Term
What enzyme releases arachidonic acid from phospholipids stored in membranes?
What are the 2 paths that arachidonic acid can take (what enzymes)? |
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Definition
Phospholipase A2 (usually quiet until activated)
It can become leukotrienes by lipoxygenase
It can become Prostacyclin, Prostaglandins, or Thromboxane by cyclo-oxygenase 1 and 2 (COX2-inducible ) |
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Term
*What enzyme is the steroid drug target?
What blocks this enzyme? |
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Definition
phospholipase A2
corticosteroids |
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Term
| Where is arachidonic acid stored? |
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Definition
| component of the phospholipid bilayer of the cell membrane, primarily on the #2 carbon of glycerol backbone |
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Term
AA conversion to prostaglandins can be inhibited by ?
AA conversion to leukotrienes can be inhibited by ? |
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Definition
AA conversion to prostaglandins can be inhibited by NSAIDs (cyclooxygenase inhibitors-must block both COX1 and COX2)
AA conversion to leukotrienes can be inhibited by lipoxygenase inhibitors |
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Term
*What is the one drug that inhibits 5-lipoxygenase (stops at arachidonic acid) but increases prothrombin time with warfarin (anticoagulant)
Where does Montelukast, Pranlukast, and Zafirlukast block? |
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Definition
Zileuton
Inhibits LTA4, LTC4, and LTB4 from bind to their receptors |
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Term
| What is the main adverse effect with Zileuton (5-lipoxygenase inhibitor)? |
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Definition
| liver disease (also a lot of drug-drug interactions) |
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Term
| What leukotriene receptor antagonist drug is orally effective, once a day, and most commonly used. Adverse effects: occasional liver abnormalities |
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Definition
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Term
Which is true and which is false concerning nonsteroidal anti-inflammatory drugs:
Lacks addictive potential
Never sedation or respiratory depression
Analgesic properties at high doses and anti-inflammatory effects at low doses |
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Definition
Lacks addictive potential - T
Never sedation or respiratory depression - F (sedation/resp depression if overdose)
Analgesic properties at high doses and anti-inflammatory effects at low doses - F (Analgesic properties at low doses and anti-inflammatory effects at higher doses) |
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Term
When there is an injury (prostacyclin or thromboxane) predominates?
When the injury heals (prostacyclin or thromboxane) predominates?
What does PGE2 AND PGF2 protect and regulate?
What inhibits the production of these chemicals? |
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Definition
thromboxane
prostacyclin (need both)
protect stomach and regulate intraocular pressure
COX-inhibitor |
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Term
(COX1 or COX2) is in GI cytoprotection, platelet activity, and renal function (found almost everywhere).
(COX1 or COX2) is inducible for inflammation, pain, fever and constitutive for renal function. |
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Definition
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Term
| What chemical Enhances bicarbonate secretion (neutralize acid), Enhances renal blood flow, Enhances blood flow to mucosal surfaces (Promotes mucus secretion, Promotes epithelial growth)? |
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Definition
| PGE (when inhibited causes stomach ulcer and cardiovascular problems) |
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Term
Platelets have (COX1 or COX2).
What is big difference between aspirin and other NSAIDS in regards to platelets? |
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Definition
COX1
Aspirin has specific target for platelets (no nuclei) and IRREVERSIBLY inhibits COX (bc it acetylates the enzyme) while other NSAIDS are reversible, so platelet is dead forever. Important to be off aspirin before surgical procedure |
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Term
| Are COX-2 selective inhibitors less problematic than non-selective NSAIDS that inhibit both COX-1 and COX-2 when it comes to renal complications? |
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Definition
| No-COX-2 selective inhibitors are no less problematic than non-selective NSAIDS that inhibit both COX-1 and COX-2. |
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Term
When taking NSAIDS and aspirin, you (increase or inhibit) the effectiveness of thiazide, loop diuretics, and ACE inhibitors. Why?
