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3. Electrolytes (Table)
Clinical Chemistry 2 (MDT 3122L)
Our Lady of Fatima University
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SODIUM (Na) * Serum/Plasma: 136-145 mmol/L * Urine (24hrs): 40-220 mmol/d * CSF: 136-150 mmo l/L DEFINITION: - also called as Natrium - most abundant Extracellular Cation (90%) - determines the osmolality of the plasma * Normal Plasma Osmolality: 295 mOsm/kg - 270 mOsm/kg composed of Sodium & associated Anions REGULATION: 1. Intake of water in response to thirst - stimulated or suppressed by Plasma Osmolality * THIRST: major defense against Hyperosmolality & Hypernatremia 2. Excretion of water - largely affected by AVP release in response to changes in Blood Volume & Osmolality 3. Blood volume status - affects Sodium excretion through Aldosterone, Angiostenin II, & ANP DETERMINATION: - Specimen: Serum, Plasma (Lithium Heparin, Ammonium Heparin, Lithium Oxalate), Urine (24hrs), Sweat - not affected by Hemolysis - Methods: 1. ION-SELECTIVE ELECTRODE (ISE) - most routinely used method 2. FLAME EMMISION SPECTROPHOTOMETRY 3. ATOMIC ABSORPTION SPECTROPHOTOMETRY (AAS) 4. COLORIMETRY - “Albanese Lein“ * Na,K—ATPase ION PUMP - used to prevent ECF & cell Sodium to reach equilibrium - moves 3 Sodium out of the cell in exchange of 2 Potassium moving into the cell as ATP is converted to ADP * HYPONATREMIA Causes: Symptoms: Treatment: - Serum/Plasma <135 mmol/L 1. ↑ Sodium Loss * 125-130 mmol/L 1. Fluid restriction & providing Hypertonic Saline - level <130 mmol/L is - Hypoadrenalism - Ketonuria - primarily Gastrointestinal * CEREBRAL MYELINOLYSIS: too rapid Clinically significant - Potassium deficiency - Salt-losing Nephropathy * <125 mmol/L * CEREBRAL EDEMA: too slow - one of the most common - Diuretic Use (Thiazides) - Diarrhea/Vomiting - (Neuropsychiatric) Headache, * BARTTER’S SYNDROME: Hyponatremia is not electrolyte disorders - Ketonuria - Severe burns Nausea, Vomiting, Lethargy, Ataxia, corrected by Fluid Restriction 2. ↑ Water retention Muscular weakness 2. Use Pharmacologic agents - Renal failure - Hepatic Cirrhosis - more severe symptoms include * CONIVAPTAN: - Nephrotic Syndrome - Congestive Heart Failure Seizure, Coma, & Respiratory - US FDA approved, AVP receptor antagonist 3. Water imbalance depression - blocks the action of AVP in the Collecting Ducts of - Excessive water intake * <120 mmol/L for 48hrs. the receptor, thus ↓ water reabsorption - SIADH - Medical Emergency - Pseudohyponatremia HYPONATREMIA BY OSMOLALITY: HYPONATREMIA WITH NORMAL RENAL FUNCTION: HORMONES AFFECTING SODIUM LEVELS: 1. LOW OSMOLALITY 1. ALDOSTERONE 24hr SERUM URINE URINE SERUM CAUSE URINE - ↑ Sodium loss - promotes absorption of Sodium Na Na OSMOLALITY K Na - ↑ Water restriction - promotes Sodium retention & Potassium ↑ 2. NORMAL OSMOLALITY 2. ATRIAL NATRIURETIC FACTOR (ANF) Overhydration ↓ ↓ ↓ ↓ N/↓ - ↑ Non-sodium Cations - Severe Hyperkalemia - blocks Aldosterone & Renin secretion Diuretics ↓ ↓ ↑ ↓ ↓ - ↑ Gamma-globulins - Severe Hypermagnesia - inhibits action of Angiostenin 1 & Vasopressin SIADH ↓ ↑ ↑ ↑ N/↓ - Lithium excess - Severe Hypercalcemia Mildly Adrenal Failure N --↑ ↑ - Hyperproteinemia - Pseudohyponatremia * FRACTIONAL EXCRETION - Hyperlipidemia - Pseudohypokalemia - quantity of a substance excreted in the urine expressed as the Bartter’s ↓ ↓ ↑ ↓ ↓ Syndrome 3. HIGH OSMOLALITY fraction of the filtered load of the same substance - Hyperglycemia a. PRE-RENAL AZOTEMIA: F. of Sodium <0 Diabetic Hyperosmolalit ↓ N N N ↑ - Mannitol Infusion b. ACUTE TUBULAR NECROSIS: F. of Sodium > 0 y * HYPERNATREMIA - Serum/Plasma >145 mmol/L - results from excess loss of water relative to sodium loss, ↓ sodium intake & retention Causes: 1. Excess water loss - Diabetes Insipidus - Renal Tubular Disorder - Prolonged Diarrhea - Profuse Sweating - Severe burns 2. ↓ Water Intake - Older persons - Infants - Mental impairment 3. ↑ Intake or Retention - Hyperaldosteronism - Sodium Bicarbonate excess - Dialysis fluid excess Symptoms: - >160 mmol/L is associated to 60-75% mortality - Fever, Nausea, Vomiting, Irritability, Restlessness, Muscle Twitching, altered Mental Status, Seizure, Hyper-reflexes, Difficult Respiration, ↑ Thirst Treatment: - correction of underlying condition that caused Water depletion or Sodium retention - must be corrected gradually because too rapid correction of Serious Hypernatremia (>160 mmol/L) can induce Cerebral Edema and Death - Maximal rate: 0 mmol/L HYPERNATREMIA RELATED TO URINE OSMOLALITY: * <300 mOsm/kg - Diabetes Insipidus * 300-700 mOsm/kg - Partial defect in AVP release or response to AVP - Osmotic Diuresis * >700 mOsm/kg - loss of thirst - insensible loss of water - Gastrointestinal loss of Hypotonic fluid - excess intake of Sodium CHLORIDE (Cl) DEFINITION: - most abundant Extracellular Anion - chief counter ion of Sodium - maintains Osmolality, Blood volume, & Electric Neutrality - shifts secondarily to a movement of Sodium or Bicarbonate - excreted in the urine & sweat - excessive sweating stimulates Aldosterone secretion, which acts on the sweat glands to conserve Sodium & Chloride * CHLORIDE SHIFT - a.k. “Hamburger shift”or “Hamburger Phenomenon” named after Jakob Hamburger - maintains Electroneutrality * Plasma/Serum: 98-107 mmol/L * Urine (24hr): 110-250 mmol/d CLINICAL APPLICATIONS: - disorders are often a result of the same causes that disturb Sodium levels because Chloride passively follows Sodium * HYPERCHLOREMIA - may result when there is an excess loss of Bicarbonate because of GI losses, RTA, Metabolic Acidosis * HYPOCHLOREMIA - may result when there is excess loss of Chloride from prolonged vomiting, Diabetic Ketoacidosis, Aldosterone deficiency, & Pyelonephritis BICARBONATE (HCO3) * Plasma/Serum: 23-29 mmol/L (Venous CO2) DEFINITION: - second most abundant Extracellular Anion - major component of Buffering system in the blood - Total CO2 comprises of Bicarbonate ion, Carbonic Acid (H2CO3), and dissolved CO2 - 90% of Total CO2 is HCO3: its measurement is indicative of HCO3 level - Regulation: 80% of HCO3 is reabsorbed in the Kidneys CLINICAL APPLICATION: * ACID-BASE BALANCE - causes