Potassium serum levels

Pharmacology Potassium participates in a number of essential physiological processes, such as maintenance of intracellular tonicity and a proper relationship with sodium across cell membranes, cellular metabolism, transmission of nerve impulses, contraction of cardiac, skeletal, and smooth muscle, acid-base balance, and maintenance of normal renal function. Normal potassium serum levels range from 3.5 to 5 mEq/L. 

Hypersensitivity to these agents depressed sodium or potassium serum levels marked kidney and liver disease or dysfunction suprarenal gland failure hyperchloremic acidosis adrenocortical insufficiency severe pulmonary obstruction with inability to increase alveolar ventilation since acidosis may be increased (dichlorphenamide) cirrhosis (acetazolamide, methazolamide) long-term use in chronic noncongestive angle-closure glaucoma. 

Mild (5.S-6.5 mEq/L) to moderate (6.5-8 mEq/L) potassium blood level increases may be asymptomatic and manifested only by increased serum potassium concentrations and characteristic BOS changes such asdisappearance of P waves or Rereading (widening) of the QRS complex. 

Drug/Lab test interactions Urine glucose and serum cholesterol levels may increase. Decreased serum levels of potassium, T3, and a minimal decrease of T4 may occur. 

Monitoring Carefully monitor standard hypercalcemia-related metabolic parameters, such as serum levels of calcium, phosphate, magnesium, and potassium following pamidronate and zoledronic acid initiation. Also, closely monitor electrolytes, creatinine as well as CBC, differential and hematocrit/hemoglobin. Carefully monitor patients who have preexisting anemia, leukopenia or thrombocytopenia in the first 2 weeks following treatment. 

Drugs that may affect triamterene include ACE inhibitors, cimetidine, and indomethacin. Drugs that may be affected by triamterene include amantadine and potassium preparations. Triamterene will interfere with the fluorescent measurement of quinidine serum levels. 

Parameters to monitor Perform the following laboratory tests prior to and periodically during lithium therapy Serum creatinine complete blood count urinalysis sodium and potassium fasting glucose electrocardiogram and thyroid function tests. Check lithium serum levels twice weekly until dosage is stabilized. Once steady state has been reached, monitor the level weekly. Once the patient is on maintenance therapy, the level may be checked every 2 to 3 months. 

Absorption - Peak serum levels occur approximately 1 hour after oral use. Parenteral penicillin G (sodium and potassium) gives rapid and high but transient blood levels derivatives provide prolonged penicillin blood levels with IM use. 

Most patients should eat a diet with no added salt because of associated hypertension or edema. In dialysis patients, sodium intake should be reduced in patients who gain excessive weight between dialysis. Potassium restriction is not usually necessary until oliguria supervenes. Dialysis patients, however, should be educated to what foods are high in potassium, such as citrus foods, nuts, bananas, in order to avoid very high serum levels of potassium before each dialysis. Water restriction may be necessary if predialysis hyponatremia becomes prominent. 

Potassium, serum digoxin level prior to therapy... 

AMIODARONE POTASSIUM-SPARING DIURETICS Risk of T levels of eplerenone with amiodarone risk of hyperkalaemia directly related to serum levels Calcium channel blockers inhibit CYP3A4-mediated metabolism of eplerenone Restrict dose of eplerenone to 25mg/day. Monitor serum potassium concentrations closely watch for hyperkalaemia... 

The presence of depressed sodium and/or potassium blood serum levels... 

Willis (Wll), using a potassium hollow cathode tube instead of the commonly employed discharge lamp, determined potassium in blood serum. At the 1 50 dilution no interference was encountered from calcium, magnesium, and phosphate at serum levels, but sodium gave a small enhancement. The sodium interference was controlled by the addition in excess of sodium chloride or of the disodium salt of EDTA to samples and standards alike. 

Urinary potassium and magnesium losses are anticipated consequences of AmB therapy. Some of the losses can be compensated for with increased dietary intake, while others will require oral or intravenous replacement. It should be recognized that the serum levels of these ions do not necessarily correlate with the total deficit, as the plasma levels tend to be conserved while cellular stores are becoming depleted. In general, potassium and magnesium supplements should be given to all patients and the amounts increased if the... 

