Diuretics causing

Hyperaldosteronism is a syndrome caused by excessive secretion of aldosterone. It is characterized by renal loss of potassium. Sodium reabsorption in the kidney is increased and accompanied by an increase in extracellular fluid. Clinically, an increased blood pressure (hypertension) is observed. Primary hyperaldosteronism is caused by aldosterone-producing, benign adrenal tumors (Conn s syndrome). Secondary hyperaldosteronism is caused by activation of the renin-angiotensin-aldosterone system. Various dtugs, in particular diuretics, cause or exaggerate secondary peadosteronism. 

Each year in the United States, about 30 million prescriptions for potassium supplements are written for people with hypertension (high blood pressure). These supplements are often prescribed with diuretics. Diuretics cause increased urination and reduce the volume of retained fluids in the body, thus reducing blood pressure. Explain why potassium supplements are prescribed. 

Diuretics cause numerous adverse effects and metabolic abnormalities, with severity linked to diuretic potency. A particularly worrisome adverse effect in the setting of HF is... 

Diuretics cause the body to release excess fluids. They are used to help people with congestive heart failure and high blood pressure, as excess fluid makes heart failure and high blood pressure worse. When someone does not have one of... 

Drugs acting only on the distal tubule (however complete the resulting block of sodium resorption at that site) are limited, in the effect obtainable, by the comparatively small contribution to total sodium reclamation made by this portion of the nephron. For example, even at their activity peak, thiazide diuretics cause the elimination of only 8 per cent of the total filtered sodium [302, 303] Very much higher proportions of filtered sodium would be expected to contribute to diuresis if the mechanisms of the loops of Henle could be blocked (this has, in fact, proved to be the case in that frusemide and ethacrynic acid are both capable of clearing up to 20 per cent of filtered sodium [302, 304-6]). 

This potassium sparing diuretic causes a moderate increase in excretion of sodium and bicarbonate ions in urine, and it raises excretion of potassium and ammonia ions. It has little effect on urine volume. 

The molecular mechanism of diuretics acting as antihypertensive agents is not completely clear however, use of diuretics causes a significant increase in the amount of water and electrolytes excreted in urine, which leads to a reduction in the volume of extracellular fluid and plasma. This in turn leads to a reduction of cardiac output, which is the main parameter responsible for a drop in arterial blood pressure and venous blood return. Cardiac output is gradually restored, but the hypotensive effect remains, possibly because of the reduced peripheral resistance of vessels. It is also possible that diuretics somehow lower vascular activity of noradrenaline and other factors of pressure in the organism. Methods of synthesizing thiazide diuretics used for hypertension are described in the preceding chapter. Chapter 21. 

Physalis angulata L. Ku Zhi (Groundcherry) (fruit, leaf) Hystonin.60 Overdose may cause dizziness. Antifebrile, laxative, diuretic, causing uterine contractions. 

Portulaca oleracea L. Ma Chi Xian (Purslane) (aerial part) Potassium salts, catecholamines, norepinephrine, dopamine, vitamin A, vitamin B, magnesium.33 49 Antibacterial, diuretic, causes vasoconstriction, stimulates uterine and intestinal smooth muscle contraction. 

The sulfonamide diuretics cause problems through excessive excretion of potassium which diffuses into the urine as Na+ is removed in the distal tubule. This cation exchange is prevented by a different type of diuretic, triamterene (198), which was developed by following the observation that xanthopterin (199) affects renal function. The pyrazine amiloride (200) also increases Na+ output and spares K+, and is used in conjunction with chlorothiazide. It has been shown to reduce the electrical potential gradient along which K+ migrates into the lumen of the tubule. 

Uses Acute CHF, ischemic cardiomyopathy Action Inotrope w/ vasodilator Dose IV bolus 0.75 mg/kg over 2-3 min maint 5-10 mcg/kg/min, 10 mg/kg/d max i if CrCl <10 mL/min Caution [C, ] Contra Bisulfite allergy Disp Inj SE Monitor fluid, electrolyte, renal changes Interactions Diuretics cause significant hypovolemia T effects OF cardiac glycosides EMS Avoid diuretic use, can cause profound hypovolemia incompatible w/ dextrose solns monitor ECG for hypokalemia (flattened T waves) OD May cause profound hypotension use IV fluids w/ caution d/t fluid buildup in lungs, pressors may be used... 

Because diuretics cause an overall water weight loss, they are often abused by individuals with eating disorders such as anorexia and bulimia. They may also be misused (and sometimes abused) by athletes to make weight for certain classes of competition (i.e., wrestling). 

The NaCl transport system in the luminal membrane of the thick ascending limb is a Na+/K+/2CF cotransporter (Figure 15-4). This transporter is selectively blocked by diuretic agents known as "loop" diuretics (see below). Although the Na+/K+/2CF transporter is itself electrically neutral (two cations and two anions are cotransported), the action of the transporter contributes to excess K+ accumulation within the cell. This results in back diffusion of K+ into the tubular lumen and development of a lumen-positive electrical potential. This electrical potential provides the driving force for reabsorption of cations—including Mg2+ and Ca2+—via the paracellular pathway (between the cells). Thus, inhibition of salt transport in the thick ascending limb by loop diuretics causes an increase in urinary excretion of divalent cations in addition to NaCl. 

