Osteo arthritis Flashcards
What is the MC joint disease, and leading cause of disability in the US
Osteoarthritis aka DJD
A disease of cartilage with progressive destruction of articular cartilage
OA involves
the entire diarthrodial joint;
articular cartilage, synovium, capsule, and sunchondral bone; surrounding muscles, and ligaments
What happens in OA
Chondrocyte fails to maintain proper balance between cartilage formation and destruction= Loss of cartilage in the joint, local inflammation, pathologic changes to underlying bone, and further damage to cartilage triggered by affected bone
S/Sx of OA are
joint pain (*MC) and tenderness (worse w/ activity) decreased ROM weakness joint instability disability NO soft tissue swelling crepitus
OA typically involves
hips knees spine IP joints CMC joints
Confirmatory radiograph findings for OA (x-ray) are
Decreased joint space
Subchondral sclerosis
Subchondral cysts
Osteophytes (bone spurs)
What nodes are associated with OA
Herbeden’s nodes: DIP joints
Bouchard: PIP
What are the types of OA
Primary: MC, idiopathic
Secondary: 2/2 RA, inflammatory arthritis, trauma, metabolic or endocrine disorder, congenital factors
Non-pharm therapy for OA includes
Exercise (ROM and surrounding muscle strength) Weight loss (esp if weight bearing joints involved)
Pharm Tx for OA includes
Simple analgesics: APAP, tramadol, duloxetine, +/- narcotics
NSAIDS: non-selective if low risk for GI complications. if at risk, may ad PPO or H2 antagonist, OR, give COX specific NSAID
Ancillary and surgical Tx for OA includes
Splints Canes or other orthotics Corticosteroid injections Hyaluronic acid injections arthroscopic surgery osteotomy total joint replacement
What does pain in OA come from
activation of nociceptive nerve endings w/in a joint, by mechanical or chemical irritants; distention of synovial capsule
Pain is not related to the destruction of cartilage!
What can cause distention of the synovial joint capsule
increased joint fluid
microfracture
periosteal irritation
damage to ligaments, synovium, or meniscus
In the arachadonic acid cascade, where do certain analgesics work
NSAID, ASA: inhibit cyclooxygenase
Corticosteroids: inhibit phospholipase= stop the cascade
What treatment is generally expected for pain relief in knee and hip OA
APAP (up to 4g daily in divided doses)
BUT, must monitor well because of Tylenol’s effect on the liver
If this fails, try a topical or oral NSAID
What is the normal way the renal system works
Increases renin-angiotensin axis & Increased SNS activity
=renal vasoconstriction
=compensatory vasodilation (renal PG)
=normalized renal function
How do NSAIDs affect the kidneys
They block prostaglandins necessary in compensatory vasodilation, so you maintain renal vasoconstriction
This eventually leads to reduced renal function
ADE of NASIDs include
CNS: HA, tinnitus CV: HTN, edema, fluid retention, +/- CHF GI: abd pain, n/v, +/- ulcers Heme: thrombocytopenia Hepatic: abn LFT Pulm: asthma Skin: rash, pruritis Renal: insufficiency and failure
When taking NSAIDs, you should monitor
CBC
SrCr
Hepatic transaminase levels
How can you reduce GI toxicity when taking NSAIDs
Use nonacetylated salicylates (choline magnesium, pepto bismol)?
COX-2 selective inhibitors
add Misoprostol or a PPI
If you use ASA concomitantly, it defeats the purpose of the GI protective effort
How can you reduce GI toxicity when taking NSAIDs
Use nonacetylated salicylates (magnesium trisalicylate, pepto bismol)?
COX-2 selective inhibitors
add Misoprostol or a PPI
If you use ASA concomitantly, it defeats the purpose of the GI protective effort
Who are topical NSAIDs recommended for?
Patients >75 y/o, to decrease the risks of systemic toxicity
MC: Ketoprofen
Other options in treating OA are
Tramadol
Intraarticular injections of corticosteroids
Duloxetine (cymbalta- Tx nerve pain and depression)
