food and water
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| def homeostasis | the state of equilibriums in the internal environment of the body
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| during normal metabolism the body produces many what | kacids
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| the acids the body produces alter the what | internal environment of the body
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| water content of body: water makes up how much of the body; what is transported in water; what cells contain less water | 60%;salts,nutrients, and wastes; fat cells
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| why are older adults and infants at higher risk for fluid related problems | due to the fact older adults water content is less and infants is more
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| body fluid compartments: what are the two major fluid compartments of the body; def intracellular; def extracellular;2/3 of the bodies water is located where; | intracellular and extracellular fluid; fluid within the cells; fluid outside the cells; in the cells
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| body fluid compartments: extracellular fluid is aka; what is the fluid between the cells; | interstitial fluid; interstitial fluid;
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| body fluid compartments: where is 1/3 of body water located; | in the extracellular fluid
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| functions of body water: body fluids are in constant motion doing what; | transporting nutrients, electrolytes, and oxygen to cells and carrying waste products away from the cells, regulating body temp;
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| calculating fluid gain or loss: one liter of water weighs what; | 2.2 lbs;
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| electrolytes: def; def of ions; def of cations; def of anions | are substances whose molecules dissociate or split into ions when placed in water; electrically charged particles; are positively charged ions; neg. charged particles
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| electrolytes: give example of cations; give example of anions | sodium, potassium, calcium,magnesium; bicarbonate, chloride, and phosphate, most proteins
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| def osmolarity | a measure of the total solute concentration per liter of solution
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| def of solvent; def of solute | substance that is capable of dissolving a solute; substance that dissolves into a solvent
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| def of a solution | homogeneous mixture of solutes dissolved into a solvent
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| electrolytes: in the ICF what is the most common electrolyte; what is most common electrolyte in ECF | potassium and phosphate; sodium and chloride
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| movement of electrolytes: movement occurs how; | from areas of high concentration to areas of low concentration and to areas of opposite charge
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| movement of electrolytes: diffusion- def; active transport- def; | the movement of molecules from area high concentration to area low concentration; molecules move against the pressure gradient energy required for this
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| what is the energy source for active transport | ATP
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| movement of electrolytes: def osmosis; | the movement of water between two compartments separated by semipermeable membrane
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| osmotic movement of fluid: def isotonic; def hypotonic; def hypertonic | fluids with the same osmolarity as the cell interior; solutions which the solutes are less concentrated than the cells are; those with solutes more concentrated than cells
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| the __ and __ are normally isotonic to eachother | ICF and ECF
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| if a cell is surrounded by hypotonic fluid what happens | water moves into the cell causing it to swell and possibly to burst
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| if a cell is surrounded by hypertonic fluid what happens | water leaves the cell to dilute the ECG the cell shrinks then
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| def hydrostatic pressure hydrostatic pressure decreases when | is the force with in a fluid compartment; as the blood moves through the arteries until it is pushed into the capillary bed
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| oncotic pressure: def; | the pressure exerted by collied in solution
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| the movement and direction of fluid movement in the capillaries are determined by what 4 things | capillary hydrostatic pressure, plasma oncotic pressure, interstitial hydrostatic pressure, interstitial oncotic
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| shifts of plasma to interstitial fluid: when does fluid accululate to the interstitium; | if venous hydrostatic pressure rises, plasma oncotic pressure decreases or interstitial oncotic pressure rises or if lymph is interrupted
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| shift of interstitial fluid to plasma: fluid is drawn into the plasma space when; how does this happen; | whenever there is an increase in the plasma osmotic or oncotic pressure; w/ admin of colloids, dextran, mannital, hypertonic solution
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| fluid spacing: term that describes what; def 1st spacing; def 2nd spacing; def 3rd spacing | the distribution of body what; the normal distribution in the ICF and ECF conpartments; abnormal accumulation of interstitial fluid; trapped and essentially unavailable for functional use
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| ex third spacing; | ascites
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| hypothalamic regulation: body fluid deficit or increase is sensed by the hypothalamus and this in turn stimulates what; what does ADH due; so if ADH is suppressed do we urinate more or less | thirst and the antidiuretic hormone release; causes the renal distal tubules to reabsorb water if there is a water deficit or it is suppressed and more water is released if there is excess; more
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| pituitary regulation of water balance: the pituitary is under what part of the bodies control; what factors increase the release of ADH; factors that reduce the release of ADH | the hypothalamus; stress, n/V, nicotine, morphine, post surgery due to stress; diabetes insipidus
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| syndrome of inappropriate antidiuretic hormone: what is it | causes an abnormal amount of ADH production causing water retention, decrease plasma osmolarity and decreased urine output
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| cortisol: what is it; in large doses what does it retain; what does it elevate; | glucocorticoid;; sodium; glucose;
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| aldosterone: in large doses what does it retain; what does it excrete ; what excretes it; | retain sodium; potassium; adrenal cortex;
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| renal regulation: what are the primary organs for regulating fluid and electrolyte balance; how much urine should be produced a day on average; what happens when kidneys do not function well | the kidneys; 1.5 L; the cannot maintain fluid and electrolyte balance resulting in edema, phosphorus retention , acidosis
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| cardiac regulation of water: increased atrial pressure (volume) and high serum sodium levels causes the release of what; what doe natriuretic peptides do; | natriuretic peptides; suppress secretion of aldosterone, renin, and ADH and action of angiotensin II thus more water excreted and decrease in BP and blood volume
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| gastrointestinal regulation of water: what is average daily intake of H20; diarrhea and vomiting prevent reabsorbtion of what from GI tract; this lack of reabsorbtion leads to what | 2000-3000 ml; water; fluid loss
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| insensible water loss: def; how much water is lost each day from this; what is sensible water loss; | vaporization from the lungs and skin assists in regulating body temp; 900 ml; excessive sweating by fever, high environmental temps
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| gerontologic considerations of fluids: why is there a decrease in glomerular filtration; what are hormonal changes | due to structural changes in the kidneys and decrease in renal blood flow; decreased renin, aldosterone, increase ADH and ANP
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| gerontologic considerations of fluids: loss of subq tissue leads to what; | increased loss of moisture through the skin;
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| normal serum electrolyte values: what is potassium; what is magnesium; what is sodium; what is calcium; bicarbonate; chloride; phosphate | 3.5-5; 1.5-2.5; 135-145; 4.5-5.5; 22-26; 96-106; 2.8-4.5
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| ECF volume imbalance: the deficit is aka; excess is aka; | hypovolemia; hypervolemia;
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| ECF volume imbalance: deficit- what are abnormal losses of fluid; def dehydration | diarrhea, fistula drainage, hemmorage, polyuria, inadequate intake, plasma in interstitial fluid shift (from a burn); loss of pure water alone w/o loss of sodium
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| ECF volume imbalance: deficit- clinical manis; | restlessness, drowsiness, lethargy, confusion, thirst, decreased skin turgor, postural hypotension, increased pulse, decrease urine output, increased RR, wt loss;
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| ECF volume imbalance: deficit- what is tx; | to correct cause and replace water and electrolyte
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| ECF volume imbalance: excess- causes; CMs | excessive intake of fluids, heart failure, renal failure, primary polydipsia, SIADH, cushing syndrome, long term use corticosteroids; HA, confusion, lethargy, peripheral edema, distended neck veins, inc. BP, polyuria, crackles, SOB, muscle spasms, wt gain
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| ECF volume imbalance: excess- tx; how are fluids removed;k | removal of fluids; diuretics and fluid restrictions
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| nursing interventions for fluid/volume issues: what should IandO include; why should CV changes be monitored | oral,IV, tube feedings, retained irrigants, urine, woundtube drainage, vomit, diarrhea; prevent or detect complications from fluid and electrolute imbalances;
