• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key

image

Play button

image

Play button

image

Progress

1/45

Click to flip

45 Cards in this Set

  • Front
  • Back
When does RA present?
Mostly in adults, peak incidence in 4th-6th decades, Women predominant.
Which gene is the primary susceptibility haplotype in seropostive RA?
HLA-DR4, except in Black Americans.
What is the initial presentation of RA?
Morning stiffness over 30 min, gradual onset of fatigue and weightless are the presenting symptoms. Progresses to joint pain with swelling tenderness, and stiffness AFTER INACTIVITY. Symptoms are bilateral!
How does elderly-onset RA differ from younger-onset RA?
Presents similarly to polymyalgia rheumatica, abrupt onset of shoulder and hip joint inflammation, more weight loss, involvement of large and small joints, and greater disease activity.
How do patients with RA and SLE present? Which serum factors are present?
RF, ANA, and dsDNA are all present. THey have deforming, symmetrical inflammatory polyarthritis involving small joints, and radiographic evidence of deterioration.
Which joints are characteristically affected in RA?
PIPs, MCPs, wrists, elbows, shoulders, hips, knees, ankles, and MTPs
What is the pathogenesis of RA? How does it start?
Exudative Phase first: PMNs move into the joint space between the endothelial cells. They release inflammatory mediators which superficially erode the cartilage. Next is Chronic Inflammatory Phase: prolonged PMNs activate synovial cells to produce enzymes to degrade cartilage and bone. The 1-3 cell synovial layer becomes 6-10 layers thick. Capillary destruction and thrombosis occur.
What cells are found in rheumatoid synovitis?
5,000-75,000 WBC, and PMN predominance.
What role does RF play in Rheumatoid Synovitis?
Synthesized by B cells and Plasma cells. It is an IgM Ab directed against IgG. Plays role in complement activation and PMN activation. Most with RA have RF, but not always.
When RA progress, it becomes chronic and granulomatous Pannus in the synovium, which invades and erodes adjacent tissue. What factors does the Pannus produce?
IL-1, TNF, PGs, PDGF, Substance P, transferrin, IL-2
Which radiographic findings are suggestive of extra-articular RA?
Wide space between atlas and axis, subluxations of cervical vertebrae, narrow disc spaces without osteophytosis.
Where are Rheumatic Nodules found in RA?
Points of pressure such as olecranon process, extensor aspects of the finger joints, achilles tendon, and occiput in bedridden patients. They have central necrosis with connective tissue cells around the periphery.
What is the most frequent cause of neuropathy in RA?
entrapment of nerves by thickened inflammatory tissue.
When Vasculitis is associated with RA, which serum factors are expected?
High RF, Low Complement.
Which extra-articular RA symptoms are associated with low complement?
Sjogrens, leg ulcers, Felty's, neuropathy, pulmonary involvement
Which syndrome consists of RA with splenomegaly and neutropenia?
Felty's (associated with low complement)
What is the most common pulmonary manifestation of RA?
Pleural effusion and pleural thickening. Predisposing factors are male gender over 45 with the presence of nodules. They also have a low glucose content, which is characteristic of TB and malignancy.
What is unique about the presentation of RF negative RA?
It is often asymmetric. anti-CCP may be present in RF negative affected patients.
What are the goals of RA therapy?
Control disease activity, Decrease Pain, Optimize Function, Reduce Joint Dysfunction
Why is RA treated more aggressively now than in the past?
NSAID toxicity, more effective DMARDs, long term smoldering of disease can lead to poor functional outcome, there are now prognostic indicators of poor outcome (like multiple joints, extra-articular features, early impairment, radiographic features.)
Methotrexate treats RA. How should it be monitored and administered?
Given once a week. Monitor LFTs because hepatic fibrosis is a concern. Shouldn't be used in someone with lung, liver, kidney or EtOH problems. Given with folic acid to reduce mouth ulcers. Can cause congenital malformations. Should only be give with NSAIDS if on a low dose
Methotrexate is the main drug used for RA. Another is Hydroxychloroquine for mild/moderate disease. What are some adverse affects?
Take 200 mg twice daily, Retinopathy is a cumulative risk, patients can relapse after several years, G6PD deficiency can lead to hemolysis.
How are corticosteroids used in RA treatment?
Low dose in conjunction with DMARDs. Combination therapy is either DMARDs plus NSAIDs or corticosteroids.
Which factors affect RA prognosis?
Onset after 65 achieves remission and requires minimal medication after 1-2 years of therapy. But if female and earlier age of onset in the presence of erosions, less chance of remission.
