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WVC 2 chapt 13 Iggy
WVC 2 Chapt 13 Iggy
| Question | Answer |
|---|---|
| The ECF includes | interstitial fluid (third space”) • blood, lymph, bone, and connective tissue water • transcellular fluids. 15 L or .333 of total body fluid |
| Transcellular fluids include (ECF) | •cerebrospinal fluid • synovial fluid • peritoneal fluid • pleural fluid. |
| ICF contains | .666 (about 25 L). |
| Why is H20 needed | to deliver dissolved nutrients, electrolytes, and other substances to all organs, tissues, and cells. |
| Solvent is | the water portion of fluids. |
| Filtration, diffusion and osmosis are | the 3 processes needed to maintain normal fluid balance. |
| Filtration is | FLUID through a cell or BV membrane. Hydrostatic pressure differences on both sides of the membrane cause filtration. |
| Diffusion is | free movement of SOLUTE across a permeable membrane. |
| Diffusion is regulated by | the movement (collisions) of partials (solute) in an area of higher concentration (steepness) to an area of lower concentration |
| Diffusion occurs across a | select cell membrane. Membranes are selective to a particular solute. |
| Facilitated diffusion or facilitated transport is | diffusion across a cell membrane that requires the assistance of a membrane-altering system (e.g., insulin & Na). |
| Osmosis is | the movement of water only through a selectively permeable (semipermeable) membrane. (Effects the concentration of the particles.) |
| Factors for osmosis | the overall concentration of particles in solution, solubility, and the amount of membrane available for osmosis. |
| OsmolARity is the number of | milliosmoles in a LITER of solution |
| OsmolALity is the number of | milliosmoles in a KILOGRAM of solution. |
| The normal osmolARity | 270-300 mOsm/L. Best fx occurs closer to 300. |
| Isosmotic, normonic and isotonic mean | body fluids have concentrations of 270-300 |
| Fluids w/concentrations >300 | hyperosmotic, or hypertonic (>osmotic pressure than isotonic and pulls water from isotonic space. |
| Examples of hypertonic solution | 2% saline IV solution, can lyse blood vessels |
| Isotonic IV solutions | 0.9% saline or D5W (5% dextrose) |
| Hypotonic solutions | <270 mOsm/L. water is pulled from the hypo-osmotic fluid space into the isosmotic fluid space. |
| Hypertonic solution is any solution | >350 mOms/L |
| Isotonic is any solutions | 275-295 mOms/L |
| What factors influence lymph circulation | skeletal muscle movements, breathing, and a peristalsis-like motion in the lymph vessels. |
| The amount and distribution of body fluids is effected by | age, gender and the amount of body fat |
| Minimum amount of urine needed to excrete toxic waste (obligatory urine output) | 400-600 mL. |
| Insensible water loss | water loss via skin, lungs and stool (not measurable) |
| Normal insensible water loss in a healthy adult | 500 to 1000 mL/day. |
| Aldosterone, antidiuretic hormone (ADH), and natriuretic peptide (NP) | hormones that help control water balance |
| Aldosterone is | •secreted by the adrenal cortex whenever sodium level in ECF is decreased. •Aldosterone prevents both water and sodium loss. |
| How does aldosterone work | secreted when Na levels decrease causing the kidney to reabsorb Na & H20 from the urine back into the blood. It also prevents blood K levels from becoming too high |
| What effect does aldosterone have on blood osmolarity & BV | causes it to increase. |
| Vasopressin or ADH (Antidiuretic hormone) is produced | in the brain and stored in the posterior pituitary gland |
| ADH works directly on | kidney tubules and collecting ducts, making them more permeable to water. (more water reabsorbed & returned to blood, decreasing blood osmolarity by making it more dilute) |
| What happens when blood osmolarity decreases (↓Na) | ADH release is inhibited →H20 loss via urine. ↓ H20 in ECF |
| Natriuretic peptides (NPs) are | secreted in cells that line the atria of the heart (atrial natriuretic peptide [ANP]) and the ventricles of the heart (brain natriuretic peptide [BNP]). In response to ↑BP & BV |
| The effects of NP are | opposite of aldosterone. NP INHB re-absorption of NA & ↑glomerular filtration→increased urine output. |
| The outcome of NP is | decreased circulating blood volume and decreased blood osmolarity. |
