Being an outstanding physician and lifelong learner requires stoking the flames of clinical curiosity. In Chiefs’ Inquiry Corner (CIC) we attempt to succinctly answer actual clinical questions that have been raised on the wards and in the clinics of NYU’s teaching hospitals. Our answers are not meant to be all encompassing or practice changing but rather to serve as springboards for further exploration. For those of us with short attention spans, we hope CIC satisfies that craving for a morsel of knowledge in a digestible format.
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Beta blockers (BBs) have fallen out of favor as first-line, or even second-line, treatment options for hypertension. And as patients’ medical regimens gradually drop BBs, concerns may arise about the rebound phenomenon we learn in medical school. With chronic beta blocker therapy, there is an upregulation of receptors, which can lead to an adrenergic surge if BBs are abruptly stopped. This is particularly seen with short-acting BBs. So, how do we prevent an adrenergic surge and appropriately taper? We don’t really know, as there haven’t been many studies. One study from back in 1982 compared a propranolol taper over 6 to 9 days versus over 2 weeks and found no difference in blood pressure. Beta-adrenergic receptors have half-lives of 1.5 days, so tapering with halved doses every two to three days to allow for downregulation appears to be one reasonable approach.
Conventional wisdom suggests that patients must be vitamin D replete prior to the initiation of antiresorptive therapy. The reason is such: while all bisphosphonates are osteoclast inhibitors, several older agents, such as etidronate, also have a small inhibitory effects on osteoblasts. Therefore, there was a theoretical concern that in patients with vitamin D deficiency, who have high PTH levels, that the osteoclast inhibitory effect would be blunted by the effects of PTH, while the osteoblast inhibitory effect would be unchecked, resulting in lower efficacy of treatment and a higher risk for osteomalacia after bisphosphonate initiation. However, newer agents, such as alendronate, have no inhibitory effect on osteoclasts. Moreover, the safety and efficacy of alendronate therapy in vitamin D deplete patients has been shown in a large RTC. At the end of the day, it is safe to start vitamin D and alendronate concurrently in these patients, as opposed to waiting for vitamin D repletion prior to bisphosphonate initiation.
References: Bisphosphates and Vitamin D Deficiency
Both calcium chloride and calcium gluconate can be used in the treatment of hyperkalemia. Calcium gluconate is less irritating and less likely to cause necrosis at the injection site, but calcium chloride has the theoretical advantage of faster onset as calcium gluconate theoretically needs to be hepatically metabolized in order to release the active elemental form of calcium. However, in a study of adults undergoing liver transplant, subjects were given an equivalent dose of calcium by calcium chloride or calcium gluconate, and ionized calcium concentration were measured at short intervals. An equivalent rapid increase in calcium levels was detected with the administration of both medications at 1 min, with a slow downtrend after, suggesting this theory may not be correct.
References: Calcium Administration During Liver Transplant