Hypokalemia alkalosis causing

Regardless of the cause of the hypokalemia, potassium supplements usually are provided to diminish the symptoms and complications. Caution is taken with potassium supplements to avoid excess. If hypokalemia is caused by alkalosis, particular caution is taken with supplements because the correction of alkalosis will cause potassium to shift hack out of the cells, and supplements could result in a potassium excess. 

The use of CA inhibitors as diuretics is limited by their propensity to cause metabolic acidosis and hypokalemia. Their use can be indicated in patients with metabolic alkalosis and secondary hyperaldosteronism resulting for example from aggressive use of loop diuretics. Furthermore, CA inhibitors are effective dtugs to produce a relatively alkaline urine for the treatment of cysteine and uric acid stones as well as for the accelerated excretion of salicylates. Perhaps the most common use of CA inhibitors is in the treatment of glaucoma. 

Liddle s syndrome is an autosomal dominant disorder that is caused by persistent hyperactivity of the epithelial Na channel. Its symptoms mimic aldosterone excess, but plasma aldosterone levels are actually reduced (pseudoaldosteronism). The disease is characterized by early onset arterial hypertension, hypokalemia, and metabolic alkalosis. 

Acid-base and electrolyte balance High therapeutic dose especially when used in rheumatic fever, stimulates respiration and causes respiratory alkalosis. Reduction in bicarbonate and potassium level reduces the buffering capacity of the extracellular and intracellular fluid. Hypokalemia may lead to dehydration and hypernatremia. They also interfere with carbohydrate metabolism resulting in accumulation of pyruvic acid and lactic acid. 

It is important to note that, even more than in heart failure, overly aggressive use of diuretics in this setting can be disastrous. Vigorous diuretic therapy can cause marked depletion of intravascular volume, hypokalemia, and metabolic alkalosis. Hepatorenal syndrome and hepatic encephalopathy are the unfortunate consequences of excessive diuretic use in the cirrhotic patient. 

Sodium Polystyrene Sulfonate (Kayexalate) [Potassium Removing Resin] Uses Rx of T K+ Action Na+/K+ ion-exchange resin Dose Adults. 15-60 g PO or 30-60 g PR q6h based on serum K+ Peds. 1 g/kg/dose PO or PR q6h based on serum K+(given w/ agent, eg, sorbitol, to promote movement through die bowel) Caution [C, M] Contra T Na+Disp Powder, susp SE T Na+, vl K+, Na retendon, GI upset, fecal impaction Interactions T Risk of systemic alkalosis W/ Ca- or Mg-containing antacids EMS Monitor ECG for hypokalemia (flattened T waves) OD Not systemically absorbed but may cause hypokalemia and die associated effects (muscle weakness, confusion) and bowel obstruction symptomatic and supportive... 

Several relatively common disorders result in aldosterone secretion abnormalities and aberrations of electrolyte status. In Addison s disease, the adrenal cortex is often destroyed through autoimmune processes. One of the effects is a lack of aldosterone secretion and decreased Na+ retention by the patient. In a typical Addison s disease patient, serum [Na+] and [CL] are 128 and 96 meq/L, respectively (see Table 16.2 for normal values). Potassium levels are elevated, 6 meq/L or higher, because the Na+ reabsorption system of the kidney, which is under aldosterone control, moves K+ into the urine just as it moves Na+ back into plasma. Thus, if more Na+ is excreted, more K+ is reabsorbed. Bicarbonate remains relatively normal. The opposite situation prevails in Cushing s disease, however, in which an overproduction of adrenocorticosteroids, especially cortisol, is present. Glucocorticoids have mild mineralocorticoid activities, but ACTH also increases aldosterone secretion. This may be caused by an oversecretion of ACTH by a tumor or by adrenal hyperplasia or tumors. Serum sodium in Cushing s disease is slightly elevated, [K+] is below normal (hypokalemia), and metabolic alkalosis is present. The patient is usually hypertensive. A more severe electrolyte abnormality is seen in Conn s syndrome or primary aldosteronism, usually caused by an adrenal tumor. Increased blood aldosterone levels result in the urinary loss of K+ and H+, retention of Na+ (hypernatremia), alkalosis, and profound hypertension. 

