RA and OA

Ah, the vague, but widely heard of rheumatoid arthritis.  How is it different from osteoarthritis?  What causes it?  What does "autoimmune" mean?  How does it work?  How do we treat it?


ETIOLOGY/PATHOLOGY OF RHEUMATOID ARTHRITIS:

The working hypothesis is: a genetically predisposition patient becomes exposed to an antigen (varies), which causes the body to produce an abnormal looking IgG.  Abnormal or not, this IgG is still part of the patient's own immune system.  The normal immune system sees this weird IgG and freaks out, thinking it's an invader and attacks it with another antibody (another IgG), this one is the "autoantibody," which is also known as "rheumatoid factor" and it binds together with the abnormal IgG and antigen, making one big clump that deposits all over the synovial membranes and cartilage in the joint.  This whole thing is called an immune-complex reaction.

The "autoimmune" comes from the fact that the weird blue IgG is being attacked by the purple IgG.  In science, "auto" means "self" or "same," as in the antibodies both made by one person are attacking each other.

It is interesting to note that the antigen-antibody complex (the red-blue, and the red-blue-purple) is too small to be removed by the mononuclear phagocytosis, so all of these clumps of teenie-tiny antigen-antibodies are deposited in tissue. This causes a complement activation, which is just a fancy way of saying that an inflammatory process is created that amplifies the inflammatory process--ultimately it causes cell membrane rupture (normally it would cause pathogens to explode, but in this case, it's normal cell exploding all over the place, and normal cell bits being presented as antigens to perpetuate the inflammation).


RA VS. OA
So, what's osteoarthritis?  If your joints hurt in the morning, is that OA?  But RA has flareups in the morning, too, right?  And they both involve the swelling of joints to an extent.  And you take NSAIDs--but there's also other medications for RA, right?

(This is what cool people do in cafès.  They make lists of comparisons between similar diseases.  Yup.)

The details differentiating rheumatoid arthritis from osteoarthritis are so various and extensive it's maddening, however, if you understand the etiologies and the A&P, it's actually pretty straightforward.  The biggest point to understand is that rheumatoid arthritis is a systemically inflammatory disease that causes symmetrical cartilage and bone destruction whereas osteoarthritis is a non-inflammatory (with the exception of secondary localized inflammation) diseases involving cartilage destruction from repetitive motion, and impact, which causes uneven bone growth called 'spurs.'  I have osteoarthritis in my right knee from a seriously bad fall while hiking, and then ignoring the injuring and playing water polo for an entire season.  I wish I had a copy of my old MRI because the bone spurs are wicked.  Here's a picture of a shoulder joint with bone spurs:

http://utahshoulderknee.com/images/stories/shoulder/shoulder_impingement/bone_spur_removed.jpg

See how bumpy the surface is?  It's not supposed to look like that.  If you understand that osteoarthritis is caused by repetitive motion, you can see how the osteoarthritis would be localized to the joints being abused.  It may or may not be symmetrical (depending on the action, for example, if you're someone who stomps on a shovel with you right foot all day, you might develop some bone spurts on just your right foot, or it could be symmetrical like in the knees of an overweight runner), and rest and splinting would improve the pain.  If there is inflammation from secondary synovitis (a marker of advanced OA) you might feel that the joints are "squishy," like a water balloon, but there may be some joint hypertrophy from all the spurs developing--and those are called Heberden's (DIP) and Bouchard's (PIP)--but they're not nearly as gigantic as RA joints.

Rheumatoid arthritis, on the other hand, is an autoimmune disease, so you would have systemic symptoms, such lab values (increased RF, CRP, ESR, ANA, and WBC), and lung (bronchitis, pleursy, pleural effusion), heart (pericarditis, pericardial effusion, and cardiomyopathy), spleen (Felty's syndrome) skin (Sjögren's syndrome), and other extra-articular symptoms ( photosensitivity, itchy/dry eyes and mouth, scleral nodules/cataracts, muscle fiber degeneration--seriously, everything).  It has hallmark bilateral symptoms of swan neck subluxation, Boutonnière's, ulnar drift, and hallux valgus.  The patient may have a decreased appetite, so oftentimes the weight is subpar.

TREATMENT OF OA and RA:

I'll start with OA treatment since it's simpler.  Essentially the treatment is pain management with:
1) Tylenol (no synovitis)
2) NSAIDs (synovitis)
3) topical analgesics like trolamine salicylate and capsaicin
4) heat/cold compresses (heat for chronic, cold for acute/flareups, always, always, always) and splinting/braces
5) glucosamine chondroiton (contraindicated with shellfish allergy)
6) intraarticular injections of glucocorticoids and hyaluronic acid (to rebuild cartilage--made from chicken combs, so contraindicated with egg allergies) until you can't manage the pain and deterioration anymore, and you
6) progress to the final stage of surgery for joint replacement.

