Yu, Yan – Hypercalcemia – Clinical Findings – FINAL.pptx
Hypercalcemia: Clinical FindingsAuthor: Yan YuReviewers:David WaldnerSean SpenceGreg Kline** MD at time of publicationLegend:Published May 7, 2013 on www.thecalgaryguide.comMechanismPathophysiologySign/Symptom/Lab FindingComplicationsHypercalcemia(serum [Ca2+] > 2.5mmol/L)Na+ channels on neuronal membranes become more resistant to opening (resists Na+ influx)Cognitive dysfunctionIf precipitation occurs in the urinary tract…Fatigue? contractility of GI tract smooth muscle? K+ movement out of TAL epithelial cells into the tubule lumen Alters charge balance across the cell membraneCa2+ precipitates with PO43- throughout the bodyDetected by the Ca-Sensing-Receptor (CaSR) on Thick Ascending Limb (TAL) epithelial cells? neuronal action potential generationSluggish neuronal activity…? appetiteConstipationFlank painInhibit insertion of Renal Outer Medullary K+ (ROMK) channels on TAL’s luminal membrane? K+ in TAL lumen to drive Na+/Cl- reabsorption through the Na-K-Cl Cotransporter (NKCC)? Na/Cl in tubule lumen ? osmotically draws water into lumen? drinking (polydipsia)? Urine volume (polyuria)Rationale for the CaSR-pathway: ECF has enough Ca2+, no need for more K+ to be excreted into the tubule lumen to create a more + charge there that drives Ca2+ reabsorptionBehavior compensates to prevent dehydrationKidney stones (nephrolithiasis)Constantly feeling full because of reduced GI motilityCa2+ directly inhibits the insertion of aquaporin channels in the collecting duct membraneLess water reabsorbed into the renal vasculatureMore water remains in the tubule filtrateMuscle Weakness…in central nervous system:…at neuromuscular junction:A rhyme to help you recall the manifestations of one specific cause of hypercalcemia, primary hyperparathyroidism:Bones (Calcium levels are high often due to ? resorption from bones)Stones (? Calcium-containing kidney stones)Groans (GI and skeletal muscle issues) Psychic Moans (Cognitive dysfunction from neuronal disturbances)Note: sick/ICU patients have ? serum albumin, due to ? synthesis from a sick liver. Their lab Ca2+ values can be “normal”, but they may be truly hypercalcemic (more “free Ca2+”, less “albumin-bound Ca2+”). Correct this by adding 0.2mmol/L to the lab Ca2+ value for every 10g/L drop of albumin below 40g/LNote: “Total Ca2+” in the blood is either “free”, or bound to albumin. The lab value measures the “Total Ca2+”, but it is the “free Ca2+” that carries out Ca2+’s functions and determines if someone is hyper- or hypo-calcemic.
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