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NURS 500 Patho Ch 3

Patho 500 Ch 3 Fluid, electrolytes, acid base

total body water is 40% ICF & 20% ECF---the 20% ECF includes these systems 20% TBW broken into 15% intersititial and 5% intravascular
total body water 60% of total body weight
water moves mostly by osmosis and hydrostatic p across pmem
movement across capillary wall defined by starling hypothesis=Net filtration = forces favoring filtration – forces opposing filtration
figure 3-1 osmotic pressures pull water from weaker to stronger concentration
alterations in water movement --> edema accumulation of fluid in interstitium
edema caused by - finish from 3-3 Increase in capillary hydrostatic pressure--- Losses or diminished production of plasma ---decreased capialbumin Increases in capillary permeability Lymph obstruction (lymphedema)
Thirst perception - water balance thirst perception regulated by osmolality receptors and baroreceptors----also by ADH secretion
Na Primary ECF cation Regulates osmotic forces Roles Neuromuscular irritability, acid-base balance, and cellular reactions
Cl Primary ECF anion Provides electroneutrality
Na/Cl balance maintained by Renin-angiotensin-aldosterone system Aldosterone Natriuretic peptides Atrial natriuretic peptide Brain natriuretic peptide Urodilantin (kidney)
alterations in Na/Cl/Water balance - isotonic alterations Total body water change with proportional electrolyte change Isotonic volume depletion Isotonic volume excess
hypertonic alterations Hypernatremia Serum sodium >147 mEq/L Related to sodium gain or water loss Water movement from the ICF to the ECF Intracellular dehydration Manifestations: intracellular dehydration, convulsions, pulmonary edema, hypotension, tachycardia
more hypertonic alterations Water deficit Dehydration Pure water deficits Renal free water clearance Manifestations Tachycardia, weak pulse, and postural hypotension Elevated hematocrit and serum sodium levels
even more hypertonic alterations Hyperchloremia Occurs with hypernatremia or a bicarbonate deficit Usually secondary to pathophysiologic processes Managed by treating underlying disorders
hypotonic alterations Hyponatremia Serum sodium level <135 mEq/L Sodium deficits cause plasma hypoosmolality and cellular swelling Pure sodium deficits Low intake Dilutional hyponatremia Hypoosmolar hyponatremia Hypertonic hyponatremia
more hypotonic alterations Water excess Compulsive water drinking Decreased urine formation Syndrome of inappropriate ADH (SIADH) ADH secretion in the absence of hypovolemia or hyperosmolality Hyponatremia with hypervolemia Manifestations: cerebral edema, muscle twitchig, HA
even more hypotonic alterations Hypochloremia Usually the result of hyponatremia or elevated bicarbonate concentration Develops due to vomiting and the loss of HCl Occurs in cystic fibrosis
wow, more hypotonic alterations wow - maybe there's not any more
K characteristics Major intracellular cation Concentration maintained by the Na+,K+ pump Regulates intracellular electrical neutrality in relation to Na+ and H+ Essential for transmission and conduction of nerve impulses, normal cardiac rhythms, and skeletal/sm contract
K levels effects these systems Changes in pH affect K+ balance Hydrogen ions accumulate in the ICF during states of acidosis. K+ shifts out to maintain a balance of cations across the membrane. Aldosterone, insulin, and catecholamines influence serum potassium levels
hypokalemia Potassium balance described by changes in plasma potassium levels Causes: reduced potassium intake, increased potassium entry, and increased potassium loss Manifestations Membrane hyperpolarization causes a decrease in neuromuscular excitability, skele
hyperkalemia Hyperkalemia is rare due to efficient renal excretion Caused by increased intake, shift of K+ from ICF, decreased renal excretion, insulin deficiency, or cell trauma
mild hyperkalemia Hypopolarized membrane, causing neuromuscular irritability Tingling of lips and fingers, restlessness, intestinal cramping, and diarrhea
severe hyperkalemia The cell is unable to repolarize, resulting in muscle weakness, loss of muscle tone, flaccid paralysis, cardiac arrest
Calcium functions Most calcium is located in the bone as hydroxyapatite Necessary for structure of bones and teeth, blood clotting, hormone secretion, and cell receptor function
phosphate functions, and relative to Ca most phosphate (85%) located in the bone Necessary for high-energy bonds located in creatine phosphate and ATP and acts as an anion buffer Calcium and phosphate concentrations are rigidly controlled Ca++ x HPO4– – = K (constant) If concentration of
