RA Flashcards
Definitions to be aware of
arthraliga v arthritis
monoarthritis
polyarthritis
oligoarthritis
Arthralgia
- joint PAIN only
- no evidence of inflammation
Arthritis
- joint inflammation
- joint structural damange
- (does not NEED to have pain)
Monoarthritis: a single joing
oligoarthritis: 2-4 joints
polyarthritis: 5+ joints
inflammatory v non-inflammatory arthritis
characteristics which will help point towards 1 over the other
Inflammatory arthritis
- joint inflammation or damange which is driven by immune system underlying factors
- could be autoimmune, infectious or crystalline causes
- thingk rhemu. related
Non-inflammatory arthritis
- joint inflammation or damange which is not due to an underlying rheum. or inflammatory process
- typically due to age, degeneration, injury/trauma or mechanial issues
- think osteoarthritis!
________________________ characterisitcs
pain worse in the morning : think inflammatory
pain worse at night/evening: think non-inflammatory
pain improved with activity: think inflammatory
worsened with activity: think non-inflammatory
joint swelling: think inflammatory
morning stiffness?
think inflammatory if > 60 mintues
think non-inflammatory if < 30 minutes
Rheumatoid Arthritis (RA)
etiology
risk factors (genetic, environmental & antibodies)
Etiology
- chronic, systemic inflammatory disorder : MCC of inflammatory arthritis
- location of pathology: synovium of the joints= forming a pannus
Risk Factors
Genetic
- MHC region for specific HLA-DR genes: shared epitope of DR4 and DR1
Environmental
- smoking
- inhaled particles (silica dust, coal, pollultion)
- bacterial in mucosa & viruses (EBV, CMV, parvovirus B19)
- low SES
Autoantibodies
- ACPAS: antibodies to cirullinated protein anitgens
- the ACPA’s attack the citrillated proteins creating this inflammatory reaction in specific locations
Progression of the RA disease from preclinical –> established disease
Susceptible stage
- pt has the predisposition to RA; but no signs/symptoms
PreClinical Stage
- asymptomatic autoimmune: start to increse in flammatory factors, CRP, cytokines, etc. = beginning the creation of the autoantibodies (RF and ACPA)
- turns into early symptomatic stages here = start of inflammatory infilteration within the joint
Early RA
- autoantibodies continue to proliferate and infiltrate the joint synovium and synovidal membrane
Estalblished RA
- the autoimmune cells are increasing in infiltration of the joint space
- now detecatble formation of the pannus and hyperplasia of the lining
what is the Pannus of RA
Pannus: the inflammed, proliferative layer of the synovium which is a charateristic of RA
- the autoantibodies (ACPAs) proliferatre here and create inflammation
- this pannus has the ability to infilterate the bone and cartilage therfore cuasing destruction of the joint
Pannus made of what WBCs
- mononuclear cells (CD4+ t lymphs, macrophages, plasma cells, B cells and dendritic cells
- few neutrophils therefore you can now it will be noninfection (however the SYNOVIAL FLUID may have PMNs)
- the synovium becomes thick and boggy with edematous projections of villous formations in toth ebone and cause breakdown
Diagnosis of RA: Joint involvement
RA is symmetrical involvement: meaning both left and right joints involved but also symmetric within the joint itself
Often of the small joints, commonly
- PIP
- MCP
- NEVER EVER THE DIP
- MTP
- C-spine (C1&C2)
- wrists
- knees
- shoulder
Diagosis of RA
- joints
- antibodies
- inflammatory marks
- time
diagnosis of 6+ on the scale indicates RA
Joints
- more commonly small joints & multiple of them
Antibodies
- + RF (not NEEDED)
- + ACPA
Inflammatory: acute phase reactants
- CRP or ESR
Timing
- lasting > 6 weeks (chronic condition)
Joint Abnormalities on Exam associated with RA
these are less common now as we tend to catch diseases early and these are often a presentation with late stages
Boutonniere’s deformity: flexed PIP, extended DIP
Swan Neck: extended PIP, flexed DIP
Ulnar Deviation of the fingers: due to sublux. of the MCP joints and weakening of the ligaments
Hitchhicker Thumb: hyperextension of the IP joint on thumb leading to exxagerated adduction
“Piano” key ulnar head: destroyed ulnar collateral ligament leads to floating styloid head in wrist
Odontoid Process C1-C2 subluxation: as there is synovial membrane here that gets inflammed and pushes
Extra-Articaular Manifestations of RA
carpel tunnel syndrome
- interstitial lung disease/pulmonary fiberosis
- Subcutaneous rhumatoid nodules (dissapate with treatment of RA: exception that methotrexate can cause these)
- scleritis & episcleritis
- pericarditis
- pleuritis & pleural effusions & pulmonary nodules
- Sjogrens (2ndary)
- never kidney!!!!