What are the clinical manifestations of gout?
recurrent acute attacks of arthritis, monosodium urate deposition in joint, monosodium urate crystals depositing in kidneys, uric acid urolithiasis due to excess uric acid secretion, and hyperuricemic nephropathy
What is the normal level of uric acid in serum?
7.5-8.0 mg/dl, above this is hyperuricemia. Uric acid is less soluble in blood at lower temperatures, which explains why symptoms are worse in areas with reduced blood flow.
Difference b/w primary and secondary gout?
primary gout is hyperuricemia caused by genetic error of excess production or impaired excretion. secondary gout is hyperuricemia from an acquired disease state.
How is an individual characterized as a uric acid overproducer?
Excrete 600mg in 24 hours after a five day purine restricted diet. (less than 15% of gout patients.) Others could be with HGPRTase deficiency (Lesch Nyhan Syndrome)
What is the basis of hyperurecemia for 75-90% of individuals with primary gout?
Diminished renal clearance of uric acid. It is also an important cause for secondary hyperuricemia.
What is the pathogenesis of acute gouty arthritis?
Shedding of urate crystals (microtophi) in the synovial fluid from articular cartilage or precipitation of new crystals. Can occur from sudden increase in urate concentration, or from mechanical stresses. However, remember that urate crystals are ALWAYS present in synovial fluid of gouty arthritis.
What is the onset of a gouty attack? Who does it affect?
40-60 y/o Male, in the middle of the night. Even untreated, the attack is self-limiting, lasts 3-7 days, and then the patient is asymptomatic. Attacks can get progressively worse until the patient gets persistent gout.
What tests can you do to diagnose chronic gout?
Synovial aspiration will show PMNs and bright yellow needle shaped crystals on a dark background on polarizing microscopy. Radiographic features are cortical indentations or erosions with sharply defined sclerotic margins due to tophi in adjacent soft tissues.
What are the renal complications of hyperuricemia?
Urate nephropathy: prteinuria, loss of urine concentration ability, HTN, azotemia, due to crystals in the interstitium of the kidney. Acute hyperuricemic nephropathy is characterized by oliguria and renal failure due to crystal's tubular destruction. Teat with hydration and allopurinol. Urolithiasis: stones are a mix of uric acid and calcium oxalate, correlates with the amt of uric acid excreted in urine.
How is asymptomatic hyperuricemia managed?
No treatment because it doesn't affect renal function, and a uric acid lowering agent requires lifelong therapy(expensive, SE)
How is acute gouty arthritis treated?
Colchicine, NSAIDs, corticosteroids. Colchicine can be used for low dose prophlaxis. Do not use allopurinol because it can precipitate another acute attack!
How is chronic gouty arthritis treated?
Only after an acute attack has resolved, you can give allopurinol (xanthine oxidase inhibitor). Keep the dose low in the presence of renal failure, and allopurinol reduces metabolism of Warfarin, 6-mercaptopurine, and azathioprine, so it could lead to toxicity of those drugs. SE of allopurinol are nausea, diarrhea, drug fever, hepatotoxicity, vasculitis, nephritis, rash. Esp bad in those with renal insufficiency
When can uricosuric agents be used for patients with chronic gout?
When they have normal renal function and hyperuricemia that excretes less than 700 mg of uric acid/day. Probenecid SE are headache, nausea, anorexia, skin rash, nephrotic syndrome, hepatic necrosis, aplastic anemia. Sulfinpyrazone can cause BM suppression. An acute attack prophylaxis must still be used after the uric acid levels have gone down.
Which joint is affected first in gout?
First MTP joint (base of big toe)
Which joint is affected first in pseudogout?
knees
What is the difference b/w gout and pseudogout?
pseudogout has calcium-pyrophosphate crystals, and has a more subacute onset. Also affects knees first, whereas gout affects big toe first.
What diseases are associated with pseudogout(CPPD)?
Hyperparathyroidism(elevated Ca levels,) low PO4, low Mg, familial hypocalciuric hypercalcemia, hemochromatosis, hypothyroidism. OA can also facilitate crystal deposition in pseudogout.
How is pseudogout definitively diagnosed?
aspiratino f synovial fluid which will show positively birefringent calcium pyrophosphate crystals in the leukocytes. Should also be cultured for infectious agents.
In the work up for gout or pseudogout, why should you do a culture?
Because it could be a septic joint.
How are pseudogout attacks treated?
Colchicine, NSAIDs, corticosteroids, just like acute gouty arthritis. Make sure you rule out septic joint first!
How is gout pain different from OA pain?
Gout pain-due to inactivity, morning stiffness over 30 minutes. OA pain due to activity, morning stiffness less than 30 minutes.