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Bio 203
Electrolytes
| Question | Answer |
|---|---|
| sodium functions | *membrane potentials *Action potentials *nerve transmission *muscle contraction *cotransport of ions across membranes |
| Potassium functions | *intracellular fluid balance *pH balance by trading places with H+ *RMPs and APs *neuromuscular excitation |
| sodium primary cation of | almost 1/2 osmolarity of ECF, most abundant extracellular cation |
| hypernatremia causes | *suspect dehydration *hypersecretion of aldosterone *osmotic diuresis *diabetes insipidus |
| hypernatremia s/s | *neuromuscular excitability *muscle twitching, etc *if dehydrated, then dec. bp |
| hyponatremia causes | *suspect hypotonic hydration (water intoxication) *usually corrected by kidneys bwo ANP/BNP |
| hyponatremia s/s | *cellular edema *neuronal APs disturbed *confusion, coma, death |
| acidosis leads to | hyperkalemia (H+ goes into cell, K+ goes out) |
| alkalosis leads to | hypokalemia |
| hyperkalemia causes | *suspect dehydration *renal failure *crush injury (affected cells leak K *diminished aldosterone (less K secr *acidosis *transfusion reaction (K+ leaks out of lysed RBCs) |
| hyperkalemia s/s sudden onset causes | *crush injury *IV push of K+ |
| hyperkalemia s/s sudden onset | *sudden increase in extracellular K+ makes nerve & muscle cells abnormally excitable bwo *K+ moving rapidly into cell, increases RMP to move cell closer to threshold |
| hyperkalemia s/s slow onset cause | decreased aldosterone (decreases sodium reabsorption, less K+ secretion, therefore more K+ in body) |
| hyperkalemia s/s slow onset | *nerve & muscles become less excitable bwo *inactivation of v-gated Na+ channels |
| normokalemia effect on membrane potential | K+ concentrations in equilibrium, equal diffusion into and out of cell--> normal RMP |
| hyperkalemia effect on membrane potential | elevated ECF K+, less K+ diffusion out of cell, elevated RMP (cells partially depolarized) --> cells more excitable |
| hypokalemia effect on membrane potential | reduced ECF K+ concentration, greater diffusion of K+ out of cell, reduced RMP (cells hyperpolarized) --> cells less excitable |
| K+ leaky channels corrected by | cells leak K+ continually by diffusion, K+ transported back into cell by NaK-ATPase |
| Clinical manifestation- hyperkalemia sudden onset | *morbid cardiac arrhythmias (v-tach, fibrillation) *bwo: gradient for diffusion is lost, more K+ stays in cell --> cell closer to threshold --> muscles/nerves hyperexcitable |
| Clinical manifestation - hyperkalemia slow onset | *muscle weakness *slow cardiac arrhythmias *both bwo non-intuitive process *slow depol of cell inactivates V-gated Na+ channels --> no APs --> nerve/muscles less excitable |
| clinical manifestation - severe hyperkalemia | *cells can't repolarize --> *muscle paralysis *cardiac arrest (heart block) |
| hypokalemia causes | *chronic emesis/diarrhea/laxatives *hypersection of adosterone *Loop diuretics (Lasix) *Alkalosis *correction of DKA with insulin |
| how does hypersecretion of aldosterone effect K+ | too much sodium reabsorbed --> more K secreted |
| how do loop diuretics like Lasix affect K+ | K+ is 'wasted', not reabsorbed |
| how does alkalosis affect K+ | H+ comes out of cells, K+ goes into cell |
| how does DKA correction effect K+ | with insulin administraton, glucose is permitted into cells ALONG WITH K+ |
| hypokalemia effect on cell | K+ moves out of cell to correct ECF deficit --> hyperpolarization --> decreased neuromuscular excitability |
| hypokalemia clinical s/s | *muscle weakness *severe heart arrhythmias *depressed reflexes |
| Chloride functions | *major contributor of ECF osmolarity *required to make stomach acid HCL *CO2 transport in blood bwo Cl- shift *tends to follow Na+, indirectly regulated by same hormones as Na+ |