| Actual dehydration | too little intake or too much output |
| Relative dehydration | water shifts from the plasma into the interstitial space. |
| Risk associated with aging for dehydration | less total body water •↓ thirst sensation ↓motor skills needed for ingesting fluids • (DRUGS) diuretics, antihypertensives, and laxatives |
| Isotonic dehydration | ICF remains normal, loss is from ECF only |
| Cardiovascular changes associated with dehydration | ↑HR • ↓BP • ↓PP • pulses are weak and easy to block •orthostatic hypotension |
| Respiratory changes of dehydration | ↑ RR (hypoxia). The increased respiratory rate is an attempt to maintain oxygen delivery. |
| Skin changes in dehydration | color, moisture, and turgor. Turgor is less reliable in aging adult |
| Where do you assess for turgor in an older adult | sternum |
| Neurologic changes with dehydration | Δ in LOC and sometimes a low grade fever |
| For every degree (Celsius) increase in body temperature above normal, a minimum of an additional | 500 mL of body fluid is lost. The older adult begins to lose more body water at lower levels of fever. |
| Renal changes in dehydration | specific gravity >1.030 •odor •dark color |
| Normal person’s urine output below _______ is a cause for concern | 500 mL/day |
| Fluid loss is considered any weight loss over | half pound per day |
| Lab values in dehydration | ↑H&H •↑ serum osmolarity, glucose, protein, blood urea nitrogen, and various electrolytes (hemoconcentration). |
| Goal of dehydration management is | prevent injury •prevent further fluid losses • ↑fluid compartment volumes to normal ranges. |
| NIC fluid management | •IV therapy, as prescribed. •Give fluids, as appropriate. •Promote oral intake •Distribute the fluid intake over 24 hours, as appropriate. •Encourage significant other to assist patient with feedings, as appropriate. •Offer snacks, as appropriate. |
| Teaching for UAP with dehydration | offer 2 to 4 ounces of fluid every hour. Stay w/pt and report amount |
| The two most important areas to monitor during rehydration are | pulse rate and quality and urine output. |
| Hypotonic solution | >0.9% saline |
| Isotonic solutions | Ringer's lactate •0.9% saline •D5W (5% dextrose in H20) |
| Isotonic dextrose and saline solution | 5% dextrose in 0.225% saline •5% dextrose in water (D5W) |
| Hypertonic dextrose and saline solution | 10% dextrose in water (D10W) •5% dextrose in 0.9% saline •5% dextrose in 0.45% saline •5% dextrose in Ringer's lactate |
| CARDIOVASCULAR CHANGES in fluid overload | • ↑PR • Bounding pulse quality • Full peripheral pulses • ↑BP • ↓PP • ↑central venous pressure • Distended neck and hand veins • Engorged varicose veins • Weight gain |
| RESPIRATORY CHANGES with fluid overload | • ↑ RR • Shallow respirations • ↑dyspnea with exertion or in the supine position • Moist crackles present on auscultation |
| SKIN AND MUCOUS MEMBRANE CHANGES w/fluid overload | • Pitting edema in dependent areas • Skin pale and cool to touch |
| NEUROMUSCULAR CHANGES w/fluid overload | • Altered LOC • Headache • Visual disturbances •Skeletal muscle weakness • Paresthesias |
| GASTROINTESTINAL CHANGES w/fluid overload | • Increased motility • Enlarged liver |
| Labs w/fluid overload | serum electrolyte values are normal •↓H&H and serum protein levels may result from excessive water in the vascular space (hemodilution). |
| Risks associated w/fluid overload | pulmonary edema and heart failure, skin breakdown, |
| How often do you monitor for fluid overload | every 2 hours |
| Specific gravity below ______ indicates fluid overload | 1.005 |
| The best indicator of fluid retention and overload is | |
| Metabolism can account for no more than a half pound of weight gain in one day. Each pound of weight gained (after the first half pound) equates to | 500 mL of retained water. |
| Instruct the patient to call his or her health care provider for more than | a 3-pound gain in a week or more than a 1- to 2-pound gain in 24 hours. |
| Cations have | positive charges |
| Anions have | negative charges. |
| Sodium (Na+) | 136-145 mEq/L |
| Potassium (K+) | 3.5-5.0 mEq/L |
| Calcium (Ca2+) | 9.0-10.5 mg/dL |
| Chloride (Cl−) | 98-106 mEq/L |
| Magnesium (Mg2+) | 1.3-2.1 mEq/L |
| Phosphorus (P) | 3.0-4.5 mg/dL |
| Serum protein | 7-8 g/L |
