Hypocalcemia (Low Calcium) - Managing Side Effects - Chemocare
If the patient has a low albumin-corrected serum calcium or ionized calcium Hypoalbuminemia: Calcium correction — Calcium in serum is bound to the total calcium concentration by approximately mg/dL ( mmol/L). Mg absorption is not regulated; balance is maintained by renal excretion. Magnesium Each g of albumin binds mg of calcium. Complexing anions. Ionised Ca is inversely related to serum albumin; Total serum Ca is Ca is adjusted by mg/dL for every 1G/dL change in serum albumin).
Intracellular K diffuses passively across cell membranes; the magnitude of K transmembrane diffusion determines transmembrane electrical potential. As a rule of thumb, for each 0. Hyperosmolality may cause extracellular K shifts, such as in severe hyperglycemia and after rapid intravenous administration of sodium bicarbonate. Plasma K concentration may rise as much as 0. Extracellular concentration of K 3.
The two pathways of excretion of K are intestinal and renal. Renal K excretion is tightly regulated to maintain balance between intake and output and stable K body contents.
In adults, intake and output is usually equal and approximately 1. Renal K excretion is primarily stimulated by three factors: Increase in serum K concentration Increase in serum aldosterone concentration. Aldosterone increases the number of open apical cell sodium channels; increased Na reabsorption increases the electronegativity of the lumen and therefore enhances K secretion. Enhanced delivery of sodium and water to the distal secretory site. A K load is usually excreted in the urine in 6 to 8 hours in patients with normal renal function.
Virtually all the K excreted in the urine is K secreted in the renal tubules; virtually all filtered K is reabsorbed completely in the proximal tubule and thick ascending loop of Henle TALH. Renal excretion of K is regulated by modifying K tubular secretion.
Renal tubular handling of K is closely associated with renal control of acid-base equilibrium Renal tubular handling of K is tightly regulated by the renin-angiotensin-aldosterone axis. K filters freely across the glomerular filtration membrane. The remaining K in tubular fluid is virtually completely reabsorbed in the thick ascending loop of Henle, in a process that can be inhibited by loop diuretics.
Apical secretory K channels recycle K intra- and extracellularly and maintain an intratubular-positive transepithelial electrical gradient, which favors Ca and Mg reabsorption. In the distal and cortical collecting tubule two morphologically distinct cells, the principal cells PC and the intercalated cells IC are responsible for K secretion and reabsorption, respectively.
IC are capable of significant reabsorption of K during periods of K depletion. Apical entry of Na via the epithelial Na channel ENaC generates a lumen-negative transepithelial potential that drives K exit via apical channels. Distal K secretion is critically dependent on distal Na delivery In the distal nephron, K is recirculated such that K secreted in the cortical collecting duct is reabsorbed in the outer and innner medullary collecting duct and secreted into the thin descending loop of Henle medullary K recycling.
This recirculation causes high medullary K concentration and contributes to a lumen-negative transepithelial gradient that favors K secretion. Mediates baseline K secretion and is stimulated by increased tubular flow such as in volume expansion or diuretic therapy; mediates adaptive increases in K excretion. Mediates flow-stimulated K secretion in connecting tubule and cortical collecting duct. Regulates distal K transport.
Disorders of K, Mg, and Calcium balance - Cancer Therapy Advisor
Sodium delivery Extracellular volume expansion or diuretic administration enhances K secretion. Concurrent reabsorption of Cl- reduces transepithelial electrical gradient and limits K secretion.
The normal adult value for calcium is 4. Calcium is important for healthy bones and teeth, as well as for normal muscle and nerve function. If your blood test results show hypocalcemia, your doctor may check your albumin level as well. A corrected calcium level will be higher if the albumin is low. There are many causes of hypocalcemia, these include; Vitamin D deficiency Magnesium deficiency Alcoholism Biphosphonate therapy - drugs used to treat high blood calcium levels or pills used to treat osteoporosis.
Ionized Calcium Test
Certain types of leukemia or blood disorders A complication of chemotherapy, tumor lysis syndrome, occurs when your body breaks down tumor cells rapidly, after chemotherapy.
This may cause hypocalcemia, high blood potassium levels, and other electrolyte abnormalities. This is very serious, and if your blood test results indicate you suffer from it, your doctor or health care provider will need to closely monitor you during this time.
Drugs such as diuretics, estrogens replacement therapy, fluorides, glucose, insulin, excessive laxative use, and magnesium may also lead to hypocalcemia. Certain things in your diet, like caffeine, phosphates found in soda popand certain antibiotics may make it difficult for you to absorb calcium. Vitamin D, however, helps you to absorb calcium in your body. The most common sign of hypocalcemia is what is called "neuromuscular irritability. If your blood test results indicate hypocalcemia, you may notice muscle cramps in your legs or your arms.
The symptoms of hypocalcemia you experience may relate to how fast or how slowly the fall in blood calcium levels occur. If you have long-standing low blood calcium levels, you may notice no symptoms of hypocalcemia.
If you have an "acute" or sudden drop in your blood calcium level, you may notice more twitching. You may notice, with mildly lowered blood calcium levels, numbness and tingling of your fingers and toes.
You may notice that you are depressed, or more irritable if you have mildly low hypocalcemia. With severely lowered blood calcium levels, you may become confused or disoriented.
Your heart muscle may contract irregularly due to the electrolyte disturbance.