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| nursing interventions for fluid/volume issues: how is pulse in excess; when are neck veins distended; when is HR elevated; | bounding; when increase in volume; in fluid deficit;
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| nursing interventions for fluid/volume issues: when is there pulmonary congestion; why is there an in RR with fluid loss | when there is excess of volume; b/c decreased tissue perfusion resulting in hypoxia
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| nursing interventions for fluid/volume issues: what should be assessed neurologically | LOC, pupillary responses to light, voluntary movement of extremities
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| nursing interventions for fluid/volume issues: an increase in 1 K of weight would equal __ amount in fluid retention; what is term when there is a lag in skin turgor for ECF deficit; why is routine oral care important; | 1000 ml; tenting; to comfort those on fluid restriction and management of fluid volume excess
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| nursing interventions for fluid/volume issues: why should edematous tissue be elevated; | to promote venous return and fluid reabsorption;
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| nursing interventions for fluid/volume issues: a nasogastric tube should always be irrigated with ___ and never with __; why should NG tube never be irrigated with water; | isotonic saline solution, water; b/c water causes diffusion of electrolytes into the gastric lumen from mucosal cells and the lytes are then suctioned away
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| sodium imbalances: what absorbs sodium from food; how does sodium leave the body; what regulates sodium balance; aldosterone does what; | GI tract; through urine, feces and sweat; the kidneys; promotes the reabsorption from the renal tubules
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| hyp0natremia: causes; | excessive sodium loss, gi loss, renal loss(diuretics, adrenal insufficiency),skin losses- burns; fasting diets, excessive water gain, excessive hypotonic fluids, HF, SIADH;
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| hyp0natremia: CMs with decreased fluid volume; CMs with increased fluid volume; | irritability, confusion, dizziness, termors, coma, dry mm, postural BP, tachycardia, thread pulse, clammy skin; Ha, apathy, confusion, seizures, coma, N/V, diarrhea, st gain, increased BP
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| Hypernatremia: causes | excessive sodium intake- IV fluids, near drowning in salt water, hypertonic tube feedings, inadequate water intake, excessive water loss, osmtic diuretic therapy, diarrhea, diabetes insipidus, cushings syndrome, DM uncontrolled
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| Hypernatremia: cms with decreased fluid volume; CMs with increased fluid volume | restlessness, agitation, coma, intense thirst, swollen tongue, sticky mm, postural bp, wt loss, weakness; restlessness, agitation, twitching, seizures, intense thirst, flushed skin, wt gain, peripheral edema,increase bp,
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| Sodium: what would sodium levels be if .. . there was a water deficit; sodium deficit;isotonic ecf deficit; water excess; sodium excess; isotonic ecf excess | hypernatremia; hyponatremia; normal sodium; hyponatremia; hypernatremia; normal
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| Hypernatremia: this causes what type of osmolarity; hyperosmolarity causes water to shift where; when water shifts outside of cells what happens to cells; as plasma osmolarity increases what center is stimulated in the hypothalamus | hyperosmolarity; outside of the cells; they dehydrate; thirst center
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| Hypernatremia: is symptomatic hypernatremia rare or common; what is tx; over rapid correction of this can result in what | rare; underlying cause; cell swelling and cerebral edema;
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| hyponatremia: results from loss of sodium containing what; this does what to the fluid osmolarity; with hypoosmolarity fluid shifts where; retention of water causes what | fluids or water excess; it becomes hyposmolarity; into the cells; lowers sodium concentration
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| hyponatremia: s/s of this are directly r/t what; s/s are first seen where; what tx is often all that is needed | cellular swelling; CNS; fluid restriction;
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| potassium imbalances: 98% of the bodies K+ is located where; | in the cells;
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| how does the sodium potassium pump maintain high sodium levels ECF and high k+ levels outside the cells; this process is fuelled by what | it pumps sodium out and k+ in; ATP
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| potassium imbalances: why are neuromuscular and cardiac function commonly affected by potassium imbalances | b/c the ratio of ECF potassium to ICF potassium gives the potential for nerve and muscle cell
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| potassium imbalances: potassium moves into the cell when; k+ leaves the cell when; where in body is primary route for k+ loss; | with tissue formation; tissue breakdown; the kidneys
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| potassium imbalances: what happens if kidney function is impaired; factors that cause sodium retention cause k+ to be lossed or gained; large urine volumes = large __ volumes | toxic levels of k+ are retained; lossed; k+ volumes
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| potassium imbalances: factors that cause k+ to move from ecf to icf; factors that cause k+ to move from icf to ecf | insulin, alkalosis, stress, coronary ischemia, beta blockers, rapid cellbuidling; acidosis, trauma to cells, exercise, dig, beta blockers
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| hypokalemia: causes- what are the 3 main ones; ex of k+ losses; ex of shift of k+ into cells; ex lack of k+ intake | potassium loss, shift potassium into cells, lack of k+ intake; gi losses, renal losses, skin losses, dialysis; increased insulin, alkalosis, tissue repairs, increased epi; sarvation, low k+ diet, no k+ in parental fluids if npo
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| hypokalemia: CMs; | fatigue, muscle weakness, leg cramps, N/V, paralytic ileus, softflabby muscles, decreased reflexes, weak pulse, polyuria, hyperglycemia;
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| hypokalemia: ECG changes- what does ST segment look like; what does Twave look like; what type dysrhythmias seen, what is HR, | depressed; flattened; ventricular- pvcs; bradycardia
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| hyperkalemia: what are the 3 main causes; ex of excess k+ intake; ex ofshift of k+ out of cells; FAILURE to eliminate k+ ex; | excess k+ intake, shift k+ out of cells, failure to eliminate k+; excessive parenteral admin, k+ containing drugs, k+ salt substitutes; acidosis, tissue catabolism, crush injury, tumor lysis; renal disease, k+ sparring diuretics, adrenal insufficiency, AC
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| hyperkalemia: CMs; | irritability, anxiety, abdominal cramps, diarrhea, weakness of lower extremities, paresthesias, irregular pulse, cardiac arrest if hyper kalemia sudden
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| hyperkalemia: ECG changes- what does T wave look like; what is PR interval like; what is ST segment like; what happens to P wave; what happens to QRS; what are dysrhythmias | tall tented T waves; prolonged; depressed; loss of P wave; widening QRS; V fib, V standstill;
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| hyperkalemia: what is the most common cause; what drugs reduce the kidneys ability to excrete k+; | renal failure; k+ sparring diuretics, ACE inhibitors,
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| hyperkalemia: this increase the concentration of k+ where; what are initial s/s; what muscle is effect 1st; what happens to cardiac depolarization | outside the cell; cramping leg pain, weekness of skeletal muscle; leg; it is decreased
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| hyperkalemia: why does ab cramping and diarrhea occur; | b/c of hyperactivity of smooth muscle
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| hyperkalemia: why is there a risk for injury; to resolve oral intake of what should be limited; how is elimination of k+ increased; | r/t lower body muscle weakness; potassium; diuretics, dialysis, ion exchange resins;
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| hyperkalemia: how is potassium forced from the ecf to the icf; how is the membrane excitability reversed | admin iv insulin along with glucose so pt does not become hypoglycemic; by admin calcium gluconate
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| hypokalemia: what is most common cause; release of aldosterone causes what; | abnormal losses from kidney or GI tract; k+ excresion in the urine;
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| hypokalemia: how does low magnesium cause k+ depletion; | low plasma mag stimulate the renin release which increased aldosterone levels which results in k+ excretion;
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| hypokalemia: what does metabolic alkadosis do | cause k+ to shift into cells in exchange for hydrogen
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| hypokalemia: is the cell less or more excitable | les
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| hyperkalemia: is the cell less or more excitable; can it effect resp muscles | more ; no
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| hypokalemia: what is impaired cardiac wise; low k+ results in what toxicity of what med; s/s first noted where; can it effect respiratory muscles; what happens to GI motility | impaired repolarization; dig; in weakness legs; yes; it decreases
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| hypokalemia: why is pt at increased risk for injury; tx; | muscle weakness; by giving k+ supplements;
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| calcium imbalances: calcium is obtained how; calcium combines with what; where is it concentrated; as calcium levels increases what decreases; as calcium levels decrease what increases; the calcium-phosphorus relationship is what type of relationship | from ingested foods; phosphorus; the skeletal system; phosphorus; phosphorus; and inverse one
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| calcium imbalances: what is the function of calcium; | transmission of nerve impulses, myocardial contractions, blood clotting, formation of teeth and bone, muscle contraction;
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| calcium imbalances: what are the 3 forms of calcium; what is the common protein it binds to | free/ionized, bound to protein, complexed with phosphate, citrate or carbonate; albumin
