DJD, Gout & Pseudogout Flashcards
A type of inflammatory arthritis that is caused by uric acid crystal deposition in the joints?
Gout; can be monoarticular or pauci-articular.
Prevalence of Gout?
- 3% of men and 0.6% of women.
- -Postmenopausal women.
- -Peak onset in 4th decade of life.
- -More frequent in AA men than Caucasians.
Pathophysiology of Gout?
High uric acid levels due to overproduction or under-excretion – crystallization occurs (esp. distal joints) – incites a violent immune response w/a large amount of inflammatory cells and cytokines.
- *Prolonged or frequent events can lead to bony erosions.
- *Prolonged attacks or hyperuricemia can also lead to deposits of crystals called “Tophi.”
What are Tophi?
Deposits of crystals in the joints, usually caused by Hyperuricemia.
Predisposing conditions to Gout?
Renal insufficiency or renal transplant, High purine diet, Psoriasis (high cell turnover), Medications (HCTZ, Cyclosporine, ASA).
Some of the things pt’s say to describe a gout flare/attack?
“I woke up, and my foot was twice its size.”
“I thought I must have sprained it.”
“I can’t stand to have a sheet touch it.”
“I’ve got the gouch.”
“It went away from that foot but then spread to this knee.”
History provided by a pt about a typical flare…
- Affects one (80%) or two joints.
- Very swollen, red, hot to the touch.
- can affect the tendons.
- Whole hand or whole foot can be affected.
- Extremely painful.
- May be unable to ambulate.
- Lasts a week +/-, then goes away.
Gold Standard diagnosis of Gout?
Crystals in joint fluid and biopsy of tophus.
Other diagnostics for Gout?
**Typical history is suggestive.
- Uric Acid Levels:
- -During flare…can be low or normal.
- -High Uric Acid levels do not actually = gout; only 1 in 4 w/hyperuricemia will get gout.
- -Monitor uric acid level to assess response to treatment.
What is Podagra?
Gout of the foot, esp. the big toe.
What is Tophaceous Gout?
A chronic form of gout; Nodular masses of uric acid crystals (tophi) are deposited into different soft tissue areas of the body.
Laboratory findings in Gout?
- Elevated ESR/CRP.
- Fluid analysis = elevated WBCs (thousands).
- Urate crystals – needle-shaped.
- Uric acid not helpful “acutely.”
Treatment GOAL in Acute Gout?
Reduce inflammation and pain.
Treatment GOAL in Chronic Gout?
Reduce uric acid level.
Treatment of ACUTE Gout?
- Steroid injection – if one joint involved.
- NSAIDs.
- Systemic Steroids.
- Colchicine.
- NO Allopurinol initiation!!
- -It worsens acute gout.
- -But, continue it if the pt is already taking it.
Treatment of ACUTE Gout?
- Steroid injection – if one joint involved.
- NSAIDs.
- Systemic Steroids.
- Colchicine.
- NO Allopurinol initiation!!
- -It worsens acute gout.
- -But, continue it if the pt is already taking it.
Treatment of Chronic Gout?
“Does the patient need urate lowering therapy?”
YES if….
- -Frequent flares (2-4/yr).
- -Tophi.
- -Radiographic erosions from gout.
- -Urate kidney stones.
What is the 1st line treatment for Chronic prophylactic therapy?
Allopurinol = blocks formation of uric acid.
- added when gout is quiet.
- titrated slowly.
- uric acid level monitored to determine response to treatment.
- add Colchicine for 1st 4-6 months of treatment (blocks white cell immune response).
Other medications used as Prophylactic therapy in Gout?
- Probenecid = enhances urinary excretion, but have to drink 2 L H2O daily, no ASA.
- Febuxostat (Uloric).
- Peglitocase (Krystexxa) infusion.
What is considered the therapeutic level of uric acid?
<6, but if Tophi present, then <5.
> 90% of gout cases are primary or secondary?
