Presentation on theme: "Fluid and Electrolyte Disorders. Functions of Body Fluids Transports gases, nutrients, and wastes Help to generate the electrical activity needed to power."— Presentation transcript:
Fluid and Electrolyte Disorders
Functions of Body Fluids Transports gases, nutrients, and wastes Help to generate the electrical activity needed to power body functions Takes part in the transforming of food into energy Maintains the overall function of the body
Distribution of Body Fluids Intracellular compartment (ICF) –Consists of fluid contained within all of the billions of cells in the body –Larger of the two compartments, with approximately two thirds of the body water in healthy adults –High concentration of K + Extracellular compartment (ECF) –Contains the remaining one third of body water –Contains all the fluids outside the cells, including that in the interstitial or tissue spaces and blood vessels –High concentration of Na +
Composition of the ECF, Plasma, and Interstitial Fluids Large amounts of sodium and chloride Moderate amounts of bicarbonate Small quantities of potassium, magnesium, calcium, and phosphorus
Composition of the ICF Almost no calcium Small amounts of sodium, chloride, bicarbonate, and phosphorus Moderate amounts of magnesium Large amounts of potassium
Question Which ion is in the highest concentration in the ICF? a.Na + b.K + c.Cl - d.Ca 2+
Answer a.Na + b.K + : Potassium is the most abundant ion of the ICF and is responsible for the membrane potential. c.Cl - d.Ca 2+
Diffusion and Osmosis Concentration gradient –Difference in concentration over a distance Diffusion –The movement of charged or uncharged particles along a concentration gradient from an area of higher concentration to one of lower concentration Osmosis –The movement of water across a semi-permeable membrane from the side of the membrane with the lesser number of particles and greater concentration of water to the side with the greater number of particles and lesser concentration of water
Tonicity The osmotic pressure gradient of two solutions separated by a semipermeable membrane Solutions can be classified according to whether or not they cause cells to shrink. –Isotonic: neither shrink nor swell –Hypotonic: swell –Hypertonic: shrink
Physiology of water balance Na + retention causes this volume to expand Na + loss causes this volume to decrease Water moves freely within intracellular and extracellular compartments, keeping osmolality equal
Edema Edema = Accumulation of water in interstitial space Collections of fluid in body cavities –Hydrothorax – serous fluid in the thoracic cavity –Hydroperitoneum (ascites) –Hydropericardium fluid in the pericardial sac Anasarca = severe, generalized edema with profound subcutaneous edema
Pathophysiology of Edema The normal flow of fluid through the interstitial space depends on four factors: –Capillary hydrostatic pressure that filters fluid from the blood through the capillary wall –Oncotic pressure exerted by the proteins in the blood plasma –Permeability of the capillaries –Presence of open lymphatic channels that collect some fluid forced out of the capillaries by the hydrostatic pressure of the blood and return the fluid to the circulation
Mechanism of Edema Formation Increased hydrostatic pressure –Reduced plasma oncotic pressure –Decreased lymph outflow (lymphatic channel obstruction –Increased capillary membrane permeability –Retention of water and salts
Hydrostatic pressure increases due to: Venous obstruction: –thrombophlebitis (inflammation of veins) –hepatic obstruction tight clothing on extremities prolonged standing Salt or water retention –congestive heart failure –renal failure
Increased Hydrostatic Pressure
Decreased plasma oncotic pressure: ↓ plasma albumin liver disease protein malnutrition plasma proteins lost in: glomerular diseases of kidney hemorrhage, burns, open wounds idiopathic edema –protein leakage from capillaries
Lymphatic channels blocked Surgery –Breast carcinoma with lymph node removal Blocked lymphatics –Hematologic conditions –Parasitoses
Lymphatic obstruction Caused by thread-like parasitic worm – filaria (filariasis) transmitted by mosquitoes
Effects of Edema Swelling –Pitting –Increased body weight –Functional impairment –Pain –Impairment of arteriole circulation –Other complications
Clinical Consequences of Edema In skin edema may cause poor wound healing or poor clearance of infection Edema in a closed space such as the calvarium can cause increased pressure, which may cause herniation of the brain
Acute pulmonary edema Definition: An increase in pulmonary extravascular water, which occurs when transudation or exudation exceeds the capacity of lymphatic drainage.
Stages of pulmonary edema Interstitial pulmonary edema Cresentic alveolar filling Alveolar flooding Airway flooding With gradual onset these may be identifiable clinically, however with fulminant disease progression may be obscured There is usually prodromal stage in which lymphatic drainage is increase, though there is no detectable increase in lung water
Stages of Cardioigenic Pulmonary Edema Stage 1 –Elevated LA pressure causes distention and opening of small pulmonary vessels Stage 2 –Fluid and colloid shift into the lung interstitium from the pulmonary capillaries, but an initial increase in lymphatic outflow efficiently removes the fluid.