Don't be fooled--just because the treatment is simpler, doesn't mean the disease is better--it just means there's not much that can be done.  Basically, the patient has to find low impact sports and listen to his body.  There has to be a happy medium of weight loss but also refraining from working so hard that the joints become irritated and painful.  I played co-ed waterpolo, swam competitively, played rugby (for just one year--I was starting to mentally mature enough--or maybe just hurting enough--to realize I only had one body), and practiced martial arts.  Plus, I was a nursing assistant on an end-stage Alzheimer floor.  I don't think I have a single joint in my body that doesn't have some kind of damage.  I was talking to my pediatrician who, when I mentioned how I regret wearing my body out on water polo, nodded with some chagrin and said, "Sometimes it got frustrating bandaging you up enough so that you could go back to the same thing that broke you in the first place."  I have crepitus like nobody's business.  I literally snap, crackle, and pop.  My body hurts--it's why I can't sit still in class.  And I take 800 Ibuprofen every night to get my body to stop aching enough to fall asleep.  Every.  Night.  On bad days, I wear bilateral wrist splints to sleep.  If I could go back in time...  I digress.

Treatment of rheumatoid arthritis is multifaceted.  Yes, you want to deal with the pain, but you also want to stop the progression of the disease because once it starts, it progresses rapidly, and it's irreversible.  It's nearly impossible to memorize all of the medications that treats RA, and it's very hard to understand why you would even want to take some of them (gold salts aka auranofin?  Really?), but I scribbled out a picture of how each medication class intervenes in the pathophysiology of the disease, and it helps me to remember why each medication has its classification.  Don't worry, they're only the ATI medications, and they're only generic names.

Excuse the scribbles.  After poring over my drug book, medsurg book and ATI book,  I wasn't in the mood
to make a clean copy.  Rule of thumb: if you see "-mab" there's a good chance it's a DMARD.

Basically, you should definitely know that there are disease modifying antirheumatic drugs, of which methotrexate is the go-to first line of defense for early RA.  Methotrexate is an immunosuppressant, and cytotoxic.  Recall, methotrexate is given with extrauterine pregnancies to abort the embryo before it can rupture the fallopian tube, and it's also a chemotherapeutic agent.   Now, since it's a chemo-agent, you can remember that chemo patients have immunosuppression/pancytopenia due to bone marrow suppression, hepatic fibrosis, ulcerative stomatitis (s/s of toxicity, which is basically what chemotherapy is), and obviously fetal death.

After that, there are a plethora of immune system/cytokine antagonists, some of which are antibiotic (given as immunosuppressants).

Here's a list of DMARs from Wikipedia, all nicely charted out:

http://en.wikipedia.org/wiki/Disease-modifying_antirheumatic_drug

The only medication I'm going to expand on are the TNF antagonists (etaercept, infliximab, and adalimumab)because they're SO COOL.  Basically, they're like decoy free-floating TNF receptors look-alikes that bind to TNF and prevent it from increasing inflammation in the joint.  Seriously, the person/people who made this is/are brilliant.  Treatment with TNF antagonists aren't without risks.  TNF antagonists are given via IV, so SQ infiltration and irritation is always a risk, plus there's a risk of Stevens-Johnson type of skin reactions, heart failure and blood dyscrasias (any drug that messes with cell development is going to put you at risk for blood dyscriasis).  Since we're messing with the WBCs and the complement system, be aware that any dormant infections can rear their big green heads, so TB and hepatitis B patients can have flareups with the immune system being dampened.

Other than that, there are adjuvants that are rarely used, like auranofin (adverse affect of pruritus and stomatitis, renal toxicity, blood dyscrasias, and hepatitis--but all medications affect the kidneys and liver, so basically all of you have to remember is blood dyscrasias).  Plus you have glucocorticoids, like prednisone, that can cause Cushings-like symptoms.

The pain management is very similar to that of OA, NSAIDS, compresses, topical analgesics.  Once the disease becomes severe enough, surgical joint replacement is necessary.

REFERENCES:
Brucher, L., Dirksen, S.R., Harding, M.M., Heitkemper, M.M., & Lewis, S.L.  (2014).  Medical Surgical Nursing (pp. 174, 212, 1568-1576) St. Louis, MO: Elsevier Mosby.

Sommer, S., Johnson, J., Roberts, K., Redding, S., Churchill, L., Ball, B., Henry, N. J., Leehy, P., & Roland, P.  (2013). RN Adult Medical Surgical Nursing.  9th Ed. (pp. 803-806) Leawood, KS: ATI.

Lippincott 2013 Nursing Drug Handbook