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PHYS 2 Electrolytes
Physiology
| Question | Answer |
|---|---|
| Basic Cell Functions | - Nutrition and O2 acquisition - Use nutrition and O2 to make energy - eliminate waste - synthesize proteins - control of exchange with extracellular space - movement of materials within cell - respond to environment - reproduction |
| What are the exceptions to the cell function of reproducing? | gametes and nerves |
| Extracellular fluid components | plasma and interstitial fluid |
| t/f: stability equals unchanging | false |
| Homeostatically Regulated Factors | - concentration of nutrients, co2, and o2 - concentration of waste products - changes in pH of ECF ** - concentrations of water and electrolytes ** - volume and pressure of plasma (ECF compartment) - temperature - hormone levels - blood sugar |
| Homeostatic control systems must | 1. detect deviations from normal 2. integrate information 3. make adjustments needed to restore homeostasis |
| Intrinsic homeostatic control system | built into the organ |
| Extrinsic homeostatic control system | initiated outside of the target organ that affects the target organ |
| 3 types of homeostatic control systems | negative feedback, positive feedback, and feedforward |
| negative feedback system | a reaction that causes a decrease in function that occurs in response to a stimulus |
| positive feedback system | output amplifies a change to continue to move in the direction of the initial change-- must have a way out |
| feedforward mechanism | response in anticipation of a change |
| positive feedback examples | - oxytocin and uterine contractions - estrogen surge prior to ovulation |
| feedforward example | increased insulin in response to food in the digestive tract |
| total body water percentage of body weight | 60% |
| what fraction of total body water is the intracellular fluid | 2/3 |
| what fraction of total body water is the extracellular fluid | 1/3 |
| what fraction of total body water is the plasma | 1/15 |
| what fraction of total body water is the interstitial fluid | 4/15 |
| t/f: there would be no oncotic pressure without protein anions | true |
| t/f: there is a selective barrier between interstitial fluid and intracellular fluid | true |
| how is fluid balance regulated by the ECF volume? | - maintains blood pressure - salt balance regulates this |
| how is fluid balance regulated by the ECF osmolarity? | - prevents shrinking and swelling of cells - water balance regulates this |
| what happened to the plasma when the red blood cells were introduced to a hypotonic solution? | fluid rushed into the red blood cells which caused them to burst |
| how many liters of filtrate are formed each day? | 180 liters |
| what is the glomerular filtration rate? | 125 mL/min |
| how much urine is produced per minute in an adult? | 1 mL per minute |
| constricting the afferent arteriole will cause what in the glomerulus? | decrease glomerular capillary blood pressure, decrease net filtration pressure, decrease GFR |
| dilation the afferent arteriole will cause what in the glomerulus? | increase glomerular capillary blood pressure, increase net filtration pressure, increase GFR |
| what do granular cells do? | produce renin |
| what does the macula densa do? | sense salt balance |
| when arterial blood pressure is decreased and detected by the baroreceptors what are the two short term adjustment pathways? | increase sympathetic activity which will either: 1. increase cardiac output to increase arterial blood pressure 2. cause generalized vasoconstriction to increase the total peripheral resistance to increase arterial blood pressure |
| when arterial blood pressure is decreased and detected by the baroreceptors what is the long term adjustment pathway? | increase sympathetic activity → generalized arteriolar vasoconstriction → constrict the afferent arterial → decreases glomerular capillary pressure → decrease GFR → decreases urine volume → increases conservation of fluids and salt → increase arterial BP |
| t/f: the liver produces renin | false |
| what does the liver produce? | angiotensinogen |
| how is angiotensinogen converted into angiotensin 1 and what produces that converting substance? | renin secreted by the kidney |
| how is angiotensin 1 concerted into angiotensin 2 and what produces it? | angiotensin-converting enzyme (ACE) produced by the lungs |
| how does angiotensin 2 affect the adrenal cortex? | produces aldosterone |
| angiotensin 2 produces what 3 things? | vasopressin, thirst, and arteriolar vasoconstriction |