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| calcium imbalances: what is the active form ; how much of serum calcium is ionized | he ionized form; about half
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| calcium imbalances: total calcium is what; serum pH changes effects total calcium or ionized calcium; decrease in plasma pH does what to calcium; | all the serum calcium; ionized only; decreases calcium binding to albumin;
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| calcium imbalances: so if calcium does not bind to albumin bc decrease in pH this causes more ___ type of calcium in body; | ionized;
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| calcium imbalances: does albumin levels effect total calcium; does albumin levels effect ionized calcium levels; low albumin lowers or raises plasma calcium; | yes; no; lowers;
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| calcium imbalances: calcium balance is controlled by what; parathyroid hormone is aka; PTH is produces by what; | parathyroid hormone, calcitonin, vit D; PTH; the parathyroid gland;
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| calcium imbalances: what stimulates the release ofPTH; def bone reabsorption; | low serum calcium levels; movement of calcium out of the bones;
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| calcium imbalances: what does PTH do; | increases bone reabsorption, increase GI absorption of calcium, and increases renal tubule reabsorption of calcium
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| calcium imbalances: what produces calcitonin; what stimulates the release of calcitonin; calcitonin apposes the action of what; what does calcitonin do; | the thyroid gland; high serum calcium levels; PTH; lower serum calcium levels- does opposite of PTH;
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| calcium imbalances: how is Vit D formed; what does Vit D do with calcium | through the action of ultraviolet rays on a precursor found in the skin or ingested in the diet; helps absorb calcium in the GI tract
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| Hypercalcemia: what are the majority of cases caused by; what is the 2nd most common cause; why do malignancies lead to hypercalcemia; | hyperparathyroidism; malignancies (from cancer); b/c of bone destruction;
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| Hypercalcemia: excessive calcium leads to reduced excitability of what; | muscles and nerves;
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| Hyp0calcemia: what are causes of decreased total calcium; what are causes of decreased ionized calcium; | chronic renal failure, hypoparathyroidism, vit D def, mag def, acute pancreatitis, loop diuretics, diarrhea,decreased serum albumin; alkalosis
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| Hypercalcemia: what are causes of increased total calcium; what are causes of increased ionized calcium; | multiple myeloma, prolonged immobilization, hyperparathyroidism, vit D overdose; acidosis
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| Hyp0calcemia: what are cms; | easy fatigue, depression, anxiety, confusion, numbness and tingling in extremities, hyperreflexia, chvostek's sign, trousseau's sign, laryngeal spasm, tetany
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| Hyp0calcemia: ECG changes- what happens to ST segment; what happens to QT interval; what dysrhythmia occurs | elongation; prolonded; v. tach
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| Hypercalcemia: what are cms | lethargy, weakness, depressed reflexes, decreased memory, confusion,anorexia, n/v, bone pain fx, polyuria, coma, dehydration
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| Hypercalcemia: ecg changes- what happens to ST segment; what happens to QT interval; what is dysrhythmia | shortened; shortened; ventricular dys
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| Hypercalcemia: why is there a risk for injury; what is best tx; what type of I infusion should be used; how much should pt drink a day | do to neuromuscular changes; promoting exretion of calcium in urine with diuretic; isotonic; 3000=4000 ml;
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| Hypercalcemia: why is synthetic calcitonin given; what is drug given for hyper due to malignancy | to lower serum calcium levels; aredia
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| hypocalcemia: how does pancreatisis cause hypocalcemia; why can multiple blood transfusions cause it; | fatty acids combine with calcium ions decreasing calcium levels; b/c the anticoagulant in it is citrate and it binds with calcium;
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| Hypocalcemia: low calcium allows what to move into thecells; the result of sodium moving into the cells is termed what; def tetany; | sodium; tetany; it is trousseau's sign, chvosteks sign
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| hypocalcemia: def chvosteks sign; def trousseaus sign; | contraction of facial muscles in response to tap over the facial nerve in front of ear; carpal spasms induced by inflating a BP cuff and it is obvious w/I 3 min;
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| hypocalcemia: why is there a risk for injury; what is goal of tx; why is calcium not given im; | b/c of tetany and seizures; treat the cause; can cause severe local reaction;
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| magnesium imbalances: where is most of it located in the body; it functions as a coenzyme in the metabolism of what; what regulates it; cms of it are often mistaken for what other imbalance; | in the bone; carbs and proteins; gi absorption and renal excretion and factors that regulate calcium; calcium;
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| hypomagnesemia: causes; most common cause; cms | diarrhea, n/v, chronic alcoholic, impaired GI absorption, malnutrition, large urine out, ng suction; prolonged fasting and starvation; confusion, hyperactive DTR,tremorsand seizures,
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| hypermagnesemia: causes; most common cause; cms; | renal failure, adrenal insufficiency, excessive adm of mag; increased mag intake accompanied with renal failure; lethargy, drowsiness, n/v, DTR are lost, resp. and cardiac arrest
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| acid base imbalances: when are acids produced; what do bases do to the acids; | during metabolism; the neutralize them;
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| pH: the acidity or alkalinity depends on the concentration of what ions; increase in h+ =__; decrease in h+ = ____; | h+; acidity; alkalinity;
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| pH: what does it mean by it is a logarhythm; what is the range; what is neutral; what # is acidic; what # is alkaline; what is blood; | that it increases by 10 fold or decreases by 10 fold; 1-14;7; <7; >7; pH 3.35-3.45 slightly alkaline;
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| def acidemia | signifyingan arterial blood pH of < 7.35
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| def acidosis | process that adds aicd or eliminates base from fluids
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| def alkalemia | sign arterial blood pH of more than 7.45
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| def alkalosis | process that adds base or eleiminates acidfrom the body fluids
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| def anion gap | reflection of normally unmeasured anionsin the plasma
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| def buffer | substance that reacts with an acid or base to prevent a large change in pH
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| regulating pH: what are the 3 ways the body regulates it; what is fastest- how fast; what is slowest- how slow; what is mediacore- speed | buffer systems, respiratory system, and renal system; buffers-immediately; respiratory-minutes max effect in hours; renal- 2-3 days
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| regulating pH: buffer system- they change strong acids into ___; they also bind to acids to do what; what are the buffers of the body; what is a buffer made of; function of buffer; | weaker acids; neutralize them; carbonic acid, acid-bicarbonate, monohydrogen, intracellular and plasma protein; a weak ionized acid or a base and salt; to minimize effects of acids on the body and excrete it in urine
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| regulating pH: buffer system- buffers cannot maintain pH with out functioning what | renal and resp systems
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| regulating pH: resp system- how do lungs maintain normal pH; decreased resp causes more ofwhat in blood; increased CO2 leads to increased what; | by excreting CO2 and water; CO2; h+;
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| regulating pH: resp system- what center in brain is alerted with increased CO2; the medulla signals body to do what; respiration is inhibited when | the resp center in the medulla; increased rate and depth of breathing; when medulla senses low CO2 or h+;
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| regulating pH: more co2 = more ____ | h+
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| regulating pH: renal system: what are the 3 mechanisms of acid elimination; why do kidneys excrete acidic urine; what is pH of urine; what happens if there is renal failure | excreting small amount h+ in tubules, combining h+ with ammonia, excretion of weak acids; b/c it removes portion of acid cellular metabolism; 6 from 4-8; loses ability to correct pH alterations
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| respiratory acidosis: this is an excess ofwhat; this occurs with hypo___; hypoventilation is caused by a buildup of what; a build up of CO2 causes what to build up in the blood; as carbonic acid dissociates what is then freed; | carbonic acid; hypoventilation; CO2; carbonic acid; h+;
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| respiratory acidosis: h+ decreases or increases pH; what do the kidneys do to compensate; cms | decreases it; it conserves bicarb and secretes increases in h+; confusion,drowsy, decreased BP, ha, coma, vfib, hypoventilation
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| respiratory acidosis: causes; what is plasma pH; what is PaCO2; what is HCO3; what is urine pH | COPd, barbiturate orsedative OD, severe PNA, atelectasis, resp muscle weakness,hypoventilation; low; high; normal or high; less then 6
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| respiratory alkalosis: this is a deficit in what; this occurs with hyper___; most common cause; is the ventilation rate increased or decreased | carbonic acid; ventilation; hypoxemia from acute pulmonary disorders; increased
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| respiratory alkalosis: increased ventilation rate leads to what; cms | decreased carbonic acid and alkalosis; lightheaded, tachycardia, n/v, tetany, seizures, hyperreflexia,
