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Angiotensin converting enzyme NSAIDs

Figure 38.1. Sites of renal damage, including factors that contribute to the kidney s susceptibility to damage. ACE - angiotensin converting enzyme NSAID-nonsteroidal anti-inflammatory drugs HgCl2 - mercuric chloride (adapted from Color Atlas of the Diseases of the Kidney, Vol. 1, Berl, T., Bonventre, J.V., 1998, with permission). Figure 38.1. Sites of renal damage, including factors that contribute to the kidney s susceptibility to damage. ACE - angiotensin converting enzyme NSAID-nonsteroidal anti-inflammatory drugs HgCl2 - mercuric chloride (adapted from Color Atlas of the Diseases of the Kidney, Vol. 1, Berl, T., Bonventre, J.V., 1998, with permission).
ACE, Angiotensin converting enzyme NSAIDs, nonsteroidal antiinflammatory drugs. [Pg.1708]

E.g., angiotensin converting enzyme inhibitors, angiotensin receptor blockers, and NSAIDs... [Pg.158]

The most potentially serious drug interactions include the concomitant use of NSAIDs with lithium, warfarin, oral hypoglycemics, high-dose methotrexate, antihypertensives, angiotensin-converting enzyme inhibitors, fi-blockers, and diuretics. [Pg.28]

Exposure after this point may result in growth retardation, CNS or other abnormalities, or death (e.g., nonsteroidal antiinflammatory drugs [NSAIDs], angiotensin-converting enzyme inhibitors [ACEIs], and tetracycline derivatives). [Pg.367]

Diclofenac is a non-steroidal anti-inflammatory drug. NSAIDs interact with both angiotensin-converting enzyme inhibitors, such as enalapril, and beta-adrenoceptor blockers, such as atenolol, resulting in antagonism to the hypotensive reaction, leading to a hypertensive reaction. NSAIDs interact with... [Pg.118]

Hyperkalaemia, not surprisingly, is the most important side effect of these drugs and can be dangerous in patients who are taking K-i- supplements or other K-i--sparing diuretics. Concomitant use of angiotensin-converting enzyme (ACE) inhibitors and NSAIDs can also exacerbate hyperkalaemia. [Pg.208]

Nephrotoxicity is caused by drugs that principally affect the renal hemodynamics of the patient depended on vasodilator prostaglandin biosynthesis or angiotensin converting enzyme (ACE) mediated vasoconstriction drugs causing nephrotoxicity include NSAIDs (fenprofen), ACE inhibitors (captopril, and cyclosporin). [Pg.400]

NSAIDs should be avoided in patients with chronic renal insufficiency due to the risk of inducing further kidney damage. In patients at risk, acute renal feilure can occur after a single dose of drug. Risk fectors include dehydration, hypertension, congestive heart failure, concomitant use of angiotensin-converting enzyme inhibitors, and advanced age. [Pg.102]

ACE-I, indicates angiotensin-converting enzyme inhibitor SSRI, selective serotonin receptor inhibitor NSAID, non-steroidal anti-inflammatory drug OA, osteoarthritis. [Pg.1909]

Abbreviations NSAID = nonsteroidal anti-inflammatory drugs, PG = prostaglandin, RBF = renal blood flow, GFR = glomerular filtration rate,HTN = hypertension, DM = diabetes mellitus, = potassium, RAA = renin-angiotensin- aldosterone, CHF = congestive heart failure, AGE = angiotensin-converting enzyme, SLF = systemic lupus erythematosis. [Pg.424]

Examples angiotensin converting enzyme (ACE) inhibitors, cyclosporine, nonsteroidal antiinflammatory drugs (NSAIDs) Tubular obstruction... [Pg.1479]

ACE, angiotensin-converting enzyme H, histamine LO, lipoxygenase MAO, monoamine oxidase NSAID, non-steroidal anti-inflammatory drug... [Pg.197]

ACE angiotensin-converting enzyme CNS central nervous system COPD chronic obstructive pulmonary disease DPIs dry-powder inhalers EDTA ethylenediamine tetraacetic acid EDA Eood and Drug Administration EEVi forced expiratory volume in 1 second HIV human immunodeficiency virus IPS idiopathic pneumonia syndrome NSAIDs nonsteroidal anti-inflammatory drugs... [Pg.588]

NSAIDs interfere with the antihypertensive action of angiotensin-converting enzyme inhibitors the other drugs listed enhance the blood pressure-lowering effects of captopril and other members of the pril drug family. The answer is (C). [Pg.537]

Celecoxib is currently indicated for the relief of signs and symptoms of osteoarthritis and rheumatoid arthritis and to reduce the number of adenomatous colorectal polyps in familial adenomatous polyposis as an adjunct to usual care. Celecoxib is at least as effective as naproxen in the symptomatic management of osteoarthritis and at least as effective as naproxen and diclofenac in the symptomatic treatment of rheumatoid arthritis, and it is less likely to cause adverse Gl effects. Celecoxib appears to be effective in the management of pain associated with both of these arthritic conditions, but effectiveness in acute or chronic pain has not been fully demonstrated. Unlike aspirin, celecoxib does not exhibit antiplatelet activity. Concomitant administration of aspirin and celecoxib may increase the incidence of Gl side effects. Another notable potential drug interaction with celecoxib is its ability, like other NSAIDs, to reduce the blood pressure response to angiotensin-converting enzyme inhibitors. A more detailed discussion of the chemical, pharmacological, pharmacokinetic, and clinical aspects of celecoxib is available (81). [Pg.1482]

M, metaboiism S, at or near site of action IV, intravenously MHS, malignant hyperthermia syndrome ALA, aianine ICU, intensive care unit CNS, central nervous system MAOI, monoamine oxidase inhibitor, NSAID, non-steroidal anti-inflammatory drug ACE, angiotensin in-converting enzyme 5-HT, 5-hydrox ryptamine. [Pg.272]


See other pages where Angiotensin converting enzyme NSAIDs is mentioned: [Pg.449]    [Pg.178]    [Pg.362]    [Pg.886]    [Pg.336]    [Pg.338]    [Pg.61]    [Pg.427]    [Pg.627]    [Pg.784]    [Pg.1698]    [Pg.95]    [Pg.287]    [Pg.413]    [Pg.439]    [Pg.513]    [Pg.449]    [Pg.112]    [Pg.225]    [Pg.23]    [Pg.356]   
See also in sourсe #XX -- [ Pg.427 , Pg.430 , Pg.438 ]

See also in sourсe #XX -- [ Pg.287 , Pg.289 , Pg.297 ]




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