Mineralocorticoids help control the body s water volume and concentration of electrolytes, especially sodium and potassium. Aldosterone acts on kidney tubule cells, causing a reabsorption of sodium, bicarbonate, and water. Conversely, aldosterone decreases reabsorption of potassium, which is then lost in the urine. [Note Elevated aldosterone levels may cause alkalosis and hypokalemia, whereas retention of sodium and water leads to an increase in blood volume and blood pressure (see p. 180). Hyperaldosteronism is treated with spironolactone (see p. 232).]... 

Intracellular redistribution of is illustrated by the fall in plasma IC that occurs following insuiin therapy for diabetic hyperglycemia. The cells must take up as a consequence of glucose transport. Redistribution hypokalemia is also a feature of alkalosis, in which K moves from ECF into the cells as H moves in the opposite direction. In addition, the renal conservation of m the distal tubule occurs at the expense of ions. On the other hand, severe intracellular IC depletion may also cause alkalosis, as shifts intracel-lularly. Catecholamines and states of endogenous or pharmacological P-adrenergic excess have a similar effect. 

Hypokalemia is common in the patient with liver failure who has normal renal function. Poor nutritional intake and vomiting may initiate this disorder. Severe vomiting may lead to volume contraction metabolic alkalosis, with increased renal excretion of potassium. Secondary hyperaldosteronism, seen in the liver failure patient with intravascular depletion, also increases renal excretion of potassium. Loop diuretic therapy causes increased renal excretion of potassium, whereas diarrhea from lactulose therapy increases fecal excretion of potassium. All these conditions can lead to profound hypokalemia. Therefore, potassium requirements in the liver failure patient receiving specialized nutritional support often are increased substantially. 

The thiazide diuretics, also called sulfonamide or ben-zothiadiazide diuretics, vary in their actions. For instance, the potency of hydrochlorothiazide (Hydro-Diuril and Esidrix) is ten times greater than that of chlorothiazide (Diuril), but the drugs have equal efficacy. The duration of action of hydrochlorothiazide, which is 6 to 12 hours, equals that of chlorothiazide. On the other hand, chlorthalidone (Hygroton) has a duration of action lasting 48 hours. Some thiazide derivatives inhibit carbonic anhydrase, which is unrelated to their diuretic activity. Those that are active in this respect may, at sufficient doses, have the same effect on bicarbonate excretion as does acetazola-mide. They cause a moderate loss of sodium (5 to 10% of the filtered load), chloride, and water, and the clearance of free water is impaired. They may cause metabolic alkalosis (resorption of bicarbonate and loss of hydrogen ions), hyperuricemia (enhanced resorption of uric acid), or hyperglycemia (due to directly inhibited insulin release and to hypokalemia). 

These actions on electrolyte transport, in the kidney and in other tissues e.g., colon, salivary glands, and sweat glands), appear to account for the physiological and pharmacological activities that are characteristic of mineralocorticoids. Thus, the primary features of hyperaldosteronism are positive Na balance with consequent expansion of extracellular fluid volume, normal or slight increases in plasma Na+ concentration, hypokalemia, and alkalosis. Mineralocorticoid deficiency, in contrast, leads to Na+ wasting and contraction of the extracellular fluid volume, hyponatremia, hyperkalemia, and acidosis. Chronically, hyperaldosteronism can cause hypertension, whereas aldosterone deficiency can lead to hypotension and vascular collapse. 

Primary Hyperaldosteronism Caused by adrenal adenoma which secretes aldosterone. Results in hypertension, hypokalemia, metabolic alkalosis, suppressed renin. 

Loop or high-ceiling diuretics causes a vasodilatory effect and increase renal blood flow before diuresis. The most common side effects are fluid and electrolyte imbalances such as hypokalemia, hyponatremia, hypocalcemia, hypomagnesemia, and hypochloremia. Hypochloremic metabolic alkalosis may result. Orthostatic hypotension can also occur. Thrombocytopenia, skin disturbances, and transient deafness are seen rarely. Prolonged use can cause thiamine deficiency. 

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