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| respiratory alkalosis: cause; what causes hyperventilation; what causes stimulated resp center | hyperventilation, stimulated resp center, mechanical hyperventilation; hypoxia, pulmonary emboli, anxiety, fear, pain, fever; septicemia, encephalitis, brain injury
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| respiratory alkalosis: what is plasma pH; what is PaCO2; what is HCO3; what is urine pH; | high; low; normal or low; more than 6;
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| metabolic acidosis: what is there a deficit of; what are the 2 ways it occurs; what are examples of acid acculilation; | base bicarbonate; from an acid build up in body other then carbonic acid or when bicarbonate is lost from body fluids; ketoacids with DKA and lactic acid accum with shock
🗑
|
||||
| metabolic acidosis: ex of loss of a bicarbonate; what does the lungs do in response to this; what type resp does ptdevelop | severe diarrhea; increase CO2 excretion in the lung; kussmaul;
🗑
|
||||
| metabolic acidosis: causes; what is plasma pH; what is PaCO2; what is HCO3; what is urine pH | DKA, lactic acidosis, starvation, severe diarrhea, renal failure, shock; low; normal or low; low; les then 6
🗑
|
||||
| metabolic acidosis: cms | drowsiness, confusion, ha, coma, decreased BP,dysrhythmias,n/v and d, deep rapid resp
🗑
|
||||
| metabolic alkalosis: what is there and excess of ; this occurs from what 2 things; why does bod decrease resp rate | base bicarbonate; loss of a acid or gain of a bicarbonate; to increase plasma CO2;
🗑
|
||||
| metabolic alkalosis: ex of loss of an acid; ex of gain of a bicarbl | prolonged vomiting; ingestion baking soda
🗑
|
||||
| metabolic alkalosis: causes; what is plasma pH; what is PaCO2; what is HCO3; what is urine pH | severe vomiting, excess gastric suctioning, diuretic therapy, potassium deficit; high; normal or high; high; more then 6;
🗑
|
||||
| metabolic alkalosis: cms | dizziness, irritable, nervous, tachucardia, dysrhythmias, n/v and anorexia, tetany tremors, tingling fingers, msuclecramps seizures, hypoventilation
🗑
|
||||
| blood gas values: what is normal arterial and venous pH; what is normal PaCO3;what is normal HCO3; HCo3 is aka | 7.35-7.45; 22-26; bicarbonate
🗑
|
||||
| hydrostatic pressure is aka | BP
🗑
|
||||
| so if hydrostatic pressure is greater then oncotic pressure what occurs | edema
🗑
|
||||
| what composes extracellular fluid | interstitial, lymph, plasma, cavities
🗑
|
||||
| why are burn pt have extreme risk for shock | protein is pushed into interstitial and then oncotic pressure is reversed and substances are pulled out
🗑
|
||||
| what is difference between diffusion and osmosis | diffusion movement of solutes and osmosis movement of h2o
🗑
|
||||
| what 3 types of fluid movement is passive; what fluid movement is active | diffusion, facilitated diffusion and osmosis; active transport
🗑
|
||||
| osmosis: the movement is always from ___ concentration to __ concentration; | dilute to more concentration;
🗑
|
||||
| osmolarity: measures the concentration of what; increase of osmolarity means increase in what; decrease of what; | solutes in plasma and urine; and solutes; blood volume;
🗑
|
||||
| normally ICF and ECF are ___ tonic | isotonic
🗑
|
||||
| protein content: more of it is in where- the vascular space or the ECF | vacular (ICF) space
🗑
|
||||
| hypotonic moves from dilute to concentrated of concentrated to dilute | dilute to concentrated
🗑
|
||||
| hydrostatic pressure: it is the force of fluid where; what is it in blood vessels; this is the major force that pushes water out of where | in fluid compartments; the BP generated by the contraction of the heart; the capillary system
🗑
|
||||
| oncotic pressure: is aka __ pressure; it is pressure excerted by what; ex of a colloid; colloids pull what | osmotic; colloids; protein; fluids
🗑
|
||||
| fluid shifts: water follows what 2 things; increase in EFC osmolarity moves water where; if increase in EFC osmolarity what happens to cells | salt and sugar; out of the cells; they shrink
🗑
|
||||
| fluid shifts: increase in solutes of EFC = increase in what; decrease in ECF osmolarity moves water where; what happens to cell when there is an decrease in ECF osmolarity | solutes; into the cell; the cells swell
🗑
|
||||
| fluid shifts: increase in ICF osmolarity moves water where; increase in ICF causes cells to what | into the cells; cells swell;
🗑
|
||||
| fluid shifts: decrease in ICF causes cells to what; decrease in icf causes water to move where | shrink; to the tissues
🗑
|
||||
| aldosterone secretion: what does it retain; what follows the retention of salts; | Na+; water;
🗑
|
||||
| oral fluid and electrolyte replacement: imbalance tx is directed to correcting what; glucose provides what obsorption where; | the underlying cause; sodium obsorption to the small intestines;
🗑
|
||||
| oral fluid and electrolyte replacement: what would skin look likefor na+ excess; what would skin look like for na+ deficit; bounding pulse could indicate shift of fluid to where; what shift of fluid could it be if there was a rapid weak thready pulse | flushed dry skin; clammy cold skin; institial fluid to plasma; shift of plasma fluid to the interstial
🗑
|
||||
| oral fluid and electrolyte replacement: what lyte imbalance could it be if there was a rapid irregular weak pulse; what lyte imbalance could it be if there was a slow weak irregular pulse | severe k+ deficit; severe k+ excess
🗑
|
||||
| hypotonic solution- common hypotonic solutions; | saline 0.45%;
🗑
|
||||
| maintainance fluids are usually what; why are hypotonic solutions used as maintainence fluids; | hypotonic solutions; b/c most fluid losses are hypotonic;
🗑
|
||||
| hypotonic solution- they have the potential to do what to cells; what are s/s of cellular swelling; | swelling; alterations of mental changes;
🗑
|
||||
| hypotonic solution- %5 dextrose in water is considered what really; how does %5 dextrose become hypotonic; the dextrose helps prevent ketosis from what; why cant pure water be IV | isotonic; the dextrose is quickly metabolized and the net result is free water which is hypotonic; starvation; b/c it would cause hemolysis of RBCs
🗑
|
||||
| isotonic solutions: this solution expands only in the what; is there a net loss or gain in the ICF; this is the ideal fluid replacement for a pt with would type of fluid deficit; ex; | ECF; no loss or gain in the ICF; ECF; lactated ringers;
🗑
|
||||
| isotonic solutions: what is the saline is isotonic; 0.9% saline has a sodium concentration that is a bit higher than what; excessive admin of isotonic NaCL results in elevated ___ levels; | 0.9% saline; plasma; sodium and chloride levels;
🗑
|
||||
| hypertonic: this initially raises the osmolarity of what; it treats what; why should these be used with caution; what frequent monitoring should be done; | ECF; hypovolemia and hyponatremia; risk for intravascular fluid volume excess; BP, LS and serum sodium levels;
🗑
|
||||
| why are additives added to IV solutions | b/c there may be specific loss
🗑
|
||||
| plasma expanders: what do they do; list the colloids; | they stay in the vascular space and increase the osmotic pressure; protein solutions like plasma, albumin, commercial plasma;
🗑
|
||||
| blood transfusion: why are packed RBCs giving; packed RBCs pull fluid where; whole blood can cause circulatory overload with; | they have the advantage of giving the patient primarily RBCs; into the ICF; circulatory overload b/c of the excess fluid volume;
🗑
|
||||
| BMI: what is healthy BMI ; what is ideal; what is overweight; what is obese; how is it calculated; | 18-25; 22; 25-30; >30; wt in lbs x 700/ ht in inches/ ht in inches again
🗑
|
||||
| nutritional assessments lab value: good lab values to know; | Hgb, BUN, creatinine, urine/serum clearance, prealbumin, albumin, transferrin;
🗑
|
||||
| nutritional assessments lab value: 60% of protein in body is what; 40% of protein in body is what; albumin levels will be increased if blood is concentrated or dilute | albumin; globulin; concentrated
🗑
|
||||
| nutritional assessments lab value: total lymphocyte count- what is it; what counts suggests malnutrition; | the % of lymphs x WBC; <1800;
🗑
|
||||
| def of anemia of chronic disease | they have iron studies but do not use it
🗑
|
||||
| def serum iron | circulating protein bound iron
🗑
|
||||
| def transferrin | protein that transports iron
🗑
|
||||
| respiratory imbalances effect what concentrations | carbonicacid concentrations
🗑
|
||||
| metabolic imbalances affect what | the base bibarbinate
🗑
|
||||
| acidosis is caused by an increase in what; an increase in carbonic acid is termed what; acidosis is also caused by a decrease in what; what is a the term for a decrease in bicarbonate; | carbonic acid; resp. acidosis; bicarbonate; metabolic acidosis;
🗑
|
||||
| alkalosis can be caused by a decrease in what; a decrease in carbonic is termed what; alkalosis can be caused by an increase of what; what is the term for an increase in bicarbonate | carbonic acid; respiratory alkalosis; bicarbonate; metabolic alkalosis
🗑
|
||||
| iron studies: serum iron shows what; what does transferrin show; what does TIBC show; | circulating protein bound to iron; protein that transports iron; all protein that binds and transports iron
🗑
|
||||
| iron studies: what does transferrin saturation show; | better indicator of iron available for erythropoiesis
🗑
|
||||
| calculating caloric needs: obesity is > __% above BMI; how are protein needs calculated; how much protein is needed for someone weighing 100 kg; | 20%; wt in kg x 1gram of protein; 100gram (100kg x1)
🗑
|
||||
| calculating caloric needs: what is protein calculation for stage 2 decub, fx, cancer, ambulation; | wt in kg x 1.25 grams
🗑
|
||||
| calculating caloric needs: what is calculation of protein for stage 3 decub and albumin <3; | wt in kg x 1.5 grams;
🗑
|
||||
| lab tests: total protein- total protein is the combo of what 2 proteins; increased total protein could mean what; decrease in total protein could mean what; | albumin and globulin; hemoconcentrated; malnurished
🗑
|
||||
| labs: Albumin- what is normal albumin level; what is normal globulin level; if pt serum calcium is low, what other lab should be checked before concluding that calcium is low; why should albumin be checked if calcium is low; | 2.5-5; 2.3-3.4; albumin; if albumin is low calcium could be low b/c it binds with albumin, but if albumin is high and calcium is low- there is truly low calcium
🗑
|
||||
| what is the best way to know someones fluid status | is pt weight
🗑
|
||||
| nutritional supplements: why is gut used first; | b/c we don't want the gut mucosa to atrophy, it is less expensive, less risk, less complicated;
🗑
|
||||
| nutritional supplements: what type of tube feeding increases risk for aspiration | NG tube feeding
🗑
|
||||
| nutritional supplements: how does nurse know how many calories per ML; 2 cal/mL are given to what ppl | the bottle will read cals/ml usually 1/1; ppl with fluid restriction
🗑
|
||||
| changes in peristalsis: does SNS response slow or increase peristalsis; what is needed until bowel function returns to normal; why are PPIs given; ex of a PPI | it slows peristalsis; NPO or NG; to decrease the stress related mucosal damage; omeprazole
🗑
|
||||
