Lecture 3 Water, Sodium, and Potassium Balance PDF

The importance of water, sodium, and potassium balance Pixabay.com 1. Body Fluid Compartments 60% of the human body is water Water and sodium balance is essential 2 compartments: ICF and ECF ECF: blood and interstitial fluid Water and sodium location in the body Water...

The importance of water, sodium, and potassium balance Pixabay.com 1. Body Fluid Compartments 60% of the human body is water Water and sodium balance is essential 2 compartments: ICF and ECF ECF: blood and interstitial fluid Water and sodium location in the body Water follows sodium Sodium loss- water loss- dehydration 1/3 of 2/3 of The kidneys regulate ECF volume water water 2. Changes in water and sodium amounts Imagine: Loss or gain of 5L of pure water Loss of sodium (+ loss of 5 L of water) Dehydration Gain of sodium (+ gain of 5 L of water) Consequences of loss of fluid from individual compartments ICF: cell dysfunction (lethargy, confusion, coma) ECF: dehydration Loss of blood 3. Osmolality assesses water balance The measure of the number of solute particles per unit of solvent No identity of solutes Concentrated substances= high osmolality Dilute specimens = low osmolality Movement of water keeps the osmolality the same ICF=ECF Consider an increase in osmolality of the blood Hypothalamus stimulates ADH secretion Consequence? Measured versus calculated 3.1 Calculation of osmolality Derived from sodium, BUN, and glucose Simplest formula: Serum osmolality [mmol/Kg] = 2 X serum [sodium] [mmol/L] When serum concentrations of urea and glucose are NOT within the reference intervals Serum osmolality = (2 x [Na + ]) + (BUN/2.8) + (glucose/ 18) Osmolal GAP (measured – calculated) = less than 10 mOsm/Kg Wikimedia Commons, 2024 Osmometers measure serum and urine osmolality 3.2 Osmolality Clinical significance Reference range Serum: 275 – 295 mOsm/Kg Urine: 300 - 900 mOsm/Kg Homeostasis Values can be affected Diseases (diabetes insipidus), medications https://www.pacehospital.com/diabetes- types-symptoms-causes-and-complications and poisons can affect the osmolality values Changes in the amount of solute or solvent – changes in osmolality < 240 mOsm/Kg > 320 mOsm/Kg – immediate intervention 4. Electrolytes Na+, K+, Cl-, and HCO3- ions Function Na+ (major extracellular fluid cation) K+ (major intracellular fluid cation) Osmotic pressure is created by ions inside and outside of cells Pixabay.com Electrolytes are commonly measured in plasma/serum The kidneys reabsorb/excrete water and electrolytes Loss of sodium/potassium along with proportional loss of water= constant electrolyte concentration Clinical information + laboratory results 4.1 Electrolyte Regulation Water and sodium levels vary often Homeostatic mechanisms prevent changes in fluid compartments The ECF volume must be maintained for survival Water remains constant because of ADH (AVP) ADH system Hypothalamus senses differences in osmolality in ECF High osmolality Low osmolality Sodium 5. Sodium and its physiological regulation Sodium source Table salt Most is in ECF Total body sodium does not vary in health Sodium drop? Sodium increase? Sodium regulation: 2 hormones Renin-angiotensin-aldosterone system (RAAS) Triggered by decrease in ECF volume Atrial natriuretic peptide system (ANP) Triggered by increase in ECF volume Effects of Low Sodium 5.1 Fluid Changes and Sodium Imbalances Hyponatremia General causes of hyponatremia Water retention Sodium depletion If sodium is lost, water is lost Decrease in ECF may occur ❖In hyponatremia, hypovolemia strongly indicates sodium depletion 5.2 Assessment and management of hyponatremia Excess of water or little sodium? Symptoms of hyponatremia Nonspecific symptoms (e.g. lethargy, headache, confusion, dizziness) No history of fluid loss, water retention is likely Symptoms of decreased ECF and blood volume Sodium depletion 5.2 Assessment and management of hyponatremia ❖Clients with Edema Causes Heart failure or hypoalbuminemia Increase aldosterone Consequences Increased ECF volume Treatment depends on volume status Hypovolemic clients (sodium depleted) Normovolemic clients (retaining H2O) – no water Edematous clients (retaining Na+ and H2O)- diuretic Effects of High Sodium 5.4 Fluid Changes and Sodium Imbalances Hypernatremia Clinical characteristics: Hypernatremia may be associated with: normal sodium sodium depletion Low ADH sodium gain Hypernatremia is most commonly due to water loss Treatment Hypernatremia