| Low serum sodium levels inhibit the secretion of | ADH and NP and trigger aldosterone secretion. |
| Problems caused by hyponatremia involve two mechanisms | reduced excitable depolarization and cellular swelling |
| ACTUAL SODIUM DEFICITS causes | • Excessive diaphoresis • Diuretics (high-ceiling diuretics) • Wound drainage (especially gastrointestinal) • Decreased secretion of aldosterone • Hyperlipidemia • Renal disease (scarred distal convoluted tubule) • Nothing by mouth • Low-salt diet |
| RELATIVE SODIUM DEFICITS (DILUTION) causes | • Excessive ingestion of hypotonic fluids • Psychogenic polydipsia • Freshwater submersion accident • Renal failure (nephrotic syndrome) • Irrigation with hypotonic fluids • Syndrome of inappropriate ADH secretion • Hyperglycemia • HF |
| SS of hyponatrema | Δ in LOC •muscle weakness •N/V •diarrhea •hyperactive bowel sounds •Δ in cardiac output. •orthostatic hypotension |
| The priority for nursing care of the patient with hyponatremia is | monitoring the patient's response to therapy to prevent hypernatremia and fluid overload. |
| Severe hyponatremia may be treated with small-volume infusions of | hypertonic (2%-3%) saline. |
| Treatment of hyponatremia occurs with fluid excess | mannitol (Osmitrol), or conivaptan (Vaprisol). Assess hourly for signs of excessive fluid loss, potassium loss, and increased sodium levels. |
| Hyponatremia caused by inappropriate secretion of antidiuretic hormone (ADH) includes agents that antagonize ADH, such as | lithium and demeclocycline (Declomycin). |
| When serum sodium levels are high, what occurs | severe cellular dehydration |
| ACTUAL SODIUM EXCESSES causes | • Hyperaldosteronism • Renal failure • Corticosteroids • Cushing's syndrome or disease • Excessive oral sodium ingestion • Excessive administration of sodium-containing IV fluids |
| RELATIVE SODIUM EXCESSES causes | • Nothing by mouth • Increased rate of metabolism • Fever •Hyperventilation • Infection • Excessive diaphoresis • Watery diarrhea • Dehydration |
| SS of hypernatremia | ↓in attention span •confusion •lethargy •twitching •↓deep tendon reflexes •muscle weakness •↓HR •↑PR •↑BP •↓cardiac output |
| Hypotonic IV infusions, usually 0.225% or 0.45% sodium chloride, are prescribed for | hyponatremia caused by fluid loss |
| Hypernatremia caused by poor renal excretion | furosemide (Lasix), bumetanide (Bumex). Assess the patient hourly for symptoms of excessive losses of fluid, sodium or potassium. |
| Foods that are high in K | meat, fish and some vegitables |
| Foods that are lowest in K | eggs, milk, bread, cereal and grains |
| The normal ICF potassium level is about | 140 mEq/L (mmol/L). |
| Kidney excretion of potassium is enhanced by | aldosterone. |
| Actual potassium depletion occurs when | potassium loss is excessive or when potassium intake is not adequate to match normal potassium loss. |
| Relative hypokalemia occurs when | total body potassium levels are normal but the potassium distribution between fluid spaces is abnormal. |
| ACTUAL POTASSIUM DEFICITS causes | • Inapp/excessive drugs • Inc. secretion of aldosterone • Cushing's syndrome • Diarrhea • Vomiting • Wound drainage (GI) • Prolonged nasogastric suction • Heat-induced excessive diaphoresis • Renal disease impairing reabsorption of potassium • NPO |
| RELATIVE POTASSIUM DEFICITS causes | • Alkalosis • Hyperinsulinism • Hyperalimentation • Total parenteral nutrition • Water intoxication • IV therapy with potassium-poor solutions |
| Drugs that can increase K loss via kidneys | diuretics, corticosteroids, and betaadrenergic agonists or antagonists |
| Hypokalemia increases the sensitivity of the cardiac muscle and may result in | digoxin toxicity, even when the digoxin level is within the therapeutic range. |
| SS of hypokalemia | ↓RR •hyporeflexia •muscle weakness •↓HR •↓PR or increased•orthostatic hypotension •altered mental status •hypoactive bowel tones •ECG changes in the heart, including ST-segment depression, flat or inverted T waves, and increased U waves. |
| The priorities for nursing care of the patient with hypokalemia are | ensuring adequate oxygenation •patient safety for falls prevention •prevention of injury from potassium administration •monitoring the patient's response to therapy. |
| Maximum IV infusion rate for K | 5 to 10 mEq/hr •never to exceed 20 mEq/hr under any circumstances. |
