A summary of normal magnesium homeostasis, and an overview of the manifestations, etiologies, diagnostic evaluation, and treatment of both hypomagnesemia and hypermagnesemia.
Has been largely ignored in most clinical circumstances the reasons we tend to ignore magnesium disorders is twofold. we have limited understanding the significance and frequency of i’ll summarize the extent of what we do know. before discussing pathology and about 50 percent is in the intracellular which is the biologically active form. the consequence of the fact that
With total body magnesium content. let’s as with all electrolytes, homeostasis begins the gi tract, passive diffusion from the gi lumen, through the tight junctions between the bones act as a reservoir for huge amounts of magnesium. magnesium is freely filtered through the glomeruli of the kidneys, where most is in the thick ascending limb of the loop of henle. as with
The gut, reabsorption of sodium and chloride here. it is also dependent upon overall, there are no known hormones or enzymes that’s not to say there aren’t any. just that we don’t understand them yet. however, what regulation we do know about occurs mostly in the renal tubule where a number of metabolic derangements and thus lead to hypomagnesemia include low potassium,
High calcium, high magneseium (obviously), and a low serum ph. this is a good time to transition to hypomagnesemia. as hypomagnesemia is rarely seen in isolation from other electrolyte abnormalities, it’s difficult to attribute specific symptoms to it. for example, concurrent hypokalemia can lead to cardiac arrhythmias. which can manifest as tremors, fasciculations,
And tetany. and both hypertension and coronary artery disease, though a casual relationship in a similar manner, despite occasional claims to the contrary there are probably no specific abnormalities of the waveforms on the ekg that are specifically suggestive of hypomagnesemia. however, there are conditions in which hypomagnesemia these include acute myocardial infarction,
Prolonged qt syndrome, and may also increase the risk of a-fib in the general population. there are a large number of causes of hypomagnesemia. most commonly seen alcoholics. it is also observed in patients there’s also a very rare disorder called primary familial but which presents in infancy as hypocalcemia that’s responsive to iv this secondary hypocalcemia is believed
Lowering pth secretion and increasing pth resistance. detail in my video on normal calcium and phosphate physiology. which normally are largely reabsorbed later on in the gi tract. and those with extensive inflammatory by far, the most varied general category of etiologies cisplatin, and calcineurin inhibitors are all classic causes of hypomagnesemia. as mentioned
Earlier, hypercalcemia and hyperkalemia both inhibit magnesium reabsorption in the renal tubules. any process that causes a prominent osmotic diuresis which can be seen in uncontrolled alcohol is thought to cause transient tubular dysfunction, finally, there are a handful of rare familial renal magnesium wasting syndromes. caused by a defect in the thiazide-sensitive
Sodium chloride co transporter in the distal tubule, which also results in very rare genetic defects affecting the claudin 16 protein lastly, in the miscellaneous category is pancreatitis, of retroperitoneal fat. and magnesium can be quickly drawn up from the serum moving on to the diagnostic evaluation of hypomagnesemia, if it’s not, one can calculate the fractional
Excretion of magnesium. the 0.7 term here accounts for the fact that only about 70 percent of excessive renal losses. if it’s less than 2 percent, when it comes to the treatment of hypomagnesemia, on one level, one reason for this is abrupt increases in serum mag, as which greatly predisposes to arrhythmias, oral repletion is usually preferred. although it’s a common
Practice to give iv mag relatively quickly, a practical question that quickly comes up and which is literally it’s common practice to replete serum mag to high normal levels, possible exceptions to this, that is, patients to still replete above 2 include those with acute mis, those with active arrhythmias, in patients who are either elderly and/or have renal impairment,
I feel like because hypermagnesemia is often more abrupt and iatrogenic, and not from other concurrent electrolyte disorders as with which can progress to complete heart block and even asystole, the etiologies of hypermagnesemia are pretty minimal. are sort of regulated, and if they aren’t working properly, that it may have absorbed from the gut. the next mechanism of
Hypermagnesemia it can be from excessive iv infusion, which can be seen during the treatment in which appropriate treatment almost and finally, can be from magnesium containing enemas, and in fact, magnesium containing enemas are contraindicated the only significant miscellaneous mechanism is tumor lysis syndrome, or in response to initiation of chemotherapy, suddenly die
In general, the hypermagnesemia from this will be relatively minor issue the diagnostic evaluation of hypermagnesemia is the easiest i personally have never encountered a patient with hypermagnesemia who the treatment of hypermagnesemia depends upon the patient’s renal function. if the patient has chronic kidney disease with a gfr on the order a 15 to 45, a combination of
Normal saline and furosemide should be sufficient, if the patient has chronic kidney disease with a gfr under 15 finally, in a setting of acute, life-threatening hypermagnesemia, know a lot more about this electrolyte but from a clinical standpoint, potassium disorders
Transcribed from video
Magnesium Disorders By Strong Medicine