| TPN: aka; when is it used; what are the ingredients; what type of solution is it; | total parental nutrition; used when gut cannot be used; glucose, amino acids, trace elements, vitamins and electrolytes; hypertonic;
🗑
|
||||
| TPN: what percent of glucose is it; what vein is it given in; | >20% glucose; the central venous line
🗑
|
||||
| PPN: it has what percent dextrose; aka; what kind of vein is it given in; | <20%; peripheral parental nutrition; peripheral vein
🗑
|
||||
| TPN: what to assess; what should be looked at on bottle; can blood products, piggybacks or push meds be given with TPN; is it a drip or pump; why is pt weaned off of it; | wt, I/O, mucus membranes, elastic skin turgor, VS, lung sounds, CBG, electrolytes balanced, follow labs; the expiration date and time; no; always a pump; sudden stopping can increase change of rebound hypoglycemia
🗑
|
||||
| TPN: why is pt at risk for hypoglycemia post TPN; why is pt at risk for hyperglycemia; | b/c TPN has a lot of dextrose; during TPN hyperglycemia can occur b/c of high dextrose content
🗑
|
||||
| TPN: why is there a risk for pneumothorax; what are other risks; | r/t insertion of the CVC; infection, air embolus, hyperglycemia, hypoglycemia, psychological problems r/t decreased oral stimulation
🗑
|
||||
| assessment of fluid status: what should be assessed | wt,I&O, JVD, MM, skin turgor, LS, edema
🗑
|
||||
| lipids: are they given with TPN'; it prevents what deficiencies; they contral hyper___; it is __tonic; 20% has __cals/ ml; 10% has __cals/ml | yes; fatty acid ones; glycemia; isotonic; 2 cals; 1 cals
🗑
|
||||
| TPN: does it have fats in it; what 2 substances does it only have in it; | no; protein and glucose;
🗑
|
||||
| lipids: s/s of allergy; what labs should be monitored; what pt should not take this; why must it be given slowly 12-24 h; | fever, chills, back pain, chest pain; tryglycerides and cholesterol; metabolism probs, pancreatitis, liver disease, egg allergy too fast may report n&V,temp
🗑
|
||||
| access for TPN and PPN: CVC- where should end of catheter end up; how many lumens are there; can blood be drawn from it; | in the superior vena cava; 1-3 lumens; yes
🗑
|
||||
| access for TPN and PPN: PICC- can RN insert; can bp or lab be drawn in that arm; | yes; no;
🗑
|
||||
| does pt need tpn or EN: 26 yo with ulcerative colitis scheduled for colectomy; 74 yo with stroke and impaired swallowing; 56 yo alcoholic with impaired liver function and minimal oral intake | tpn b/c she is preoperative; EN; EN
🗑
|
||||
| does pt need tpn or EN: 35 yo with with a tracheo-esophageal fistula; 28 yo with DM and gastroparesis; 22 yo with traumatic brain injury on mechanical ventilation; | TPN there would be a hard time putting the tube down; TPN; TPN;
🗑
|
||||
| does pt need tpn or EN: 45 yo with pancreatitis and pancreatic pseudocyst; | TPN- but no lipids
🗑
|
||||
| body water: the majority of fluid in body is located where; what is normal serum osmolarity; is the serum osmolarity more or less then normal if pt is dehydrated; is the serum osmolarity more or less then normal if the pt is overloaded | in the ICF; 275-295 mOsm/l; more then normal; less then normal
🗑
|
||||
| calculating fluid needs: what is average persons intake; our body regulates fluids by our sense of what; fluid needs are unreliable for what 2 type of ppl | 1500-2000 ml/day; thirst; the elderly and very young;
🗑
|
||||
| calculating fluid needs: fluid loss is from what; how do you calculate fluid needs; why do we third space fluids; how much urine should be output an hour | burns, diarrhea, fistula wound drain, Lasix, DKA, sweat; 30 ml x IBW or OIBW; capillaries damaged, lymph obstruction, plasma proteins are decreased; 30 mL
🗑
|
||||
| Stress response: ADH- a decrease of BP, decrease of volume, decrease osmolarity causes what to stimulate the pituitary to secrete ADH; when ADH is secreted what happens to the renal tubules; release of ADH U/O increases or decreases | osmoreceptors in the hypothalamus; they reabsorb H20; decreases
🗑
|
||||
| Stress response: ADH- release of ADH causes increase or decrease of BP; release of ADH causes increase or decrease of volume; | increase of BP; volume
🗑
|
||||
| Stress response: Aldosterone- regulates what 2 things; renin is found where; renin converts angiotensinogen to what;angi I is converted to what; angiotensin II stimulates the secretion of what; where is aldosterone made | Na and H20; in the liver; angiotensin I; angiotensin II; aldosterone; in the adrenal cortex;
🗑
|
||||
| Stress response: aldosterone- it absorbs what; it excretes what | Na and H20; ecretion of k and H and peripheralvasoconstriction
🗑
|
||||
| Stress response: ANS- what is found in the carotid and aortic arch that sense changes in what; the baroreceptors trigger the ANS to do what; | BP and volume; respond to the increase or decrease in blood volume
🗑
|
||||
| Stress response: ANS- an increase in volume causes the receptors to do what; a decrease in volume activates the SNS and this does what | stretch and PSNS is activated and it vasodilates; increase HR and vasocontriction
🗑
|
||||
| Stress response: glucocorticoids- they promote the reabsorption of what; they elevate what | Na and H2O in kidney; blood sugar
🗑
|
||||
| Stress response: prostaglandins- when is it released; release of this decreases what; | with the vasocontraiction of renal vessels; blood volume
🗑
|
||||
| causes of post op third spacing | lymph obstruction, decreased plasma proteins, fluid overload, ascites, pleural space pericardial space, joint cavities
🗑
|
||||
| guidelines for parenteral fluids: why should calcs be done at prep; | to prevent errors;
🗑
|
||||
| def of crystalloids | solutions with small molecules that flow easily from vascular into cells and tissues
🗑
|
||||
| isotonic fluids: def; is there a fluid shift | same osmo as body fluids; no
🗑
|
||||
| hypertonic fluids: def; fluids move where; does it increase serum osmo or decrease it | increase serum osm; from intracellular to exstracellular; increase it
🗑
|
||||
| hypotonic fluids: def; does it increase or decrease serum osmolarity; do fluids move into or out of the cell; | fluids shifts from extracellular to intracellular and interstitial; decrease; into the cell;
🗑
|
||||
| colloids: def; are they hypertonic or hypotonic; | they are plasma expanders and they stay in the vascular space; hypertonic;
🗑
|
||||
| whole blood: is it hypo are hyper tonic | hyper
🗑
|
||||
| TPN: is it hypo or hyper tonic | hyper
🗑
|
||||
| tube feedings: is it hypo or hyper tonic | hyper
🗑
|
||||
| calculating IV solutions: how do you do it; | 4kcal/gm of CHO;
🗑
|
||||
| NG tube for decompression: causes a loss of what; | k+
🗑
|
||||
| BMP lab norms: norm BS; norm Na+; norm k+; norm Cl; norm CO2; norm BUN; norm Cr | 60-110; 135-145; 3.5-5; 96-106; 22-30; 5-25; .5-1.5
🗑
|
||||
| PEARLS: wherever k+ goes what follows; wherever Na+ goes what follow; calcium and magnesium act like a ___ id there is too much; changes in Na+ cause what changes; | Mg+; water goes; sedative; brain changes
🗑
|
||||
| acid base: increase in k+ causes acidosis or alkalosis; decrease in k+ causes alkalosis or acidosis; | acidosis; alkalosis;
🗑
|
||||
| what is the normal ratio of bicarb/carbonic acid; | 20:1;
🗑
|
||||
| carbonic acid is controlled by what; bicarb is controlled by what; | the lungs; the kidneys;
🗑
|
||||
| PaCO2: <35 is acidic or alkaline; is >45 acidic or alkaline | alkaline; acid
🗑
|
||||
| HCO3: <22 is acid or alkaline; >26 is acidic or alkaline | acidic; alkaline
🗑
|
||||
| anion gap: helps to differientiate what; what is 90% circulating cations; what is 85% of the circulating anions; what is range | diff between acidotic conditions; Sodium; chloride and bicarbonate; 8-14
🗑
|
||||
| isotonic fluids: the concentration of dissolved particles are similar to what; does the solution remain in the ECF or ICF; name them; | plasma; ECF; 0.9% NS, 5% DW, ringer's solution
🗑
|
||||
| hypotonic solutions: how does fluid shift; does it stay in the ECF or ICF; give ex; does it have a higher or lower solute concentration | from the ECF to the ICF; ECF; 0.45% NS, 0.33% ns, 0.2% ns, 2.5% DW; lower solute concentration
🗑
|
||||
| hypertonic solution: where does fluid shift; is there a higher or a lower solute concentration | from the ICF to the ECF; higher solute concentration; 3% ns, 5% ns, D5LR, D10W, D20W, D50W, 5%D&0.45%ns;
🗑
|
||||
| if k+ is lowered is that alkalosis or acidotic | alkalosis
🗑
|
||||
| k+: it is hypo if it is <___; it is hyper if it is >___; | 3.5; 5;
🗑
|
||||
| K+: hypo- why do kidneys escrete large amounts of urine; tx; can acidosis or alkalosis cause this | b/c kidneys become less sensitive to ADH so excrete; k+ foods, parenteralreplacement of k+, minotr iv site for infiltration, I/O; alkalosis
🗑
|
||||
| k+:hyper- is there more or less peeing; what should be restricted; could acidosis or alkalosis cause this; | less peeing; k+ foods; acidosis
🗑
|
||||
| Na+: hypo- this causes cellular edema which leads to what 3 things; what should d/ced immediately; | cerebral edema, weakness, muscle cramps; diuretics;
🗑
|
||||
| Na+: hyper- what should be restricted; what hormone increased excretion could cause this; | Na+; aldosterone
🗑
|
||||
| hypochloremia: what is cause; does it occur with what ABG issue; s/s; tx | follows Na losses, overhydration; metabolic alkalosis; neuromuscular excitability, slow/shallow resp, decreased bp, tatany; underlying cause, replace K+, seizure precautions
🗑
|
||||
| hyperchloremia: what ABG issue does it occur with; causes; s/s; what is IV tx; why should we monitor safety | metabolic acidosis, Na+ gain, dehydration; weakness, lethargy, deep rapid breathing; NaHCO3 IV, ringers lactate IV; b/c decreased LOC
🗑
|
||||
| calories per IV bag: percentage on IV bag is written as a fraction how; how determine how many mL are admin to pt a day; | ex: 25% would be written over 100 like 25/100 or x/100; if order says x ml/hr times it by 24 (ex: 100 ml/hr equals 2400 ml/day)
🗑
|
||||
| calories per IV bag: how to break down CHO, Proteins, fats- 1 CHO= __kcals; 1 Protein = __kcals; 1 fat= ___ kcals; | 4 kcals; 4 kcals, 9 kcals
🗑
|
||||
| calories per IV bag: ex: what is kcal for 25% dextrose; | 25/100 x 2400 ml/day x 4kcals/gm = 2400 kcals
🗑
|
||||
| diets: how many calories in general diet; | 2000-3000 kcals;
🗑
|
||||
| tube feeding: what is the biggest cause of diarrhea; what is used for diarrhea tx | ABX; kaopectate
🗑
|
||||
| sodium is found outside or inside the cells of the body; potassium is found inside or outside the cells of the body | outside the cells; inside the cells
🗑
|
||||
| high potassium is most common in the failure of what organ | kidneys
🗑
|
||||
| ___ + ____ =bicarbonate + hydrogen | water + carbon dioxide
🗑
|
||||
| what organ regulates CO2; what organ regulates bicarbonate | lungs; kidneys
🗑
|
||||
| how does bicarbonate help post metabolism | it helps buffer the acids that build with metabolism
🗑
|
||||
| diabetic ketoacidosis: what deficiency does this person have; this deficiency causes what; does this occur with type 1 or type 2 dm; what age group is it most common in; | insulin; dehydration; type one; young adults;
🗑
|
||||
