fatal, more common in men
ABx treatment for infectious arthritis
nafcillin + mysin (only 3 days due to ototoxicity)
ancef
vancomycin
may need debridment
how is cuteneous lupus diagnosed
where will you usuallly see lesions
does it scar?
DX by skin biopsy because ANA is usually negative
face, scalp, arms, upperchest
it can
muscle biospy findings associted with myositis
perivascular infiltrate of inflammatory cells
used to rule out inclusion body myositis
what is a definitive test for RA
CCP test, if its high you have RA
T/F 90% of drug included lupus will go away
common causes
what is the common presentation
true
progainamide, isoniazid, TNF blockers
inflammation of serous membranes (pericarditis, peritonitis, etc)
two less frequent systems affected by wegeners
skin (nodules, palpable purpura, ulcerations)
arthritis
telangiectasias
red spidery veins commonly seen on the nose, mouth, and chin; part of CREST syndrome
ESR >100 means what likely conditions
GCA
wegeners granulomatosus
lymphoma
mets to bone
what is this
what is the prognosis
a type of limited scleroderma know as morphea
generally it has very good outcomes
musculoskeletal conditions associated with limited scleroderma
polyarthralgias common but not very inflammatory
no fricition rubs
mostly confined to hands
lower respiratory conditions associated with wegener’s granulomatosus
SOB, hemopytsis, cavitating lesions, tracheal lesions
ANA Profile (patterns)
Sm (smith)
SSA
SSB
RNP
SLE, UCTD (speckled)
Sjogrens, SLE (speckled)
Sjogrens (speckled)
UCTD, SLE (speckled)
podagra
gout attacking the first MTP joint of the foot
dactylitis
swollen fingers
osteoarthritis treatment
weight loss
exercise
nsaids
joint injections (steroid or synovial fluid)
joint replacement
ankylosing spondylitis Dx
Elevated ESR and CRP
HLA-B27 +
sacroilitis and bamboo spine on radiograph
most common bacteria causing infectious arthritis
staph, strep, gram negative bacilli
Systemic lupus erythematosus treatment
exercise
sunblock
NSAIDs
antimalarials
topical or oral steroids
MTX
Rheumatoid factor (RF) test for
what might increase RF without underlying pathology
inflammation, COPD, HCV, Lupus
age
secondary raynauds can be caused by what rheumatic disease
scleroderma
SLE
polymoysitis
sjogren
vasculitis
why would you test someone who SLE for APA
when they present with some kind of clotting probelm
calcium pyrophosphate dihydrate (CPPD)(pseudogout) Dx
CPPD crystals in joint fluid (positively bifringent)
fine, linear calcifications on xray
where is synovitis usually found with Lupus
similar to RA, small joints of the hands and feet
relationships between raynauds and PSS
usually present first with skin changes to follow
increased risk of gangrene or infarct
usually seen at 1 or 2 fingers
those who don’t have it have worse surivival
Sjogren syndrome treatment
keeping the eyes/mouth/vagina moist
pilocarpine can increase saliva flow
cyclosprine for eye symptoms
labs to monitor the progression of SLE
smith antigen antibodies
double stranded DNA antigens
depressed compliment
clinical factors associated with gout
more than on acute arthritis attack
development of maximal inflammation within 1 day
monoarticular arthritis
painful or swollen joint
erythema
suspected tophus
hyperuricemia
subcortical cysts without erosions
psychological management of PFS
stress management
biofeedback
relaxation
group/individual therapy
negative findings on PE for PFS
positive
muscle weakness, neurological exam, joint exam
trigger points, mild swelling, skin tenderness on pinch, hyperemia of skin
differentiate between GI involvement with limited vs PSS
uncommon to have lower GI involvement in limited
commonly has biliary cirrhossi
Granulomatosis with polyangiitis clinical presentation
usually presents with upper and lower respiratory symptoms with glomerulonephritis that takes place over 4-12 months
T/F low dose aspirin is bad for gout
true, it can exacerbate but high dose aspirin is a useful therapy
CXR findings associated with wegener’s granulomatosus
lung biopsy
nodules and cavititing infiltrate
necrotizing granulomatous process
giant cell arteritis treatment
should you wiat for biopsy before treatment
immediate high dose steroids with a 1-2 month duration
no
drugs for PFS
tricyclic antidepressants
muscle relaxers
SSRI
SNRI
antianxiolytics
gabapentin
tramadol
narcotics
types of uveitis
how do you differentiate
anterior, intermediate/posterior
anterior will have redness and dilated cillary vessels that go right up to the iris
posterior will have more vision defects (blurred vision, floaters0
what is the only condition that is treated with indomethacin
gout and pseudogout
polymyalgia rheumatica treatment
low dose corticosteroids for up to one year
treatment of psoriatic arthritis
NSAIDs work for mild cases
methotrexate, biologic DMARDS, TNF inhibitors for severe cases
surgery for end stage arthropathy
corticosteroids and antimalarials should be avoided
C-Reactive Protein tests for
what can confound the results
general marker for inflammation (RA, PMR) that is more specific than ESR
truncal obestity