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55 Cards in this Set
- Front
- Back
Intracellular Fluids
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2/3rds of the body's water. it is rich in potassium K+, magnesium, phosphate, and proteins |
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Extracellular Fluid
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Interstitial (80% between cells) and Intravascular ( 20% inside the blood vessels) 1/3rd of the body fluid. rich in sodium, chloride, and bicarbonate. |
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Transcellular
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1% of body fluid in peritoneal, pleural, and pericardial cavities cerebrospinal cavities fluid in joint spaces, lymph system, eyes, and gastrointestinal tract |
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Osmosis
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the movement of fluid (water) across a semipermeable membrane from an area of lower concentration to an area of high concentration. to achieve equilibrium |
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Hydrostatic (push) pressure VS Osmotic (pull) pressure
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hydrostatic push- water and solutes blood push fluid from intravascular to interstitial osmotic pull - water proteins and electrolytes pull fluid from interstitial to intravascular |
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Tonicity
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3 classifications- isotonic solutions. hypotonic solutions, hypertonic solutions |
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Isotonic Solutions |
equal solute concentrations, cause no fluid shifts 0.9% saline, lactated ringer
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Hypotonic solutions
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lower solute concentrations, causing fluids to shift out from intravascular to intracellular 4.5% saline |
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Hypertonic solution
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5% dextrose in 0.9% saline, 3% saline |
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fluid loss
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feces insensible losses (breathing, perspiration, etc |
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Thirst Mechanism
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Triggeredby decreased blood volume and increased osmolarity (solute concentration) |
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Antidiuretic hormone |
Promotesreabsorption of water in the kidneys |
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Aldosterone |
Increasesreabsorption of sodium and water in the kidneys |
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Atrial natriuretic peptide |
stimulatesrenal vasodilatation and suppresses aldosterone, increasing urinary output |
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Edema
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Excess fluidin the interstitial space |
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Hypervolemiaor fluid volume excess |
Excess fluidin the intravascular space |
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Waterintoxication |
Excess fluidin the intracellular space |
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Fluid Excess
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•Manifestations:peripheral edema, periorbital edema, anasarca, cerebral edema, dyspnea,bounding pulse, tachycardia, jugular vein distension, hypertension, polyuria,rapid weight gain, crackles, and bulging fontanelles •Diagnosis:history, physical examination, daily weights, measurement of intake and output,blood chemistry, urine analysis, and complete blood count •Treatment:wearing compression stockings, administering diuretics, restricting sodium andfluids, maintaining high Fowler’s position, and hypertonic solutions |
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causes of Fluid Excess
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•Excessivesodium or water intake –High-sodiumdiet –Psychogenicpolydipsia –Hypertonicfluid administration –Freewater –Enteralfeedings •Inadequatesodium or water elimination –Hyperaldosteronism –Cushing’ssyndrome –Syndromeof inappropriate antidiuretic hormone –Renalfailure –Liverfailure –Heartfailure |
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types Fluid Deficit
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uDehydration uHypovolemiaor fluid volume deficit uDecreasedfluid in the intravascular space |
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causes of fluid deficit
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Excessive fluid or sodiumlosses Gastrointestinal losses Excessive diaphoresis Prolonged hyperventilation Hemorrhage Nephrosis Diabetes mellitus Diabetes insipidus Burns Open wounds Ascites Effusions Excessive use of diuretics Osmotic diuresis Inadequate fluid intake poor oral intake inadequate iv fluid replacement |
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Fluid Deficit
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Manifestations:thirst, altered level of consciousness, hypotension, tachycardia, weak and threadypulse, flat jugular veins, dry mucous membranes, decreased skin turgor,oliguria, weight loss, and sunken fontanelles Diagnosis:history, physical examination, measurements of intake and output, dailyweights, blood chemistry, urine analysis, and complete blood count uTreatment:indentifyand manage underlying cause along with fluid replacement |
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Electrolytes in body
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sodium (Na+) Chloride (Cl-) Potassium (K+) Calcium (Ca++) Phosphorus (P) Magnesium (Mg++)
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Electrolytes
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important in muscle and neural activity and in acid base and fluid balance Anions- Negatively charged |
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Sodium (Na+)