| diabetic ketoacidosis: what begins to break down; what are these things broken down into; what hormones break these down; | muscle,fat, and livers; sugar and fatty acids; glucagon, growth hormone, adrenaline;
🗑
|
||||
| diabetic ketoacidosis: what are the fatty acids converted to; what is the process of the fatty acids to ketones called; what should the normal metabolism of the body be; | ketones; oxidation; carbs for fuel;
🗑
|
||||
| diabetic ketoacidosis: what is the fuel in this dx; why does increase in sugar occur; as bs rises what do the kidneys do | fat for fuel; b/c insulin is unavailable to transport sugar into the cells; they dump extra sugar into urine;
🗑
|
||||
| diabetic ketoacidosis: since kidneys are trying to get rid of sugar is there an increase or decrease of urine; what % of total body fluids are lost; what electrolytes are lost | increase of urine; 10%; k+ and sodium
🗑
|
||||
| diabetic ketoacidosis: most common causes that this happens in type 1 dm; | infections from diarrhea, vomiting, high fever, missed inadequate insulin, newly dx dm;
🗑
|
||||
| diabetic ketoacidosis: s/s; | excessive thirst, frequent urination, general weakness, vomiting, loss of appetite, confusion, adominal pain, sob, sry skin mouth, increased hr, decreased bp,fruity odor of breath;
🗑
|
||||
| intracellular fluid volume excess: aka; fluid gain is ___ (>,< or equal to) solute gain; fluid moves how; fluid moving into the cells causes them to become what; when cells are overloaded what do they do; | hypoosmolar ECF; >; extracellular to intracellular; overloaded; they swell;
🗑
|
||||
| intracellular fluid volume excess: s/s | convulsions, behavior changes, confusion, sudden wt gain, increase SBP, decrease DBP, electrolyte washout
🗑
|
||||
| intracellular fluid volume excess: why is there s/s of confusion and coma; | b/c the brain cells are overloaded and it increases intracranial pressure;
🗑
|
||||
| intracellular fluid volume excess: causes; | water intoxication or Na deficit, excessive tap water enamas; electrolyte free IVS
🗑
|
||||
| intracellular fluid volume excess: electrolyte free IVs are __ tonic | hypotonic
🗑
|
||||
| intracellular fluid volume excess: tx- what iv to give; what should be restricted; meds; what assessment should be done; | hypertonic IV fluids; oral fluids; Lasix; neuro checks
🗑
|
||||
| extracellular fluid volume excess: aka; fluid gain is ___ (>,< or equal to) solute gain; what becomes overloaded; what spacing can occur; | iso-osmolar; equal to; EC space and Vascular space; 3rd spacing;
🗑
|
||||
| extracellular fluid volume excess: s/s; what are s/s of pulmonary edema | wt. gain, inc BP, dependent edema, pulmonary edema, JVD, ascites, dyspnea, rales
🗑
|
||||
| extracellular fluid volume excess: causes- why does hypervolemia cause it; why are burns and surgery an issue | r/t increased NaCl IV, heart or renal failure, liver disease; fluid shifts 2-3 days after these things
🗑
|
||||
| extracellular fluid volume excess: what meds are given; what should be restricted; nursing intventions | diuretics; Na+; lungsounds, increase HOB, monitor labs and lytes
🗑
|
||||
| intracellular fluid volume deficit: aka; fluid loss is ___ (>,< or equal to) solute loss; the fluid moves where; what happens to the cells; | hyperosmolar ECF; >; from intracellular to extracellular space- moves out of the cells; they are dehydrated and shrink;
🗑
|
||||
| intracellular fluid volume deficit: s/s; why is there an increased temp | thirst, oliguria, increase spec gravity, twitching andconvulsions, flushing, inc temp, wt loss, tenting turgor, dry mouth; due to water is needed to regulate temp
🗑
|
||||
| intracellular fluid volume deficit: causes- why does cellular dehydration cause it; who gets dehydrated cells; who gets increased water loss; | r/t dec. fluid intake, increased water loss, confused, weak elderly; hyperventilation, fever, kidney unable to concentrate urine;
🗑
|
||||
| intracellular fluid volume deficit: what IV fluids are given; | hypotonic fluids;
🗑
|
||||
| extracellular fluid volume deficit: aka; fluid loss is ___ (>,< or equal to) solute loss; extracellular fluid becomes hyper or hypovolemic; this can lead to what serious thing; | iso-osmolar loss; equals; hypo; shock and CV collapse;
🗑
|
||||
| extracellular fluid volume deficit: are lytes lost; | yes;
🗑
|
||||
| extracellular fluid volume deficit: s/s- what is the first sign of severe CV symptoms; other s/s; | postural hypotension; tenting turgor, dec wt, dry skin, mucous membrane dry, oliguria, nausea, weakness, inc. specific gravity dec. u.o., tachycardia
🗑
|
||||
| extracellular fluid volume deficit:causes- what causes dehydration; | r/t fluid loss from GI wound drainage diaphoresis, hemorrhage and decreased fluid intake and from initial fluid shifts from trauma or burns
🗑
|
||||
| extracellular fluid volume deficit: tx- what IV fluids are given; | NaCl fluids;
🗑
|
||||
| fluid movement: decreased serum osmolarity is dilution or concentration; decreased serum osmolarity is doe to an increase in what hormone secretion; | dilution; ADH;
🗑
|
||||
| fluid movement: decreased serum osmolarity is caused by what | RT surgery, stress, narcotic
🗑
|
||||
| fluid movement: increased aldosterone secretion causes what to be retained; when sodium is retained what else is retained | sodium; waterl
🗑
|
||||
| thirst: what stimulates it; why is thirst stimulated; | the hypothalamus; a drop in blood volume and increase in serum osmolarity;
🗑
|
||||
| kidneys: they control the excertion of what | H20 and lytes
🗑
|
||||
| renin-angiotensin-aldosterone system: renin is released when; renin release causes what else to be released; angiotensin I is converted to what; | when there is a decrease in blood flow stimulates the release of renin; angiotensin I; angiotensinII;
🗑
|
||||
| renin-angiotensin-aldosterone system: then do vessels vasoconstrict of vasodilate; when the vessels vasocontrict what happens; | vasoconstrict; there is a release of aldosterone;
🗑
|
||||
| ADH: aka; does it want to save or get rid of H2O; what releases ADH; | antidiuretic hormone; save H2O; the posterior pituitary
🗑
|
||||
| ANP: aka; when is it released; when this is released what does it inhibit | atrial natriuretic peptide; with atrial stretch; renin and aldosterone
🗑
|
||||
| fluid movement: what causes fluid to move; increase in plasma osmotic pressure increases the concentration of what; increase of plasma osmotic pressure is done by the admin of what meds | increased plasma osmotic pressure, increase plasma oncotic pressure, increase tissue hydrostatic pressure; solutes; mannitol, dextran, hypertonic solutions
🗑
|
||||
| fluid movement: increase in plasma oncotic pressure causes what to pull fluids; what meds cause the increase in plasma oncotic pressure | protein; admin of colloids like IV albumin
🗑
|
||||
| fluid movement: what is an example of and increase in tissue hydrostatic pressure | compression stockings
🗑
|
||||
| intracellular fluid volume excess: what is the serum osmolality; why is Lasix given | it is <275; to eliminate water and retains Na;
🗑
|
||||
| second spacing is fluid where; 3rd spacing is fluid where | interstitial spacing;spacing in the cavity
🗑
|
||||
| intracellular fluid volume deficit: why are fluids given slowly | avoid increased intracranial pressure
🗑
|
||||
| extracellular fluid volume deficit: why is there postural hypotension and tachycardia; | when the heart does not have enough blood volume it speeds up circulation to give body what it needs
🗑
|
||||
| DKA: causes; why doesDM become out of control; what is the process of breaking down fats called; | Type 1 DM, illness, infection,stress, inadequate insulin doses; b/c of increased insulin needs; lipolysis;
🗑
|
||||
| DKA: why does the pH drop; what are the acids; ketones results from the breakdown of what; why does body not fats for fuel | when hydrogen ions accumulate from ketones; ketones; fats for fuel; b/c there is no glucose
🗑
|
||||
| DKA: there is a deficit in ___; insulin is used to transport ___ into the cell; there is lots of glucose where; there is no glucose where; ketones accumulate in what 2 places | insulin; glucose; in the ECf; ICF; the blood and urine
🗑
|
||||
| acidosis happens when the buffering systems of the kidneys and the lungs fail to due what | to restore the pH to the homeostatic range of 7.35-7.45
🗑
|
||||
| HHS: the s/s are r/t what; | dehydration;
🗑
|
||||
| in both DKA and HHS there is a huge diuretic effect b/c water follows ___; what tries to eliminate glucose; what fluid shift is this; | glucose; the kidneys; iso-osmolar fluid volume deficit;
🗑
|
||||
| HHS: causes of HHS; does pt produce ketosis; why is there no ketosis; what type of DM; what age; r/t impaired what | osmotic diuresis,extracellular fluid depletion; no; b/cbody can produce enough insulin to prevent ketosis; type 2; 60 yo; thirst
🗑
|
||||
| DKA and HHS: what is the key difference between DKA and HHS; what type of ketone gives pts the fruity breath | the prescence of ketones; acetone;
🗑
|
||||
| kussmail respirations: body tries to use to blow off what; blowing off CO2 is a way for the body to try to return what backto normal in DKA; | CO2; bodies pH
🗑
|
||||
| DKA and Hhs: why is there an elevated Blood glucose | it happens as body attempts to compensate for cellular starvation b/c glucose can't get in cell w/o insulin
🗑
|
||||
| DKA andHHS: why is serum osmolarity much higher; why are there neuro s/s; neuro s/s can be misinterpreted for what; | due to increase in solutes and loss of fluids; due to intracellular volume deficits as well as pH abnormalities; a CVA
🗑
|
||||
| DKA and HHS: what are the classic s/s that are evident in both in the early stages | polydipsia, polyphagia, polyuria
🗑
|
||||
| DKA: s/s are related to what; what is pH; what is BG; are there ketones | dehydration an decreased pH; <7.3; 200-1500; yes
🗑
|
||||
| HHS: what are s/s r/t; what is BG; are there ketones; is there an increased serum osmolarity | dehydration; 600-2000; none or sometimes minimal; yes
🗑
|
||||
| DKA: s/s- what do vs look like; is there increased or decreased LOC; what is turgor; where is pain | orthostatic hypotension, tachycardia; decreased; tented; abdominal pain
🗑
|
||||
| HHS: does it have more or less severe neuro s/s; does it have more or fewer early s/s; pt often c/o having an increase in what | more; fewer; urination
🗑
|
||||
| DKA: potassium problems- acidosis is an excess of what ions; the body moves what into the cell and pushes what out of the cell during acidosis; how isk+ then lost; | H ion; H ion in and k+ out; lost by osmotic diuresis through urination with sugar and water loss too;
🗑
|
||||
| DKA: if k+ is pushed out into the ECF will the levels initially be higher or lower; what helps make the sodium potassium pump function; | higher; insulin;
🗑
|
||||
| what belongs in the cell sodium or potassium; what belongs outside the cell; these pt almost always need what supplement | potassium; sodium; k+
🗑
|
||||
| DKA: what solution is given 1st; why is normal saline given 1st; where does ns stay to begin with; | normal saline; it is isotonic and will stay where we put it to begin; in the vascular space
🗑
|
||||
| DKA: why is it important to give NS IV right away; why is dextrose given; | so that the body can perfuse to all the vital organs; to prevent hypoglycemia
