RENAL 09: EVERYTHING ELSE Flashcards
Potassium is abundant inside, or outside cells?
INSIDE CELLS
What are the clinical names for high and low potassium
hyperkalemia; hypokalemia
where does most of our potassium come from?
Diet (5-10% is excreted in feces, but rest is absorbed)
what critical problem occurs right after potassium is absorbed?
It’s going to be high in ECF; this is bad because if we go too high with potassium this is hyperkalemia and you can get neurological or cardiac symptoms. Therefore, as soon as you get absorption you move that potassium into cells
What are the critical hormones in moving potassium into cells? There are 3
Epinephrine
Insulin
aldosterone
How much of our potassium is reabsorbed?
Around 85% (but remember, a lot of potassium will also be secreted so it goes back in the pee pee tube later on)
Where is the majority of potassium reabsorbed
proximal tubule (just like with sodium), with the thick ascending limb of the loop of henle being a close second
Range of K excretion
1-110% of filtered load - this shows the high variation in how much we can get rid of depending on how much we’re secreting
Normal potassium excretion (ex, not under very high potassium in blood plasma and closer to a balance – you have NOT just eaten a banana)
15%
Where is potassium secreted into the tubular system?
Late distal tubule nd collecting duct (primarily LDT) from crossing principal cells
Process of potassium secretion into the tubular system
We set up a drive in two ways:
1: ENaC (sodium channel) is going to put sodium into the distal tubule cell. This is going to be pumped out through the NKA. That sodium channel pulling sodium out of the distal tubule creates a quite negative charge in this area.
2. As sodium is pumped out through NKA into the blood, K is pumped into the distal tubule cell from the NKA. This creates excess of potassium in the cell, and the cell wants to push it out. It does this through K channels on apical membrane that allow Potassium to escape into the tubular fluid along an electro(set up by ENaC)chemical (Set up by NKA) gradient.
What are the 3 considerations of potassium secretion?
Pump (NKA), electrochemical gradient, permeability of the cell to potassium (channel availability)
what is the effect of aldosterone on K?
K wasting - it would insert more NKA into principal cells, so you increase potassium in cells which pushes K in the direction of secretion.
How does epinephrine affect the K balance in the body?
Epinephrine will bind to adrenergic receptors. on the skeletal muscle (high in alpha receptors) this will lead to K release. In cells with B2 receptors, this can lead to uptake of K.
What is insulin effect on K levels in cells
Decreases ECF K - it’ll shift K into cells especially liver (elevation after a meal with bananas is transient)
Plasma osmolarity affect on K
Hyposmolarity - this will cause cells to swell (water following salts). This means the K inside will be diluted, so this drives the force of K to move into them.
In hyperosmolarity, the cells will shrink and so this concentrates the K inside, and increases the driving force moving the potassium outside of the cells.
What happens to K in the case of cell lysis
Potassium is high inside cells, so when cells burst, this is released into the surrounding fluid. Severe trauma such as burns or crush injury can lead to this.
I something is a K-wasting diuretic, what is it effectively doing? - also nclude what is special about loop diuretics
You need to think Upstream.
Diuretics which act on the thick ascending limb block sodium reabsorption upstream. This is going to mean you have more Na going through ENaC, therefore K is pumped into cell and driven out into urine. There’s also a greater flow rate in general, meaning that K is diluted in the lumen of the tubule so this is a chemical gradient as well
Loop diuretics also inhibit the reabsorption of potassium itself because it blocks the Na/K/Cl transporter
Why are some diuretics potassium sparing?
Again, think about where they act; they are acting on cells affected by aldoterone (principal cells). These inhibit ENaC, thereby reducing drive for NKA and reducing electical drive as well