changes in the Bicarbonate & CO2 level * METABOLIC ACIDOSIS (↓ HCO3) - Compensated by: Hyperventilation - Effect: ↓ pCO2 * METABOLIC ALKALOSIS (retained HCO3) - Compensated by: Hypoventilation - Effect: ↑ pCO2 DETERMINATION: - Specimen: Serum, Plasma, (Lithium Heparin), Urine (24hrs), Sweat - Collection of Sample: Marked Hemolysis may result to ↓ of Chloride due to dilutional effect - Methods: 1. ION SELECTIVE ELECTRODE (ISE) 2. AMPEROMETRIC-COULOMETRIC TITRATION - “Cotlove Chloridometer” 3. MERCURIMETRIC TITRATION - “Schales & Schales” - Indicator: Diphenylcarbazone - End product: HgCl2 (Blue Violet) 4. SPECTROPHOTOMETRIC METHODS - Mercuric Thiocyanate (Whitehorn Titration Method) - Ferric Perchlorate DETERMINATION: - Specimen: Serum, Plasma (Lithium Heparin) - Methods: Total CO2 Determination 1. ION SELECTIVE ELECTRODE: pCO2 electrode 2. ENZYMATIC METHOD MAGNESIUM (Mg) * Serum: 0-1 mmol/L * Colorimetric: 1.26-2 mmol/L DEFINITION: REGULATION: - second most abundant Intracellular Cation - fourth most abundant Cation - essential cofactor of >300 enzymes - significant findings are associated with Cardiovascular, Metabolic, & Neuromuscular disorders * Forms: 1. Free Mg/Ionized form: 55% 2. Protein-bound Mg: 30% 3. Complexed w/ Ions: 15% - Kidneys can readily absorb Mg in deficiency status or excrete excess Mg in overload states - Mg regulation appears to be related to Sodium & Calcium * HYPOMAGNESEMIA HORMONES AFFECTING MAGNESIUM LEVELS: 1. PTH - ↑ reabsorption of Mg in the Kidney & Intestine 2. ALDOSTERONE & THYROXINE - apparently have opposite effect on PTH - ↑ excretion of Mg Cause: 1. ↓ Intake - Poor diet; Starvation - prolonged Magnesium Therapy - Chronic Alcoholism 2. ↓ Absorption - Vomiting - Malabsorption Syndrome - Diarrhea - Surgical resection of Small Intestine - Neonatal - Nasogastric suction - Congenital - Laxative abuse - Primary - Pancreatitis 3. ↑ Excretion (Renal) - Tubular disorder - Glomerulonephritis - Pyelonephritis 4. ↑ Excretion (Endocrine) - Hyperthyroidism - Hyperparathyroidism - Hypercalcemia - Hyperaldosteronism - Diabetic Ketoacidosis 5. ↑ Excretion (Drug-Induced) - Diuretics (Furosemide) - Antibiotics (Gentamicin) - Digitalis (Cardiac Glycoside) 6. Miscellaneous - Pregnancy - excess lactation Symptoms: 1. Cardiovascular - Arrhythmia - Hypertension - Digitalis toxicity 2. Psychiatric - Agitation - Depression - Psychosis 3. Neuromuscular - Weakness - Cramps - Tremors - Ataxia - Seizure - Tetany - Paralysis - Coma 4. Metabolic - Hyponatremia - Hypokalemia - Hypocalcemia - Hypophosphatemia DETERMINATION: - Specimen: Serum, Plasma (Lithium Heparin), Urine (24hr) - Mg conc. in the RBC is 10x > than in the ECF - Oxalate, Citrate, & EDTA are unacceptable because they will bind to Mg - Methods: 1. COLORIMETRIC a. CALMAGITE: (+) Reddish-Violet b. FORMAZAN DYE c. METHYTHYMOL BLUE 2. ATOMIC ABSORPTION SPECTROPHOTOMETRY - reference method 3. DYE-LAKE METHOD - Titan Yellow Dye (Clayton Yellow / Thiazole Yellow) Treatment: 1. Oral intake for Magnesium lactate, Magnesium oxide, or Magnesium Chloride, or an Antacid that contains Magnesium 