Clin Path - Electrolytes

drraythe's version from 2015-04-18 21:33

intro and Na+

Question Answer
When we think of Na, we should think of what ratio?TB Na+ / TB H2O
First thing you should think of when you see K+Think shifting of extracellular (ECF) & Intracellular (ICF) K+. If that's not the case, then think of total body K+ inc or dec
First things to think about when you see Cl-?Think “follows Na+” for electrical balance (or H+in acid-base)... AND that it is Exchanged for HCO3-(or other anions) for electrical neutrality
first things to think about when you see HCO3- (bicarbonate)?Think acid-base status
how does she explain/define metabolic alkalosis?inc [HCO3-] associated with loss of H+ or HCO3- production
how does she explain/define metabolic acidosis?dec [HCO3-] associated with too much H+ (inc production or dec loss) or HCO3- loss
how does HCO3- relate to various types of CO2 levels?[HCO3-] is apprx equal to [total CO2 content] but is NOT EQUAL to PCO2 (partial pressure of CO2)
what are the 1st, 2nd, and 3rd ECF spaces?(1st) intravascular (2nd) interstital (3rd) body cavities
how do most elecrolytes move, and why?usually move in PAIRS (one + and one -) to keep things ELECTRICALLY NEUTRAL (ex: Na+ and Cl- usually move together)
How is serum Na+ controlled? (2)(1) by regulation of blood VOLUME, because if blood volume dec, then---> RAS aka RAAS (renin-angiotension-(aldosterone) system) is activated to INC Na retention. Also ADH is stimulated so that there is inc H2O retention(=attempting to restore blood volume) (2) Regulated by plasma OSMOLALITY. an inc in osmolality stimlates more AHD (which inc water retention) and also stimulates thirst centers (Which inc water intake) (=attempting to dilute solutes)
The RAS/RAAS is what? is stimlated by what, and causes what to happen?Renin-Angiotensin System. STIMULATED BY: Hypovolemia, hyperkalemia, or hyponatremia. This causes an inc in the renin-angiotensin response, which inc aldosterone release by adrenal glands(--> inc renal resorption of Na+ and Cl- and inc renal secretion of K+)
what part of the kidney does the RAAS stimulate? what is the net result (of solutes and charges)aldosterone works on the distal tubule, and the next result of solutes/charges in plasma is +3 Na+, -2 K+, +1 Cl- which means it is still electrically neutral, however, you gained +2 solutes which increases osmolality
what is ADH? what triggers it to be released? what does it do?Anti-Diuretic-Hormone, aka vasopressin. ADH is stimulated by HyPOvolemia or by hyPERosmolality. This causes inc water resorption in the distal nephron and an inc USG(bc youre taking the water out of the urine and leaving the solutes behind). It ALSO stimulates the thirst center, and causes inc intake of water. This all basically leads to a replenishment of blood vol and a dilution of solutes (she also had Note: ADH promotes urea resorption)
three major mechanisms for HYPERnatremia?(1) dec water intake (2) increase in "pure" water loss (only lose water and nothing else) (3) the water loss is just GREATER THAN the Na loss. ( (4) Rarely, there is steep inc intake of Na, from salt poisoning or hyperaldosteronism)
when are some times you'd get a "pure" loss of water? (which would lead to hypernatremia)diabetes insipitus (almost totally pure loss of water, USGref is <1.007) or water vapor loss from a fever
when would there be a situation where thered be H2O loss > Na+ loss?in OSMOTIC diuresis (such as glucosuria). (or osmotic diarrhea)
what are the two major mechanisms for HYPOnatremia?(1) Edematous states (H2O retention > Na+ retention) (2) Dehydration states (Na+ loss > H2O loss)
hyponatremia--> edematous states. what are some examples of when this happens?heart failure, cirrhosis, nephrotic syndrome..both Na and H2O are being retained, but H2O much more than Na
hyponatremia--> dehydration. What are some situations where this happens?Renal loss of Na (Hypoadrenocorticism, obligated loss with anions, diuretics, medullary dz) Intestinal loss (diarrhea, intestinal sequestration, maybe vomiting) and cutaneous loss in sweating (horses)
Hypoadrenocorticism causes hyponatremia in what two ways?dec aldosterone (a Na saving hormone) and also dec INHIBITON of ADH (which means there is more ADH) which means inc water retention which dilutes remaining Na
what are some anions that Na+ would be obligatorily lost with in renal excretion? (body is trying to stay electrically neutral)Ketones, HCO3-(in metabolic alkalosis), with lactate(inc in hypoxia)
how does diarrhea and sweating cause a hyponatremia?in both of these, you lose water AND Na, and then you are hypovolemic, so you drink water (only replacing water) and then you retain that water bc of the ADH since you were hypovolemic, so your Na that was remaining and was never replaced was diluted, so you get a HYPOnatremia
how does a 3rd space loss (like a uroperitoneum) cause a hyponatremia? (situation that does not fit the Na/H2O ratio concept)ureter tears--> urine spills into ab. cavity. Na in Urine is in a lower conc than in blood (bc Na is pulled out of the plasma filtered in the glom in the ascending loop) so then the blood Na notices there is a low conc in the urine in the urine in peritoneum, so diffuses across gradient and then you have hyponatremic blood
how can a hyperglycemia cause a hyponatremia?a marked hyperglycemia will cause an osmotic gradient which will pull the water out of cells and into the extracellular space, diluting the Na that is there. which means that the blood Na will follow the gradient to try to compensate. ALSO glucouria-->solute diuresis---> inc water in urine means inc Na in urine--> hyponatremia
normonatremia DISORDERS can happen when both Na and H2O inc or when Na and H2O dec. Ex of when they both inc?"Edematous normonatremia." when Na and H2O are equally retained in things like heart failure, cirrhosis, nephrotic syndrome. (can also cause hyponatremia if more H2O is retained than salt)
what is the most common type of dehydration, with regards to Na?normonatremic dehydration is most common
normonatremia DISORDERS can happen when both Na and H2O inc or when Na and H2O dec. Ex of when they both dec?like all of the dehydration mechanisms before (renal loss, intestinal loss, cutaneous loss) except the Na and water are lost in equal proportion, which is the MORE COMMON OCCURANCE
what can cause a "pseudohyponatremia"?Lipemia or marked hyperproteinemia


