Advanced Laboratory Evaluation PDF

Advanced Labs 6/27/2024 Advanced Laboratory Evaluation Patti Parker, PhD,APRN,CNS,ANP,GNP,BC 1 Topics for Disc...

Advanced Labs 6/27/2024 Advanced Laboratory Evaluation Patti Parker, PhD,APRN,CNS,ANP,GNP,BC 1 Topics for Discussion Disorders of Sodium Disorders of Calcium Disorders of Phosphorus Disorders of Magnesium Disorders of Proteins – Serum and Urine Uncommon Anemias 2 2 Patti Parker, PhDc, CNS, A/GNP 1 Advanced Labs 6/27/2024 Disorders of Sodium Hypernatremia Hyponatremia SIADH 3 3 Hypernatremia Plasma Na+ >145 mEq/L, caused by a deficit of H2O relative to solute Mortality of 40-60% Hypernatremia implies hyperosmolality of ECF, which results in H2O moving out of intracellular spaces until cellular tonicity to that of ECF 4 4 Patti Parker, PhDc, CNS, A/GNP 2 Advanced Labs 6/27/2024 Risk Factors Vomiting Diarrhea Renal disease Taking loop diuretics Burns Excessive sweating 5 5 Pathogenesis Usually caused by excess loss of H2O from body that is not adequately replaced Most common cause of hypernatremia from osmotic diuresis is hyperglycemia, seen in nonketotic hyperosmolar hyperglycemic coma of diabetes 6 6 Patti Parker, PhDc, CNS, A/GNP 3 Advanced Labs 6/27/2024 Pathogenesis [con’t] Renal insufficiency can prevent maximally concentrated urine, predisposing to Na+ When H2O deficit exists, hypernatremia occurs without disturbance in Na+ balance – Excess sweating– H2O loss 7 7 Pathogenesis [con’t] Diabetes insipidus is a defect in production or release of ADH by posterior pituitary – Patient cannot secrete a concentrated urine – Thirst is okay, patient develops Na+ if they do not have access to H2O 8 8 Patti Parker, PhDc, CNS, A/GNP 4 Advanced Labs 6/27/2024 Hypernatremia Common in the elderly, related to – Inability to access H2O – Impaired thirst – Impaired renal concentrating ability – Increased insensible H2O loss 9 9 Hypernatremia Diagnosis Treatment – Signs and Symptoms – H2O replacement Thirst is primary goal CNS Symptoms – If patient – Brain stem shrinkage cannot drink– IV – Confusion with D5W – Neuromuscular irritability – Seizures – Coma 10 10 Patti Parker, PhDc, CNS, A/GNP 5 Advanced Labs 6/27/2024 Principle Causes of Hypernatremia Hypernatremia with Hypernatremia with Hypernatremia with Hypovolemia Euvolemia Hypervolemia [ TBW and Na+; greater  [ TBW; near normal body Na+] [ Na+; normal or TBW] in TBW] Extrarenal Vomiting Extrarenal Tachypnea Hyper-tonic Hypertonic losses Diarrhea losses Fever IV fluids Saline Burns Excess NaHCO3 Excess sweating TPN sweating Renal losses Intrinsic Renal losses Central DI Mineralo- Adrenal tumor renal disease Nephrogenic DI corticoid secreting Osmotic deoxycorti- excess diuresis costerone [glucose, Congenital urea, adrenal mannitol] hyperplasia Loop diuretics Other Inability to Iatrogenic access H2O Primary hypodipsia Reset osmostat 11 11 Hyponatremia Plasma Na+ Na+ is lost than H2O – Protracted vomiting, severe diarrhea – Sequestration of fluid in 3rd space is replaced with free H2O or treated with hypovolemic IVF Significant ECF loss results in release of ADH, causing H2O retention by kidneys and  hyponatremia 15 15 Euvolemic Hyponatremia TBW is  and there is no significant change to total body Na+ Dilutional hyponatremia can occur from  H2O intake without Na+ retention in presence of renal failure, Addison’s disease, myxedema or nonosmotic ADH secretion [stress, post-op and certain drugs] – Chlorpropamide, Tolbutamide, Opioids, barbiturates, Vincristine, Clofibrate, Carbamazepine 16 16 Patti Parker, PhDc, CNS, A/GNP 8 Advanced Labs 6/27/2024 Hypervolemic Hyponatremia Increase in TBW and total body Na+ content CHF and Liver Failure Decrease in effective circulating volume causes release of ADH and angiotensin II – Hyponatremia results from antidiuretic effect of ADH on kidneys and direct impairment of renal H2O excretion by angiotensin – Decreased GFR and stimulation of thirst by angiotensin II also potentiates development of hyponatremia 17 17 Effects on CNS Brain cellular H2O  in acute and chronic hyponatremia – As a result of  brain electrolyte content, the  in brain H2O content in chronic hyponatremia is less than would be expected Symptoms of CNS dysfunction are more common and greater in acute hyponatremia 18 18 Patti Parker, PhDc, CNS, A/GNP 9 Advanced Labs 6/27/2024 Principle Causes of Hyponatremia Hyponatremia with Hypovolemia Hyponatremia with Euvolemia Hyponatremia with [ TBW and Na+; greater [ TBW; near normal total Hypervolemia [relative]  of Na+] body Na+] [ total body Na+; relatively greater  in TBW] GI Vomiting Syndrome of inappropriate Congestive Heart Failure Diarrhea ADH secretion 3rd Pancreatitis States that Postop narcotics Hepatic cirrhosis spacing Peritonitis increase Pain Small bowel release of Emotional stress