🗑
|
||||
| DKA: why do hypotonic fluids need to be given slowly; | to prevent rapid fluid shifts causing brain cells toswell;
🗑
|
||||
| DKA tx: what is the first priority; what Iv fluid; how is insulin admin; what should be monitored; | fluid; NS first then 0.45 NaCl; IV; BG, k+ levels and neuro changes
🗑
|
||||
| HHS: does it need a greater or lesser fluid replacement; what should IV fluids be; is insulin IV; is | greater;IV NS at rapid rate then 0.45 NaCl; yes; lesser; BS, lytes and neuro status
🗑
|
||||
| HHS and DKA: when is D5 given; | when BG is <250 or else pt becomes hypoglycemic
🗑
|
||||
| ADH: where is it produced; where is it secreted; does increased or decreased serum osmolatity cause the release of ADH; increased serum osmolatity is increased or decreased solutes; | in the hypothalamus; by the pituitary; increased; increased;
🗑
|
||||
| ADH: when ADH is released what do kidneys do; brain tells the kidneys not to do what; | the increase water reabsorption; diurese;
🗑
|
||||
| adh is aka | vasopressin
🗑
|
||||
| ADH: not enough and what happens; with out ADH is there a FV overload or deficit | water is not reabsorbed in kidneys tubules so large amounts of dilute urine are formed; deficit
🗑
|
||||
| ADH: too much ADH and what happens; with too much ADH is the urine concentrated or dilute; is there a FV excess or deficit | there is an excess amounts of water reabsorbed in kidney tubules; concentrated; excess
🗑
|
||||
| ADH: not enough of ADH is ____; too much ADH is ____; | diabetes insipidus (DI); syndrome of Inappropriate ADH secretion (SIADH)
🗑
|
||||
| ADH secretion: baroreceptors are stimulated by what; osmoreceptors are stimulated by what; | decreased blood volume; increased osmolality;
🗑
|
||||
| How to remember SIADH; How to remember DI; | SIADH (stinking inappropriate ADH- just too much) DI -ADH (darn inadequate ADH- just not enough)
🗑
|
||||
| SIADH: makes too much what; it saves too much what; | ADH; water
🗑
|
||||
| DI: not enough what; it eliminates too much what | ADH; water
🗑
|
||||
| DI: causes- def; neurogenic causes; ex of neurogenic causes | inadequate synthesis, release or response to ADH; lesionthat interferes with ADH synthesis or release; tumor, head injury, surgery, CNS infection
🗑
|
||||
| DI: nephrogenic cause def; nephrogenic ex; why is there excessive thirst | adequate ADH but impaired response in kidneys; renal disease, drugs; /t lesions in thirst center or psych dx
🗑
|
||||
| SIADH: def; ex of causes; | it is released in spite of low or normal plasma osmolality; malignancy, head injury, meds, lung disease PEEP
🗑
|
||||
| DI: pt experience a large amount of dilute urine since there is no what; | ADH to save water;
🗑
|
||||
| SIADH: can cause dilutional hyponatremia why; | the sodium is dilute b/c water is being retained;
🗑
|
||||
| DI: is it r/t DM; is the spec gravity low or high; what is serum osmolality high or low; is serum sodium high or low; what poly s/s are there; all this peeing can lead to what; | no; low; high; high; polyuria and polydipsia; intracellular deficit;
🗑
|
||||
| DI: what will s/s represent | dehydration
🗑
|
||||
| SIADH: why is there wt gain; what is specific gravity high or low; is serum osmolality high or low; s/s; | b/c of fluid retention; high; low; n/v, abd cramps, muscle twitching and weakness, confusion, seizures, cerebral edema possible;
🗑
|
||||
| SIADH: it depends on how low what goes; | sodium goes;
🗑
|
||||
| DI: tx- what type of fluid replacement should there be; what assessment should be done; | hypotonic; I&O,daily wt, urine spec gravity
🗑
|
||||
| DI tx- what med is given; | hormone replacement vasopessin (synthetic ADH hormone)
🗑
|
||||
| SIADH: tx- what is restricted; what is assessment; what fluids to give; what meds to give; | fluids; I and O, daily wt, urine spec gravity; hypertonic 3-5% saline; diuretics, declomycin;
🗑
|
||||
| SIADH: what is action of declomycin; why should HOB be elevated <10 degrees; | it blocks the effect of ADH on renal tubules; to enhance venous return and reduce baroreceptors that stimulate ADH release
🗑
|
||||
| DI: what has been lost, solutes or fluid; | fluid;
🗑
|
||||
| SIADH: what is the most important thing we can do; | restrict fluids;
🗑
|
||||
| what are the thyroid hormones | T3 and T4
🗑
|
||||
| thyroid hormones: T3and 4 regulate what | energy metabolism and growth
🗑
|
||||
| increase in thyroid hormone increases or decreases metabolism | increases
🗑
|
||||
| thyrotoxic crisis: what is thyrotoxicosis; | physiologic effects of hypermetabolic state results from excess circulation of T3 and 4
🗑
|
||||
| thyrotoxic crisis: what is the most common cause; is it common; can it be fatal | graves disease; no; yes
🗑
|
||||
| Myxedema coma: this is caused by what; what happens to body processes- do they slow or speed up | not enough thyroid hormone in the body; slow
🗑
|
||||
| thyroid functions test: hyperthyroidism- is T4 high or low; is T5 high or low; is TSH high or low; | high; high; low
🗑
|
||||
| what does ths stand for | thyroid stimulating hormone
🗑
|
||||
| thyroid functions test: hypothyroidism- is T4 high or low; is T3 high or low; is TSH high or low; | low, low; elevated or low
🗑
|
||||
| TSH: what does hormone do | asks body to produce more T3 and T4
🗑
|
||||
| thyrotoxic crisis: is aka; what is temp; what is BP; what is HR; is pt hyper or hypo ventilating; is skin hot or dry; is CNS increasingly irritably or sluggish; is person confused | thyroid storm; very high 106; high; high; hyper; hot; increasingly irritable; yes
🗑
|
||||
| Myxedema coma: what is temp; what is BP; what is HR; does pt hyper or hypo ventilate; is skin hot or cold; is CNS more or less sensitive | hypothermia; hypotension; bradycardia; hypo;cool skin; dec. CNSm hard to awaken,paranoid
🗑
|
||||
| thyrotoxic crisis: what assessment should be done; what med is given; why are beta blockers given; why is cool blanket given; what other meds are given | cardiac; antithyroid med PTU or Tapazole; to lower BP; to decrease temp; steroids, glucose and fluids
🗑
|
||||
| Myxedema coma: what assessment should be given; what med should be givin; why is pt put on ventilation; why warm blanket; what should be monitored | cardiac; levothyroxine IV; due to hypoventilation; to warm body; fluid balance, anemia
🗑
|
||||
| Liver: how many lobes; what important BVs are located here; def of lobules; | 2; hepatic artery and portal vein; they are the functional units of hepatocytes around a vein
🗑
|
||||
| liver: what are the functions: what does it metabolize; it __ meds and alcohol; what does it synthesis and secrete; | carbs, proteins, fats steriods; detoxifies them; bile;
🗑
|
||||
| liver: what does it store; what does it breakdown/phagocyte; | glycogen, vitamins, minerals, fatty acids, amino acids; RBCs, WBCs, bacteria, particles
🗑
|
||||
| cirrhosis: def; rate of progression depends on what | a progressive disease characterized by destruction of liver cells and tissues caused by fibrosis and disorganized nodular regeneration; the cause
🗑
|
||||
| compare types of cirrhosis: what is the most common type in N america; is alcohol hepatotoxic; in alcoholic how can malnutrition cause it; | alcoholic; yes; malnutrition causes scar tissue to form around portal area
🗑
|
||||
| compare types of cirrhosis: post necrotic- aka; this is caused by complications from what; why is this the most common type in the world; there is massive necrosis from what; | post hepatic; viral, toxic, autoimmune hepatitis; due to viral hepatitis; hepatotoxins;
🗑
|
||||
| compare types of cirrhosis: biliary- def; what can it be caused by; what is the key symptom; | chronic partial or complete obstruction of bile duct; tumors, gallstones, chronic pancreatitis;jaundice
🗑
|
||||
| compare types of cirrhosis: cardiac- is this rare of common; results from what severe disease; right heart failure causes a backup into where; the backup into the liver causes what | rare; CHF; the liver; pressure and liver tissue damage
🗑
|
||||
| cirrhosis: what could be common s/s; what is abdominal pain described as; what will skin color be | vomiting bright red, increasing fatigue, anorexia, SOB, flatulence, abdominal pain, swelling of abdomen, generalized itching, bruising; dull and aching; jaundice
🗑
|
||||
| jaundice: what blocks the bile duct; when bile duct is compressed this reduces the ability to conjugate and excrete what; what is released when RBCs are destroyed; hemoglobin breaks down into what; | connective tissue; bilirubin; hemoglobin; bilirubin;
🗑
|
||||
| Jaundice: bilirubin is transported to the liver be what; once in liver bilirubin isconverted into a ___ soluble form; why is it converted into a water soluble form; what is this process called; jaundice can form if what fails; | albumin; water; to be excreted into the bile; conjugation; conjugation;
🗑
|
||||
| s/s of cirrhosis: why would we find abrasions on the skin; would would be found on face; itching can result from an accumulation of what; | from itching; spider angiomas; bile salts;
🗑
|
||||
| spider angiomas: they are dilated what; what is the cause; when the liver is dysfunctional what continues to circulate | small dilated BVs; the livers inability to detoxify circulating estrogen; different hormones
🗑
|
||||
| cirrhosis: what are 2 s/s of endocrine dysfunction; def of palmer erythema; what is cause of palmer erythema; | palmar erythema, and gynecomastia; reddened areas that blanch with pressure on hands; caused by increase in circulating estrogen
🗑
|
||||
| cirrhosis: gynecomastia- what is the cause; if liver cannot adequately metabolize aldosterone what could be retained | from increased levels of steroid hormones; sodium and water
🗑
|
||||
| cirrhosis: s/s of bleeding; why do ppl bleed; spenomegaly destroys what in the blood; this distruction of platelets is termed what; | vomiting blood, nosebleeds, bruises; less clotting factors and splenomegaly low levels of vit k,; blood cells and platelets; thrombocytopenia;
🗑
|
||||
| cirrhosis: low levels of vit k causes less absorption and storage of what; why is there poor RBC production | fat; this it RT folic acid and protein deficiencies
🗑
|
||||
| cirrhosis: TPO is aka; what does TPO do; what produces TPO; if liver is bad what happens to TPO; many __ factors are synthesized by what; | thrombopoietin; stimulates the bone marrow to produce platelets; the liver; there is not enough and bone marrow is not stimulates to produce more and bleeding risks are increased; the liver;
🗑
|
||||
| cirrhosis: portal hypertension- scarring and changes to liver structure create compression and obstruction of flow through where; the obstruction of flow in portal system creates what; what are changes dueto increased pressure; why are there collateral ve | the portal system; portal HTN; increased venous pressure, splenomegaly, systemic HTN, large collateral veins; bodies attempt to reduce pressure, and divert flow of volume;
🗑
|
||||
| cirrhosis: what is the name of collateral veins | varices
🗑
|
||||
| cirrhosis: portal HTN- is HTN where; what makes up the portal system; the portal system drains what; | in the portal system;circulation thru the pancreas, gallbladder, GI tract, liver and spleen; the GI tract, the spleen and the surface veins of the abd.
