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77 Cards in this Set
- Front
- Back
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What drug inhibits the formation of LTs by inhibiting 5-lipoxygenase? |
Zileuton |
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What drug acts by blocking LT receptors? |
Zafirlukast |
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What drugs have the most potent anti-inflammatory properties?
Why? |
Corticosteroids
Block phospholipase A2 production of AA, thus you can't make LTs or PGs (COX & 5-lipo pathways) |
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(COX-1/COX-2) is involved in the inflammatory response |
COX-2
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(COX-1/COX-2) is the homeostasis "housekeeper" & helps maintain vascular permeability, glomerular perfusion, & has cytoprotective GI functions |
COX-1 |
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TXA2 & ______ have opposite effects & are normally present in equal amounts during homeostasis (part of COX-1 path)
What does each do? |
TXA2 & PGI2 (prostacylin)
TXA2- vasoconstriction & platelet aggregation
PGI2- vasodilation & inhibition of aggregation |
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How do NSAIDs serve as an analgesia? (MOA) |
block COX production of PGs--> inhibit PGs from lowering pain threshold & inc pain sensitivity--> inc pain threshold & reduced nociceptor sensitization |
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How do NSAIDs serve as an antipyretic (anti-fever)? (MOA) |
block COX production of PGs--> inhibit PG in hypothalmus from altering thermostat & causing fever--> reset hypothalamic thermostat--> reduce fever |
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How do NSAIDs serve as an anti-inflammatory? (MOA) |
Directly Block COX-2 (inflammatory pathway): inhibit PG production inhibit inflammatory cascade & chemotaxis reduce edema stabilize lysosomal enzymes |
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4 Clinical signs of inflammation: |
1. Erythema (vasodilation--> redness & heat) 2. Edema (exudation of fluid) 3. Tenderness (hyperalgesia) 4. Pain |
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3 Phases of the Inflammatory Response: |
1. Acute transient phase= local vasodilation & inc. capillary premeability 2. Delayed, subacute phase= chemotaxis & phagocytosis 3. Chronic proliferative phase= degneration & fibrosis |
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In the chronic proliferative phase of inflammation, tissue degeneration and fibrosis occurs why? |
Because of the lysosomal and proteosomal enzymes |
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T/F
NSAIDS & aspirin inhibit COX-2 & COX-1 |
TRUE
(only COX-2 inhibitors are specific for COX-2) |
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List the COX inhibitors (NSAIDs) by increasing affinity for COX-2 affinity. |
Indomethacin |
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T/F |
False! |
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Low dose aspirin is indicated for....(clinical uses) |
-coronary artery disease -deep vein thrombosis -unstable angina -myocardial infarction & stroke
**anti-platelet effects |
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Why is aspirin NOT used for fever, inflammation, pain, like other NSAIDs? |
requires very high doses & causes the WORST GI distress (of all NSAIDs) |
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What effect does low & high doses of aspirin have on uric acid secretion at the proximal tubule? |
low dose (81 mg): uric acid secretion decreased
high dose (300 mg): uric acid secretion increased |
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What will happen in a patient w hyperuricemia & gout if they take low dose aspirin? |
gouty attack!!
aspirin precipitates hyperuricemia
(high dose is NOT effective in reducing hyperuricemia either*)
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In what patients is aspirin (acetylsalicylic acid) contraindicated? |
COPD/asthma (bronchoconst d/t increased LTs) |
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Aspirin is contraindicated in children w/ viral infections because it can cause ___________ |
Reye's syndrome = liver dysfunction & encephalopathy--> fatal |
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Aspirin: toxicity/SE |
GI distress/bleed hypersensitivity Bronchoconstriction (due to unopposed LTs) Renal dysfunction (PG inhibition= dec perfusion)
overdose= Salcicylism= tinnitus (ringing) & vertigo |
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Q: 24 yr old experiencing headaches, has been taking inc. doses of aspiring. One night after taking a large dose, he becomes confused & seizures. Pt presents to ER w/ serum salicylate level of 130 mg/dL. What should be administered? |
A: Bicarbonate
normal serum salicylate= 30-40 mg/dL 130 mg/dL = aspirin overdose aspirin is a weak acid, need a base = bicarbonate to ionize aspirin & enhance excretion |
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What is the DOC for anti-pyresis in children? |
Acetaminophen (paracetamol) |
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Which NSAID is indicated for anti-pyresis & analgesis ONLY?
