Tuesday Na and K Flashcards
normal body stores of K
how much can the kidney get rid of in a day at max?
3000 to 4000 meq
(50 - 55 meq per kg)
98% is intracellular
kidney can get rid of like 400 meq/day max
if you are seeing a dialysis patient with weak legs what do you think
kigh K
EKG changes of hypokalemia
DISCLAIMER: THIS WAS MY WAY OF REMEMBERING IT, IT MAY NOT BE 100% ACCURATE FOR PR INTERVAL PROLONGATION
PR interval prolongation (hypokalemia -> bigger gradient of K on the inside of the cell compared to the outside (it’s like as if your Na/K pump is working TOO well) -> increased membrane potential -> takes longer to depolarize -> signal takes longer to travel from atria to ventricles)
ST depression (as a result of increased membrane potential)
Flattened or inverted T wave
U - wave (due to repolarization of the septum as a different time that the ventricular wall. slower depolarization may cause this) (U OK? -> U waves with hypOKalemia)
QRS widening (similar reason as PR elongation)
EKG changes of hyperkalemia
PR prolongation
elevated T waves
widened QRS
when are you fucked
when you are hyperkalemic and then get a metabolic acidosis
because the way you get rid of H+ is by antiporting it with K+
loop diuretics do what to potassium
block NKCC, cause you to excrete more
get hypokalemia
where is aldosterone made in the body
adrenal cortex
chronic hypokalemia does what to the kidneys
interstitial fibrosis
increasing catecholamines/beta agonists will do what to your potassium
cause hypokalemia
metabolic alkylosis due to vomiting can do what to your potassium levels
can cause COMPENSATORY hypokalemia
compensatory holding onto H+, the K+/H+ antiporter wastes all your K
if you have more “distal flow” in the kidney, what is going to happen to your potassium?
hypokalemia
more distal flow means you absorbed less in the proximal tubule, where you absorb with NKCC pumps
(loop diuretics would cause increased distal flow and hypokalemia)
Eating what would cause hypokalemia in someone who is on a loop diuretic
eating more salt.
you would get even more distal flow and then the Na would be sucked up in the distal region and the potassium would be excreted even MORE
having low magnesium does what to your K and how
it causes hypokalemia
magnesium normally inhibits ROMK channels.
no Mg and you potassium spills out (can be aggrivated by intake of sodium)
metabolic acidosis due to diarrhea/laxative can do what to your potassium levels
causes PRIMARY hypokalemia
K+ follows HCO3- out of the GI tract when you poop
which can cause rhabdo - hyper or hypokalemia
hypo
insulin will take up potassium into the cells. what else does this?
catacholamines (that work on beta- adrenergic receptors)
Three main causes of increase in serum K if total body K is normal
muscle or tissue breakdown
insulin deficiency with hyperglycemia
metabolic acidosis
common drug that can cause high potassium
ace inhibitors (lack of aldosterone causes the Na/K antiporter to stop)
what do NSAIDs do to you aldosterone levels?
NSAIDS block prostaglandin
prostaglandins cause the juxtaglomerular cells lining the afferent arterioles to release renin, activating the renin–angiotensin–aldosterone system, to increase blood pressure.
no prostaglandins means no aldosterone
addisons
adrenals can’t make mineralcorticoids
get lack of aldosterone and cortisol (which is actually a glucocorticoid)
what do you think if someone’s potassium is 6.5-7 with no EKG changes
their sample may have been hemolysed, a lab error causing increased serum K in the plasma that isn’t actually in vivo
having hyponatremia will do what if you have hyperkalemia
it will make it worse because you won’t be secreting K with the Na/K antiporter
Tx for hyperkalemia and why
FIRST: antagonize
Calcium IV: antagonizes the effects of hyperkalemia on muscle cells in minutes
THEN: move into cells
glucose and insulin: shifts K into the cells
Bicarb: making them alkalemic shifts K into the cells via the K+/H+ antiporter
LATER…excrete
Loop diuretic
kayexalate
dialysis
spironolactone does what to your potassium
hyperkalemia
spironolactone is an aldosterone receptor antagonist (THIS IS NOT THE SAME AS AN ARB. ARBS ARE ANGIOTENSIN RECEPTOR BLOCKERS like losartan)
so it blocks the Na/K antiporter
values for hyper and hypo natremia
less than 135 or more than 145
where is ADH made
produced in the hypothalmus supraoptic and paraventricular nuclei
get stored in secretary granules that move down to the posterior lobe of the pituitary
Describe what is meant by non osmotic stimuli of ADH
Non osmotic sources of stimulation for ADH secretion
Come from baroreceptors for hypovolemia
can cause retention of water even if you have a low osmolality
used to keep the brain perfused and BP up in hypovolemia
what does ADH bind to
V2 receptor
makes aquaporin 2 move into the luminal membrane
does the kidney think the body is volume (overloaded or depleted) when on a diuretic
kidney can think that the body is volume depleted because you are getting rid of sodium on a diuretic
urine osmolality of sodium can range from _____ -______
can dilute to 50 - can concentrate to about 1400
use 50-1000 for her calculations though for the test i guess……..
when do you declare someone oliguric
when someome is making less that 500-600 cc of urine a day
pseudohyponatremia
when you have a low sodium but your plasma osmolality is normal
states of high protein (like multiple myeloma) or high lipids (like high triglycerides) or high sugar ( like mannitol to treat cerebral swelling)
high urine sodium means the kidneys are behaving as if the body is fluid _____ (expanded or depleted)
expanded
how much water do you have to drink in order to overcome the renal capacity to excrete water
10-15 liters
what are you thinking if someone is hyponatremic, urine osmolarity >100, UNa+ is less than 10
their body is trying to retain sodium so that they retain water. This is normal for hypovolemia
can be because of GI loss, burns, diuretics (late), cortisol deficiency
what are you thinking if someone is hyponatremic, urine osmolarity >100, UNa+ is less than 10 but they are volume expanded
they probably have edema, but the kidney thinks that they are volume depleted due to hyponatremia, so the kidney is trying to retain sodium inappropriately (because it is not perfused)
may be due to CHF/cirrhosis/nephrosis
what are you thinking if someone is hyponatremic, urine osmolarity >100, UNa+ >10, and volume depleted
this is a salt wasting nephropathy.
rarer, can be seen with diuretics (early), adrenal insufficiency, hypothyroidism
what are you thinking if someone is hyponatremic, urine osmolarity less than 100
probably primary polydypsia, beer potomania, or tea and toast syndrome
they are getting rid of excess water to correct hyponatremia
THEY ARE NOT VOLUME DEPLETED SO THEY DON’T CONCENTRATE THEIR URINE
what are you thinking if someone is hyponatremic, urine osmolarity >100, UNa+ >10, and volume appropriate or expanded
syndrome of inappropriate ADH secretion (SIADH) classically from lung cancer, also
how do you treat someone who is hyponatremic and volume expanded
restrict free water intake or treat state of poor perfusion (diuretics)
when would you give an ADH antagonist and what are they called
the “vaptans” target V2 receptors
hyponatremia with volume expansion
use them in an effort to get free water off
what is the maximum rate of correction of hyponatremia
.5 meq/liter/hour
what common-ish drug is known to cause nephrogenic diabetes insipidus?
lithium
need to give them just water, not saline
