OA Flashcards
What is OA
Wear and tear of cartilage
Where does OA affect
Mainly weight bearing joints, lower spine, knees
What are the symptoms of OA
Morning stiffness lasts LESS than an hour
Joint ache not usually swelling
Restricted function
What are the risk factors of OA
Obese
Long term strain
Previous joint injury
What is the diagnosis of OA
Pain history and examination of joints
X-ray - joint space loss (more space lost worse pain and mobility)
What is lifestyle advice of OA
Weight loss
Exercise (swimming build up muscle)
Engage with supportive therapy’s (physio)
What is the treatment of OA
1st line paracetomol
2nd line NSAIDS
3rd line opioids
Physio, occupational therapy, splints, build up muscle
C/I and cautions of NSAIDS (ibuprofen and naproxen)
Don’t buy any OTC NSAIDS or aspirin
GI risk
CV risk
Renal risk
MXT
Warfarin
Paracetamol overdose
Paracetomol oxidised by CYP enzymes
- when therapeutic dose is taken, 10% of it is converted into NAPQI
- NAPQI is very reactive and unstable
- forms NAPQI it is TRPA1 stimulant
- if overdose of paracetamol then more NAPQI will be formed and this is toxic
-NAPQI is toxic as it reacts with the proteins in the liver and will eventually lead to liver damage
NSAID
Oral admin inhibits COX1 in the GI tract
COX1 acts upon arachidonic acid into producing thomboxord, leukotrienes, prostaglandins and prostacyclin which helps to maintain the integrity of the gastric mucosa. W/o this causes erosion over extended periods of time, which means the stomach acid irritates the GI tract causing pain and disturbances.
In the stomach the carboxylate form of the drug which is water soluble will be converted to the carboxylic acid form which is more lipophilic that can diffuse the gastric mucosa and gets further than it normally would. As the PH rises, if it gets towards the actual true lining of the GI tract it will lose an acidic proton which causes additional pain to the patient
