Potassium plasma

In long-term treatment, the thia2ides may produce hypokalemia, hyperglycemia, hypemricemia, and a 5% increase in plasma cholesterol indapamide has been shown not to increase plasma cholesterol or Hpids at therapeutic doses (21—23). The decrease of plasma potassium, ie, hypokalemic effect, is dose-dependent, and can be avoided if high doses are avoided (24,25). Thia2ides can cause hyponatremia in patients with large water intake while on the dmg (26,27) hyponatremia may be associated with nausea, vomiting, and headaches. 

Gibb I., Evaluation and assessment of new disposable strip for determination of plasma potassium concentration, J. Clin. Pathol. 1987 40, 298. 

Chemistry Plasma urea Plasma sodium Plasma potassium Plasma creatinine... 

Hypokalaemia occurs when the plasma-potassium level falls below 3.0 mmol/L Hypokalaemia may occur following loop or thiazide diuretic therapy. Patients at risk of developing hypokalaemia are often prescribed potassium supplements to counteract the potassium loss caused by the diuretic therapy. Symptoms of hypokalaemia include muscle weakness and cramps. Severe cases may lead to muscle paralysis and respiratory failure. 

The side-effects of cardiac glycosides are mostly caused by electrophysiological/neuronal phenomena. Gastro-intestinal adverse reactions are probably triggered by effects on the central nervous system. Various types of cardiac arrhythmias are caused by the influence of the drugs on nodal tissues in the heart. The risk of arrhythmia is strongly enhanced by low plasma potassium concentrations. 

As a result of the narrow therapeutic range overdosage of digoxin readily occurs, in particular in patients with low plasma potassium levels. Special attention should therefore be paid to the combination of digoxin with drugs causing hypokalemia, such as diuretics. 

Plasma potassium should be monitored carefully. The retention of sodium together with water will consequently be followed by weight gain and oedema. 

Keilani T, Danesh FR, Schlueter WA, Molteni A, Batile D. A sub-depressor low dose of ramipril lowers urinary protein excretion without increasing plasma potassium. Am J Kidney Dis 1999 33 450-7. 

The catecholamines can play an important role in the short-term regulation of plasma potassium levels. Stimulation of hepatic a-adrenoceptors will result in the release of potassium from the liver. In contrast, stimulation of (32-adrenoceptors, particularly in skeletal muscle, will lead to the uptake of potassium into this tissue. The (32-adrenoceptors are linked to the enzyme Na"", K+ adenosine triphosphatase (ATPase). Excessive stimulation of these (32-adrenoceptors may produce hypokalemia, which in turn can be a cause of cardiac arrhythmias. 

Early after-depolarizations and the associated ventricular arrhythmia can be prevented or suppressed by the appropriate adjustment of plasma potassium and/or magnesium concentrations. Lidocaine or procainamide may be effective for termination of the arrhythmia. 

In addition to the angiotensin II effects, aldosterone secretion is regulated by increased plasma potassium levels.75,83 Presumably, elevated plasma potassium serves as a stimulus to increase aldosterone release, thus causing increased potassium excretion and a return to normal plasma levels. Finally, there is evidence that ACTH may also play a role in aldosterone release. Although ACTH is primarily involved in controlling glucocorticoid secretion, this hormone may also stimulate mineralocorticoid release to some extent.75... 

Hematological Effects. A 62-year-old victim accidentally exposed to molten barium chloride had a depressed plasma potassium level and an increased plasma barium level when admitted to the hospital (Stewart and Hammel 1984). No studies were located regarding hematological effects in animals after dermal exposure to barium. 

Hypokalemia is commonly seen in cases of acute barium toxicity and may be responsible for some of the symptoms of barium poisoning (Proctor et al. 1988). Plasma potassium should be monitored and hypokalemia may be relieved by intravenous infusion of potassium (Dreisbach and Robertson 1987 Haddad and Winchester 1990 Proctor et al. 1988). 

Animals are placed in appropriately-sized metabolism cages for an appropriate period of time to allow collection of an adequate volume of urine (for large animals only a few hours may be needed for rodents, 12-24 hours might be required). To preserve the quality of the urine specimens, the collection vial must have a small neck (to prevent evaporation of water) and it should be surrounded by wet ice or frozen cold packs to ensure the urine is maintained at 4 °C for the duration of the collection period (Emeigh Hart and Kinter 2005). At the end of the collection period a blood sample is obtained under appropriate anesthesia (note the use of C02 will falsely elevate plasma potassium levels and render the method inaccurate) for determination of electrolyte and creatinine levels. 

An adult contains about 3 g of potassium. The plasma level is maintained within narrow limits by the kidney which can efficiently conserve or excrete potassium according to need. Abnormally low plasma levels cause muscle irritability and weakness together with potentially dangerous cardiac arrhythmias. Similar changes can also occur with abnormally high plasma potassium levels, thus making potassium determination one of the more important investigations in clinical medicine. 

Aldosterone secretion is also stimulated by increased plasma potassium concentration. Potassium is secreted into the urine in exchange for reabsorption of sodium in the distal nephron. Aldosterone also promotes secretion of hydrogen ions from the distal tubule according to the acid-base status of the... 

Q4 Potassium concentration is mainly controlled by the steroid hormone aldosterone. Aldosterone release from the adrenal cortex can be stimulated by either decreased plasma sodium or by increased plasma potassium concentration. An increase in aldosterone secretion causes retention (reabsorption) of sodium in the distal nephron in exchange for secretion of potassium into the urine. The amount of potassium excreted by the kidney is influenced by the acid-base status of the body. In alkalosis, potassium excretion increases, whereas in acidosis it is decreased. In the distal nephron H+ and K+ compete for excretion in exchange for the reabsorption of sodium. Insulin also affects plasma potassium concentration because it promotes the movement of potassium from the plasma into cells. 

Kevin s [K+] is somewhat higher than the normal range and a high plasma potassium concentration could account for his weakness and possibly contributes to his nausea. However, the increased plasma urea concentration, which Kevin also shows, is known to cause nausea and vomiting and is more likely to be responsible for these symptoms. 

As for digitoxin. Low plasma-potassium increases digoxin toxicity which may occur at therapeutic concentrations. 

A key factor for successful MHD operation is the degree of interaction between plasma potassium seed and the slag medium. Using slag activity data from the present studies, it is possible to predict conditions under which plasma seed will be continuously depleted by slag absorption of alkali. Plante et al. ( ) presented similar arguments earlier, based on their data for the binary oxide systems. A more definitive analysis can now be made from the present data on complex synthetic and actual slag systems. 

A vasoconstrictor should not be used for nerve block of an extremity (finger, toe, nose, penis). For obvious anatomical reasons, the whole blood supply may be cut off by intense vasoconstriction so that the organ may be damaged or even lost. Enough adrenaline (epinephrine) can be absorbed to affect the heart and circulation and reduce the plasma potassium. This can be dangerous in cardiovascular... 

Adrenergic mechanisms have a role in the physiological control of plasma potassium concentration. The biochemical pump that shifts potassium into cells is activated by the P -adrenoceptor agonists (adrenaline, salbutamol, isoprenaline) and can cause hypokalaemia. Pj-adrenoceptor antagonists block the effect. 

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