| Because rapid infusion of potassium can cause cardiac arrest, potassium is not given by | IV push. |
| In sever hypokalemia, how often do you monitor oxygenation | hourly. Muscles respond at the slightest stimuli (cardiac arrest) |
| ACTUAL POTASSIUM EXCESSES causes | • Overingestion •Na substitutes •K Cl- •Rapid infusion of K-containing IV solution •Bolus IV K injections • Transfusions of whole blood or packed cells • Adrenal insuff (Addison's disease, adrenalectomy) • Renal failure • K-sparing diuretics |
| RELATIVE POTASSIUM EXCESSES causes | • Tissue damage • Acidosis • Hyperuricemia • Uncontrolled diabetes mellitus |
| SS of hyperkalemia | bradycardia •hypotension •ECG (tall, peaked T waves, prolonged PR intervals, flat or absent P waves, and wide QRS complexes.) •muscle twitching •parenthesis •N/V •diarrhea |
| Hyperkalemia caused by renal failure occurs with | elevated serum creatinine •↑blood urea nitrogen •↓ blood pH •normal or low H&H levels. |
| The priorities for nursing care of the patient with hyperkalemia are | monitoring to prevent cardiac complications • patient safety for falls prevention • monitoring the patient's response to therapy •health teaching. |
| What is used to get potassium from the ECF into the cell | insulin. IV fluids containing glucose and insulin are prescribed to help decrease serum potassium levels (hypertonic) |
| What hormone is secreted to increase Ca levels from the bone | parathyroid hormone (PTH) is released from the parathyroid glands. This stimulates vitamin D activation to help increase intestinal absorption of dietary calcium, inhibiting kidney calcium excretion, and stimulating kidney calcium reabsorption. |
| What causes serum Ca to decrease when it’s too high | TCT thyrocalcitonin |
| DIETARY MANAGEMENT OF HYPERKALEMIA,YOU SHOULD AVOID | • Meats, esp. organ meat & preserved meat• Dairy • Dried fruit• Fruits high in K(Bananas, Cantaloupe, Kiwi, Oranges) • Vegs high in K( Avocados, Broccoli, Dried beans or peas, Lima beans, Mushrooms, Potatoes (white or sweet), Seaweed, Soybeans, Spinach) |
| FOOD YOU MAY EAT W/HYPERKALEMIA | Eggs• Breads• Cereals •Sugar •Fruits low in K,Apples, Apricots, Berries, Cherries, Grapefruit, Peaches, Pineapple • Veg low in K, Alfalfa sprouts, Cabbage, Carrots, Cauliflwer, Celery, Eggplant, Green beans, Lettuce, Onions, Peas,Peppers,Squash |
| ACTUAL CALCIUM DEFICITS | • Inadequate oral intake of Ca• Lactose intol• Malabsp syndromes •Celiac •Crohn's• Inadequate intake of vitamin D • End-stage kidney disease • Renal failure—polyuric phase • Diarrhea • Steatorrhea • Wound drainage (especially gastrointestinal) |
| RELATIVE CALCIUM DEFICITS | • Hyperproteinemia • Alkalosis • Calcium chelators or binders • Citrate • Mithramycin • Penicillamine • Sodium cellulose phosphate (Calcibind) • Aredia • Acute pancreatitis • Hyperphosphatemia • Immobility • Removal or destruction of parathyroid glands |
| Actual calcium loss (a reduction in total body calcium) occurs when | the absorption of calcium from the GI tract slows or when calcium is lost from the body. |
| Relative calcium loss causes | total body calcium amounts to remain normal while serum calcium levels are low. This problem occurs when the unbound calcium in the body is reduced or when parathyroid gland function is decreased. |
| SS of hypocalcaemia | Charlie horses, Paresthesias, tetany, prolonged ST interval and a prolonged QT interval, Palmar flexion–(positive Trousseau's sign), Facial muscle response–(positive Chvostek's sign), hyperactive bowel sounds, osteoporosis |
| NIC hypocalcaemia | seizure precautions, increased dietary intake of Ca w/vit D for absorbtion, environmental stimulation control, mag sulfate & muscle relaxers for spasms, protect fragile bones |
| Hypocalcaemia causes | excitable tissues to be less sensitive to normal stimuli, thus requiring a stronger stimulus to function (heart, muscles, nerves, and intestinal smooth muscles, causes faster clotting times) |
| ACTUAL CALCIUM EXCESSES | • Excessive oral intake of calcium • Excessive oral intake of vitamin D • Renal failure • Use of thiazide diuretics |
| RELATIVE CALCIUM EXCESSES | • Hyperparathyroidism • Malignancy •Direct invasion cancers of breast, lung, prostate, & osteoclastic bone and multiple myeloma) •Indir resorption (liver cancer, small cell lung, & adrenal gland)• Hyperthyroidism •Immobility •glucocorticoids •Dehydration |