Why is warfarin affected? |
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Definition
inhibit effectiveness because decreasing renal blood flow
Warfarin affected because inhibiting CYP450 metabolism
Also inhibits renal clearance |
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Term
Aspirin, sodium salicylate, salsalate, sulfasalazine, Indomethacin, sulindac, Tolmetin, diclofenac, ketorolac, Ibuprofen, flurbiprofen, ketoprofen, fenoprofen, oxaprozin, Naproxen, Piroxicam, meloxicam, Nabumetone
What type of drug are these?
How do they work? |
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Definition
NSAIDS
most of them are acids, so they look like arachidonic acid and will competively bind to COX to diminish formation of prostaglandins |
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Term
| *What is the only non-selective irreversible inhibitor of COX1 and 2 that reduces pain, body temperature, and very short half-life |
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Definition
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Term
At (low, medium, or high) dose of aspirin you get anti-inflammatory effect
At (low, medium, or high) dose of aspirin you analgesic, antipyretic effect
At (low, medium, or high) dose of aspiring you get decrease platelet aggregation |
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Definition
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Term
| Should you give a child aspirin or tylenol to reduce their fever during a viral infection? |
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Definition
| Tylenol- data shows Reye's syndrome (rapid liver degeneration & encephalopathy) |
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Term
What is the main ingredient in Advil and motrin?
Is it (reversible or irreversible) COX inhibitor? |
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Definition
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Term
| What is the main problem with ibuprofen? |
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Definition
| Acute renal failure and interstitial nephritis |
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Term
| What is the main ingredient in Aleve and is non-selective COX inhibitor? |
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Definition
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Term
What is given for postoperative inflammation of cataract surgeries?
What is given before to inhibit intraoperative miosis? |
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Definition
NSAIDS:
Diclofenac
Flurbiprofen |
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Term
| What are effective inhibitors of cyclo-oxygenase and prostaglandin induced inflammation |
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Definition
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Term
| What are some adverse effects of NSAIDS |
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Definition
gastropathy and ulcers
decreased GFR, renal insufficiency
renal sodium retention [HBP, CHF]
platelet inhibition
headache, cognitive dysfunction, tinnitus |
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Term
| What selective COX-2 inhibitor is still on the market (because the others were withdrawn due to thrombotic events) but is expensive and doesn't work well? |
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Definition
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Term
| How is acetaminophen different from aspirin/NSAIDS? |
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Definition
lack of potent anti-inflammatory and platelet inhibitory effects, weak inhibitor of cyclooxygenase in peripheral tissues
Good for fevers |
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Term
How is acetaminophen metabolized?
What is the most serious concern with large dose of acetaminophen?
What do you use to treat an overdose of acetaminophen? |
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Definition
In the liver by glucuronidation or glutathione conjugation
hepatic toxicity (liver failure)
acetylcysteine (like glutathione with a cysteine group) |
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Term
| What is the condition where you get recurrent episodes of acute arthritis because elevated blood and urinary uric acid level causes deposits of monosodium urate crystals in synovial fluid and tissues where macrophages can't get to? (Formation of uric acid stones in the kidney) |
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Definition
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Term
How can you treat gout?
What is the enzyme that breaks down uric acid? Do humans have it? |
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Definition
anti-inflammatory and anti-uric acid drug (xanthanide oxidase)
uricase- humans lack |
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Term
What increases excretion of uric acid by increasing renal excretion
What are 2 IMPORTANT drugs that do this, which is more potent, and when are they given? |
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Definition
Uricosurics
Probenecid and Sulfinpyrazone-more potent (given when uric acid levels are lower than normal in urine) |
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Term
| How does probenecid and sulfinpyarzone work in increasing uric acid output? |
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Definition
| Effects active transport sites in middle segment of proximal tubule responsible for reabsorption of uric acid |
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Term
| What drug inhibits xanthine oxidase, and is the drug of choice of treatment of chronic tophaceous gout especially in the presence of renal insufficiency? |
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Definition
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