(NO anti-inflammatory effects) |
Acetominophen |
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T/F |
True!
(no significant GI side effects) |
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Q: 20 yr old women ingest 100 acetaminphen tablets (500 mg each) in a suicide attempt. She seams healthy until 2 days later she develops massive hepatic failure. What is the primary mechanism responsible for failure? |
A: depletion of intracellular reduced glutathione
*normally very high levels, takes a long time to burn through all of it (& symptoms to develop), toxic metabolites accumulate in addition to breakdown causing liver failure |
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How are NSAIDs used in RA? |
As an adjunct only, never 1st line. They do NOT reduce progression of joint disease in RA. ONLY tx symptoms |
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Which NSAIDs are used for the symptomatic tx of gout, RA, arthritis & osteoarthritis? |
Ibuprofin Naproxen |
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Which NSAID is an effective analgesic for OA & musculoskeletal sprains by providing BOTH central & peripheral pain relief? |
Diflusinal |
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This analgesic drug is 4x more potent than Aspirin, but it has LESS efficacy. What is it? |
Diflusinal
(also has similar anti-platelet effects at low dose) |
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What drug would you give to someone who needs a chronic NSAID, but has underlying GI distress? |
Celecoxib |
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___________ is the ONLY (specific) COX-2 inhibitor on the market |
Celecoxib |
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Celecoxib is contraindicated in ANY underlying _________ pathology. |
Cardiac |
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How does chronic use of NSAIDs relate to HTN?
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Causes Na+ retention, so it may decrease the efficacy of anti-HTN diuretics.
*especially in Geriatric pts |
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Why are patients with renal dysfx susceptible to nephrotoxicity with NSAIDs?
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Because decreased PG synthesis leads to decreased renal perfusion
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What is the ONLY NSAID that can be used in patients w/ renal dysfunction? |
Sulindac |
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Sulindac is indicated in what? |
Acute AND long-term tx of: |
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Which drug is known for its 2 active components with an extended duration of action (up to 24 hours)? |
Sulindac |
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What NSAID is an alternate to opiods (narcotics) in post-op analgesia? |
Ketorolac
(almost equipotent to opiods in post-op analgesic) |
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Ketorolac should never be taken more than 5 days. Why? |
Can cause severe GI bleeding!
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List strongest to weakest Analgesic effects: naproxen aspirin ketorolac ibuprofen |
Ketorolac > Naproxen > Ibuprofen > Aspirin |
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Half-lifes of which NSAIDs allow for once daily dosing?
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Naproxen (14 hrs) |
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What NSAID is indicated for closure of the PDA? |
Indomethacin
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Indomethacin is highly indicated in what instances?
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RA |
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Indomethacin has prominent __________, ____________ and __________ activity. |
Anti-inflammatory, anti-pyretic, and analgesic |
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T/F
With indomethacin, you need high doses daily. |
False! |
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Piroxicam and Meloxicam have good affinity for (COX-1/COX-2) & are indicated in what? |
COX-2
Long-term tx of: |
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Which drug is known for concentrating in the synovial fluid? |
Diclofenac |
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Dicolfenac is highly selective for COX-2 & may be used long-term in......
