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Parenteral Nutrition Components, Admixture and Administration
Published in Michael M. Rothkopf, Jennifer C. Johnson, Optimizing Metabolic Status for the Hospitalized Patient, 2023
Michael M. Rothkopf, Jennifer C. Johnson
PN formulas that contain large quantities of electrolytes, particularly sodium and potassium, will have higher osmolarity. As a rule, sodium and potassium salts have an osmolarity of about 2 mOsm/mEq. But the phosphate salts are notable exceptions. Potassium phosphate has an osmolarity of about 2.5 mOsm/mmol and sodium phosphate about 4 mOsm/mmol. The remaining micronutrients generally play a minor role in the osmolarity of the PN.
Electrolyte and Acid-Base Disturbances
Published in John K. DiBaise, Carol Rees Parrish, Jon S. Thompson, Short Bowel Syndrome Practical Approach to Management, 2017
Lingtak-Neander Chan, Berkeley N. Limketkai
IV potassium supplementation is highly effective, although it carries risks. The most serious risk associated with IV potassium is arrhythmia, which is closely associated with the rate of infusion. As a general rule, the rate of potassium infusion should never exceed 10 mEq/hour in the absence of continuous electrocardiographic monitoring. Infusion rates >10 mEq/hour should be given only in settings with continuous cardiac monitoring, such as the intensive care unit. Rates above 20 mEq/ hour are highly irritating to peripheral veins. An infusion rate >40 mEq/hour is not recommended. The preferred vehicle in delivering potassium is saline solution, as infusing large amount of dextrose may stimulate insulin release, which would drive plasma potassium intracellularly. Potassium acetate should be considered in patients with hypokalemia who also have metabolic acidosis or a bicarbonate deficit. Similarly, potassium phosphate can be used in hypokalemic patients with concomitant hypophosphatemia. To maximize potassium retention, serum magnesium concentration should be monitored and deficiency corrected.
Phosphate
Published in Linda M. Castell, Samantha J. Stear (Nottingham), Louise M. Burke, Nutritional Supplements in Sport, Exercise and Health, 2015
Although in most instances the supplementation of various phosphate sources (sodium, calcium or potassium phosphate) in athletes is innocuous, the following should be noted: oral supplementation with phosphate may cause gastrointestinal distress, leading to cramping, diarrhoea and/or vomiting. In addition, excessive phosphate loading may place unnecessary strain on the kidneys and, as a result, any athletes with known kidney disorders should refrain from using this supplement.
Investigation of the inhibition of eight major human cytochrome P450 isozymes by a probe substrate cocktail in vitro with emphasis on CYP2E1
Published in Xenobiotica, 2019
Guru R. Valicherla, Amrut Mishra, Srinivas Lenkalapelly, Bhupathi Jillela, Femi M. Francis, Lakshman Rajagopalan, Pratima Srivastava
All incubation mixtures contained microsomal protein 0.2 mg/mL, 1 mM NADPH, 100 mM potassium phosphate buffer (pH 7.4), and individual substrates or probe substrate cocktail (tacrine, diclofenac, S-(+)-mephenytoin, dextromethorphan, midazolam, bupropion, paclitaxel, and chlorzoxazone) in a total volume of 100 µL. Potassium phosphate buffer was prepared fresh weekly by adding 13.98 g of dibasic potassium phosphate and 2.7 g of monobasic potassium phosphate in 1000 mL water and pH adjusted to 7.4. The substrates were used at concentrations equal to their respective Km values: 5 µM for tacrine, diclofenac, paclitaxel, bupropion, dextromethorphan, 2 µM for midazolam, 30 µM for S-(+)-mephenytoin and 200 µM for chlorzoxazone. The final concentrations of methanol, acetonitrile and DMSO for the cocktail incubation conditions were 0.075%, 0.1% and 0.4% respectively. Samples were preincubated for 15 min at 37 °C in shaking water bath (Julabo SW23). The reaction was initiated by the addition of NADPH. Incubation was carried out for 5 min (CYP3A4) and 17 min for remaining isoforms. The reaction was terminated by adding 150 µL ice cold ACN containing internal standard (IS, telmisartan, and metoprolol). Samples were vortexed for 5 min at 900 rpm using Plate Mixer (Mix Mate) and centrifuged for 5 min at 4000 rpm to pellet the precipitated protein. The 150 µL supernatant was transferred to phenomenex plates containing 150 µL water and vortexed for 5 min at 900 rpm. The half diluted samples were analyzed by using LC-MS/MS.
A practical guide to the interpretation of PK/PD profiles of longer-acting analogue insulins. Part one: The principles of glucose clamp studies
Published in Journal of Endocrinology, Metabolism and Diabetes of South Africa, 2018
Oppel BW Greeff, Jacob John van Tonder, Kershlin Naidu, Alicia McMaster, Alet van Tonder, Rashem Mothilal
After an overnight fast, a 20% dextrose solution and/or rapid-acting insulin is administered intravenously to reach clamp glucose and insulin target. Insulin is administered to suppress endogenous insulin and hepatic glucose production. Potassium phosphate may also be administered to prevent hypokalaemia.15 Once the clamp target has been reached, infusion of rapid-acting insulin is gradually tapered off and discontinued prior to administration of the long-acting study insulin. The long-acting study insulin is administered at a predetermined dose. Blood samples are collected at regular intervals to determine blood glucose and plasma insulin concentrations. Based on the blood glucose levels determined, the glucose infusion rate is adjusted to maintain clamp target.7,8
A rare case of parental iron-induced persistent hypophosphatemia
Published in Journal of Community Hospital Internal Medicine Perspectives, 2020
Abigayle Sullivan, Theresa Lanham, Adam Rubin
At the time of her first infusion, serum phosphate was 3.6 [ref: 2.5–4.5] mg/dL. One week later, the patient was hospitalized for fatigue, weakness, and lightheadedness. Her symptoms were attributed to a urinary tract infection. Interestingly, serum phosphate was noted to be 1 mg/dL and was repleted with 21 mmol of potassium phosphate. The patient’s serum phosphate level was not reassessed until hospitalization, just prior to her third scheduled ferric carboxymaltose infusion, and was <1 mg/dL. The patient’s severe hypophosphatemia was corrected with a total of intravenous [IV] sodium phosphate 60 mmol, IV potassium phosphate 151 mmol, oral monobasic and dibasic sodium and potassium phosphate 3,750 mg, and calcitriol 0.25 mcg daily over the course of 5 days.