| how does vasopressin correct a decrease in arterial blood pressure, a decrease in NaCl, and a decrease in ECF volume? | increases water reabsorption by kidney tubules which conserves water |
| how does thirst correct a decrease in arterial blood pressure, a decrease in NaCl, and a decrease in ECF volume? | increases fluid intake |
| t/f: arteriolar vasoconstriction is used to correct a decrease in arterial blood pressure, a decrease in NaCl, and a decrease in ECF volume | true |
| how does aldosterone affect the kidneys? | increases sodium reabsorption by kidney tubules (& Cl passively) and conserves Na and Cl, the Na then osmotically holds more water in ECF which conserves more water to correct a decrease in arterial blood pressure, NaCl, and ECF volume |
| a decrease in arterial blood pressure, a decrease in NaCl, and a decrease in ECF volume causes what? | increase in renin, angiontensin 1, angiotensin 2, and aldosterone in adrenal cortex |
| how does a increase in plasma potassium do to aldosterone? | increase |
| how does aldosterone affect potassium tubular secretion and urinary excretion? | increase tubular secretion and increase urinary excretion |
| how does aldosterone affect sodium tubular secretion and urinary excretion? | increase tubular secretion and decrease urinary excretion |
| what produces vasopressin? | hypothalamus |
| where does vasopressin work? | at the basolateral membrane in the distal and collecting tubules |
| what does vasopressin do? | open water channels and brings filtrate osmolarity to 1200 mOsm |
| what type of urine is produced without vasopressin? | hypotonic (dilute) |
| what type of urine is produced with low levels of vasopressin? | isotonic |
| what type of urine is produced with high levels of vasopressin? | hypertonic (concentrated) |
| what does MAP depend on? | cardiac output and total peripheral resistance |
| what does cardiac output depend on? | heart rate and stroke volume |
| what does heart rate depend on? | parasympathetic activity (decrease), sympathetic activity and epinephrine (increase) |
| what is stroke volume increased by? | sympathetic activity and epinephrine, and venous return |
| what is venous return affected by? | sympathetic activity, skeletal muscle pump, respiratory pump, cardiac suction, and blood volume |
| what is blood volume affected by? | passive bulk-flow fluid shifts between vascular and interstitial fluid compartments and salt and water balance |
| what is salt and water balance controlled by? | vasopressin and renin-angiotensin-aldosterone system |
| what does total peripheral resistance depend on? | arteriolar radius* and blood viscosity |
| how is arteriolar radius affected? | local metabolic control (skeletal muscle activity) and extrinsic vasoconstrictor control |
| how is blood viscosity affected? | number of red blood cells |
| what are external vasoconstrictor controls? | sympathetic activity and epinephrine and vasopressin and angiotensin 2 |
| t/f: venous valves mechanically prevent backflow of blood to increase venous return | true |
| how does cardiac suction effect increase venous return? | decrease pressure in the heart to increase pressure gradient |
| how does pressure imparted to blood by cardiac contraction increase venous return? | increase in venous pressure to increase pressure gradient |
| how does an increase in sympathetic vasoconstrictor activity increase venous return? | increase in venous pressure to increase pressure gradient and decrease venous capacity |
| how does the skeletal muscle pump increase venous return? | increase in venous pressure to increase pressure gradient |
| how does the respiratory pump increase venous return? | decrease pressure in chest veins to increase pressure gradient |
| how does an increase in blood volume increase venous return? | increase venous pressure to increase pressure gradient |
| bulk flow net exchange pressure equation | (Pc + π IF) - (π p +Pif) |
| t/f: when bulk flow net exchange pressure is positive it indicates reabsorption | false |
| what does a negative bulk flow net exchange pressure indicate? | reabsorption |
| role of bulk flow | maintain blood pressure via filtration and reabsorption of fluid |
| t/f: we can tolerate a range in sodium levels | true |
| t/f: we can tolerate a range in calcium and potassium levels | false |
| what hormone will change the concentration of sodium in the ECF but not the total amount of sodium in the ECF? | Vasopressin |
| roles of sodium | - osmotic agent - establish RMP - Depolarize excitable membranes - Co-transport (glucose and AA) - Acid/Base & electrical neutrality |
| what is typically used to control sodium by lowering it? | Natriuretic Peptides (ANP and BNP) |
| what do ANP's do? | promote sodium loss or vasopressin production |