due to pure water loss – water/ dextrose 5% Clinical evidence of dehydration (reduced ECF) - sodium Sodium overload (diuretic + H2O) Skin turgor Potassium Source 98% in intracellular space Functions Pixabay.com Indirect effect of aldosterone Effects of Low Potassium 6. Fluid Changes and Potassium Imbalances Hypokalemia Clinical characteristics Increased losses Redistribution of K+ into cells Causes of hypokalemia History is important E.g., Vomit, diarrhea, diuretics, metabolic alkalosis No mechanism to conserve potassium (NO aldosterone) Clinical consequences of hypokalemia Symptoms in excitable tissues Muscle weakness, hyporeflexia, and cardiac arrythmias Treatment Oral and IV potassium 6. Fluid Changes and Potassium Imbalances Hyperkalemia Potassium balance is tightly kept 98% of potassium is inside of cells Tissue damage Potassium excretion is determined by: ▪ Glomerular filtration rate (GFR) ▪ Plasma potassium concentration Causes of hyperkalemia E.g., decreased excretion, hypoaldesteronism, metabolic acidosis, potassium intake (supplements) Consequences of hyperkalemia Cardiac arrest Treatment (e.g., insulin (K+ + glucose into cells), dialysis in refractory hyperkalemia) 7. Investigation of Renal Function Renal functions Electrolyte/water, acid-base, by-products protein, nucleic acid Renal function= glomerular and tubular function ❖Glomerular function Glomerular filtration rate (GFR) Reduced glomerular function has been associated with disease progression ❖Tubular function analysis No single measure of tubular function (ability to concentrate urine is commonly affected= water reabsorption) Urine osmolality Vs. serum osmolality Too similar= no reabsorption of H2O 7.1 Specific Tubular Defects- Kidney Stones (calculi) Common cause of obstruction in the urinary tract Biochemical analysis of renal stones Why stones have formed Types of stones: Calcium phosphate (hyperparathyroidism/ renal tubular acidosis) Magnesium, ammonium and phosphate (UTIs) Oxalate - hyperoxaluria Uric acid – by-product of purines Cystine – genetic disorder (cystinuria- excretion of cystine) 7.2 Acute Kidney Injury (AKI) Acute Kidney Injury (AKI): Rapid decline in kidney function over hours to days Causes Prerenal Postrenal Renal Clinical Biochemistry Patterns: 1.Serum creatinine 2.Urine output (oliguria or anuria) 3.Estimated glomerular filtration 7.3 Chronic Kidney Disease (CKD) Chronic Kidney Disease (CKD): Gradual and irreversible loss of kidney function over months to years Clinical Biochemistry Patterns: 1.Serum Creatinine 2.Urine Output https://hganalytics.com/chronic-kidney-disease-stages/ 3.Estimated glomerular filtration 7.4 Kidney dysfunction Azotemia: (lab finding) Elevated levels of nitrogen-containing compounds in blood Clinical Implications: Azotemia often indicates impaired kidney function It can result from various causes Uremia: (clinical syndrome) Systemic effects of kidney failure Build up of waste products Clinical Implications: 1.It reflects significant kidney damage and often requires medical intervention 2.It may affect multiple organs and systems 7.5 Renal Function and Abnormalities ❖BUN (Blood Urea Nitrogen) ✓Clinical Significance: 1.Elevated BUN (e.g., kidney dysfunction, dehydration) 2.Low BUN levels (e.g., liver disorders) ❖Creatinine: ✓Clinical Significance: 1.Elevated creatinine (e.g., kidney dysfunction, muscle disorders) 2.Low creatinine levels (e.g., muscle atrophy) ❖Uric Acid ✓Clinical Significance: 1.Elevated uric acid (e.g., kidney dysfunction, excess purine consumption) - it may lead to gout) 2.Low uric acid levels (e.g., kidney or liver disease) 7.8 Gout Clinical syndrome characterized by hyperuricemia and recurrent acute arthritis Chemical basis of gout Accumulation of uric acid crystals in joints/tissues Origin- byproduct of the breakdown of purines Crystallization- high uric acid levels lead to crystallization and deposit in joints Clinical relevance Symptoms- Sudden, severe joint pain Triggers- dietary choices (e.g., purine rich food, such as meat) Treatment- medications and lifestyle changes 7.9 The Urinalysis: a diagnostic tool for multiple myeloma and nephrotic syndrome ❖Multiple Myeloma Overflow of proteinuria (clone of plasma cell) Presence of Bence Jones Proteins (light chain fragments of immunoglobulin)- it may be detected in urine Hematuria ❖Nephrotic Syndrome (damage to glomeruli leading to:) Massive Proteinuria: (>3 grams/day) Hypoalbuminemia Increased fluid in interstitial space (edema)