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NURS 500 Patho Ch 3
Patho 500 Ch 3 Fluid, electrolytes, acid base
| Question | Answer |
|---|---|
| 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 |
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lorrelaws
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