| what happens to ECF volume and blood pressure if you increase salt retention? | increase ECF volume and increase BP |
| where are ANP's synthesized? | right atrium/ventril |
| in what way do ANP's control stimulation? | - atrial stretch (volume expansion) - constrictor agents that increase BP - high salt diets - atrial tachycardia |
| where are ANP receptors found? | endothelium of the vasa recta |
| what is the mechanism of action for ANP? | increased cGMP; inhibits adenyl cyclase |
| what are the actions of ANP? | - natriuresis & diuresis - increase GFR without increasing BP - decrease angiotensin 2 induced aldosterone release - relax the pre-constricted renal vasculature |
| what does a decrease in angiotensin 2 induced aldosterone do? | decrease renin release and decrease synthesis of aldosterone |
| what is the main role of ANP? | lower total sodium in the body |
| what hormones or tissues are used to raise sodium levels? | aldosterone, adrenal glands, vasopressin |
| where is aldosterone found? | distal tubule and collecting duct |
| what is aldosterone's function? | retain sodium (and water with vasopressin) and eliminate potassium |
| what is aldosterone secretion increased by? | activation of the renin-angiotensin-aldosterone system |
| t/f: the renin-angiotensin-aldosterone system is affected by both sodium AND potassium | true |
| t/f: if vasopressin is present with aldosterone, only sodium will be reabsorbed | false |
| where are adrenal glands found? | embedded in a capsule of fat on top of each kidney |
| what three zones does the outer adrenal cortex consist of? | zona glomerulosa, zona fasciculata, zona reticularis |
| what hormone is found in the zona glomerulosa? | aldosterone |
| what hormone is found in the zona fasciculata? | cortisol and sex hormones: androgens and estrogens |
| what hormone is found in the zona reticularis? | cortisol and sex hormones: androgen and estrogens |
| what hormones are secreted by the adrenal medulla? | epinephrine and norepinephrine |
| t/f: progesterone adds to sodium retention | true |
| what is the main role of vasopressin? | alter sodium concentration but not the total amount |
| t/f: vasopressin reabsorbs sodium and has no effect on water reabsorption | false |
| how does vasopressin alter sodium concentration? | increase water reabsorption through the addition of aquaporin channels (APQ-2) in the distal nephron |
| t/f: if you have no vasopressin, you will be fine | false |
| hyponatremia | low amount of sodium |
| isotonic hyponatremia | normal osmolarity but have a low amount of sodium |
| how does isotonic hyponatremia occur? | other substances are contributing to the osmolarity than only sodium-- other substances compensate for the low sodium levels |
| hypertonic hyponatremia | high osmolarity with a low amount of sodium |
| one example of hypertonic hyponatremia | diabetes (started compensating but haven't finished) |
| hypotonic hyponatremia | low osmolarity and low amount of sodium |
| how does hypertonic hyponatremia occur? | other substances have started to contribute to the osmolarity but have not finished compensation |
| what is hypovolemic hypotonic hyponatremia? | low volume, low osmolarity, and low sodium |
| what is hypervolemic hypotonic hyponatremia? | high volume, low osmolarity, and low sodium |
| what is isovolemic hypotonic hyponatremia? | normal volume, low osmolarity, and low sodium |
| t/f: hypovolemic hypotonic hyponatremia is a small problem and easy to resolve | false (BAD) |
| what causes hypervolemic hypotonic hyponatremia? | too much of the wrong fluids (pancake dog) |
| how does isovolemic hypotonic hyponatremia occur? | no compensation by other substances |
| clinical signs of hyponatremia | - muscle cramps - nausea and vomiting - confusion, lethargy, coma, & seizures |
| clinical signs of hyponatremia at a concentration of below 125 mEg/L and above 120 mEq/L | mental and motor depression |
| clinical signs of hyponatremia at a concentration of below 120 mEq/L and above 105 mEq/L | seizures |
| clinical signs of hyponatremia at a concentration of below 105 mEq/L | death |
| clinical signs of hypovolemic hypotonic hyponatremia | increased BUN with normal creatine levels which both indicate renal function and small volumes of hypertonic urine with little sodium |
| what does an increase in blood urea nitrogen indicate? | kidneys are not filtering |
| how would you determine dehydration based off of blood work? | increased blood urea nitrogen (BUN) with normal creatine levels |
| clinical signs of hypervolemic hypotonic hyonatremia | edema (SQ fluids)- water retention as a result of sodium retention 12-15 L excess |