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occular specifics
- dry eye (keratoconjunctivitis sicca) & dry mouth!
- corneal metl, scleromalacia perforans and peripheal ulcerative keratitis = occular emergency
common “syndromes” associated with RA to know (Caplan, Felty & rhematoid vasculitis)
Caplan’s Syndrome
- invovles multiple nodules within the lungs of RA pts. who are coal miners: a pneumoconiosis in the setting of RA)
Felty’s Syndrome
- RA (if left untreated)
- neutropenia
- spelnomegaly
- commonly see nonhealing ulcers
Rhematoid vasculitis
- inflammed vessels cause damange to nerve and vessels
- lead to infaract and mononueritis multiflex (footdrop) in pt with RA vasc.
RA: Lab Findings
side note on what rheumatoid factor is
CBC: can show anemia of chronic disease
ESR/CRP: usually elevated
RF (rheumatoid factor) : usually elevated (70% of pts.) but doesnt NEED to be
Anti-CCP: postive in 60% of pts. (the ACPA specific for RA)
- more specific for RA than RF is
- helpful to show RA vs. other arthritis
- can be indicative of severe disease
remember, labs dont NEED to be positive to show disease, but can point in the right direction if they are
_________________________
RF: Rheumatoid Factor
- a autoantibody against a fragment of immnoglobin G (antibody against an antibody)
- the autoantibody can come from any other antibodies: most commonly arising from IgM then going to attack a part of IgG
- RF does not flux. with clinical state of disease and is not diagnostic of RA
Radiologic Findins of RA (these can help differentiate between RA and OA)
RA Radiographic findings
- periarticular osteopenia
- **symmetry!!! within the joint cavity and of the joints bilaterally & narrowing
- marginal/periarticualr erosions**
(no osteophytes: that would show OA)
________________________________________
Mariginal Erosoin: eating away of the bone in closest proximity to the pannca or the synovum; bare areas aka areas where the synovium is direclty in contact with the bone iwhtout a protective layer of cartilage
Periarticualr osteopenia: see bone degeneration around the joint (more translucent on radiograph)
narrowing: symmetrical narrowing of the joint space, leading to bone sitting on top of bone
MRI (sens.) can also be done and US to see inflammation v. arthralgia
General Treatment Stragety for RA
- treat early: to avoid those worsening complications
- treat to target: aim for low disease activity or remission of disease
Disease Activity SCores: CDAI and DAS-28 to help gauge pt. and provider management and expectation of disease treatment
if results land in moderate to high = continue treatment if not; can taper
Role of Steroids & DMARDS in RA treatment
Steroids are for short-term management of inflammation and pain only
- ideally, should start a steroid to control pain and inflammation first & then taper it down
- as you taper the steroid down, you should but upping the DMARD
DMARD: disease modifying anti-rheumatic drugs
- conventiional synthetic, targeted syntehtic and biologics avalible
- the pt. are put on some and it is a trial and error to see best effect
common ones include
- methotrexate: majority on this
- hydroxychloraquine : some
- -umabs = antibodies treatement
- AVOID: tofacitinub (BBW for stroke)
Symptoms of RA
Systemic: fever, WL, fatique
- can have signs of extra-articualr disease
joint pain: early AM stiffness gets better throughout the day
- polyarthriris, symmetric
- common in the small joints of hands and feet most commonly
