Arthritis

Published on 16/06/2015 by admin

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CHAPTER 21 Arthritis

I. Osteoarthritis

1. Osteoarthritis (OA), also called degenerative joint disease, is marked by the breakdown of cartilage that lines the ends of most limb bones. This type of cartilage is known as articular cartilage, and it serves to cushion the bones and allow painless joint movement. Because OA affects the articular cartilage, patients with OA experience pain and reduced mobility in their joints. OA may affect any joint in the body, but it occurs most often in fingers, spine, and weight-bearing joints. Individuals with OA often experience inflammation around the affected joint, which is caused by bits of cartilage that break off and aggravate the synovial tissue lining the joints.

2. Besides cartilage loss, OA is characterized by irregular thickening and remodeling of bone. The synovial tissue may bulge out of joints to form cysts (commonly known as Baker cysts), or become hardened with fibrous tissue overgrowth (a condition known as sclerosis). Bony protrusions, called bone spurs or osteophytes, may also form. These pathological changes result in increased blood flow and joint inflammation.

C. Signs and symptoms

1. OA may affect any joint in the body; however, because it develops slowly, many patients do not experience symptoms right away. The pain and inflammation in OA is typically less severe and more localized than that of rheumatoid arthritis (RA), another form of arthritis that is more systemic.

2. Common symptoms of OA

a. Joint pain (arthralgia)

b. Swelling and/or stiffness in a joint (especially after not moving for a while); stiffness in morning lasts < 30 minutes.

c. Joint discomfort before or during a change in the weather (such as conditions of low pressure and high humidity)

d. Bony lumps on the fingers

e. Loss of joint flexibility

3. When individuals have OA, the cells that form cartilage (called chondrocytes) cannot efficiently repair the damaged cartilage. Thus, OA represents a failure of the chondrocyte to maintain proper balance between cartilage formation and destruction. Instead, new bone grows alongside the existing bone, causing small lumps to form. Although these lumps cause minimal pain, they may be disfiguring and limit the joint’s mobility.

2. Pharmacologic

a. Acetaminophen (Tylenol): The American College of Rheumatology has recommended acetaminophen as first-line therapy for osteoarthritis of the hip or knee.

(1) Dose, maximum 4 g/day

(2) Adverse effects: Hepatotoxicity may occur.

b. Nonsteroidal anti-inflammatory drugs (NSAID)

(1) Mechanism of action

(a) Decrease production of prostaglandins

(i) Nonselective inhibitors of cyclooxygenase (COX)-1 and COX-2

(b) Increase vascular permeability and sensitivity to the release of bradykinins

(c) Inhibits formation of prostacyclin and thromboxane, resulting in reduced platelet aggregation

(2) May be used if patients fail to respond to acetaminophen

(3) Adverse effects

(a) Abdominal pain

(b) Gastrointestinal (GI) bleeding

(d) Hypersensitivity reactions

(e) Renal or hepatic impairment

(f) Impaired bone marrow function

(g) Platelet aggregation

(4) Primarily metabolized in liver by cytochrome P-450 (CYP) 2C9 and excreted in urine

(a) Indomethacin, sulindac, and piroxicam undergo enterohepatic circulation resulting in a prolonged half-life (avoid in the elderly)

(5) Contraindications

(a) Active peptic ulcer disease

(b) Renal disease

(c) Heart failure

(6) NSAID examples

(a) Salicylates (aspirin)

(b) Propionic acids (ibuprofen [Motrin], naproxen [Aleve, Naprosyn], oxaprozin [Daypro], ketoprofen [Orudis])

(c) Acetic acids (diclofenac [Voltaren], etodolac [Lodine], indomethacin [Indocin])

(i) Diclofenac is available for topical use.

(d) Oxicams (piroxicam [Feldene])

(e) COX-2 inhibitors (celecoxib [Celebrex])

(i) Mechanism of action: inhibits COX-2, thereby impairing the transformation of arachidonic acid to prostaglandins, prostacyclin, and thromboxanes

(ii) Rofecoxib (Vioxx) and valdecoxib (Bextra) were removed from marketing due to safety concerns.

(iii) Adverse effects: similar adverse event profile to other NSAID; linked to an increased risk of serious heart-related side effects, including heart attack and stroke. Selective COX-2 inhibitors have also been shown to increase the risk of stomach bleeding, fluid retention, kidney problems, and liver damage.

c. Glucocorticoids

(1) Systemic glucocorticoids are not used for osteoarthritis

(2) Intraarticular injections may be used in patients who do not respond to NSAID or for whom NSAID are contraindicated.

(a) Examples: triamcinolone acetonide, triamcinolone hexacetonide, methylprednisolone

d. Hyaluronic acids

(1) Used for osteoarthritis of the knee in patients who do not respond to NSAID therapy or who have a history of gastric ulcer disease

(2) Examples: sodium hyaluronate (Hyalgan, Supartz, Nuflexxa), hylan G-F 20 (Synvisc)

e. Other analgesics

(1) Tramadol (Ultram): 50–100 mg can be administered as needed for pain relief every 4–6 hours, not to exceed 400 mg/day (immediate release)

(a) Mechanism of action: centrally acting synthetic analgesic

(b) Adverse effects: risk of seizure

(2) Opioids, such as codeine, oxycodone, or propoxyphene may be used short term in patients with acute pain exacerbations.

f. Topical pain relievers

Used for localized pain control at a specific joint. Topical NSAID generally considered more effective than topical capsaicin.

(1) Capsaicin 0.025% cream

(2) Trolamine salicylate (e.g., Aspercreme, Sportscreme, Icy Hot, Ben-Gay)

(3) Methylsalicylate (e.g., Exocaine and Gordogesic)

(4) Topical NSAID: e.g., diclofenac (Voltaren Gel)

g. Alternative therapies

(1) Glucosamine/chondroitin combination is most studied, particularly in patients with OA of the knee; may help with pain relief.

(a) Patients should be taking at least 1.5 g of glucosamine daily. Significant pain benefit may not occur in all patients. Does not appear to limit progression of OA in the joint.

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