Thiazides drug interactions with

Which of the following is unlikely to cause a drug-drug interaction with the thiazides ... 

Drug interactions with orally administered drugs (warfarin, thiazides, digoxin, etc.)... 

Other drugs that may interact with cardiac glycosides include the following Albuterol, amphotericin B, beta-blockers, calcium, disopyramide, loop diuretics, nondepolarizing muscle relaxants, potassium-sparing diuretics, succinylcholine, sympathomimetics, thiazide diuretics, thioamines, and thyroid hormones. 

Sulfonylureas In acute poisoning with sulfonylureas, the stomach should be washed and treated with activated charcoal, and hypoglycemia must be treated. Sulfonylureas interact with oral contraceptives, thiazide diuretics, corticosteroids, adrenaline, chlorpromazine, ACE inhibitors, some NSAIDs, antihistamines, anticoagulants, MAOIs, antidepressants, and many other drugs. Care must be exercised when treating with sulfonylureas. 

Corticosteroids interact with barbiturates, carbamazepine, phenytoin, primidone, frusemide, thiazide, NSAIDs, antidiabetics, and antihypertensive drugs. Benzquinamide hydrochloride is incompatible with chlordiazepoxide, diazepam, and some barbiturates. Care should be exercised when handling bisacodyl to avoid contact with skin and mucosal membranes. 

Interactions. Several types of drug interfere with lithium excretion by the renal tubules, causing the plasma concentration to rise. These include diuretics (thiazides more than loop type), ACE inhibitors and angiotensin-11 antagonists, and nonsteroidal anti-inflammatory analgesics. Theophylline and sodium-containing antacids reduce plasma lithium concentration. The effects can be important because lithium has such a low therapeutic ratio. Diltiazem, verapamil, carbamazepine and pheny-toin may cause neurotoxicity without affecting the plasma lithium. Concomitant use of thioridazine should be avoided as ventricular arrhythmias may result. 

The drug most commonly used in clinical practice that can produce immune thrombocytopenic purpura is heparin. Other examples are sulfonamides, thiazide diuretics, chlorpropamide, quinidine, and gold. These types of immune thrombocytopenic purpura are reversed when the drug is withdrawn. Molecular mechanisms for the formation of specific drug-dependent antibodies appear to be very similar. The glycoproteins on the platelet surface interact with the drugs to form neo-epitopes. Subsequent... 

The exact mechanism for reduction of arterial blood pressure by diuretics is not certain. Initially, the drugs decrease extracellular volume by interacting with a thiazide-sensitive Na-Cl cotransporter in the kidney, leading to a fall... 

Most of the renal tubular reabsorption ofU occurs in the proximal tubule. Nevertheless, Id retention can be increased by any diuretic that leads to depletion of Na, particularly the thiazides (see Chapter 28). Renal excretion can be increased by administration of osmotic diuretics, aceta-zolamide or aminophylline, and triamterene. Spironolactone does not increase the excretion of LiL Some nonsteroidal anti-inflammatory agents can facilitate renal proximal tubular resorption of Id and thereby increase concentrations in plasma to toxic levels. This interaction appears to be particularly prominent with indomethacin, but also may occur with ibuprofen, naproxen, and COX-2 inhibitors, and possibly less so with sulindac and aspirin. A potential drug interaction can occur with angiotensin-converting enzyme inhibitors, causing lithium retention (see Chapter 29). 

One of the best-known lithium interactions is the clinically relevant reduction of renal lithium clearance by combined administration of the drug with diuretics. Special caution is advised when long-term thiazides are combined with lithium. The potassium-sparing diuretics such as spironolactone can also increase plasma... 

The use of NSAID in patients with essential and renovascular hypertension is complicated largely because of negative interaction with other drug therapy. An important exception to this observation may be sulindac, a NSAID with the putative unique property of inhibiting only extrarenal PG synthesis However, the selective nature of sulindac s inhibition of PG synthesis has been disputed Sulindac potentiates, rather than antagonizes, the antihypertensive effect of thiazides in patients with essential hypertension. However, there are case reports of nephrotic syndrome, sometimes associated with acute interstitial nephritis, related to sulindac therapy. ... 

