Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
23 Cards in this Set
- Front
- Back
|
What occurs to the joints in osteoarthritis? |
The cartilage wears away and we get bone rubbing on bone |
|
|
What occurs in rheumatoid arthritis? |
The synovial membrane becomes very inflamed and we start bone erosion |
|
|
What causes rheumatoid arthritis? |
Inflammation is generally good, because it clears out an infection In RA we get a imbalance of pro-inflammatory cytokines and autoimmunity |
|
|
What is the chief transcription factor in inflammation? |
NF-kB |
|
|
NSAIDs can stop inflammation but what do they not do? |
Prevent the progress of injury (just covering up problem) |
|
|
In addition to preventing inflammation what do NSAIDs control? |
Pain (because eicosanoids are known to stimulate peripheral sensory neurons) Fever |
|
|
What is the primary site of action for NSAIDs? |
Cyclooxygenase |
|
|
How does the effect of ASA change with dose and how do the pharmacokinetics change? |
At low doses (300mg-1g) ASA will primarily suppress pain - At this dose it does not saturate the metabolic enzyme and therefore obeys first order kinetics (rate increases with dose) At High doses (4-6g/day) ASA will primarily suppress inflammation - At this dose the metabolic enzyme is saturated and it will only obey zero order kinetics and has a long half-life (12 hours) |
|
|
What is the effect of ASA on the gut? |
It can reduce PG activity here which has a protective effect and the salicylate can accumulate in the mucosa |
|
|
What is the purpose of enteric coated ASA? |
ASA dissolves in the stomach and is said to increase gastric ulcers because of inhibiting PG activity Enteric ASA is supposed to not dissolve until later in the tract although this just means its effects will be noticed there |
|
|
Why is ASA sometimes administered with misoprostol? |
Misoprostol is a PGE1 analog and therefore it may provide some gastric protection when taking ASA (although it can also produce systemic side effects) |
|
|
What is dangerous about ASA for asthmatics? |
It increases leukotriene activity which can cause bronchoconstriction and inflammation in the airways |
|
|
What are other alternatives to ASA? |
Indomethacin (RA treatment), naproxen and ibuprofen |
|
|
What are common symptoms of steroids (glucocorticoids)? |
Weight gain, moon face, buffalo hump, increased hair, acne, and thin extremities |
|
|
What is a first line DMARD? What is its mechanism |
Methotrexate, it is an anti-folate that therefore reduces purine synthesis and pro-inflammatory cytokines |
|
|
What is Etanercept? |
It is a novel biologic that inhibits TNF-a It is a recombinant protein that can bind two molecules of TNF-a |
|
|
What is a common side effect of a TNF-a inhibitor? |
Increases risk of infection
|
|
|
What is Rituximab? When is it used? |
It is an antibody against CD20 on B-cells and by binding kills the B-cells. It is only used if Etanercept is not successful |
|
|
What is Tofactinib? |
It is an inhibitor of JAK3 that is responsible for transcription of many cytokines (interleukins) It is either used with MTX or if MTX doesn't work |
|
|
What is the cause of Gout? What is the treatment goal? |
It is caused by buildup of uric acid crystals in the joints. The goal of treatment therefore is to increase excretion of uric acid or reduce production |
|
|
What is responsible for producing uric acid in the body? |
Hypoxanthine is converted by xanthine oxidase into xanthine and then once more into uric acid |
|
|
What is a treatment for reducing biosynthesis of uric acid? |
Treat with oxypurinol (also called alloxanthine) can inhibit xanthine oxidase Also has a very long half life of one full day |
|
|
What are the roles of Probenecid and Sulfinpyrazone? |
They are both used to increase the excretion of gout by reducing its proximal tubule reabsorption (therefore increase its tubule excretion) |
