Term
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Definition
| about 60% of body weight in adults, about 50% of body weight in women, about 75% of body weight in full-term newborns. percentage decreased with age due primarily to the relative increase in body fat that occurs with normal aging. |
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Term
| why aging adults are more prone to dehydration |
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Definition
| as the kidneys age, the tubules become less responsive to antidiuretic hormone (ADH) and tend to lose too much water. the excess water loss is accompanied by a decrease in thirst mechanisms |
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Term
| mechanism by which fluid distribution between interstitial and intracellular compartments occur |
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Definition
| osmosis. distribution of fluid btwn the vascular and interstitial compartments is the net result of filtration across permeable caplillaries. in contrast, the distribution of fluid btwn the interstitial and intracellular compartments occurs by osmosis rather than by filtration. |
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Term
| where the largest volume of fluid is excreted in a normal/healthy person |
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Definition
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Term
| When the release of ADH from the posterior pituitary gland will occur |
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Definition
| factors that cause this release include increased osmolality of the extracellular fluid, decreased circulating fluid volume, pain, nausea, and physiologic and psychological stressors. ADH causes reabsorption of water in the distal tubules in the kidneys, thus decreasing fluid excretion. |
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Term
| Main cause of extracellular fluid volume deficit |
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Definition
| removal of sodium containing fluid from the body. removal of sodium containing fluid from the extracellular compartment is usually from removal from the body. however, it can be caused from third spacing (peritoneal cavity or fluid accumulation into the bowels). Although it remains in the body, the fact that it is no longer a part of the extracellular fluid will result in a deficit. |
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Term
| what are the clinical manifestations of extracelluar fluid volume deficit |
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Definition
| weight loss, dizziness, flat neck veins, and postural blood pressure drop. Oliguria will result from the body trying to conserve the fluid it already has to prevent additional fluid loss. |
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Term
| clinical manifestations of extracellular fluid volume excess are |
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Definition
| sudden weight gain, edema, and manifestation of circulatory overload such as bounding pulse, distended neck veins, crackles, dyspnea, pulmonary edema. |
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Term
| the concentration of this cation indicates serum osmolality |
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Definition
| sodium reflects osmolality of blood. normal concentration is 135-145 mEq/L. |
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Term
| what do serum potassium levels tell us? |
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Definition
| the ratio of intracellular to extracellular K+ level is a major determinant of the resting memb. pot. of musc. cells. in hypokalemia, both smooth and skeletal musc are hyperpolarized and are thus less reactive to stimuli, resulting in abdominal distention, diminished bowel sound, hypotension, weakness, and flaccid paralysis. the opposite is true for hyperkalemia which results in intestinal cramping and diarrhea. low and high KT produce skeletal muscle weakness in an ascending pattern in the lower extremities first, with flaccid paralysis. |
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Term
| clinical hypocalcemia versus hypercalcemia |
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Definition
| Ca2+ imbalances alter normal neuromuscular irritability. clinical manifestations of hypocalcemia are those of increased neuromuscular irritability, and hypercalcemia cause decreased neuromuscular irritability. |
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Term
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Definition
| deficiency in this cation is similar to those for Ca2+. chronic alcoholism is a major risk factor for hypomagnesemia. this indicates decreased Mg intake, incrased urinary Mg excretion. this often results in hypokalemia. to correct this, Mg needs to be taken. hypomagnesemia causes decreased activity of the enzyme responsible for driving Na+/K+ pump. ultimately, intracellular K+ will decrease in the myocardium. |
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Term
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Definition
| caused by factors that decrease phosphate intake, shift phosphate from extracellular fluid into cells, increase phosphate excretion, and cause loss of phosphate through abnormal routes. |
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Term
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Definition
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Term
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Definition
| as indicators – pCO2 is the indicator of the respiratory component of the acid-base balance. HCO3- is the indicator of the renal component of acid-base balance. |
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Term
| buffers as a line of defense against pH disorders |
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Definition
| the relative amounts of acids and bases contained within the body are used to determine pH. HCO3- buffers are found in the extracellular space. phosphate buffers are found in the intracellular space and in urine. hemoglobin buffers are found inside erythrocytes. protein buffers are found in intracellular and vascular compartments. |
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Term
| controlling carbonate levels |
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Definition
| if too much acid is present, bicarbonate binds H+ to form carbonic acid and carbonic anhydrase excretes it through the respiratory system in the form of CO2 and water. |
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Term
| ratio of bicarbonate ions to carbonic acid in normal human body |
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Definition
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Term
| result of carbonic acid accumulation in blood |
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Definition
| the respiratory sys adjusts the amt of carbonic acid that remains in the body when there’s an excess. therefore the rate and depth of resp will increase so that excess carbonic acid is removed. however, too little carbonic acid in blood will result in decreased respiration rate inorder to retain the acid until it is present in normal amounts. It is chemoreceptors that sense the changes in these PCO2 levels. |
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Term
| buildup of nonvolatile acids in blood |
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Definition
| the pH disorder is not corrected, however it is compensated for by adjusting the pH back to normal. other blood chemistry values will be made abnormal during this process. this respiratory compensation reaction takes several hours. |
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Term
| Acids that kidneys excrete |
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Definition
| lactic acid, phosphori acid, hydrochloric acid and other acids except carbonic acid, which is excreted by the lungs. |
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Term
| How kidneys neutralize metabolic acidosis or alkalosis |
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Definition
| to correct metabolic alkalosis, the kidneys slow acid excretion to allow acid levels to accumulate to normal. to correct metabolic acidosis, the kidneys decrease acid retention to allow the body to return to normal leveles. |
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Term
| How does the kidney modify H+ to maintain proper serum metabolic pH? |
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Definition
| HCO3- is returned to the blood simultaneously at the glomerulus during acid excretion for each H+ that’s secreted into the renal tubular fluid. Net H+ excretion is accomplished by attaching it to ammonia. |
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