Urinary Protein to Creatinine Ratio (Prot:Crt)u is aka?
what should you know about creatinine levels (key concept)
Basically a CONSTANT amount of crt is produced by muscle each day(via degredation of creatine), and that constant amount is excreted by the kidneys each day. HOWEVER, the amount of H2O excreted by the kidneys on any given day changes, so, the [crt] that is excreted varies with amount of H2O excreted.
under physiological conditions, if Crt is dec, what should you think about protein? If there is renal damage, THEN what does the prot:crt ratio look like?
under normal circumstances, if creatinine clearance decreases, then protein should be decreased too (bc crt readily passes filtration barrier). If more protein enters urine through damaged glomeruli then rate of glomerular protein excretion is increased compared to Crt
so, in short, Urinary excretion of protein can be assessed by comparing.... ?
urine protein & creatinine concentrations on a random sample.
what do you use the (Prot:crt)u ratio to determine? what stipulations must you follow?
you can determine the severity of the glomerular proteinuria ( severity of protein loss due to glomerular leakage of plasma proteins) BUT!!!!!!!! you need to exclude ALL OTHER CAUSES OF PROTEINURIA, such as prerenal, tubular, hemorrhagic))
what is the (Prot:crt)u for healthy dogs? border line values? Glomerular proteinuria?
(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
for hyperchloridemia, just know that is increases in the ways Na does, WITH Na. or,
if HCO3- (bicarb) dec, then you will see inc Cl- (or inc A-, like lactate or AcAc)
what are the three mechanisms of hypochloremia?
(1) Dec of Cl- happens concurrently with Na+ (so, if you have too much water it dilutes Na+ and Cl-, OR, you lose Na+ and Cl- and water, and then only regain water, it's diluted.) (2) If you inc conc of HCO3-, you will DEC conc of Cl- (there is a HCO3- and Cl- shuttle which exchanges then in stomach, kidney, intestine) (3) inc in [uA-] will cause a dec in Cl-, --> Cl- and H+ are excreted as renal compensation for acidemia
Hyponatremia & hypochloremia--> reiterate the situations where this happens (2)
(1) edema or transudates (water > Na and Cl retention, liek in heart failure, cirrhosis, nephrotic syndromes) (2) in dehydration/hypovolemia states (renal loss, intestinal loss, cutaneous loss, 3rd space loss)
what happens to the normal H+ and Cl- and HCO3- cycle (from other card) in Hypochloremic metabolic alkalosis (gastric)?
animal is vomiting, for instance, so the H+ and Cl- which was in the stomach does not get to the intestines to be resorbed, instead it is lost. To replace that Cl, more Cl- is taken from the blood, so bicarb is exchanged for it, which is why you have an inc level of bicarb then---> alkalosis
explain the paradoxical aciduia which happens during Hypochloremic metabolic alkalosis (gastric)
since Cl is being excreted (vomited), the animal is hypovolemic which leads to the activation of RAS which causes ann increase in aldosterone leading to an increase in renal excretion of K & H causing adicuria. This is a situation of paradoxical aciduria
What is metabolic acidosis?
a condition in which there is a dec [HCO3-] & acidemia (dec blood pH) tends to occur (pH is decreasing, may not be an acidemia)
what is inorganic metabolic acidosis?
(no carbon) acidosis. HCO3- is dec, due to impaired renal excretion of H+. impaired renal exretion means increased H in blood. so there is excess H and also the regular amount of HCO3- in the blood, so the body tries to compensate for the too much H+ by combining it with the HCO3- and making CO2 and H2O.
what is organic metabolic acidosis?
(with carbon) acidosis. HCO3- is dec, because of an increase in organic acids, like ketoacids and lactic acids.
what is metabolic alkalosis?
condition where there is inc HCO3- and alkalemia (inc blood pH) tends to occur
Hypochloremia disorders due to metabolic acidosis--> if the body wants to renally excrete H+, what happens?
The excretion of H+ also requires the loss of a Cl- and the production of a bicarbonate
*So, HYPOCHLORIDEMIA b/c of dec Na...why?
B/c Cl follows Na. IF Na dec, then Cl dec. This happens in stuff like edamatous disorders, Na+& Cl−loss (renal, intestinal, skin), uroperitoneum, and marked hyperglycemia
*So, HYPOCHLORIDEMIA with (is it inc or dec) HCO3-....why?
Cl- moves OPPOSITE of HCO3-. So when there is low Cl-, HCO3- goes up. This happens in vomiting/abomasal disorders(Lose Cl and H+ in vomit, Cl is pulled from blood to replace it, the Cl- and bicarb exchanger means you need to put a HCO3- into the blood if you took Cl- out), and if there is an inc in uA- (like lactic acid or ketones), then you will close Cl- (and H+) to try to renally compensate for the acidemia
*in short, hypochloridemia is seen with (three substances, which direction are they going in?)
inc aldosterone----> inc Na and dec K (aldosterone causes K to be excreted)
if youre thinking about K, you should be thinking about....
how 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?
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)