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112-T1 Electrolytes
| Question | Answer |
|---|---|
| sodium normal range | 135-145 mEq/L or mmol/L |
| Calcium normal range | 9-10.5 mEq/L |
| Chloride normal range | 98-106 mEq/L |
| Magnesium normal range | 1.8-2.6 mEq/L |
| Osmolarity normal range | 270-300 mOsm/L |
| Potassium normal range | 3.5-5 meQ/L |
| pH normal range | 7.35 - 7.45 |
| PaCO2 normal range | 35-45 mm Hg |
| HCO3 (bicarbonate) normal range | 22-26 mm Hg |
| causes of hypernatremia | dehydration, kidney disease, hypercortisolism (Cushing's) |
| causes of hyponatremia | fluid overload, liver disease, adrenal insufficiency, |
| causes of hyperkalemia | dehydration, kidney disease, acidosis, adrenal insufficiency, crush injuries |
| causes of hypokalemia | fluid overload, diuretic therapy, alkalosis, insulin administration, hyperaldosteronism |
| causes of hypercalcemia | hyperthyroidism, hyperparathyroidism, |
| causes of hypocalcemia | vitamin D deficiency, hypothyroidism, hypoparathyroidism, kidney disease, excessive intake of phosphorous-containing foods and drinks |
| causes of hyperchloremia | metabolic acidosis, respiratory alkalosis, hypercortisolism |
| causes of hypochloremia | fluid overload, excessive vomiting or diarrhea, adrenal insufficiency, diuretic therapy |
| causes of hypermagnesemia | kidney disease, hypoparathyroidism, adrenal insufficiency, |
| causes of hypomagnesemia | malnutrition, alcoholism, ketoacidosis |
| causes of high osmolarity | dehydration, hypernatremia, hyperglycemia |
| causes of low osmolarity | fluid overload, hyponatremia, hypoproteinemia, malnutrition, |
| ROME | respiratory opposite metabolic equal |
| uncompensated | CO2 or HCO3 is normal |
| partially compensated | nothing is normal (pH, CO2, and HCO3 are all abnormal) |
| compensated | ph is normal but CO2 and HCO3 are both abnormal |
| Hypokalemia ECG changes | prominent U wave flattened/ inverted T wave depresses ST segment |
| Hyperkalemia ECG changes | Peaked T wave ST segment elevation Prolonged PR interval widened QRS comples |
| Hypocalcemia ECG changes | prolonged QT prolonged ST severe V tach |
| Hypercalcemia ECG changes | short QT interval short ST segment widened T wave |
| Hypomagnesemia ECG changes | depressed ST segment inverted T wave prolonged QT interval |
| Hypermagnesemia ECG changes | widened QRS complex prolonged PR interval |
| Sodium/ Potassium relationship | inverse |
| Calcium/ Phosphate relationship | inverse |
| Magnesium/ Phosphate relationship | inverse |
| Calcium/ Vitamin D relationship | similar |
| Magnesium/ Calcium relationship | similar |
| Magnesium/ Potassium relationship | similar |
| calcium gluconate uses | antidote to magnesium overdose protects the heart from elevated potassium levels |
| BUN normal range | 8-20 mg/dL (Blood Urea Nitrogen) indicates kidney function. Produced from liver metabolism of proteins. Dehydration, tissue damage, liver dysfunction, and low cardiac output all can cause BUN to rise. |
| Creatinine normal range | 0.7-1.4 mg/dL Produced from muscle metabolism. Excreted solely by the kidneys. Inversely related to GFR. Elevated levels indicate acute or chronic kidney disease |
| Sodium Polystyrene Sulfonate | Kayexolate removes potassium through the GI tract |
| PTH | -increases calcium reabsorption thereby increasing calcium levels -reduces phosphate reabsorption by the kidneys thereby decreasing serum phosphate levels despite releasing phosphate with calcium from bones (osteoclasts), therefore the inverse relationship between phosphorous and calcium PTH is produced by the parathyroid gland |
| aldosterone | increases Na reabsorption and increases K and H+ excretion, thereby increasing Na and decreasing K+ and H+. It is produced by the adrenal cortex |
| SIADH | syndrome of inappropriate ADH excessive ADH is released despite low blood osmolarity |
| ADH | antidiuretic hormone is produced by the hypothalamus and stored and released by the posterior pituitary gland. it increased the reabsorption of water |
| High blood osmolarity causes osmoreceptors in the hypothalamus to _________. This stimulates thirst and triggers the posterior pituitary gland to release ADH, which is known as vasopressin. | shrink |
| order of events of ADH secretion | 1. extracellular fluid volume is decreased 2. plasma osmolarity is increased 3. Osmoreceptors in hypothalamus are activated when they shrink 4. ADH is released 5. water is reabsorbed from renal tubules |
| hypertonic solution causes | water to move out of a cell through osmosis leading to cell shrinkage |
| hypotonic solution caused | water to move into cell through osmosis leading to cellular swelling |
| normal saline | isotonic increase circulating plasma -treat shock, hyponatremia, blood transfusions, metabolic alkalosis, and hypercalcemia - do not use with heart failure or edema of hypernatremia |