or short term in..... |
long term: OA ankylosing spondylitis
short term: musculoskeletal pain post-op pain
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General NSAID side effects |
GI dysfunction Cardiovascularm(COX-2 inhib) Acute renal failure Hypersensitivity (due to inc LTs) Drug interactions (highly bound, anticoagulatns, phenytoin,sulfonamide, sulfonylureas) |
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What is the 1st line prevention of NSAID-induced GI injury? |
Use a COX-2 specific inhibitor! (Celecoxib) |
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What is the #1 drug to co-administor if there is already NSAID-induced GI injury and you want to promote healing? |
Proton Pump Inhibitor |
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What other drugs can be administered as co-therapy to prevent GI injury? |
misoprostol (may cause abortion) or H2 receptor antagonist |
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To prevent NSAID-induced GI injury, avoid concomitant use of what drug(s)? |
Anticoagulate or corticosteroid use |
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Why are NSAIDs contraindicated in pregnancy? |
esp in the 3rd trimester d/t risk of post-partum hemorrhage and delayed labor (PGs are necessary for labor!) |
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Gout or hyperuricemia is caused by accumulation of uric acid due to under-excretion or excess ___________ synthesis |
Purine synthesis
(if pts uric acid levels > 600 after 5 day abstain from purine in diet= overproduction of purine) |
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How does uric acid deposition lead to a "gouty attack"? |
uric acid crystal deposit--> neutrophils accumulate & phagotyze crystals--> LT are released--> lysosome rupture & phagocyte death--> hydrolytic enzymes released--> acute inflammation= local heat & pain |
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What is it called when gout begins to destroy the joint? |
Topheous
(extreme swelling of joint, esp toes) |
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What is the 1st line tx of an acute gouty attack? |
Immobilize! |
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What are the initial DOC's in an acute gout attack? |
NSAIDs: Indomethacin or Ibuprofen
(dose 2x day & continue until symptoms disappear, usually 24 hrs for inflam. to go down) |
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What drugs may also be considered in an acute gout attack (not 1st line)? |
Naproxen or Diclofenac |
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Which drug for gouty attack should you only use if the patient is non-responsive to NSAIDs? |
Colchicine |
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What drug inhibits mitotic spindles? |
Colchicine |
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What are the side effects of colchicine? |
It causes severe diarrhea, vomiting, and nausea. Should be avoided, and if you use it, you should only give one dose (1mg)! |
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What drug is used to decrease plasma uric acid (NOT in an acute gout attack) or as prophylaxis prior to a vacation? |
Allopurinol
(Do NOT give in attack bc it will cause uric acid to reform in another place) |
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What drug competitively inhibits xanthine oxidase? |
Allopurinol |
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Allopurinol is contraindicated in patients who are taking ________________ |
6-mercaptopurine (cancer drug)
*allopurinol inhibits 6-mercaptopurine metabolism via xanthine inhibition--> toxicity |
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Allopurinol is given prophylactically in _________ to prevent high levels of uric acid--> renal failure (tumor lysis syndrome) |
in pediatric patients before starting chemo/radiation therapy |
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T/F |
True!
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For which drug did Dr. Krishna say you should "go low, go slow" and why? |
Probenicid |
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What drug blocks proximal tubular reabsorption of uric acid?
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Probenicid |
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What drug is used to increase uric acid excretion?
(used if hyperuricemia due to under excretion) |
Probenicid |
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What drugs should be used in patients who are unresponsive to both NSAIDs and colchicine, or in patients with polyarticular involvement? |
Corticosteroids
(3rd choice bc they work much slower than colchicine) |
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Hyperuricemia/gout may be precipitated by what type of drugs? |
Diuretics (loop)
(* also precipitated by excessive alcohol) |
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In addition to appropriate diet modification & drug therapy, gout patients should ALWAYS ____________ to prevent nephrolithiasis |
maintain adequate hydration & fluid intake |
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Q: 50 yr obese male comes to ER complaining of severe pain in toe. Pain began 5 hrs after dinner of steak & beer. Serum normal except for elevated uric acid level. Aspiration of toe reveals negatively birefringent crystals. Pt is allergic to NSAIDs. What is the appropriate tx? |
A: Colchicine (single 1 mg dose) |