| symptoms of isovolemic hypotonic hyponatremia | inappropriate ADH release |
| lab evaluation of hyponatremia | - sodium < 135 mEq/L - Osmolarity dependent upon type - Urine sodium- usually low but may be high with Lasix |
| hyponatremia treatment | rate of correction should be proportional to the rate in which hyponatremia developed |
| what happens if the rate of treatment for hyponatremia is too rapid? | central pontine myleinolysis (CPM)- SHOCK- closes myelin in the pons |
| what is the pons responsible for? | blood pressure and respiratory control |
| what should the rate of treatment be for hyponatremia? | not greater than 2 mEq/L |
| what should the rate of treatment be for chronic hyponatremia? | 0.5 mEq/L |
| what kind of saline can be used for treatment of hypovolemic hyponatremia? | hypertonic saline |
| t/f: IV treatment of hyponatremia is better and less risky than oral treatment | false |
| clinical signs of hypernatremia | thirst nausea/vomiting agitation/stupor/coma sodium > 150 mEq/L |
| why do the symptoms of hypernatremia manifest as GI issues? | the brain is shrinking which decreases pressure |
| what are the causes of hypernatremia? | - dehydration/water deprivation - enteral feedings - salt loading - diabetes insipidus (central and renal) |
| central diabetes insipidus | inability to release ADH (vasopressin) |
| renal diabetes insipidus | inability to respond to ADH (vasopressin) |
| how is diabetes insipidus treated? | with ADH (vasopressin) as a nasal spray and eye drops in dogs and cats |
| why is diabetes insipidus not treated with a tablet medication? | the medication would be chewed up and used as a nutrient in the stomach instead of treating the issue |
| t/f: sports drinks are hypotonic | false |
| how can hypernatremia spiral? | due to having less water which adds nausea, which causes more water loss each time you vomit, NEED WATER, but not receiving enough (hangover) |
| treatment for hypernatremia | - free water at a corrected rate of 2 mEq/L/hour if not corrected, SHOCK would occur - Vasopressin (ADH) therapy |
| roles of potassium | -establishes RMP - repolarize membrane - co-transport with glucose and insulin - vasodilator - aldosterone release - exchanged for H+ at kidneys |
| t/f: a potassium imbalance requires medical attention | true |
| where is potassium resorbed and secreted? | actively resorbed in proximal tubule; actively secreted by principal cells in distal and collecting tubules; intercalated cells one secretes K+ and another actively resorbs with H+ transport |
| intrinsic factors of K+ | - hyperosmolarity - exercise - cell lysis - alpha 1 |
| extrinsic factors of K+ | insulin and beta agonists (beta 2) |
| what happens to H+ when there is high ECF K+? | hold onto H+ |
| hypokalemia clinical signs | - muscle weakness (distal then central) - CNS depression - cardiac arrhythmias - increased ammonia production - serum levels <2.5 mEq/L |
| cause of hypokalemia | decreased intake, diuretic use, renal loss in alkalosis, Mg2+ deficiency, high insulin levels, metabolic alkalosis, treatment for anemia |
| t/f: an IM injection of B12 cause hypekalemia | true |
| treatment of hypokalemia | slow re-establishment of no more than 40 mEq/hour of potassium, oral is better |
| hyperkalemia clinical signs | weakness, cardiac arrhythmias, >5.5 mEq/L |
| how does hyperkalemia cause weakness? | cells are not repolarizing because they are not reaching resting which shifts it extracellularly |
| causes of hyperkalemia | - increased consumption - potassium shifts: acidosis, intravascular hemolysis, digitalis toxicity which poisons NaK pump (congestive heart failure) - decreased excretion - ACE inhibitors - NSAIDs |
| treatment of hyperkalemia | aggressive, stop all contraindicated therapy, volume replinishment, shift K+ intracellularly, calcium |
| how does calcium treat hyperkalemia | half is bound with plasma and anionic proteins, the other half is ionic and free-- increase ionized calcium increases threshold which eliminates arrhythmias quickly and stimulates aldosterone to excrete K+ |
| how does an increase in pH affect potassium, excitability, and ionized calcium | decrease potassium, increase excitability, and decrease ionized calcium |
| how do we shift K+ intracellularly | sodium bicarbonate in acidosis, regular insulin +/- glucose-- give glucose unless it is already too high which would cause an insulin coma, give saline to dilute potassium out |
| t/f: giving insulin even one time to a diabetic patient with bad kidneys to treat hyperkalemia will harm the patient majorly | false |
Created by:
k.murski
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