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Nrs 212 2.3.3

food and water

QuestionAnswer
def homeostasis the state of equilibriums in the internal environment of the body
during normal metabolism the body produces many what kacids
the acids the body produces alter the what internal environment of the body
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
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
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
body fluid compartments: extracellular fluid is aka; what is the fluid between the cells; interstitial fluid; interstitial fluid;
body fluid compartments: where is 1/3 of body water located; in the extracellular fluid
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;
calculating fluid gain or loss: one liter of water weighs what; 2.2 lbs;
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
electrolytes: give example of cations; give example of anions sodium, potassium, calcium,magnesium; bicarbonate, chloride, and phosphate, most proteins
def osmolarity a measure of the total solute concentration per liter of solution
def of solvent; def of solute substance that is capable of dissolving a solute; substance that dissolves into a solvent
def of a solution homogeneous mixture of solutes dissolved into a solvent
electrolytes: in the ICF what is the most common electrolyte; what is most common electrolyte in ECF potassium and phosphate; sodium and chloride
movement of electrolytes: movement occurs how; from areas of high concentration to areas of low concentration and to areas of opposite charge
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
what is the energy source for active transport ATP
movement of electrolytes: def osmosis; the movement of water between two compartments separated by semipermeable membrane
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
the __ and __ are normally isotonic to eachother ICF and ECF
if a cell is surrounded by hypotonic fluid what happens water moves into the cell causing it to swell and possibly to burst
if a cell is surrounded by hypertonic fluid what happens water leaves the cell to dilute the ECG the cell shrinks then
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
oncotic pressure: def; the pressure exerted by collied in solution
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
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
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
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
ex third spacing; ascites
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
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
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
cortisol: what is it; in large doses what does it retain; what does it elevate; glucocorticoid;; sodium; glucose;
aldosterone: in large doses what does it retain; what does it excrete ; what excretes it; retain sodium; potassium; adrenal cortex;
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
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
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
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
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
gerontologic considerations of fluids: loss of subq tissue leads to what; increased loss of moisture through the skin;
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
ECF volume imbalance: the deficit is aka; excess is aka; hypovolemia; hypervolemia;
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
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;
ECF volume imbalance: deficit- what is tx; to correct cause and replace water and electrolyte
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
ECF volume imbalance: excess- tx; how are fluids removed;k removal of fluids; diuretics and fluid restrictions
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;
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;
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
nursing interventions for fluid/volume issues: what should be assessed neurologically LOC, pupillary responses to light, voluntary movement of extremities
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
nursing interventions for fluid/volume issues: why should edematous tissue be elevated; to promote venous return and fluid reabsorption;
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
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
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;
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
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
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,
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
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
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;
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
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;
potassium imbalances: 98% of the bodies K+ is located where; in the cells;
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
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
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
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
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
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
hypokalemia: CMs; fatigue, muscle weakness, leg cramps, N/V, paralytic ileus, softflabby muscles, decreased reflexes, weak pulse, polyuria, hyperglycemia;
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
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
hyperkalemia: CMs; irritability, anxiety, abdominal cramps, diarrhea, weakness of lower extremities, paresthesias, irregular pulse, cardiac arrest if hyper kalemia sudden
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;
hyperkalemia: what is the most common cause; what drugs reduce the kidneys ability to excrete k+; renal failure; k+ sparring diuretics, ACE inhibitors,
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
hyperkalemia: why does ab cramping and diarrhea occur; b/c of hyperactivity of smooth muscle
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;
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
hypokalemia: what is most common cause; release of aldosterone causes what; abnormal losses from kidney or GI tract; k+ excresion in the urine;
