N245 Final
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| Distribution of Bodily Fluids: Totall ICF; ECF; plasma; interstitium | 60% of body weight; 40% ICF' 20% ECF;' 4% Plasma; 16% Interstitium
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| Serum Osmolality | Osmotic pressure of a solution expressed in osmols or milliosmols per kilogram of water
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| Osmolarity | Osmotic pressure of a solution expressed in osmoles or milliosmoles per liter of solution
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| Serum Osmolality Calculation | (Na+ X 2)+(glucose/18)+(BUN/2.8)
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| Normal range for serium osmolality | 230-300 mOSm/kg/liter
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| Tonicity | Tension that effective osmotic pressure exerts on cell size through movement of water across the cell membrane. Determined through electrolytes which cannot permeate membrane and therefore pull water out of cell via osmosis.
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| Isotonic solution | Equal water/electrolyte concentrations within and outside of cell. Water moving across membrane but no changes in cell size occurring.
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| Hypotonic solution | Concentration inside cell of electrolytes is larger than outside. Water is being pulled into cell, and cell swells.
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| Hypertonic solution | Concentration outside cell of electrolytes is larger than inside. Water is being pulled out of cell and cell shrinks.
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| Which two substances regulate fluid distribution between ECF and ICF? | Water and Sodium
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| What are the manifestations of isotonic changes in body fluids? | changes in vascular and interstitial fluid volume
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| Which manifestations reflect changes in intracellular volume? | Hyponatremia or Hypernatremia (low or high sodium levels)
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| Isotonic contraction or expansion of ECF | Result of saline deficit or excess (respectively) and therefore isotonic fluid volume deficit or excess
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| Hypotonic dilution of extracellular sodium | Hyponatremia
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| Hypertonic concentration of extracellular sodium | Hypernatremia
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| Thirst | 1-2% change in serium osmolality activates thirst; this is emergency response and it normally doesn't come to this. Increased osmolality stimulates osmoreceptors via tonicity; vascular stretch receptors monitor volume; angiotension II responds to low vol.
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| ADH/Vasopressin | ADH opens aquaporin channels at collecting duct of kidneys to allow reabsorption of water into blood. Vasopressin receptors are activated to cause vasoconstriction even in low blood volume
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| R-A-A System for regulating water and sodium | Activated by sympathetic nervous system at kidneys. Angiotensinogen converts to angiotensin 1, ACE converts angi 1 to angi 2. Angi 2 increases Na, H2O absorption, BV constrict, and increases aldosterone. Ald increases Na absorb and increases K excretion
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| Effects of Isotonic Fluid (saline) Deficit | BP declines; CO increases to compensate; Na and H2O retention increases; ADH released and thirst activated. If compensation fails: BP falls; cardiac ischemia; arrhythmias; neurons deteriorate; death.
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| Saline (isotonic fluid) Deficit compensation mechanisms | Baroreceptors sense volume deficit; sympathetic nervous system increases Na and H2O reabsorption; ADH released from pituitary to increase thirst.
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| Saline (isotonic fluid)deficit manifestations | Normal Na associated with volume loss; acute weight loss; increase in ADH (as compensation)=decreased urine output but increased urine specific gravity and osmolality; increased serum osmolality; increased thirst, hematocrit, BUN
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| Saline (isotonic fluid) deficit manifestations (cont'd) | Hypotension; Tachycardia, weak pulse; Shock; Decreased ECF volume; Impaired temperature regulation (increased body temp)
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| Saline (isotonic fluid) Excess | Increase in total body sodium coupled with proportionate water retention. Inadequate Na and H2O elimination or excessive intake to output ratio of Na or H2O.
