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;
22 Cards in this Set
- Front
- Back
|
Define inflammation
|
the bodies reaction to injury which serves to destroy, dilute or wall off both injurious agent and injured tissue -characterized by pain, redness, swelling and heat -involves many mediators (bradykinins, prostaglandins, etc) |
|
|
What role do prostaglandins play in pain pathophysiology?
|
they sensitize pain receptors by lowering the threshold of the polymodal nociceptors of C fibers -prostaglandin E2 also triggers the hypothalamus to elevate body temperature |
|
|
What is the MOA of NSAIDs?
|
inhibition of prostaglandin synthesis by inhibiting the enzyme cyclooxygenase (COX1 = constitutive, found in blood vessels, platelets, stomach, kidneys) (COX2 = inducible, in the setting of inflammation) |
|
|
Which NSAID causes irreversible inhibition of cyclooxygenase?
|
aspirin
|
|
|
Discuss the pharmacokinetics of NSAIDs.
|
absorption: well absorbed, use sustained release for chronic probs distribution: highly protein bound, readily diffuse into synovial fluid metabolism: mostly hepatic phase II (conjugation rxn); asa, nabumetone, sulindac and oxaprozin have active metabolites -nabumetone and sulindac are prodrugs elimination: urine, also via the bile; clearance reduced in elderly |
|
|
What are some therapeutic uses for NSAIDs?
|
PAIN: to moderate; acute and chronic FEVER ANTI-INFLAMMATORY: at higher doses Tylenol DOC for osteoarthritis ASA used for prophylaxis/tx of MI and stroke |
|
|
Name some adverse effects of all NSAIDs.
|
GI intolerance: dyspepsia (GI ulceration BBW) -d/t local irritation and inhibition of prostaglandin synthesis (given w/ other meds to decrease likelihood like PPIs) Prolonged bleeding time d/t blockade of platelet aggregation ARF, edema and others d/t prostaglandin role in renal blood flow: use w/caution in pts with CHF, cirrhosis, and elderly (less likely w/ nabumetone, sulindac, nonacetylated salicylates and Tylenol) Cardiovascular (BBW): increased BP, may precipitate CHF, MI, Stroke Hypersensitivity reactions: syndrome of bronchoconstriction, rhinitis and nasal polyps |
|
|
Name an adverse effect specific for salicylates.
|
salicylism: ha, dz, ringing ears, mental confusion, N/V |
|
|
Name an adverse effect specific for Tylenol.
|
can cause liver toxicity (but so can all of them. . . ) treat with N-acetylcysteine |
|
|
What is Reyes syndrome?
|
a severe disorder involving liver damage and coma associated with the use of ASA in children with viral infections
|
|
|
Toradol
|
intermediate DOA: half life 4-6hr used mainly as an analgesic - does have some anti-inflammatory properties available PO and IV/IM rapidly absorbed, oral bioavailability is 80% highly protein bound extensively metabolized with active and inactive metabolites **decrease dose for elderly, renal probs, or low weight** short term therapy only d/t increases GI ulceration and renal failure if longer |
|
|
Specific COX-2 Inhibitors
|
selective for inhibition of COX2 and cause less GI probs (but still have BBW) minimal effects on platelet aggregation use for people at increased risk for NSAID-induced ulcers (hx PUD, older, on anticoagulants, etoh, corticosteroids, smoking) |
|
|
What is the MOA of IV acetaminophen?
|
exact mechanism unknown inhibition of central prostaglandin synthesis and elevation of pain threshold |
|
|
What are the two types of corticosteroids produced by the adrenal glands?
|
glucocorticoids: cortisol; HPA axis for cortisol production - negative feedback system mineralocorticoids: aldosterone |
|
|
What is primary adrenal insufficiency?
|
"Addison's disease" defects in cortisol and aldosterone secretion |
|
|
What is secondary adrenal insufficiency?
|
defective cortisol secretion. . . induced by prior steroid intake
|
|
|
What are some physiologic and pharmacologic effects associated with glucocorticoids?
|
glucose, protein and lipid metabolism anti-inflammatory effects immunosuppressive effects also important for CV, renal, skeletal muscle, endocrine and nervous systems function |
|
|
Differentiate between different glucocorticoids.
|
short acting: cortisone, hydrocortisone intermediate: prednisone, triamcinolone long: dexamethasone -triamcinolone and dexamethasone have no sodium retaining potency -dexamethasone is the most potent anti-inflammatory |
|
|
List the adverse effects associated with withdrawal of glucocorticoid therapy.
|
-relapse of flare-up of underlying disease -acute adrenal insufficiency: ha, fever, joint pain, N/V, weight loss, hypotension; takes several weeks for HPA-axis to recover |
|
|
List the adverse effects associated with prolonged glucocorticoid therapy.
|
hypertension edema hyperglycemia glucose intolerance increased susceptibility to infection increased risk for peptic ulcers myopathy behavioral: nervous, insomnia, mood changes cataracts glaucoma osteoporosis vertebral compression fraxtures drug-induced Cushings syndrome delayed wound healing |
|
|
What side effects are seen with single doses of glucocorticoids?
|
single doses very rarely cause adverse effects tx with glucocorticoids greater than 1 week increases the risk for bad side effects |
|
|
Your patient is on a glucocorticoid and is now going to have surgery. What does this mean to you?
|
surgery is a very potent activator of the HPA axis goal is to prevent acute adrenal insufficiency crisis there is low, intermediate and high risk for pts on steroids that estimates HPA suppression glucocorticoids only need to be replaced in an amount equivalent to the normal physiologic response (endogenous cortisol secretion rarely exceeds 200mg in first 24h) minor surgery: 25mg of hydrocortisone, resume normal scedule moderate: 50-75mg for 1-2d major: 100-150mg for 2-3d |
