RA Flashcards
RF for RA
- Genetics
- infectious agent
- Sex hormones
- Smoking
- Parental Hx of substance abuse
infectious agents that cause RA
EBC
mycoplasma
Rubella
innate susceptibility but infxn causes it to switch on
sex hormones and RA
more common in women
subsides during pregnancy
less common in women taking OC
RA patho (general)
trigger sets off an autoimmune reaction in a genetically susceptible person
RA patho (8) (long)
- inflammation in synovial membrane and synovial space
- destructive enzyme activation
- reactive oxygen species form
- synoviocyte cells proliferate extensively, cross synovial membrane and get into cartilage
- synovium relates MMP that destroys cartilage and stimulate osteoclastic bone reabsorption
- pro inflammatory cytokines released cause systemic symptoms
- osteoclast activation = osteoporosis
- articular surface damage causing destruction of the bones
- fibrous adhesions = permanent joint deformities
cells that cause RA inflammation
CD4/T cells
monocytes
neutrophils
fibroblasts
enzyme destruction to which joint
cartilage
tendons
ligaments
bone
PDGF
angiogenesis into the joint
pro inflammatory cytokines RA
TNF alpha
IL-6
produce systemic symptoms
systemic symptoms caused by cytokines
weight loss
organ inflammation
fever
pathogenies of RA
- activation of pro inflammatory cytokines causing joint swelling, stiffness, destruction
- pannus acts like locally invasive bone tumor
- cytokines cause systemic inflammation symptoms and worsened comorbidities
Epidemiology of RA
F > M
MC in Native American, least common in Caribbean Black
35-50 years
Family hx
hallmark feature of RA
persistent symmetric poly arthritis that affects small joints of hands, wrists, ankles and feet
insidious onset
RA joints on PE
swelling, tenderness, warmth and decreased ROM
atrophy of interosseous muscles
worse in AM
lab eval of RA (6)
- ESR/CRP
- CBC (ACD, thrombocytosis)
- RF (non diagnostic)
- Anti-CCP
- Anti MCV
- ANA
RF
IgM against IgG
60-80% of pts with RA over course of dz but NOT specific for RA
NEITHER necessary nor specific
seropositive RA
presence of RF in serum
increased likelihood of severe erosive arthritis, rheumatoid nodules, extra-articular dz
ACPA abs include
anti-CCP abs
AntiMCV
anti-CCP Abs
MOST specific biomarker for RA but found in other dz
indicates higher likelihood of erosive arthritis and worse prognosis
ANA in RA
if NEGATIVE can help distinguish RA from SLE
joint aspiration
inflammatory fluid (>10k WBC)
- crystals, - culture
imaging study of choice
Plain fim XR
bone erosion and uniform joint space narrowing
RA on plain film
osteopenia
symmetric narrowing of joint spaces
erosions
bony crowding due to loss of cartilage
first 4 criteria for RA diagnosis (1987)
- Morning stiffness lasting at least 1 hr
- soft tissue swelling or fluid in 3 joint spaces
- at lease one area swollen in wrist, MCP, PIP
- symmetric arthritis
joints MC involved in RA
- MCP
- wrist
- PIP
also knee, MTP, joint, ankle. C spine, hip/elbow/temporomandibular joint
4 criteria for RA in 2010
- joint involvement
- serology test results
- actue phase reactant test results
- duration of symptoms
why is early diagnosis of RA essential?
high risk of permanent joint deformities
decreased ability to do ADLs
extra articular disease of RA (who gets it, MC_
fatigue, myalgia, malaise
mc in pts with seropositive RF
rheumatoid nodules (MC site)
extensors surfaces and areas of mechanical trauma
olecranon, ulna. back of heel, occiput
ocular manifestations of RA
dry eyes/MM
Uveitis
Episcleritis
Nodular scleritis (red eye, painful with movement)
list of RA organ systems affected:
- anemia (microcytic)
- infections
- GI issues (stomach and intestinal upset)
- osteoporosis
- pulmonary dz
- lymphoma
pulmonary disease and RA
increased risk of intersistial lung dz,pleuritis, pleural effusion, rheumatoid pulm nodules
Cardiac Dz in RA
CAD not attributable to typical risk factors
MI, pericardial effusion, myocardial dysfunction
MSK dz in RA
synovial cysts
tendon rupture
nerve entrapment
tenosynovitis
cervical spine dz in RA
subluxation of C1 and C2
boutonniere deformity
contracture of PIP joint and hyperextension of DIP joint
swan neck deformity
hyperextension of PIP joint and flexion contracture of DIP
tx goals of RA
control pain
preserve joint fxn
prevent joint deformity
early referral + therapy
NSAIDs in RA
pain management and improve daily fxn
do NOT inhibit disease progression/disability and NOT as sufficient as mono therapy
risk of GIB/GI ulcer, renal dysfunction, HF exacerbation
w/u prior to RA tx
CBC, Chem Panel, ESR/CRP
LFTs, viral hepatitis panel, TB screen
pharm tx of RA (list) (
- Glucocorticoids
- non biologic DMARDs
- Biologic DMARDs
glucocorticoids use in RA
- acute exacerbation
- starting DMARD
- unable to take DMARD
long term SE of glucocorticoids
weight gain
HTN
osteoporosis
hyperglycemia
when do you start DMARD?
EARLY (<6 mo) of tx is standard
vaccinations and DMARDs
pneumococcal hep A, hep B influenza vax HPV herpes zoster
pts started on DMARDs MUST be tested for”
TB
viral hep
endemic fungal infections
initial DMARD of choice
Methotrexate
therapy should be adjusted after 6 mo if incomplete response
biologic prescribing rules
all are equally efficacious
more effective than non biologics
should only give one at a time
Biologic CIs
Chronic viral hep B and C
malignancy in last 5 yrs
CHF AHA class III or IV
fungal infection/tb
biologic DMARDs and vaccines
cant receive live virus vaccine (MMR, yellow fever, intranasal, herpes zoster, varicella)
give all killed viruses
HZE live should be given before starting DMARD or Biologics
monitoring while taking DMARDS biologics
CBC, liver, renal panel, and viral hep panel at baseline and q 4 months
HF and TNF agents
CI in pts with NYHA class II or IV
ESP infliximab
RA prognosis
disabled in 10 years
typically die 10-15 years before (2.5x mortality)
MC cause of premature death
CAD
not associated with traditional risk factors
secondary to chronic inflammation
factors indicating poor RA prognosis
RF seropositivity
>30 joints involved
Extra-articular manifestation
Felty’s syndrome MC in
RF positive,
long duration of RA (>10 yrs),
extra articular manifestations
Felty’s syndrome patho
splenic sequestration and destruction of granulocytes
Felty’s syndrome triad
RA
Splenomegaly
neutropenia
tx of Felty’s syndrome
IV abx (Neuopgen)
usual RA tx
Steroids (limited efficacy)
Triple therapy
Max MTX dose
Sulfasalazine
Hydroxychloroquine
if this fails go to biologic