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| Saline Excess compensatory mechanisms | Atrial natriuretic peptide released from heart to increase Na excretion, vasodilate, inhibit aldosterone and ADH (so H2O excreted too)
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| Saline Excess manifestations | Normal serium Na; acute weight gain; Increased interstitial volume (edema); increased vascular volume (increased central venous pressure and bounding pulse)
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| Serium Electrolyte Imbalance causes | Changes in intake, output; Shifts in location (intracellular-extracellular or more or less protein-bound)
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| Hypernatremia Causes | Excessive water loss; decreased water intake; excessive sodium intake; inability to obtain water; depressed thirst response
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| Hypernatremia Manifestations | Elevated serium Na, osmolaliity, BUN, hematocrit; Increased ADH and thirst; Intracellular Dehydration; Headache, agitation, decreased reflexes, seizures, coma, tachycardia, decreased BP
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| Hyponatremia Causes | Sodium loss or water gain; inadequate sodium intake
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| Hypovolemic Hyponatremia | ECF volume abnormally decreased
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| Hypervolemic Hyponatremia | ECF volume is abnormally increased
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| Isovolemic Hyponatremia | ECF volume is equal to ICF volume
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| Hypertonic Hyponatremia | Drawing power of glucose pulls water from ICF to ECF; sodium levels diluted; seen in hyperglycemia (diabetes)
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| Hypotonic Hyponatremia | Most common! Caused by water retention. can be hypovolemic (H2O loss > Na loss and no electrolyte replacement); Euvolemic (retention of H2O w/ diluted Na; or Hypervolemic (hyponatremia + edema)
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| Hyponatremia Manifestations | Low serum Na; Low osmolality: fluid moves into neurons (cramps, weakness, headaches, depression, apprehension, personality changes, stupor, coma); anorexia, nausea, vomit, diarrhea
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| Serum Potassium | Predominantly intracellular; largely in muscle; largely excreted and regulated by kidney; controlled by aldosterone(Na retain, K excrete)
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| H/K relationship | When H ions increase inside the cell, K gets pushed out. This helps buffer but can cause hyperkalemia. Kidneys then get rid of K to prevent hyper.
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| Insulin Adminstration and Potassium | When you give insulin, acidosis corrected and H is no longer pushing K out of cell. But important to regulate K levels because may have already been pushed out and excreted, so with type 1 hypokalemia can occur.
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| Functions of Serium Potassium | Regulates resting membrane potential, controls opening of sodium channels during action potentials, regulates membrane repolarization.
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| Potassium and Membrane potential | As K increases=more positive potential (cells more excitable and rate of repolarization incrases) K decrease=more negative potenital, takes greater stimulus to excite cell and open Na channels, rate of repolarization delayed
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| Hypokalemia Causes | Inadequate intake, excessive renal losses, excessive GI losses, transcompartmental shifts (as with H ions or insulin admin)
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| Hypokalemia Manifestations | Impaired ability to concentrate urine; anorexia, nausea, vomit, constipation, ab distenstion; muscle flabbiness, weakness, fatigue, cramps, tenderness,paralysis; hypotension, increased sensitivity to DIG, dysrhythmias; confusion; metabolic alkalosis
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| Hypokalemia EKG changes | P to R prolonged; Depressed S to T segment; Low T wave; Prominent U wave; Leads to ventricular ectopy and fatal rhythms
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| Hyperkalemia Causes | Decreased renal elimination, excessive rapid administration, shifts from ICF to ECF (as with H ions)
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| Hyperkalemia Manifestations | nausea, vomit, diarrhea, cramps; weakness, dizziness, cramps at muscles; EKG changes, cardiac arrest
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| Hyperkalemia EKG Changes | P to R prolonged; Low P wave; Widened QRS; Peaked T wave; Leads to conduction delays, ventricular fibrillation
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| Calcium and Phosphorus Facts and Distribution | Absorbed at intestine, reabsorbed at kidney,, eliminated in urine. In bone: 99% calcium, 1% phosphorus; In cells: 1% calcium, 14% phosphorus; ECF: 0.1-0.2% calcium, 1% phosphorus
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| Regulation of Calcium and Phosphorus | vitamin D increases gut absorption; low cal directly activates parathyroid hormone and low phosphorus indirectly activates; calcitonin acts on kidney to remove calcium from ECF. Inverse relationship between Cal and Phos
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| ECF Calcium exists in 3 forms | Protein bound: cannot diffuse into ICF from plasma; Complexed: chelated with citrate, phosphate, not ionized; Ionized: Free to influence cellular functions
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| Calcium Roles | Enzyme rxns, membrane potentials and neuronal excitability, muscle contraction, hormone and NT release, cardiac contractility/automaticity, blood coagulation
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| Hypocalcemia Causes | Immpaired ability to mobilize calcium from bone (hypoPTH, hypoMagnesium); abnormal loss from kidney (most common)(renal failure); increased protein binding (alkalosis, increased fatty acids); decreased intake or absorption/malabsorption (vit D deficient)
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| Hypocalcemia Manifestations | increased neuromuscular excitability, cramps, seizure
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| Hypercalcemia Causes | Increased intestinal absorption, excessive vitamin D, increased bone resorption (increased PTH, malignant neoplasms, promlonged immobility), decreased elimination (thiazide diuretics, lithium therapy)
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| Hypercalcemia Manifestations | Decreased neuromuscular excitability; weakness, lethargy, CNS depression; inability to concentrate urine, kidney stones; hypertension, AV block
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