🗑
|
||||
| cirrhosis: why is the splenomegaly; | b/c the spleen is very vascular and is enlarged with the backup of flow;
🗑
|
||||
| cirrhosis: why is the systemic HTN; | b/c the heart is working against more push back and has to increase the pressure that is expels blood to make it circulate;
🗑
|
||||
| cirrhosis: varices- def; blood takes the path of least ___; what happens to these varices veins; | small vessels that get engorged due to the backup of flow into the smaller veins in the circulation that are attached to the larger vessels impacted by portal HTN; resistance; they become thin, weak twisted and much larger then there normal size;
🗑
|
||||
| cirrhosis: varices- when are they life threatening; | with the increase in pressure and resistance in portal circulation;
🗑
|
||||
| cirrhosis: vomiting of blood is caused by what; | bleeding varices;
🗑
|
||||
| hydrostatic pressure forces fluids out of where; oncotic pressure forces fluids where; | capillaries; into cappilaries
🗑
|
||||
| cirrhosis: varices- where can they develop; where is the most common place they develop; s/s of gastric varices; s/s of rectal varices; do most ppl with cirrhosis have varices; why do they bleed | esophagus, gastric, rectal, umbilical; the esophagus; hematemesis; hemorrhoids;yes; irritation, ulceration, pressure
🗑
|
||||
| what is the most common life threatening complication of cirrhosis | varices
🗑
|
||||
| cirrhosis: varices- what is the term for varices in the umbilical; def caput medusae; | caput medusae; the vessels on the abd wall get stretched and overfilled due to back pressure and it looks like medusa's snake hair
🗑
|
||||
| cirrhosis: varices- if bleeding has not occurred what is preventative tx; how is irritation reduced in the esophagus; how is irritation reduced in the gastric; how is irritation reduced in the rectal | prevent a hemmorage; diet, alcohol restriction, prevent vomiting and cough; decrease stomach acid; avoid straining with BMs, constipation
🗑
|
||||
| cirrhosis: varices- what meds are used to decrease stomach acid | histamine H@ receptor blockers, proton pump inhibitors;
🗑
|
||||
| cirrhosis: ascites- def; s/s; causes; | abnormal accumulation of fluid in peritoneal cavity; distention, discomfort, impingement on breathing;CHF, pericarditis, nephrotic syndrome,CA, pacreatitis, hepatitis, hypothyroidism
🗑
|
||||
| cirrhosis: mechanism of ascites- hypoalbuminemia- what synthesizes albumin; albumin maintains what pressure; colloid osmotic pressure pulls and keeps fluid where; with low albumin is osmotic pressure increased of reduced; | liver; colloid osmotic pressure; in the vascular space; reduced;
🗑
|
||||
| cirrhosis: mechanism of ascites- hypoalbuminemia- when osmotic pressure is reduced fluid escapes what; the fluid then stays where; | circulation; in the interstitial space;
🗑
|
||||
| cirrhosis: mechanism of ascites- scar tissue blocks what; this blocking further increases what pressure; high plasma and lymph pressure lead to what; | microvasculature; portal hydrostatic pressure and ascites; lymph leakage into the peritoneal cavity;
🗑
|
||||
| cirrhosis: mechanism of ascites- back pressure in the portal system causes high pressure where; high pressure in the capillaries pushes more fluid where; back pressure in the lymph system limits how much interstitial fluid can go where; | in the capillaries; in the tissue; taken away;
🗑
|
||||
| cirrhosis: mechanism of ascites- impaired breakdown of ADH and aldosterone leads to what retention; this leads to loss of what; what type of hyponatremia is there; | Na+ and H20 retention; k+; dilutional hyponatremia;
🗑
|
||||
| cirrhosis: mechanism of ascites- if ADH and aldosterone are not broken down by the liver will they continue to circulate; why do kidneys fail | yes; due to vasoconstriction in hepatorenal syndrome;
🗑
|
||||
| cirrhosis: ascites- what is daily assessment | daily wt, monitor B/p, monitor electrolytes, mental status, abdominal girth, I
🗑
|
||||
| cirrhosis: what would labs look like; liver enzymes are high in beginning, but why do they end up low in end stage | dec. serum albumin, anemia, inc pt/INR, in NH3, increased AST/ALT, increased bilirubin, increased urine urobilinogen, inc. alkaline phosphate; b/c the liver is so scarred it does not function enough to excrete the right amount
🗑
|
||||
| cirrhosis: tests- what does abdominal film show; what does ultrasound show; what does CT scan show; | enlarged liver and spleen; evaluates patency of splenic, partal hepatic veins; organomegaly;
🗑
|
||||
| cirrhosis: liver biopsy- what is the risk; where is it performed; what should pt do; why should blow out; | post procedure hemorrhage; at bedside; blow out and hold breath during needle aspiration; prevents lung from being punctured bc diaphragm is elevated;
🗑
|
||||
| cirrhosis: liver biopsy- what labs are needed pre procedure; what is given for high pt/inr; what is time of bedrest post procedure; s/s of hemorrhage; s/s peritonitis | CBC and coagulation profiles; vit k; 8-12 hours; tachycardia,hypotension, cool clammy skin; abdominal pain, fever
🗑
|
||||
| cirrhosis: diet- what should be constricted; what supplements; | sodium, fluid, fat; vitamins;
🗑
|
||||
| cirrhosis: ascites- drug tx: why Lasix with aldactone; what to admin for severe hypoalbuminemia; | it will release H2o and sodium, and aldactone helps retain k+; salt poor albumin
🗑
|
||||
| cirrhosis: ascites- what are nrsing dx | fluid volume excess, fluid volume deficit, imbalanced nutrition, risk for ineffective breathing patterns, ineffective health maintenance
🗑
|
||||
| cirrhosis: why should NG not be placed with varices | pt could have bleed if nicked/irritated
🗑
|
||||
| cirrhosis: varices- tx of bleed; why is sclerotherapy done; | control the bleeding, give vit k, FFP, blood products, volume replacement; it is injected to the thrombus and obliterate veing;
🗑
|
||||
| cirrhosis: sengstaken blackmore tube- what is it; | it has gastric aspirating tube, esophageal balloon, gastric balloon;
🗑
|
||||
| cirrhosis: varices- why are nonselective Bblockers given; why are octreotide given; | lowers portal venous pressure, reduces cardiac output and organ blood flow; inhibits hormones that cause vasodilation;
🗑
|
||||
| cirrhosis: meds- vasopressin- what is it; action; side effects | synthetic ADH; splachnic vasoconstriction and decreases portal blood flow and decreases portal HTN; increase BP, abd cramping;
🗑
|
||||
| cirrhosis: paracentesis- it is the last result for what; why is only 1000 ml removed; complications of rapid decompression' | severe dyspnea andanorexia from ascites; due to more than that would be too much b/c of loss of body protein in fluids; rapid fluid shifts and protein loss shock;
🗑
|
||||
| cirrhosis: paracentesis- what distress will it relieve | resp distress
🗑
|
||||
| cirrhosis: shunting- tx of what type of bleeding; it reduces what; how does it treat ascites; how is it placed | recurrent; venous pressure and decompresses varices; to reduce pressure and removes excess fluid; stenting jugular vein to vena cava to hepatic vein to portal vein
🗑
|
||||
| cirrhosis: shunting- what is bypassed; why does it increase the risk for confusion; is it a short term or long term tx; why is it done; | the liver; b/c ammonia is metabolized in liver and if liver is bypassed then person could have increased confusion; short term; pt in acute resp distress and if back up is so severe that varices are about to blow
🗑
|
||||
| hepatic encephalophathy: this is a disorder of ___ metabolism and excretion; ammonia goes to liver via portal circulation to be converted to what; the urea is then excreted where; damaged liver cannot detoxify what; | protein; urea; in the kidneys; ammonia;
🗑
|
||||
| hepatic encephalophathy: when ammonia accumulates in the bloodstream it crosses what barrier; once ammonia crosses the blood-brain barrier it becomes ___;does ammonia depress or stimulate CNS; there is an increased risk for GI bleed as body digests __ | blood-brain barrier; toxic; depress; proteins in blood
🗑
|
||||
| hepatic encephalophathy: why does body digest blood; the digestion of blood is like a ____ supplement | due to GI bleed; protein
🗑
|
||||
| cirrhosis: meds-neomycin: destroys bacteria in intestines that break down what; this thus decreases the levels of ___ available for absorption in the blood stream; | protein; NH3
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| what does NH3 stand for | ammonia;
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| cirrhosis: meds- lactulose- breakdown of the drug acidifies what; acidifying the colon increases or decreases the stools fluid content; how many stools a day should there be; this also causes the ammonia to diffuse where | the colon; increases; 2-4; to the blood;
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| cirrhosis: meds- why should there be extreme caution when using tranquilizers, narcotics, sedatives | b/c there is not enough liver tissue to metabolize them
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| cirrhosis:assessment- asterixis: aka; what happens when the wrist is dorsiflexed while holding arms straight out; why does this happen; | liver flap; it causes abnormal jerking of the hands; due to abnormal toxins in the brain
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| cirrhosis:assessment- def of fetor hepaticus; fetor hepaticus and asterixis combined indicate what | sweet fetid breath odor; decreased LOC
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| isotonic solutions: concentration of dissolved particles are similar to what body fluid; what is risk for these solutions; | plasma; fluid volume overload;
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| s/s of fluid volume overload; | bounding pulse, crackles, SOBJVD,edema,S3
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| isotonic solution: name the 3 common ones; | normal saline, lactated ringers, D5W;
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| isotonic solution: normal saline- aka; def; b/c water follows salt this solution increases the volume in what space; treatment of what; | 0.9% sodium chloride; straight up water with balanced concentrations ofsodium and chloride; intravascular space; fluid volume deficit, resusciltation;
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| isotonic solution: lactated ringers- this electrolyte content is most similar to what; for replacement of what; what pt; why is it not good for ppl with high pH; | plasma; fluids and lytes; surgical and burn pt; b/c it is converted to bicarb in liver and thus can increase pH in alkalosis pt;
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| isotonic solutions: D5W- def; why is it hard to classify; what happens when bod quickly consumes dextrose; not at good choice for whom | sugar water; it is isotonic in bottle but is quickly metabolized to become hypotonic; there is no osmotic active particles in plasma; FV def
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| hypotonic solutions: they have a lower concentration of what; infusing these solutions creates an unequal solute concentration among what; this causes fluid to shift from ___ to __; so these solutions hydrate what; they deplete what | electrolytes; fluid compartments; intravascular space tointerstitial and incracellular spaces; cells; circulatory system
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| hypotonic solutions: 0.45% NaCl, 0.2%, NaCl, D2.5W- why will dextrose be given; treat __cellular dehydration; these move fluids where; what pt; can worsen or better hypovolemia or hypotension; who should not have; | to provide calories; intracellular; into the cell;DKA; worsen; pt with increased ICP
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| hypertonic solutions: they have a higer concentration of what; this pulls fluid out of ___ into ___; could benefit pt with ___ edema; monitored for s/s of what; give examples | solutes than the intracellular fluid volume; intracellular space into ECF; cerebral; hypervolemia;3% Sodium chloride; dextrose added to isotonic orhypotonic
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| hypertonic solutions: why does adding dextrose to hypotonic or isotonic solutions make them hypertonic | the added dextrose increases the concentration of solutes in thefluid so it becomes more hypertonic than icf
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| hypertonic solutions: 3% sodium chloride- is used to treat what; how does it treat hyponatremia; what are risks; | severe hyponatremia; it raises the sodium levels in the blood and osmosis pulls fluid from intracellular space to intravascular space; intravascular volume overlaod and shrink brain cells;
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| hypotonic solutions: before giving this solutions we fill pt tank with what; why is tank filled; | isotonic solution; so pt have something in vascular space to move into the cells when we give hypotonic solutions
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| stress response: our bodies stress response causes us to hang onto fluid and it is put where; | tissues, abdomen, joints, cavity;
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| hypertonic solutions: why are they given post op; body hangs onto fluid in vascular space for how long; | stabilize BP and not cause any more shift out of vascular space; about 3 days and pt at risk for fluid volume overload;
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