Monitor electrolyte serum level (potassium, chloride, sodium). 

Magnesium deficiency is common in SBS patients with large ostomy or diarrheal losses. This deficiency should be corrected aggressively because of the correlation between low magnesium and potassium concentrations, and magnesium supplementation decreases the formation of calcium oxalate kidney stones. Serum concentrations are most commonly monitored, but urinary magnesium concentrations may decrease earlier with deficiency, and may be a better estimate of total body stores than serum levels. Oral supplementation may be difficult because it can contribute to increased diarrhea or ostomy output. However, repletion is necessary to correct potassium deficits in addition to magnesium losses. ... 

The acute renal failure is typical for acute tubular necrosis and is characterized by a urine sediment with granular pigmented casts, and benzidine positive urine often in the absence of significant hematuria. With rhabdomyolytic acute tubular necrosis the urinary sodium concentration and fractional excretion of sodium are not always increased as in classic acute tubular necrosis [99]. One half to two-thirds of patients have ohguria, which may last from hours to many weeks. During this phase of the acute renal failure, there is a very rapid rise in the serum creatinine (often > 2.0 mg/ dl/ day), and profound increases in the serum levels of a variety of solutes normally foimd in muscle or produced from muscle derived precursors. Thus, fhe levels of potassium, phosphate, and uric acid all rise dra-... 

Diuretics are not used if hypertension is the result of renal-angiotensin-aldosterone involvement because these dmgs tend to elevate the semm renin level. Hydrochlorothiazides are combined with beta blockers, and angiotensinconverting enzyme (ACE) inhibitors. ACE inhibitors tend to increase serum potassium (K) levels. When they are combined with the thiazide diuretic, serum potassium loss is minimized. 

B. Potassium should be administered cautiously in patients with impairment of intracellular transport of potassium (due to inhibition of Na-K ATPase pump with cardiac glycosides or inhibition of beta-adrenergic transport with beta blockers). Administration of potassium may lead to large incremental rises in serum levels. 

In vitro studies have shown that ketoconazole inhibits the metabolism of astemizole. Ketoconazole, and to a lesser extent itraconazole and miconazole, also appear to reduce the metabolism of terfenadine by inhibition of the cytochrome P450 isoenzyme CYP3A. " High serum levels of astemizole and terfenadine (but not its metabolites) block cardiac potassium channels leading to prolongation of the QT interval, which may precipitate the development of torsade de pointes arrhythmia (see Table 15.2 , (p.583)). The risk of cardiac arrhythmias with other non-sedating antihistamines appears to be non-existent or very much lower (see Table 15.2 , (p.583)), so any pharmacokinetic interactions do not result in clinically relevant cardiac toxicity. In fact, studies have shown that desloratadine at nine times the recommended dose, fexofenadine in overdose, and mizolastine at four times the recommended dose do not affect the QT interval. However, some questions remain about loratadine and ebastine. Additionally, some studies have reported that ketoconazole alone is associated with a small increase in QT interval, and at least one case of torsade de pointes has been reported for ketoconazole alone. Therefore the cardiac effects of ketoconazole may be additive with those of the antihistamines, and this may be important for ebastine and loratadine. 

The mineralocorticoid effects of licorice are well documented see Human pharmacological studies) (Stewart et al. 1987). Licorice may cause reversible potassium depletion and sodium retention when consumed in therapeutic dosages over a prolonged period (Bensky et al. 2004 Bradley 1992 Martindale and Reynolds 1996). Most cases of adverse events associated with licorice have been reported in persons consuming excessive amounts of licorice candies. Overdoses of licorice have been associated with temporary paralysis, loss of vision, sodium and fluid retention, hypertension, and decreased serum levels of aldosterone. Licorice-related potassium depletion has resulted in symptoms such as tachycardia, rhabdomyolysis, myopathy, and hypokalemic paralysis. These effects are attributed primarily to the action of the compound glycyrrhizin (Isbrucker and Burdock 2006). Preparations of licorice without this compound, deglycyrrhizinated licorice (DGL), are available. 

---