Primary = overproduction or under-excretion of uric acid.
Secondary causes of gout?
- Myeloproliferative diseases or their treatment.
- Meds producing hyperuricemia.
- Renal failure or renal tubular disorders.
- Lead poisoning.
- Hyperproliferative skin disorders.
- Enzymatic defects.
Form of arthritis that is caused by deposition of Calcium Pyrophosphate Dihydrate (CPPD) crystals in and around joints, articular cartilage, fibrocartilage?
Pseudogout; mimics gout symptoms.
What causes Pseudogout?
Deposition of calcium pyrophosphate dihydrate crystals.
Pathophysiology of Pseudogout?
Build up of CPP.
It is associated with OA, older age, hemochromatosis, acromegaly, hypothyroidism, hypomagnesemia, hyperparathyroidism.
Diagnosis of Pseudogout?
- Arthrocentesis.
* XRs.
Treatment of Pseudogout?
- NSAIDs.
- Corticosteroids (Injection or oral).
- Colchicine.
- Correct other diseases.
What is the most common type of arthritis? What is it?
Osteoarthritis (OA)/DJD - degeneration of bone and cartilage that often starts after age 40; usually non-inflammatory (unless erosive).
What is OA also known as?
aka: Degenerative Arthritis, degenerative joint disease, “wear and tear” arthritis.
What are the clinical features of OA?
- Pain worse w/activity and better w/rest.
- Morning stiffness <30 minutes.
- Gelling Phenomenon.
- Joint enlargement, swelling and instability.
- Crepitation.
- Limited ROM.
- Periarticular muscle atrophy.
What are the common joints affected by OA?
- DIP and CMC (carpometacarpal) joints, most common.
* PIP joints, weight bearing joints (hips, knees), vertebral joints, 1st MTP bunion.
Cornerstone treatment of OA?
- NSAIDs – but many potential side effects:
- -GI ulcers/bleeding.
- -BP elevations.
- -Fluid retention.
- -Creatinine changes.
- -heart disease.
- -CI w/blood thinners.
Non-Pharm treatment of OA?
Muscle strengthening, water exercise, joint protection, bracing/splinting, glucosamine/chondroitin (debatable efficacy).
Indications for joint replacement from OA?
Indications:
- night pain unrelieved by NSAIDs.
- major limitations in ADLs.
- major limitations in ambulation.
Osteoarthritis risk factors?
Family history, age, obesity, female, joint deformity, Hx of trauma/surgery, Hx of excessive use (sports, career).
Pathophysiology of OA?
**Diseased cartilage and not just “old age.”
-Disruption of degradation and synthesis balance – degrading enzymes are over expressed – fibrillation, erosion and cracking appear – chondrocytes are unable to keep up repair.
What happens in a normal joint?
Healthy cartilage, lubricated by synovial fluid, cushions the bones and allows them to move easily.
What happens in the diseased joints of OA?
Gaps in the cartilage can expand until they reach the bone itself – synovial fluid leaks into cracks, which can form in the bone’s surface when this replacement cartilage wears away. This causes further damage and in some cases can lead to cysts in the bone or other deformities.
What are some common joint enlargements or deformities in OA?
Bouchard’s and Heberden’s nodes, Hallux valgus and other deformities.
Diagnosis of OA?
- XR – 4 tenets:
* *joint space narrowing.
* *subchondral sclerosis (hardening of the bone just below the cartilage surface).
* *subchondral cysts (fluid-filled space inside a joint).
* *Osteophyte formation.
Other pharmacologic treatment of OA?
- Acetaminophen – can be taken in addition to NSAIDs.
- Narcotics – dependence issues; reserved for those who can’t take NSAIDs/Tylenol.
- Glucosamine/Chondroitin.
Mixed with anesthetics and no more than 3 per year in a joint?
Corticosteroid injections.
What will happen if you hit bone when placing a corticosteroid injection?
It will hurt; periosteum has nerve endings. Pull back and reposition.
