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.
Does acidosis increase K shift out of cells, or decrease?
Acidosis leads to an increase in K shifting out of cells (increase in K in ECF)
If you have an increase in diuresis (lots of tubular fluid water), what does this do to urinary flow rate? What is the effect of this flow rate on potassium secretion?
It will increase urinary flow rate, which will increase potassium secretion.
How does flow rate impact K secretion? (looking for the actual mechanism here)
two driving factors.
Assume we have high flow rate. 1, we have the luminal K being diluted from the extra fluid, so this is driving the force for K secretion gradient-wise. But also, if we are increasing sodium in the tubular fluid, this will also drive K secretion via Na movement. This isn’t as intuitive but let’s say you have a Na wasting diuretic. This will give ENaC a bigger gradient driving force, which means a more negative membrane potential on the apical side of the distal tubule principal cell which means, you bring more potassium over (electric gradient).
How does vasopressin impact potassium secretion?
If you have increased vasopressin you’re going to increase those aquaporins which will have more sodium come out of the tubule; this also means that you’re going to have more of a gradient for sodium to go into the tubule (reverse of sodium)
If we are increasing K secretion and excretion in response to high K diet, what is this referred to as?
K spilling
If we are not secreting K or excreting K due to a low K diet, what is this referred to as?
K conservation
What are the two main factors altering K secretion? (think very broad terms of K availability)
Dietary intake and diuretics