| chloride shift in RBCs | *cell gives off C02, picked up by RBC *C02 + H20 with CAH gives H2C03 *H2C03 ionizes --> H+ + HC03- *HC03- exchanges with Cl- (then H+ combines with Hb02 so O2 subsequently released to cell) |
| Hyperchloremia causes | *dehydration *aldosterone excess *too much IV saline |
| Hyperchloremia effect on cell | *acidosis - HC03- is excreted/not reabsorbed to compensate for having too many negative Cl ions in plasma |
| hyperchloremia s/s | *lethargy, weakness bwo *decreased activity at synapses |
| hypochloremia causes | *excessive emesis *diuretic causing NaCl loss (Lasix) *aldosterone deficiency |
| hypochloremia s/s | *alkalosis *muscle spasms |
| how does hypochloremia effect aklalosis | bicarb is reabsorbed if Cl- is low |
| how does hypochloremia effect muscle spasms | increased activity at synapses because of alkalosis |
| How is calcium distributed in body? | *Higher amounts in ECF *Important in ICF in small, regulated (sequestered) amounts |
| Functions of Ca | *muscular contractions/muscle tone *neurotran release *2nd messenger for many hormones, ntrans *essential in blood clotting *structural component bones, teeth |
| Causes of hypercalcemia | *hyperparathyroidism *excess calcitriol (xs VitD) *multiple myeloma & Pagent's disease *bone metastases *Acidosis |
| How does multiple myeloma and Paget's Disease affect hypercalcemia? | increased osteoclastic bone resorption/destruction |
| How does bone metastases affect hypercalcemia? | increased bone resorption releases Ca |
| How does acidosis affect hypercalcemia? | It decreases the binding of Ca to plasma proteins --> increasing free ion Ca . . .therefore can get sx of hypercalcemia even though blood Ca may be normal |
| Hypercalcemia cellular affect | reduces Na permeability of membranes --> decreases neuromuscular excitability |
| effect of hypercalcemia on sodium membrane permeability | *muscle weakness, decreased tone *depressed reflexes *lethargy, fatigue *depression, mental confusion *coma |
| hypercalcemia s/s | *cardiac arrhythmias, heart block *kidney stones *increase peptic ulcer disease *muscle weakness, decreased tone *depressed reflexes *lethargy, fatigue *depression, mental confusion, coma |
| how does hypercalcemia effect peptic ulcer disease | by increasing gastrin secretion |
| Hypocalcemia causes | *hypoparathyroidism *Vit D deficiency *renal disease *decreased intestinal absorption *blood transfusions *alkalosis |
| how does renal disease affect hypocalcemia | decreased calcitriol formation |
| what causes a decrease in intestinal absorption of Ca | diarrhea |
| how do blood transfusions affect hypocalcemia | citrate binds Ca |
| how does alkalosis affect hypocalcemia | increases the binding of Ca to plasma proteins --> decreases free ion availability --> can get sx of hypocalcemia even though total blood Ca may be normal |
| Hypocalcemia s/s | *tetany *decreased myocardial contractility *cardiac arrhythmias |
| how does hypocalcemia affect tetany | makes membrane unstable by increasing sodium permeability --> muscles/nerves hyperexcitable |
| what are s/s of tetany (hypocalcemic) | *paresthesias fingers/toes/mouth *sk muscle cramps *Carpo-pedal spasms (Trousseau's sign) *exxagerated reflexes *convulsions *could lead to laryngeal spasms-->death |
| how does hypocalcemia affect myocardial contractility | extracellular calcium needed for contraction |
| Function of magnesium | *important intracellular cation *involved in over 300 biochemical reactions, notably *fx of Na/K/ATPase pump *protein synthesis |
| What regulates magnesium | *Kidneys/calcitriol *PTH |
| How does kidney regulate magnesium | calcitriol increases reabsorption |
| How does PTH regulate magnesium | by decreasing its reabsorption |
| Hypomagnesemia s/s | *same as hypocalcemia plus *torsades de pointes (vent arrhyth) |
| Hypomagnesemia causes | *diuretics *alcoholism *malnutrition |
| Hypermagnesemia | same as hypercalcemia |
| hypermagnesemia cause | renal failure |
Created by:
lorrelaws
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