what 3 hormones regulate Ca & Phosphate? Parathyroid hormone (PTH) Increases plasma calcium levels via bone reabsorption Vitamin D Fat-soluble steroid; increases calcium absorption from the GI tract Calcitonin Decreases plasma calcium levels
Hypocalcemia Decreases the block of Na+ into the cell Increased neuromuscular excitability (partial depolarization) Muscle cramps
hypercalcemia Increases the block of Na+ into the cell Decreased neuromuscular excitability Muscle weakness Increased bone fractures Kidney stones Constipation
hyperphospatemia Osteomalacia (soft bones) Muscle weakness Bleeding disorders (platelet impairment) Anemia Leukocyte alterations Antacids bind phosphate
hyperphosphatemia - see also hypocalcemia because because high phosphate levels are related to low Ca levels
High K solutions are used when administering death penalty, causes heart to stop
magnesium characteristics Intracellular cation Plasma concentration is 1.8 to 2.4 mEq/L Acts as a co-factor in protein and nucleic acid synthesis reactions Required for ATPase activity Decreases acetylcholine release at the neuromuscular junction
hypomagnesmia Associated with hypocalcemia and hypokalemia Neuromuscular irritability Tetany Convulsions Hyperactive reflexes
hypermagnesemia Skeletal muscle depression Muscle weakness Hypotension Respiratory depression Lethargy, drowsiness Bradycardia
What is pH Negative logarithm of the H+ concentration -----Each number represents a factor of 10. If a solution moves from a pH of 7 to a pH of 6, the H+ ions have increased 10-fold.
example of pH log If a solution moves from a pH of 6 to a pH of 5, the H+ has increased 10 times
pH, who regulates acid base and why Acids are formed as end products of protein, carbohydrate, and fat metabolism To maintain the body’s normal pH (7.35-7.45) the H+ must be neutralized or excreted Bones, lungs, and kidneys are major organs involved in regulation of acid-base balance
pH how do body acids exist? Volatile H2CO3 (can be eliminated as CO2 gas) Nonvolatile Sulfuric, phosphoric, and other organic acids Eliminated by the renal tubules with the regulation of HCO3–
buffer systems exists as pairs and are Associate and dissociate very quickly (instantaneous) Buffer changes occur in response to changes in acid-base status
most important plasma buffering systems carbonic acid/bicarbonate---and HEMOGLOBIN
carbonic acid/bicarb - operates where and how Operates in the lung and the kidney The greater the partial pressure of carbon dioxide, the more carbonic acid is formed
Mechanism of carbonic acid/bicarb buffering At a pH of 7.4, the ratio of bicarbonate to carbonic acid is 20:1 Bicarbonate and carbonic acid can increase or decrease, but the ratio must be maintained
protein buffering Proteins have negative charges, so they can serve as buffers for H+
renal buffering Secretion of H+ in the urine and reabsorption of HCO3–
Buffering bwo cellular ion exchange Exchange of K+ for H+ in acidosis and alkalosis (alters serum potassium)
acid-base imbalances - overview Normal arterial blood pH 7.35 to 7.45 Obtained by arterial blood gas (ABG) sampling Acidosis Systemic increase in H+ concentration Alkalosis Systemic decrease in H+ concentration
respiratory acidosis elevation of pCO2 due to ventilation depression
respiratory alkalosis depression of pCO2 due to alveolar hyperventilation
metabolic acidosis depression of HC03- or an INCREASE in noncarbonic acids
metabolic alkalosis elevation of HC03- usually due to an ex loss of metabolic acids
compensation - renal Alters bicarbonate and H+ levels in response to acidosis or alkalosis Much slower response Excretion and/or reabsorption
compensation - respiratory Alters CO2 retention or loss in response to alkalosis or acidosis Rapid response Respiratory rate alterations
compensation occurs when When adjustments are made to bicarbonate and carbonic acid in order to maintain the 20:1 ratio and therefore maintain normal pH The actual values for bicarbonate to carbonic acid ratio are not normal but the normal ratio is achieved
correction occurs when Correction occurs when the values for BOTH components of the buffer pair (carbonic acid and bicarbonate) have also returned to normal levels
anion gap Used cautiously to distinguish different types of metabolic acidosis By rule, the concentration of anions (–) should equal the concentration of cations (+). Not all normal anions are routinely measured. Normal anion gap = [Na+ + K+ ]- [Cl– + HCO3– ]=
abnormal anion gap Abnormal anion gap occurs due to an increased level of abnormal unmeasured anion Examples: DKA—ketones, salicylate poisoning, lactic acidosis—increased lactic acid, renal failure, etc. As these abnormal anions accumulate, the measured anions have to de
Created by: lorrelaws