| 1/2 NS | hypotonic raise total fluid volume - treat ketoacidosis, sodium and chloride depletion, gastric fluid loss -use cautiously with cardiac patients; do not use with liver disease, trauma, or burns; helpful in establishing renal function |
| lactated ringers (LR) | isotonic; replaces buffers and fluid; NS with potassium, calcium, and lactate (buffer) - treats hypovolemia from 3rd-spacing dehydration, burns, lower GI tract fluid loss, often used with surgical patents, and acute blood loss |
| dextrose 5% in water | isotonic; helpful in rehydration and excretory purposes -treats fluid loss and dehydration, hypernatremia -do not use for resuscitation (causes hyperglycemia); use with caution with renal/ cardiac disease (causes fluid overload); provides calories |
| dextrose 5% in NS | hypertonic, replaces fluid sodium, chloride, and calories -treats shock, Addisonian crisis -do not use with cardiac/ renal failure (pulmonary edema) |
| dextrose 5% in 1/2 NS (D5 1/2 NS) | hypertonic, prevents hypoglycemia and cerebral edema after diabetic ketoacidosis MC postoperative fluid -in DKA, use only when glucose falls below 250 |
| dextrose 5% in lactated ringers (D5LR) | hypertonic, prevents hypoglycemia and cerebral edema after diabetic ketoacidosis -DO NOT use in newborns |
| Vomiting reflex pattern | 1. initiation of reverse peristalsis 2. contraction of abdominal muscles 3. relaxation of upper esophageal sphincter 4. closure of trachea |
| vomiting causes | metabolic alkalosis due to loss of HCL loss of H+ loss of Cl- loss of K+ loss of Na+ dehydration |
| diarrhea causes | metabolic acidosis from loss of bicarbonate loss of calcium loss of magnesium loss of potassium dehydration |
| Cushing syndrome | hypercortisolism; causes hypertension, edema, muscle weakness, and bone fragility -increased retention of sodium (hypernatremia) and fluid retention -increased secretions of potassium (hypokalemia) -increased secretions of calcium (hypocalcemia) -increased secretions of phosphate (hypophosphatemia) -increased secretions of H+ (metabolic acidosis) |
| Addison's disease | primary adrenal insufficiency; aldosterone deficiency -hyponatremia -hyperkalemia -tends toward metabolic alkalosis because of less H+ secretion (aldosterone reabsorbs sodium and excretes K+ and H+) |
| pH 7.31, CO2-50, HCO3- 25 | uncompensated respiratory acidosis |
| pH 7.47, CO2-30 HCO3-24 | uncompensated respiratory alkalosis |
| pH: 7.32 pCO2: 60 mmHg HCO3: 30 mEq/L | partially compensated respiratory acidosis |
| pH 7.47, CO2-30 HCO3 20 | partially compensated respiratory alkalosis |
| pH: 7.25 pCO2: 40 mmHg HCO3: 17 mEq/L | uncompensated metabolic acidosis: |
| pH: 7.52 pCO2: 40 mmHg HCO3: 32 mEq/L | uncompensated metabolic alkalosis |
| pH: 7.32 pCO2: 32 mmHg HCO3: 16 mEq/L | partially compensated metabolic acidosis: |
| pH: 7.48 pCO2: 46 mmHg HCO3: 34 mEq/L | partially compensated metabolic alkalosis: |
| PaO2 | 80-100 |
| phosphate normal range | 2.4 - 4.4 mEq/L |
| Ketoacidosis can lead to hypomagnesemia through several mechanisms | 1,Osmotic diuresis: The hyperglycemia in ketoacidosis causes increased urine output, leading to excessive magnesium loss through the kidneys. 2. Metabolic acidosis: The acidic state promotes magnesium shift from intracellular to extracellular space, increasing renal excretion. 3.Insulin deficiency: Insulin plays a role in magnesium reabsorption in the kidneys. Its absence contributes to increased magnesium loss. |
| why does acidosis lead to hyperkalemia? | As blood pH decreases, hydrogen ions enter cells in exchange for potassium ions. This shift maintains electroneutrality but results in increased extracellular potassium. The process is described as "potassium-hydrogen ion exchange" |
| why does alkalosis lead to hypokalemia? | In alkalosis, hydrogen ions move out of cells to buffer the alkaline blood. To maintain electrochemical balance, potassium ions move into cells, lowering serum potassium levels. |
| what buffers pH inside cells? | Proteins: Intracellular proteins, including enzymes and structural proteins, act as significant buffers. They can bind or release hydrogen ions to help maintain pH balance. Phosphate buffer system: Composed of dihydrogen phosphate (H2PO4-) and monohydrogen phosphate (HPO4^2-), this system is particularly important in the cytoplasm and organelles. |
| In red blood cells, ____________ serves as a potent buffer, capable of binding or releasing hydrogen ions as needed. | hemoglobin |
| s/s of acidosis | muscle weakness decreased cardiac contractility rapid, deep breathing (Kussmaul respirations) headache, confusion, lethargy, coma nausea, vomiting decreased deep tendon reflexes warm, flushed skin |
| s/s of alkalosis | muscle cramps, twitches, tetany atrial tachycardia shallow slow breathing dizziness, agitation, confusion, seizures nausea, vomiting hyperreflexia, positive Chvostek and trousseau tingling, numbness |
Created by:
cnblake1
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