obstruction ADH Rhabdomyolysis Burns Renal Diuretics Others Diuretics Renal Nephrotic losses Osmotic diuresis Hypothyroidism disorders syndrome [glucose, urea, Glucocorticoid Acute renal mannitol] deficiency failure Mineralocorticoid Primary polydipsia Chronic renal deficiency failure Salt-losing nephropathies 19 19 Syndrome of Inappropriate Antidiuretic Hormone Secretion [SIADH] SIADH is Etiology – Less than maximally – Actual cause is dilute urine in often unknown presence of plasma – Sustained ADH hypoosmolality and release hyponatremia – Osmotic threshold for ADH release is subnormally low – In some, ADH is not suppressed in presence of low plasma osmolality 20 20 Patti Parker, PhDc, CNS, A/GNP 10 Advanced Labs 6/27/2024 Pathogenesis of SIADH Classically, SIADH is sustained ADH release In some, ADH secretion is erratic and apparently independent of osmotic control In others, ADH levels vary appropriately with plasma osmolality, but osmotic threshold for ADH is abnormally low [reset osmostat] A small group of people have low levels of ADH, and when plasma becomes hypoosmotic, ADH is not suppressed 21 21 Diagnosing SIADH Symptoms of hyponatremia occur when plasma osmolality falls to 12 mg/dL, ionized Ca+ is almost always  Low PO4- indicates some form of hyperparathyroidism In primary hyperparathyroidism,  serum Ca+, normal PO4-; if PO4- is , it is 2nd disease If hyperparathyroidism is causing increased bone turnover, alkaline phosphatase is  Humoral Hypercalcemia of Malignancy– diagnosis is usually made by presence of PTH-related peptide 49 49 Diagnostic Tests Parathyroid Hormone Assays – Recently, PTH by IRMA [immunoradiometric assays] have improved sensitivity to detect hyperparathyroidism – Confirm with your lab that this is the current form of the PTH assay that they are running 50 50 Patti Parker, PhDc, CNS, A/GNP 25 Advanced Labs 6/27/2024 Further Evaluation Once hypercalcemia and elevated PTH are established, rule out malignancy and impaired renal status Check urinary excretion of calcium Patients with benign familial hypercalcemia from parathyroid hyperplasia do not have hypercalciuria or other complications of hypercalcemia and do not need surgery 51 51 Treatment If symptoms are mild and Ca+ 15 mg/dL 52 52 Patti Parker, PhDc, CNS, A/GNP 26 Advanced Labs 6/27/2024 The So-Called Asymptomatic Patient If patient is asymptomatic conservative approach is appropriate Most cases are associated with psychiatric and neuromuscular disturbances that are not articulated 53 53 The So-Called Asymptomatic Patient Prominent symptoms – Anxiety – Nervousness – Daytime sleepiness – Loss of energy – Crying easily – Excessive worry – Irritability – Lack of interest 54 54 Patti Parker, PhDc, CNS, A/GNP 27 Advanced Labs 6/27/2024 Therapy Rate of complications is low in the asymptomatic patient with the exception of nephrolithiasis Decision for or against surgery is based on complicating problems 55 55 Therapy Mild hypercalcemia in postmenopausal women may respond to estrogens For Vitamin D excess– Prednisone 20-40 mg/day PO usually controls the Ca+ 56 56 Patti Parker, PhDc, CNS, A/GNP 28 Advanced Labs 6/27/2024 Treatment With normal renal function– IV of 0.9% NS with KCL and Lasix to  renal excretion of Ca+ by expanding ECF, with goal of having patient void at least 3 liters/day In patients with malignancy– bisphosphonates plus NS and Lasix to inhibit osteoclasts from absorbing bone 57 57 Treatment If hyperparathyroidism is symptomatic and progressive– surgery is treatment of choice – 99m Tc Sestamibi, radionuclide agent used to “map’ tumor prior to surgery If surgical referral is done– only send patient to a surgeon experienced in parathyroid exploration 58 58 Patti Parker, PhDc, CNS, A/GNP 29 Advanced Labs 6/27/2024 Surgical vs Conservative Therapy Guidelines for Surgery – Calcium > 12 mg – Hypercalciuria >400 mg/24 hrs – Nephrolithiasis – Cystic bone disease – Overt neuromuscular disease – Decreased cortical bone density – Reduced renal function – Age 2.1 mEq/L Magnesium containing antacids – Renal impairment/failure 73 73 Hypermagnesemia Etiology Signs/Symptoms – Rare, deficient – If plasma level is 5- excretion of it in 10 mEq/L, EKG shows urine 2nd to renal prolonged PR interval, disease or renal widening of QRS and failure increased T wave – Chronic ingestion in amplitude laxatives or antacids – DTRs decrease or disappear – Hypotension – Respiratory depression – Cardiac arrest when Magnesium >12-15 mEq/L 74 74 Patti Parker, PhDc, CNS, A/GNP 37 Advanced Labs 6/27/2024 Hypermagnesemia Treatment – If severe, IV of 10% Calcium Gluconate [10-20 cc] – If renal function okay, IV Lasix can decrease Magnesium – Hemodialysis Patient/Family Education – Do not take Magnesium containing laxatives or antacids 75 75 Hypomagnesemia Plasma magnesium