Diuretics chronic

Diazoxide is a parenteral, rapid, and direct-acting vasodilating antihypertensive used in hypertensive emergencies. An IV injection can drop blood pressure by as much as 80 mmHg in 5 minutes. Unlike sodium nitroprusside, however, venous dilation is not part of its mechanism. Chemically it is a benzothiadiazide without the sulfamoyl function at the 7 position (see diuretics). In fact, diazoxide is not a diuretic. Chronic use of diazoxide reflexly increases renin release, which actually counteracts the antihypertensive effect of the drug by expanding the volume of circulating fluid. 

Calcium chloride Dimercury dichloride Hops (Humulus lupulus) extract Potassium acid tartrate Sodium succinate Sunflower (Helianthus annuus) seed oil Theobromine Theophylline Turpentine diuretic, chronic bladder problems Cubeb (Piper cubeba) oil diuretic, pharmaceuticals Ammonium acetate Hydrochlorothiazide Potassium acetate Sodium acetate anhydrous Trisodium citrate Urea... 

Galen, a physician whose views outUved him by about a thousand years, died about 200 AD. He beUeved that mercurials were toxic, and did not use any mercury compound therapeutically. However, as a result of Arabian influence, the therapeutic uses of mercury were slowly recognized by Western Europe. In the thirteenth century mercury ointments were prescribed for treating chronic diseases of the skin. Mercury and its compounds, such as mercurous chloride, mercuric oxide, mercuric chloride, and mercuric sulfide, were used widely from the fifteenth to the nineteenth centuries, and to some extent in the twentieth century. During the first half of the twentieth century, the primary therapeutic uses of mercury included bactericidal preparations, such as mercuric chloride, mercuric oxycyanide, and mercuric oxide and diuretics, such as aryl HgX (Novasural) and mercurated ahyl derivatives (14). 

Calcium channel blockers cause more pronounced lowering of blood pressure in hypertensive patients than in normotensive individuals. Generally, all calcium channel blockers cause an immediate increase in PRA during acute treatment in patients having hypertension but PRA is normalized during chronic treatment despite the sustained decrease in blood pressure. These agents also do not generally produce sodium and water retention, unlike the conventional vasodilators. This is because they produce diuretic effects by direct actions on the kidney. 

The principal mechanism of the hypotensive effect of diuretics (qv) is salt and fluid depletion, leading to reduction in blood volume (200,240). Acute effects lead to a decrease in cardiac output and an increase in total peripheral resistance. However, during chronic adrninistration, cardiac output and blood volume return toward normal and total peripheral resistance decreases to below pretreatment values. As a result, the blood pressure falls. The usual reduction in blood volume is about 5%. A certain degree of sustained blood volume contraction has to occur before the blood pressure decreases. The usual decrease in blood pressure achieved using a diuretic is about 20/10 mm Hg (2.7/1.3 kPa) (systoHc/diastoHc pressures. 

In nephrogenic diabetes insipidus the kidney s ability to respond to AVP is impaired by different causes, such as drugs (e.g. lithium), chronic disorders (e.g. sickle cell disease, kidney failure) or inherited genetic disorders (X-linked or autosomal NDI). This type of diabetes insipidus can not be treated by exogenous administration of AVP or AVP analogues. Instead, diuretics (hydrochlorothiazide combined or not with amiloride) and NSAI (indomethacin) are administrated to ameliorate polyuria. 

Acetaminophen may alter blood glucose test results, causing falsely lower blood glucose values. Use with the barbiturates, hydantoins, isoniazid, and rifampin may increase the toxic effects and possibly decrease the therapeutic effects of acetaminophen. The effects of the loop diuretics may be decreased when administered with acetaminophen. Hepatotoxicity has occurred in chronic alcoholics who are taking moderate doses of acetaminophen. 

Patients with diabetes and hypertension should initially be treated with either P-blockers, ACE inhibitors, ARBs, diuretics, or calcium channel blockers. There is a general consensus that therapy focused on RAAS inhibition by ACE inhibitors or ARBs may be optimal if the patient has additional cardiovascular risk factors such as left ventricular hypertrophy or chronic kidney disease.2,3,59,67... 

In patients with chronic kidney disease and hypertension, ACE inhibitors and ARBs are preferred, usually in combination with a diuretic.67 ACE inhibitors in combination with a thiazide diuretic are also preferred in patients with a history of... 

