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Flashcards in NSAIDs Deck (19)
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Why is the pathophysiology of prostaglandins important?

The most widely used drugs are those that inhibit the synthesis of prostaglandins. Prostaglandin inhibitors are pain, fever, and inflammatory inhibitors.


What benefit do drugs that inhibit cyclooxygenase 2 have on pain, fever, or inflammation?

Cyclooxigenase 1 and 2 are important inflammatory mediators that increase the synthesis of prostaglandins. Therefor, NSAIDs that are effective against pain, fever, and inflammation inhibit cycloxygenase 2.


What are some negative side effects of NSAIDs and why do they occur?

GI upset, bleeding problems, decreased renal function, labor interruptions. All of these are caused by inhibition of cyclooxygenase 1. Aspirin and NSAID drugs inhibit COX 1 & 2, while acetaminophen only inhibits COX 2 and does not have any of these side effects. However, acetaminophen is not an anti-inflammatory.


What causes a person to be intolerant to NSAIDs and what should they be given instead?

Ulcers (prostaglandins protect the gut), on anticoagulants (NSAIDs prevent platelets from sticking),


What produces prostaglandins?

Trauma releases arachadonic acid. This is processed into prostaglandins or into leukotrienes depending on the environment and what cell types are present. PGs are members of the Eicosanoid family, and are produced when COX 1/2 processes arachadonic acid. Thromboxanes also result from this pathway.


What do glucocorticoids do?

Glucocorticoids inhibit the production of arachadonic acid from phospholipids by phospholipase A2, thus inhibiting prostaglandin synthesis as well as leukotriene synthesis.   All of the eicosanoids would be inhibited.   Very good long term anti-inflammatory drug for asthma.


What are the actions triggered by the products of COX 1 and 2?

The products of COX 1 & 2 (prostaglandins) function in Uterine contraction, vasodilation, inhibition of platelet aggregation, gastric cytoprotection, vasodilation, decreased gastric acid production, cervical ripening, platelet aggregation.   Note that inhibiting COX 1 & 2 opposes these effects, providing therapy or causing side effects.


What enzyme produces arachadonic acid and what two enzymes process it into prostaglandins and leukotrienes?

Phopsholipase A2 converts phospholipids into arachadonic acid.   COX 1/2 converts it into prostaglandins, 5-lioxygenase converts it into leukotrienes.


What is the biochemistry and physiology of cyclooxydase 1 in terms of expression, tissue locations, physiologic role, inducers, and inhibitors

Expression: constitutive     Tissue location: GI, Platelets, kidney, vascular smooth muscle, bone     Physiological role: Inc aggregation, inc renal blood flow, vasodilation/constriction, bone formation/resorb     Inducers: baseline levels at all times     Inhibitors: NSAIDs


What is the biochemistry and physiology of cyclooxydase 2 in terms of expression, tissue locations, physiologic role, inducers, and inhibitors

Expression: Induced as needed in inflammed tissue     Tissue Locale: areas of pain, hypothalamus, fever, kidneys, endothelia     Physiologic Role: Enhance edema, heat, stress, vasodilate, anti-aggregate platelets, inc contractions     Inducers: Cytokines (IL-1, 2, INF-g) lipopolysaccharides, shear stress, GF     Inhibitors: NSAIDS


What tissues or organs do PGE2 and PGI2 affect and what do they do?

Vascular smooth muscle: cause vasodilation   GI tract smooth muscle/secretory cells: inhibit HCl secretion, increase mucous secretion, increase smooth muscle contractions   Kidney cells: increase renal blood flow, promote diuresis   Inflammatory cells: potentiate pain, edema, and fever   PGE2: Induces uterine contractions


Which prostaglandins induce contractions in uterine cells?

PGF2a and PGE2


What cytokine induces platelet agregation?

TXA2 (ThromboXin) agreggates platelets.   Just think TeXAs slowing things down.


What are the therapeutic actions and potential side effects of NSAIDs that inhibit COX 2?

Therapeutic actions: Pain relief, fever relief, reduction of inflammation.   Potential side effects: acute renal failure, thrombotic events, prolonged gestation.


What are the therapeutic actions and potential side effects of NSAIDs that inhibit COX 1?

Potential side effects: GI ulceration, prolonged bleeding time, acute renal failure


What are the effects of leukotrienes on inflammatory cell function and pulmonary/vascular smooth muscle?

LTB4: Neutrophil chemotaxis, aggreagation, and transmigration through the endothelium. (LTB4 = neutrophils)   LTC4, LTD4, LTE4: Increased vascular permeability, bronchoconstriction, vasoconstriction.   Roles in asthma, psoriasis, arthitic, allergy processes


What effects does prostacyclin have on vascular smooth muscle and platelets?

Prostacyclins cause vasodilation and platelet dis-agreggation.   This is the opposite of Thromboxanes.


What effects does Thromboxane A2 have on vascular smooth muscle and platelets?

Thromboxane A2 is a vasoconstrictor and induces the aggregation of platelets.   Acts opposite to prostacyclins.


What is the order of acetaminophen, aspirin, COX-2 select inhibitors, and NSAIDs from stongest effects on COX 1&2 to weakest?

Apsirin (Irreversibly binds COX 1&2), NSAIDs (Reversibly binds COX 1&2), COX2 Selective Inhibitors (Reversibly binds COX 2), Acetaminophen (does not bind COX 1 or 2)