Posted: February 16th, 2023
The primary hormone involved in regulating serum calcium concentrations is parathyroid hormone (PTH). High levels of PTH lead to increased mobilization of calcium from bone stores, reabsorption from renal tubules, as well as absorption from food sources. Low levels of PTH result in decreased absorption from dietary sources with a parallel decrease in reabsorption from the kidneys. Vitamin D also plays an important role in maintaining appropriate calcium levels by increasing intestinal absorption; its active form 1α 25-dihydroxyvitamin D3 increases expression of calcium transporters on enterocytes allowing increased uptake into circulation although this process is stimulated primarily by PTH rather than vitamin D alone. Finally calcitonin secreted by the thyroid gland has an inhibitory effect on bone resorption which serves to lower circulating serum calcium levels but it acts counterintuitively compared to other hormones since it induces a decrease when serum concentrations rise above normal range.
Phosphorus balance is regulated primarily through control of renal elimination however hormonal control plays a secondary yet significant role via regulation by fibroblast growth factor-23 (FGF-23) which inhibits the production vitamin D’s active form leading to decreased phosphorus resorption at distal convoluted tubules resulting in excretion with urine. Additionally FGF-23 leads directly or indirectly to phosphaturia via suppression of 1α hydroxylase enzyme activity responsible for conversion 25 hydroxyform into its more potent bioactive form thus decreasing phosphorus reabsorption even further making it available for removal via glomerular filtration rate increase due lack inhibition provided by vitamin D’s active form normally acting upon proximal convoluted tubules leading outflow concentration greater than what would be expected based solely upon GFR related parameters alone so this implies additional influence exerted through direct action FGF-23 itself beyond just mere suppression/inhibition biochemical steps needed convert 25 hydroxyform its respective bioactive derivative before efficacy can take place (i e no receptor mediated activation mechanism present without requisite metabolic step having first been completed).
Hypercalcemia occurs when serum calcium rises above 10 mg/dL whereas hypocalcemia refers any level below 8 5mg/dL respectively Both have distinct pathophysiology clinical manifestations evaluations treatments depending on underlying cause etiologic agent driving toward development particular phenomenon within given individual patient profile It should noted hypercalcemia usually results either overproduction parathyroid hormone low cortisol states seen adrenal insufficiency Addison’s disease while hypocalcemia can caused disorders involving inadequate intake activated vitamins alongside issues dependent deficiencies magnesium potassium zinc.
Clinical manifestations hypercalcemia include weakness fatigue confusion altered mental status mood changes nausea vomiting constipation abdominal pain polyuria dehydration hypotension irregular heartbeat cardiac arrhythmias seizures. Another common symptom prior diagnosis presence nephrolithiasis bladder stones. Evaluation begins complete history physical including laboratory data comprehensive chemistry panel evaluation assesses electrolytes ACR albumin calculation imaging studies rule out malignancy metastatic spread examination skeletal system all done aid diagnosis treatment plan.
Treatment depends upon severity symptoms degree elevation initiate aggressive hydrations parenteral saline solution along furosemide demeclocycline bisphosphonates order reduce associated morbidity mortality Hypocalcemic symptoms tetany cramps neuromuscular irritability general malaise nausea fatigue confusion. Evaluations same those listed previously however therapeutic approach different Oral replacement therapy prescribed supplement ionized forms amount adjustment commonly. serums ranging 4 6 – 10 2 mg dL may require intravenous repletion regenerate critically depleted locations intravascular space Treatments focus mainly repletion regimen large pharmacological doses correct relatively rapid return attained reference standards measure decreases accordingly
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