| SS of hypercalcaemia | mild increases HR, severe slows HR, severe muscle weakness and decreased deep tendon reflexes without paresthesia, altered LOC, confusion, peristalsis, constipation, anorexia, N/V, and abdominal pain are common. Bowel sounds are hypoactive or absent |
| RN actions hypercalcaemia | measure calfs d/t increase risk of blood clots. Abdomen girth increases d/t decrease in peristaltic action |
| IV used for hypercalcaemia | IV normal saline (0.9% sodium chloride) is usually given because sodium increases kidney excretion of calcium. |
| Drugs for hypercalcaemia | furosemide, plicamycin (Mithracin) and penicillamine (Cuprimine), agents that inhibit calcium resorption from bone, such as phosphorus, calcitonin (Calcimar), bisphosphonates (etidronate), and prostaglandin synthesis inhibitors (aspirin, NSAIDs). |
| non-pharm tx for hypercalcaemia | dialysis |
| Where is most phosphorus found | in bones (80%), the major anion of the iCF |
| what is phosphorus used for | activating vitamins and enzymes, forming adenosine triphosphate (ATP) for energy supplies, and assisting in cell growth and metabolism. It also functions in acid-base balance and calcium homeostasis. |
| Food sources of phosphorus include | meats, fish, dairy products, and nuts. |
| The regulation of ECF phosphorus occurs through the activity of | parathyroid hormone (PTH). ↑PTH→↓Phosphorus |
| HYPOPHOSPHATEMIA | • Malnutrition • Starvation •aluminum hydroxide–based antacid •magnesium-based antacids • Hyperparathyroidism •Hypercalcemia •Renal failure • Malignancy •Hyperglycemia •Hyperalimentation • Respiratory alkalosis •Uncontrolled DM • Alcohol abuse |
| HYPERPHOSPHATEMIA | • Decreased renal excretion resulting from renal insufficiency • Tumor lysis syndrome • Increased intake of phosphorus • Hypoparathyroidism |
| Three main processes lead to decreased serum phosphorus levels | ♦ decreased absorption of phosphorus ♦ increased excretion of phosphorus ♦ intracellular phosphorus shift |
| SS of hypophosphatemia | ↓stoke volume ♦↓cardiac output ♦peri-pulses↓♦gen muscle weakness w/o paresthesias ♦↓RR♦irritablility |
| Adults have an average total body level of ______ mg | 25 g of magnesium. stored in bones and cartilage |
| Plasma levels of free magnesium range from | 1.3 to 2.1 mg/dL, or 0.65 to 1.05 mmol/L |
| Magnesium is critical for | skeletal muscle contraction, carbohydrate metabolism, adenosine triphosphate (ATP) formation, vitamin activation, and cell growth. More in ICF than ECF |
| Extracellular magnesium regulates | blood coagulation and skeletal muscle contractility. |
| The daily magnesium requirement for adults is about | 300 mg. |
| Magnesium regulation occurs through the | kidney and the intestinal tract |
| SS of hypomagnemia | hyperactive deep tendon reflexes, numbness and tingling, and painful muscle contractions. Positive Chvostek's and Trousseau's signs, ΔLOC, depression, abdm distention, N/V, constipation |
| HYPOMAGNESEMIA | • Malnutrition • Starvation • Diarrhea • Steatorrhea • Celiac disease • Crohn's disease • Drugs (diuretics, aminoglycoside antibiotics, cisplatin, amphotericin B, cyclosporine) • Citrate (blood products) • Ethanol ingestion |
| HYPERMAGNESEMIA | • Increased magnesium intake •Magnesium-containing antacids and laxatives•IV magnesium replacement • Decreased renal excretion of magnesium resulting from renal insufficiency |
| Drugs for Mg loss | Magnesium is replaced intravenously with magnesium sulfate (MgSO4) when hypomagnesemia is severe. The IV route is used because MgSO4 causes pain and tissue damage when injected IM. |
| hyperMg | occurs above 4 g/dL. bradycardia, peripheral vasodilation (CARDIAC ARREST), and hypotension, lethargy, ↓deep tend reflx, |
| Drugs for hyperMg | loop diuretics, IV fluids and Ca to ↓cardiac SS |
| Chloride (Cl−) is the major | anion of the extracellular fluid (ECF) and works with sodium to maintain ECF osmotic pressure. |
| Chloride is important in the formation of | hydrochloric acid in the stomach. |
| The normal plasma concentration of chloride ranges from | 98 to 106 mEq/L or mmol/L |
| ______________is the anion most commonly exchanged for chloride. | Bicarbonate (HCO3−) |
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