Question Answer
how do you get K+ in your diet?you eat cells (intracellular ion)
how do you inc loss of K+?inc aldosterone----> inc Na and dec K (aldosterone causes K to be excreted)
how does insulin and epinepherine effect K+?inc K+s entry into cells
if youre thinking about K, you should be thinking K+ is always shifting from ICF to ECF (pertaining to acid-base status, and also insulin)
two major disorders of hyperkalemia are?metabolic acidosis, dec renal secretion
what causes pseudohyperkalemia?hemolysis, thrombocytosis
what are 4 main mechanisms of hypokalemia?metabolic alkalosis, prolonged anorexia, K+ loss disorders, shift into cells (due to insulin)
what is metabolic acidosis?a condition in which there is a dec in [HCO3-] & acidemia (dec blood pH) tends to occur
what is happening in INORGANIC metabolic acidosis?("no carbon") still losing HCO3- b/c metabolic acidosis. due to impaired renal excretion of H+, also have inc [PO4]
what is happening in ORGANIC metabolic acidosis?("with carbon") still losing HCO3- b/c metabolic acidosis. Ketoacidosis and lactic acidosis (have H+ and Anion- containing carbon together)
what is metabolic alkalosis?a condition in which there is a inc [HCO3-] & alkalemia (inc blood pH) tends to occur (pH is increasing, may not be an alkalemia)
how does inorganic acidosis cause an inc in plasma K+?initial pathological process is a DEC in renal excretion of H+(inorganic acidosis) which means there is more H+ in the blood. If there is more H+ in the blood, the body tries to compensate for the acidemia by putting the H+ into the cells, which means the H+ must be exchanged for K+ (electric neutrality) so there is excess K+ in the blood--> hyperkalemia.
how come kyperkalemia is not expected in organic acidosis?there are two situations. In both cases, the organic acids have a H+ and then have the carbon portion(ANION) with a (-) charge. (lactic acid is H+ and lactate-, ketones are H+ and AcAc- , H+ and Beta-HB-). (scenario 1) The H+ and A- are produced, and follow the concentration gradient into the cells. Since the H+and A- move together, they are electrically neutral, so K doesnt go out of cell. (scenario 2) H+ and A- are produced. The H+ diffuses into the cells, and is exchanged for K+ which moves into blood. The A- is then excreted in the kidney, and the K+ is obligated to follow to keep electrical neutrality. There is NO K+ increase, rather, less K+ in body overall
Two major MECHANISMS of hyperkalemia are?(1) shift from cells(inorganic acidosis) (2) inc total body K+ (typically dec renal loss)
what are some reasons that there would be a dec in renal excretion of K+? (3)(1) oliguiric states (renal failure, urinary obstruction) (2) uroperioteneum (3) addisons disease (hypoadrenocorticism)