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•Normal range 135-145mEq/L •Mostsignificant cation and prevalent electrolyte of extracellular fluid •Controlsserum osmolality and water balance •Playsa role in acid-base balance •Facilitatesmuscles and nerve impulses •Dietaryintake main source •Excretedthrough the kidneys and gastrointestinal tract |
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Hypernatremia cause
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Sodium > 145 mEq/l, Serum osmolarity increases, results in fluid shifts Excessive Sodium excessive sodium ingestion hypertonic IV saline (3% saline) administration Cushing's syndrome corticosteroid use Deficient Water decreased water ingestion loss of thirst sensation inability to drink water third spacing vomiting diarrhea excessive sweating diuretic use diabetes inspidus |
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Hypernatremia
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uManifestations:increased temperature, warm and flushed skin, dry and sticky mucous membranes,dysphagia, increased thirst, irritability, agitation, weakness, headache,seizures, lethargy, coma, blood pressure changes, tachycardia, weak and threadypulse, edema, and decreased urine output uDiagnosis:history, physical examination, blood chemistry, and urine analysis uTreatment:fluid replacement (oral or hypotonic saline solution) and diuretics |
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Causes of Hyponatremia
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sodium < 135mEq/L, serum osmolality decreases Deficient Sodium Diuretic use * Gastrointestinal losses* Excessive sweating*Insufficient aldosterone levels* Adrenal insufficiency * Dietary sodium restrictions Excessive Water Hypotonic intravenous saline (0.45% saline) * hyperglycemia* excessive water ingestion * renal failure* syndrome of inappropriate ADH * heart failure |
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Hyponatremia
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•Manifestations:anorexia, gastrointestinal upset, poor skin turgor, dry mucous membranes, bloodpressure changes, pulse changes, edema, headache, lethargy, confusion,diminished deep tendon reflexes, muscle weakness, seizures, and coma •Diagnosis:history, physical examination, blood chemistry, and urine analysis •Treatment:limit fluids and increase dietary sodium |
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Chloride
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Normal range 98-108 mEq/L Mineral electrolyte Majorextracellular anion Found in gastric secretions, pancreatic juices, bile, and cerebrospinal fluid Plays a rolein acid-base balance Dietary intake main source Excreted through the kidneys |
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Hyperchloremia causes
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Chloride >108 mEq/L Causes Increased chloride intake or exchange: hypernatremia, hypertonic intravenous solution,metabolic acidosis, and hyperkalemia Decreased chloride excretion: hyperparathyroidism, hyperaldosteronism, and renal failure |
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Hyperchloremia
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Manifestations: reflect the underlying cause Diagnosis: history, physical examination, blood chemistry, urine analysis, and arterialblood gases Treatment: identify and manage underlying cause, diuretics, and bicarbonate |
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Hypochloremia causes |
Chloride <98 mEq/L Causes Decreased chloride intake or exchange: hyponatremia, 5% dextrose in water intravenous solution, water intoxication, and hypokalemia Increasedchloride excretion: diuretics, vomiting, metabolic alkalosis, and other gastrointestinal losses |
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Hypochloremia
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Manifestations: reflect theunderlying cause Diagnosis: history, physical examination, blood chemistry, urine analysis, and arterialblood gases Treatment: identify andmanage underlying cause, sodium replacement (oral or intravenous), ammoniumchloride, and saline irrigation of gastric tubes |
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Potassium
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Normal range 3.5-5 mEq/L The primary intracellular cation Plays a rolein electrical conduction, acid-base balance, and metabolism Dietary intake main source Excreted through the kidneys and gastrointestinal tract |
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Hyperkalemia causes
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Potassium > 5 mEq/L Causes Deficient excretion: renalfailure, Addison’s disease, certain medications, and Gordon’s syndrome Excessive intake: oral potassiumsupplements, salt substitutes, and rapid intravenous administration of diluted potassium Increased release from cells: acidosis, blood transfusions, and burns or any other cellular injuries |
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Hyperkalemia
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Manifestions: paresthesia, flaccid paralysis, bradycardia, dysrhythmias, electrocardiogramchanges, cardiac arrest, respiratory depression, abdominal cramping, nausea,and diarrhea Diagnosis:history, physical examination, blood chemistry, 12-lead electrocardiogram, andarterial blood gas Treatment: correct acidosis, usually with sodium bicarbonate. Calcium gluconate. Decrease dietary potassium intake. Dialysis. Kayexalate. Intravenous fluids. Potassium-losing diuretics. Insulin |
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Hypokalemia causes
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Potassium <3.5 mEq/L Causes Excessive loss: vomiting, diarrhea, nasogastric suctioning, fistulas, laxatives, potassium-losingdiuretics, Cushing’s syndrome, and corticosteroids Deficient intake: malnutrition, extreme dieting, and alcoholism Increased shift into the cell: alkalosis and insulin excess |
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Hypokalemia
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Manifestations: muscle weakness, paresthesias,hyporeflexia,leg cramps, weak and irregular pulse, hypotension, dysrhythmias,electrocardiogram changes, decreased bowel sounds, abdominal distension,constipation, ileus, and cardiac arrest Diagnosis: history, physical examination,blood chemistry, 12-lead electrocardiogram, and arterial blood gas Treatment: identify and manage underlying cause along with potassium replacement (oral orintravenous) |