Stages of Cardioigenic Pulmonary Edema Stage 3 –As fluid filtration continues to increase and the filling of interstitial space occurs, fluid accumulates in the relatively noncompliant interstitial space. –At this stage, abnormalities in gas exchange are noticeable, vital capacity and other respiratory volumes are substantially reduced, and hypoxemia becomes more severe.
Toxic pulmonary edema Increased vascular permeability due to toxic damage of pulmonary capillaries.
High Altitude Pulmonary Edema (HAPE) Hypoxic vasoconstriction –Blood vessel leakage –Fluid builds up in the lungs
Methods for Assessing Edema Daily weight Visual assessment Measurement of the affected part Application of finger pressure to assess for pitting edema
Water and Na + Balance Baroreceptors regulate effective volume Modulating sympathetic nervous system outflow and ADH secretion Atrial natriuretic peptide Renin-angiotensin- aldosterone system –Angiotensin II –Aldosterone Gain –Water –Oral intake and metabolism of nutrients –Na + Loss –Kidneys –Skin –Lungs –Gastrointestinal tract
Regulators of Sodium The kidney is the main regulator of sodium. –Monitors arterial pressure; retains sodium when arterial pressure is decreased, and eliminates it when arterial pressure is increased –The rate is coordinated by the sympathetic nervous system and the renin-angiotensin- aldosterone system (RAAS). –Atrial natriuretic peptide (ANP) may also regulate sodium excretion by the kidney.
Physiologic Mechanisms Assisting in Regulating Body Water Thirst –Primarily a regulator of water intake ADH –A regulator of water output Both mechanisms respond to changes in extracellular osmolality and volume.
Question Which ion will have the greatest effect on the membrane potential? a.Bicarbonate b.K + c.Cl - d.Mg 2+
Answer a.Bicarbonate b.K + : Slight deviations in potassium concentration will directly change the membrane potential. c.Cl - d.Mg 2+
Disorders of ADH Expression Diabetes insipidus –Deficiency of or a decreased response to ADH –Unable to concentrate urine during periods of water restriction, leading to excretion of large volumes of urine –Neurogenic diabetes insipidus –Central diabetes insipidus Syndrome of inappropriate antidiuretic hormone (SIAH) –Failure of the negative feedback system that regulates the release and inhibition of ADH
Types of Diabetes Insipidus Central or neurogenic diabetes insipidus –Occurs because of a defect in the synthesis or release of ADH by the Hypothalamus –Usually Idiopathic but may be due to autoimmune disease such as Sarcoidosis, head trauma, or tumor Nephrogenic diabetes insipidus –Occurs because the kidneys do not respond normally to ADH
Diabetes Insipidus Excessive Urination Extreme Thirst Urine does NOT contain Glucose
Mechanisms Protecting Extracellular Fluid Volume Alterations in hemodynamic variables –Vasoconstriction and an increase in heart rate Alterations in sodium and water balance –Isotonic contraction or expansion of ECF volume –Hypotonic dilution or hypertonic concentration of extracellular sodium brought about by changes in extracellular water
Causes of Fluid Volume Excess Inadequate sodium and water elimination Excessive sodium intake in relation to output Excessive fluid intake in relation to output
Vitamin D, Calcitonin, and Parathyroid Hormone Vitamin D acts to sustain normal plasma levels of calcium and phosphorus by increasing their absorption from the intestine. Calcitonin acts on the kidney and bone to remove calcium from the extracellular circulation.
Mechanisms Regulating Calcium, Phosphorus, and Magnesium Balance Calcium, phosphorus, and magnesium are the major divalent cations in the body. They are: –Ingested in the diet –Absorbed from the intestine –Filtered in the glomerulus of the kidney –Reabsorbed in the renal tubules –Eliminated in the urine
Physiologic Calcium ECF calcium exists in three forms 1.Protein bound –40% of ECF calcium is bound to albumin. 2.Complexed –10% is chelated with citrate, phosphate, and sulfate. 3.Ionized –50% of ECF calcium is present in the ionized form.