Medications can increase the risk of hyperkalemia in patients with CKD, including angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers, used for the treatment of proteinuria and hypertension. Potassium-sparing diuretics, used for the treatment of edema and chronic heart failure, can also exacerbate the development of hyperkalemia, and should be used with caution in patients with stage 3 CKD or higher. 

Causes of hypocalcemia include hypoparathyroidism, hypomagnesemia, alcoholism, hyperphosphatemia, blood product infusion (due to chelation by the citrate buffers), chronic renal failure, vitamin D deficiency, acute pancreatitis, alkalosis, and hypoalbuminemia. Medications that cause hypocalcemia include phosphate replacement products, loop diuretics, phenytoin (Dilantin, available as generic), pheno-barbital (available as generic), corticosteroids, aminoglycoside antibiotics, and acetazolamide (available as generic).34,39,42... 

NSAIDs can cause renal insufficiency when administered to patients whose renal function depends on prostaglandins. Patients with chronic renal insufficiency or left ventricular dysfunction, the elderly, and those receiving diuretics or drugs that interfere with the renin-angiotensin system are particularly susceptible. Decreased glomerular filtration also may cause hyperkalemia. NSAIDs rarely cause tubulointerstitial nephropathy and renal papillary necrosis. 

The answer is c. (Katzung, pp 254-255.) Thiazide diuretics enhance K, Cl, Na, and Mg ion excretion Ca excretion appears to be reduced following chronic drug administration. Because thiazides inhibit NaCl re absorption in the early portion of the distal tubule, an increased load of Na and Cl ions is presented to the collecting duct, where some Na ions may be actively reabsorbed and K ions secreted, leading to increased K loss. 

Acutely, diuretics lower BP by causing diuresis. The reduction in plasma volume and stroke volume associated with diuresis decreases cardiac output and, consequently, BP. The initial drop in cardiac output causes a compensatory increase in peripheral vascular resistance. With chronic diuretic therapy, the extracellular fluid volume and plasma volume return almost to pretreatment levels, and peripheral vascular resistance falls below its pretreatment baseline. The reduction in peripheral vascular resistance is responsible for the long-term hypotensive effects. Thiazides lower BP by mobilizing sodium and water from arteriolar walls, which may contribute to decreased peripheral vascular resistance. 

Potassium-sparing diuretics may cause hyperkalemia, especially in patients with chronic kidney disease or diabetes, and in patients receiving concurrent treatment with an ACE inhibitor, ARB, NSAID, or potassium supplement. Eplerenone has an increased risk for hyperkalemia and is contraindicated in patients with impaired renal function or type 2 diabetes with proteinuria. Spironolactone may cause gynecomastia in up to 10% of patients, but this effect occurs rarely with eplerenone. 

ACE inhibitors decrease aldosterone and can increase serum potassium concentrations. Hyperkalemia occurs primarily in patients with chronic kidney disease or diabetes and in those also taking ARBs, NSAIDs, potassium supplements, or potassium-sparing diuretics. 

Sodium and water retention can occur with chronic administration. These agents are most effective when given with a diuretic to maintain antihypertensive efficacy and minimize potential edema. 

Blockers (without ISA) are first-line therapy in chronic stable angina and have the ability to reduce BP, improve myocardial consumption, and decrease demand. Long-acting CCBs are either alternatives (the nondihy-dropyridines verapamil and diltiazem) or add-on therapy (dihydropy-ridines) to /1-blockers in chronic stable angina. Once ischemic symptoms are controlled with /1-blocker and/or CCB therapy, other antihypertensive drugs (e.g., ACE inhibitor, ARB) can be added to provide additional CV risk reduction. Thiazide diuretics may be added thereafter to provide additional BP lowering and further reduce CV risk. 

Metabolic alkalosis and respiratory acidosis can occur in patients with chronic obstructive pulmonary disease and respiratory acidosis who are treated with salt restriction, diuretics, and possibly glucocorticoids. 

Nephron adaptation to chronic diuretic therapy NSAID use Heart failure... 

In general, every 1-mEq/L fall of potassium below 3.5 mEq/L corresponds with a total body deficit of 100 to 400 mEq. To correct mild deficits, patients receiving chronic loop or thiazide diuretics generally need 40 to 100 mEq of potassium. 

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