hypokalemia: how does low magnesium cause k+ depletion; low plasma mag stimulate the renin release which increased aldosterone levels which results in k+ excretion;
hypokalemia: what does metabolic alkadosis do cause k+ to shift into cells in exchange for hydrogen
hypokalemia: is the cell less or more excitable les
hyperkalemia: is the cell less or more excitable; can it effect resp muscles more ; no
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
hypokalemia: why is pt at increased risk for injury; tx; muscle weakness; by giving k+ supplements;
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
calcium imbalances: what is the function of calcium; transmission of nerve impulses, myocardial contractions, blood clotting, formation of teeth and bone, muscle contraction;
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
calcium imbalances: what is the active form ; how much of serum calcium is ionized he ionized form; about half
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;
calcium imbalances: so if calcium does not bind to albumin bc decrease in pH this causes more ___ type of calcium in body; ionized;
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;
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;
calcium imbalances: what stimulates the release ofPTH; def bone reabsorption; low serum calcium levels; movement of calcium out of the bones;
calcium imbalances: what does PTH do; increases bone reabsorption, increase GI absorption of calcium, and increases renal tubule reabsorption of calcium
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;
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
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;
Hypercalcemia: excessive calcium leads to reduced excitability of what; muscles and nerves;
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
Hypercalcemia: what are causes of increased total calcium; what are causes of increased ionized calcium; multiple myeloma, prolonged immobilization, hyperparathyroidism, vit D overdose; acidosis
Hyp0calcemia: what are cms; easy fatigue, depression, anxiety, confusion, numbness and tingling in extremities, hyperreflexia, chvostek's sign, trousseau's sign, laryngeal spasm, tetany
Hyp0calcemia: ECG changes- what happens to ST segment; what happens to QT interval; what dysrhythmia occurs elongation; prolonded; v. tach
Hypercalcemia: what are cms lethargy, weakness, depressed reflexes, decreased memory, confusion,anorexia, n/v, bone pain fx, polyuria, coma, dehydration
Hypercalcemia: ecg changes- what happens to ST segment; what happens to QT interval; what is dysrhythmia shortened; shortened; ventricular dys
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;
Hypercalcemia: why is synthetic calcitonin given; what is drug given for hyper due to malignancy to lower serum calcium levels; aredia
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;
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
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;
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;
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;
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,
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
acid base imbalances: when are acids produced; what do bases do to the acids; during metabolism; the neutralize them;
pH: the acidity or alkalinity depends on the concentration of what ions; increase in h+ =__; decrease in h+ = ____; h+; acidity; alkalinity;
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;
def acidemia signifyingan arterial blood pH of < 7.35
def acidosis process that adds aicd or eliminates base from fluids
def alkalemia sign arterial blood pH of more than 7.45
def alkalosis process that adds base or eleiminates acidfrom the body fluids
def anion gap reflection of normally unmeasured anionsin the plasma
def buffer substance that reacts with an acid or base to prevent a large change in pH
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
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
regulating pH: buffer system- buffers cannot maintain pH with out functioning what renal and resp systems
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+;
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+;
regulating pH: more co2 = more ____ h+
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
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+;
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
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
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
respiratory alkalosis: increased ventilation rate leads to what; cms decreased carbonic acid and alkalosis; lightheaded, tachycardia, n/v, tetany, seizures, hyperreflexia,
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
respiratory alkalosis: what is plasma pH; what is PaCO2; what is HCO3; what is urine pH; high; low; normal or low; more than 6;
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
what does NH3 stand for ammonia;
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;
cirrhosis: meds- why should there be extreme caution when using tranquilizers, narcotics, sedatives b/c there is not enough liver tissue to metabolize them
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
cirrhosis:assessment- def of fetor hepaticus; fetor hepaticus and asterixis combined indicate what sweet fetid breath odor; decreased LOC
isotonic solutions: concentration of dissolved particles are similar to what body fluid; what is risk for these solutions; plasma; fluid volume overload;
s/s of fluid volume overload; bounding pulse, crackles, SOBJVD,edema,S3
isotonic solution: name the 3 common ones; normal saline, lactated ringers, D5W;
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;
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;
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
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
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
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
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
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;
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
stress response: our bodies stress response causes us to hang onto fluid and it is put where; tissues, abdomen, joints, cavity;
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;
Created by: jmkettel