Calcium Gain and Loss Gains –Dietary dairy foods –Parathyroid hormone and vitamin D stimulate calcium reabsorption in the nephron. Losses –Occur when dietary intake and calcium absorption are less than intestinal secretion
Causes and Symptoms of Hypercalcemia Increased intestinal absorption –Excessive vitamin D and calcium –Milk-alkali syndrome Increased bone resorption –Increased parathyroid hormone –Malignant neoplasms –Prolonged immobilization Decreased elimination –Thiazide, lithium therapy Symptoms –Changes in neural excitability –Alterations in smooth and cardiac muscle function –Exposure of the kidneys to high concentrations of calcium
Causes and Symptoms of Hypocalcemia Causes –Impaired ability to mobilize calcium from bone stores –Abnormal losses of calcium from the kidney –Increased protein binding or chelation such that greater proportions of calcium are in the nonionized form –Soft tissue sequestration Symptoms –Increased neuromuscular excitability –Cardiovascular effects –Nerve cells less sensitive to stimuli
Role of Phosphorus in the Body Plays a major role in bone formation Essential to certain metabolic processes –The formation of ATP and the enzymes needed for metabolism of glucose, fat, and protein Necessary component of several vital parts of the cell Incorporated into the nucleic acids of DNA and RNA and the phospholipids of the cell membrane
Role of Phosphorus in the Body (cont.) Serves as an acid–base buffer in the extracellular fluid and in the renal excretion of hydrogen ions Necessary for delivery of oxygen by the red blood cells Needed for normal function of other blood cells –White blood cells and platelets
Common Causes of Hypophosphatemia and Hyperphosphatemia Hypophosphatemia –Depletion of phosphorus due to insufficient intestinal absorption –Transcompartmental shifts –Increased renal losses Hyperphosphatemia –Failure of the kidneys to excrete excess phosphate –Rapid redistribution of intracellular phosphate to the ECF compartment –Excessive intake of phosphorus
Magnesium Balance Essential to all reactions that require ATP Regulation at kidney level –Magnesium absorption in the thick ascending loop of Henle is the positive voltage gradient created in the tubular lumen by the Na + -K + - 2Cl – cotransport system Ingested in the diet Absorbed from the intestine Excreted by the kidneys
Manifestations of Hypomagnesemia Laboratory values –Serum magnesium level less than l.8 mg/dL Neuromuscular manifestations –Personality changes, athetoid or choreiform movements, nystagmus, tetany, positive Babinski Chvostek, and Trousseau signs Cardiovascular manifestations –Tachycardia, hypertension, cardiac dysrhythmias
Causes of Hypermagnesemia Excessive intake –Intravenous administration of magnesium for treatment of preeclampsia –Excessive use of oral magnesium-containing medications Decreased excretion –Kidney disease –Acute renal failure
Question Alterations in ________________ may result in hypercalcemia. a.ADH b.Na + c.Vitamin D d.K +
Answer Alterations in ________________ may result in hypercalcemia. a.ADH b.Na + c.Vitamin D: When increased, vitamin D will result in higher retention of calcium. d.K +
Assessment of Body Fluid Loss History of conditions that predispose to sodium and water losses, weight loss, and observations of altered physiologic function indicative of decreased fluid volume –Heart rate –Blood pressure –Venous volume/filling –Capillary refill rate
Psychogenic Polydipsia Compulsive water drinking Psychiatric disorders Schizophrenia Drink large amounts of water and excrete large amounts of urine. Cigarette smoking –ADH –Interferes with water excretion by the kidneys Antipsychotic medications increase ADH levels
Isotonic Fluid Volume Excess Isotonic expansion of the ECF compartment with increases in both interstitial and vascular volumes Increase in total body sodium that is accompanied by a proportionate increase in body water Causes of decreased sodium and water elimination –Renal function –Heart failure –Liver failure –Corticosteroid excess
Potassium Distribution and Regulation Intracellular concentration of 140 to 150 mEq/L The extracellular concentration of 3.5 to 5.0 mEq/L Body stores of potassium are related to body size and muscle mass. Normally derived from dietary sources Plasma potassium is regulated through two mechanisms: –Renal mechanisms that conserve or eliminate potassium –A transcellular shift between the ICF and ICF compartments
Abnormal Potassium Hypokalemia refers to a decrease in plasma potassium levels below 3.5 mEq/L. –Inadequate intake –Excessive gastrointestinal, renal, and skin losses –Redistribution between the ICF and ECF compartments Hyperkalemia refers to an increase in plasma levels of potassium in excess of 5.0 mEq/L. –Decreased renal elimination –Excessively rapid administration –Movement of potassium from the ICF to ECF compartment
Diagnosis and Treatment of Potassium Disorders Diagnosis is based on complete history, physical examination to detect muscle weakness and signs of volume depletion, plasma potassium levels, and ECG findings. Treatment –Calcium antagonizes the potassium-induced decrease in membrane excitability. –Sodium bicarbonate will cause K + to move into the ICF. –Insulin will decrease ECF K + concentration –Curtail intake or absorption, increase renal excretion, and increase cellular uptake
ADH and Aquaporin-2 Channels ADH –V 1 receptors Vasoconstriction –V 2 receptors Control water reabsorption Aquaporins