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Calcium
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Normal range 4-5mEq/L Mostly found in the bone and teeth Plays a role in blood clotting, hormone secretion, receptor functions, nerve transmission, and muscular contraction Has inverse relationship with phosphorus Has synergistic relationship with magnesium Dietary intake main source Vitamin D aids absorption Excreted through the gastrointestinal trace Regulated by Vitamin K Parathyroid hormone Calcitonin |
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Hypercalcemia causes
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Calcium > 5mEq/L Causes: Increased intake or release: calcium antacids, calcium supplements, cancer,immobilization, corticosteroids, vitamin D deficiency, and hypophosphatemia Deficit excretion: renal failure, thiazide diuretics, and hyperparathyroidism |
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Hypercalcemia
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Manifestations:dysrhythmias, electrocardiogram changes, personality changes, confusion,decreased memory, headache, lethargy, stupor, coma, muscle weakness, decreased deep tendon reflexes, anorexia, nausea, vomiting, constipation, abdominal pain,pancreatitis, renal calculi, polyuria, and dehydration Diagnosis:history, physical examination, blood chemistry, and 12-lead electrocardiogram Treatment: identify and manage underlying cause. manage symptoms. phosphate. increase mobility. calcitonin. intravenous fluids. diuretics |
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Hypocalcemia causes
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Calcium< 4 mEq/L Causes Excessive losses: hypoparathyroidism, renal failure, hyperphosphatemia, alkalosis, pancreatitis, laxatives, diarrhea, and other medications Deficient intake: decreased dietary intake, alcoholism, absorption disorders, and hypoalbuminemia |
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Hypocalcemia
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Manifestations:dysrhythmias, electrocardiogram changes, increased bleeding tendencies,anxiety, confusion, depression, irritability, fatigue, lethargy, paresthesia,increased deep tendon reflexes, tremors, muscle spasms, seizures, laryngealspasms, increased bowel sounds, abdominal cramping, and positive Trousseau’sand Chvostek’ssign Diagnosis:history, physical examination, blood chemistry, and 12-lead electrocardiogram Treatment: identify and manage underlying cause. calcium replacement (oral or intravenous). vitamin D. Phosphorus |
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Phosphorus
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Normalrange 2.5-4.5 mg/dL Mostlyfound in the bones and small amounts are in the bloodstream Playsa role in bone and tooth mineralization, cellular metabolism, acid-basebalance, and cell membrane formation Dietaryintake main source Excretedthrough the kidneys |
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Hyperphosphatemia causes
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Phosphorus> 4.5 mg/dL Causes Deficientexcretion: renal failure, hypoparathyroidism, adrenal insufficiency,hypothyroidism, and laxatives Excessiveintake or cellular exchange: cellular damage, hypocalcemia, and acidosis |
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Hyperphosphatemia
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Manifestations:rarely seen alone Diagnosis:history, physical examination, and blood chemistry Treatment: Identify andmanage underlying cause* Aluminumhydroxide or aluminum carbonate *Treathypocalcemia |
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Hypophosphatemia causes
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Phosphorus< 2.5 mg/dL Causes Excessiveexcretion or cellular exchange: renal failure, hyperparathyroidism, andalkalosis Deficientintake: malabsorption, vitamin D deficiency, magnesium and aluminum antacids,alcoholism, and decreased dietary intake |
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Hypophosphatemia |
Manifestations:similar to hypercalcemia Diagnosis:history, physical examination, and blood chemistry Treatment: Identify and manage the underlying cause Phosphorusreplacement (oral or intravenous) |
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Magnesium
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Normal range 1.8 - 2.5 mEq/L
An intravenous at cation Mostly stored in bone and muscle Plays a role in muscle and nerve function, cardiac rhythm, immune function, bone strength, blood glucose management, blood pressure, energy metabolism, and protein synthesis Dietary intake main source Excreted through the kidneys |
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Hypermagnesemia |
Magnesium >2.5 mEg/L Causes: renal failure, excessive laxative, and antacid use Manifestation similar to hypercalcemia Diagnosis history physical examination, and blood chemistry Treatment diuretics, dialysis, and intravenous calcium |
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Hypomagnesemia |
Magnesium < 1.8 mEq/L Causes inadequate intake, chronic alcoholism, malnutrition, pregnancy, diarrhea, diuretics, and stress Manifestations similar to hypocalcemia Diagnosis history physical examination, and blood chemistry Treatment magnesium replacement |
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Buffers |
Bicarbonate carbonic acid system ( most significant in ECF) Phosphate system ( high concentrations ICF ) Hemoglobin system (found in erythrocytes) Protein system ( most abundant found in both ICF and ECF) |
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Respiratory regulations |
Increased respirations release excess CO2 decreasing acid Slow respirations release less CO2 increasing acidity |
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Metabolic acidosis |
Causes bicarbonate deficit. Intestinal loss, renal loss....... Acid excess, tissue hypoxia resulting in lactic acid build up, ketoacidosis, drugs, toxins, renal retention. |