2. Magnesium sulfate (Parenteral) * HYPERMAGNESEMIA Cause: 1. ↓ Excretion - Acute or Chronic Renal failure - Hyperthyroidism - Hyperaldosteronism - Hypopituitarism 2. ↑ Intake (Mg-containing drugs) - Antacids - Enemas - Cathartics - Therapeutic (Eclampsia, Cardiac Arrhythmia) 3. Miscellaneous - Dehydration - Bone Carcinoma - Bone Metastasis Symptoms: 1. Cardiovascular - Hypotension - Bradycardia - Heart block 2. Neuromuscular - ↓ Reflexes - Dysarthria - Paralysis - Respiratory Depression 3. Dermatologic - Flushing - Warm skin 4. Metabolic - Hypocalcemia 5. Neurologic - Lethargy - Coma 6. Gastrointestinal - Nausea - Vomiting 7. Hemostatic - ↓ Thrombin generation - ↓ Platelet adhesion Treatment: 1. Discontinue Mg intake 2. Immediate Supportive Therapy for Cardiac, Neuromuscular, Respiratory, or Neurologic abnormalities CALCIUM (Ca) DEFINITION: Forms of Calcium: 1. Ionized (Active) Calcium: 50% 2. Protein-bound Calcium: 40% 3. Complexed w/ Anions: 10% * HYPOCALCEMIA * HYPERCALCEMIA HORMONES AFFECTING CALCIUM LEVELS: DETERMINATION: 1. 1,25-DIHYDROXYCHOLECALCIFEROL (1,25-(OH)-2-D3) - Specimen: Serum (Lithium Heparin) - ↑ Renal & Intestinal absorption of Ca - Methods: - ↑ mobilization of Calcium from bones 1. PRECIPITATION & REDOX TITRATION 2. PARATHYROID HORMONE a. Clark Collip Precipitation - conserves Ca by ↑ reabsorption in the Kidneys b. Ferro Ham Chloranilic Acid Precipitation - ↑ Ca level by mobilizing Bone Calcium 2. ORTHO-CRESOLPTHALEIN COMPLEXONE DYE (Colorimetric) - activates the process of Bone reabsorption a. 1 Dye: Arzeno IIII - stimulates conversion of inactivate Vitamin D to activate b. 2 Mg Inhibitor: 8-Hydroxyquinoline (Chelator) Vitamin D3 in the Kidney 3. EDTA: TITRATION METHOD 3. CALCITONIN - Bachra, Dawer, Sobel - secreted by the Parafollicular C-cells of the Thyroid 4. ION SELECTIVE ELECTRODE (Free Ca) - inhibits PTH & Vitamin D3 (Hypocalcemic Hormone) 5. ATOMIC ABSORPTION SPECTROPHOTOMETRY - Inhibits Bone Resorption - reference method - promotes Urinary excretion of Calcium 6. EMISSION FLAME PHOTOMETRY Causes: Symptoms: Treatment: - Primary Hypoparathyroidism 1. Neuromuscular irritability (Paresthesia, Muscle 1. Calcium Therapy - Hypomagnesemia cramps, Tetany, Seizure) 2. Magnesium Therapy - Hypermagnesemia 2. Cardiac Symptoms (Arrhythmia) 3. Vitamin D Therapy - Hypoalbuminemia - Acute Pancreatitis - Renal Disease - Vitamin B deficiency - Rhabdomyolysis - Pseudohypoparathyroidism Causes: Symptoms: Treatment: - Primary Hyperparathyroidism 1. Neurologic symptoms 1. Estrogen Replacement Therapy - Hyperthyroidism - mild drowsiness, depression, Lethargy, & Coma 2. Parathyroidectomy - Benign Familial Hypocalciura 2. GI symptoms 3. Discontinue use of Thiazides - Malignancy - Constipation, Nausea, Vomiting, Anorexia, Peptic 4. Salt & Water intake - Multiple Myeloma Ulcer - ↑ Vitamin D 3. Renal Symptoms - Thiazides diuretics -Nephrolithiasis & Nephrocalcinosis - ↑ Immobilization
3. Electrolytes (Table)
Course: Clinical Chemistry 2 (MDT 3122L)
University: Our Lady of Fatima University
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