The loop diuretics act promptly, even in patients who have poor renal function or who have not responded to thiazides or other diuretics. The loop diuretics cause decreased renal vascular resistance and increased renal blood flow. [Note Loop diuretics increase the Ca++ content of urine (see p. 227), whereas thiazide diuretics decrease the Ca++ concentration of the urine.]... 

Correct answer = D. Among black patients, diuretic and calcium channel blockers are more effective than ACE inhibitors or p-blockers. Diuretics are effective among the elderly. Thiazide diuretics cause hyperuricemia and can precipitate a gout attack in susceptible individuals. Thiazide diuretics increase LDL cholesterol and may increase the risk of atherosclerosis in patients with hyperlipidemia. Patients with evidence of elevated catecholamines are best treated with p-blockers. Thiazides cannot promote sodium excretion when renal function is severely impaired. The loop diuretics, such as furosemide, are used in patients with impaired renal function. 

Calcium-sparing diuretics. Diuretics that result in a relatively low rate of excretion of calcium. The sparing effect on calcium can be beneficial in hypocalcaemia. The thiazides and potassium-sparing diuretics are considered to be calcium-sparing diuretics. The thiazides cause a net decrease in calcium lost in urine the potassium-sparing diuretics cause a net increase in calcium lost in urine, but the increase is much smaller than that associated with other diuretic classes. By contrast, loop diuretics promote a significant increase in calcium excretion. This can increase risk of reduced bone density. 

LOOP DIURETICS CISPLATIN t risk of auditory toxic effects with cisplatin Loop diuretics cause tinnitus and deafness as side-effects. Additive toxic effects on auditory system likely Monitor hearing - test auditory function regularly, particularly if patients report symptoms such as tinnitus or impaired hearing... 

Potassium sparing triamterene, amiloride and spironolactone, cause 5% of the filtered sodium to be excreted. They are usefully combined with more efficacious diuretics to prevent the potassium loss, which other diuretics cause. 

The loop diuretics cause a smaller fall in serum potassium than do the thiazides, for equivalent diuretic effect, but have a greater capacity for diuresis, i.e. higher efficacy especially in large dose, and so are associated with greater decline in potassium. If diuresis is brisk and continuous, clinically important potassium depletion is likely to occur. 

Most diuretics cause hyperuricemia. Increased reabsorption of uric acid (along with other solutes) in the proximal tubule as a consequence of volume depletion is one reason however, diuretics also compete with uric acid for excretory transport mechanisms. There is a small increased risk of acute gout in susceptible subjects (73). In the large outcome trials, about 3-5% of subjects treated with diuretics for hypertension developed clinical gout... 

Davies DL, Fraser R. Do diuretics cause magnesium deficiency Br J Clin Pharmacol 1993 36(1) 1-10. 

Thiazide diuretics cause hjrperuricemia and can occasionally precipitate gout (21). They can also cause renal stones (22). Uric acid precipitation is not normally a problem, although it was with the uricosuric drug tieniUc acid. Renal vasculitis due to thiazides is rare (SEDA-18,234). 

Toxicity occurs when the herbal therapies juniper and dandelion (diuretics causing increased urination) are taken with lithium (a psychiatric medication). 

Filtered sodium is reabsorbed at the proximal tubules, the Loop of Henle, distal tubules, or in the collecting tubules. Diuretics influence tubules closest to the glomeruli, causing natriuresis (sodium loss in the urine). Diuretics cause loss of other electrolytes (potassium, magnesium, chloride, bicarbonate). Diuretics that promote potassium excretion are called potassium-wasting diuretics or potassium-sparing diuretics. 

Loop diuretics cause vasodilation, increasing renal blood flow before diuresis and making it the prime choice in diuretics for patients who have decrease kidney function or end-stage renal disease. Side effects are ... 

Greger R. Why do loop diuretics cause hypokalemia Nephrol Dial Transplant 1997 12 1799-801. 

The diuretics cause several direct as well as indirect functional and anatomic lesions in the kidney (Table 2). Reduced RBF and/or glomerular filtration rate associated with the administration of acetazola-mide, benzolamide and chlorothiazide relate to their... 

A major use of loop diuretics is in the treatment of acute pulmonary edema. A rapid increase in venous capacitance in conjunction with a brisk natriuresis reduces left ventricular filling pressures and thereby rapidly relieves pulmonary edema. Loop diuretics are also used widely for the treatment of chronic CHE when diminution of extracellular fluid volume is desirable to minimize venous and pulmonary congestion. In this regard, a metaanalysis of randomized clinical trials demonstrates that diuretics cause a significant reduction in mortality and the risk of worsening heart failure, as well as an improvement. 

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