Hemodynamic contributions to diuresis - Almost certainly, conventional diuretics prevent renal reabsorption of electrolytes by interacting with components of tubular cells. However, hemodynamic mechanisms may also be involved. Ethacrynic acid 5 86 furosemide > 7 reduce renal vascular resistance (RVH) and, thereby, enhance renal blood flow (RBF). The Increase In RBF is proportional to the level of RVR when these drugs are administered and occurs primarily in the middle renal cortex. These agents are not vasodilators in the conventional sense since they do not increase blood flow in other vascular beds nor at pressures in the kidney below the autoregulatory range . Moreover, diuresis itself does not explain the effect since thiazides 7 91 r mercurials reduce rather than increase RBF. While the natriuretic effect of ethacrynic acid and furosemide is probably supplemented by the change in RBF, its contribution appears small. Thus, increased RBF can be demonstrated for the duration of natriuresis if urine volume is replaced 2 the more normal circumstance in which a... 

Drug interactions The extent to which vitamin D supplementation alters drug effectiveness and toxicity in humans has been systematically reviewed. Bile acid sequestrants and lipase inhibitors were found to inhibit the absorption of vitamin D from the gut. Statins, rifampicin, isoniazid, hydroxychloroquine, antiepileptics, corticosteroids, immimo-suppressive and chemotherapeutic agents, antiretroviral drugs and H2 receptor antagonists interfered with vitamin D metabolism. The interaction between vitamin D and thiazide diuretics could result in hypercalcaetnia. Vitamin D supplementation decreases concentrations of atorvastatin, and could cause hypercalcaetnia in elderly individuals or tixose with compromised renal function or hyperparathyroidism [84 ]. 

Drug/Lab test interactions Thiazides may decrease serum PBI levels without signs of thyroid disturbance. Thiazides also may cause diagnostic interference of serum electrolyte, blood, and urine glucose levels (usually only in patients with a predisposition to glucose intolerance), serum bilirubin levels, and serum uric acid levels. In uremic patients, serum magnesium levels may be increased. Bendroflumethiazide may interfere with the phenolsulfonphthalein test due to decreased excretion. In the phentolamine and tyramine tests, bendroflumethiazide... 

Lithium intoxication can be precipitated by the use of diuretics, particularly thiazides and metola-zone, and ACE inhibitors. NSAIDs can also precipitate lithium toxicity, mainly due to NSAID inhibition of prostaglandin-dependent renal excretion mechanisms. NSAIDs also impair renal function and cause sodium and water retention, effects which can predispose to interactions. Many case reports describe the antagonistic effects of NSAIDs on diuretics and antihypertensive drugs. The combination of triamterene and indomethacin appears particularly hazardous as it may result in acute renal failure. NSAIDs may also interfere with the beneficial effects of diuretics and ACE inhibitors in heart failure. It is not unusual to see patients whose heart failure has deteriorated in spite of increased doses of frusemide who are also concurrently taking an NSAID. 

Renal clearance of lithium is reduced about 25% by diuretics (eg, thiazides), and doses may need to be reduced by a similar amount. A similar reduction in lithium clearance has been noted with several of the newer nonsteroidal anti-inflammatory drugs that block synthesis of prostaglandins. This interaction has not been reported for either aspirin or acetaminophen. All neuroleptics tested to date, with the possible exception of clozapine and the newer atypical antipsychotics, may produce more severe extrapyramidal syndromes when combined with lithium. 

When problems do arise they usually reflect either interactions, which with caution could have been avoided, or relative overdosage. In the course of time the recommended antihypertensive doses of diuretics have been reduced, and some adverse effects that were noted in the early years are now of less significance these include hypotension, dehydration, reduction of the glomerular filtration rate, and severe hypokalemia. Continued use of thiazides in excessive doses may reflect ignorance of their very flat dose-response curve (1). At currently recommended low doses, diuretics improve overall quality of life, even in asymptomatic patients with mild hypertension (2). The large HANE study (3) provided no evidence of superior efficacy or tolerability of new classes of antihypertensive drugs. 

Several non-steroidal anti-inflammatory drugs (NSAIDs) have been reported to interfere with the natriuretic effects of thiazides (SED-11, 423). A similar interaction is seen with tenidap, an antiarthritic cytokine modulating drug (46). The salt-retaining properties of the NSAIDs probably play the central role in this interaction. 

Lithium is also known to interact in a variety of ways with different classes of diuretic drugs. Thiazide diuretics increase serum lithium concentration by increasing reabsorption of lithium, along with that of sodium, in the proximal tubule. With potassium-sparing diuretics, conflicting results have been reported. Increased serum lithium concentrations may be seen after amiloride. However, the loop diuretic furosemide safely can be combined with lithium with no reduction in renal lithium clearance or consequent increase in serum lithium concentration (191, 192). Other diuretics, for example, carbonic anhydrase inhibitor and xanthine derivatives, decrease serum... 

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