Download Electrolytes

Electrolytes
I. The major electrolytes and where they're located
A. Intracellular (ICF) vs. Extracellular Fluid (ECF). ICF is the fluid inside cells;
ECF is the fluid outside of cells. The two primary compartments of ECF include the
interstitium and blood plasma.
B. Major ICF electrolytes: K+, Mg+, proteins-, Pi (your book uses HPO4 2-,
which is how "free" phosphate typically exists... in any event, what you need to know is
"phosphate," and that it's an anion).
C. Major ECF electrolytes: Na+, Ca2+ Cl-, proteins- in plasma (there are not
many proteins in interstitium but there are lots in plasma).
II. Fluid Balance- here, there needs to be a) enough fluid to maintain blood
volume/pressure for proper tissue perfusion, b) the proper concentration of solutes
(especially Na+) to prevent major fluid shifts from ICF to ECF and vice-versa. This is
the primary focus here.
A. Dehydration- water loss exceeds water gain. Most commonly caused by
excessive perspiration, vomitting, diarrhea. Na+ concentration of the ECF rises:
hypernatremia (although typically lots of Na+ is lost during the same types of
circumstances). ADH maximizes water retention, urine becomes very concentrate.
B. Overhydration- water intoxication. Can be caused by chronic renal failure,
endocrine problems (excess ADH), or overconsumption (typically associated with
psychological disorders). Na+ concentration of ECF falls, excess water moves into cells,
which swell (neuron swelling produces the symptoms)
III. Regulating electrolyte concentrations: electrolyte balance. Electrolytes are gained
by the diet and lost in a variety of ways: sweat, urine, feces, epithelial sloughing. It is the
electrolyte concentration of the ECF that is monitored, and adjustments are made
based on that. ECF composition can quickly effect ICF composition throughout the body,
because a major part of the ECF travels (plasma).
A. Sodium
1. Lost primarily in sweat and urine.
2. Major hormones controlling Na+ loss at the kidneys:
a. ADH- when Na+ concentration rises, ADH is released by the
posterior pituitary. ADH, as you know, causes water retention. This will
cause the concentration of Na+ in the ECF to return to normal (instead of
actually getting rid of Na+).
b. Aldosterone- when Na+ concentration drops or K+
concentration rises, aldosterone is released by the adrenal cortex. As you
know, aldosterone causes Na+ to be reabsorbed and K+ to be secreted via
counter-transport.
3. Conditions associated with Na+ imbalances:
a. Hypernatremia- A high concentration of Na+ in ECF. Among
others, symptoms include a drop in blood pressure and volume, and
eventual circulatory collapse. Hypernatremia is caused primarily by
dehydration. So the loss of blood volume associated with hypernatremia is
connected with dehydration.
b. Hyponatremia- Low concentration of Na+ in ECF. Water
intoxication: cells swell. Neurons are particularly vulnerable, and
symptoms (much like drunkenness) reflect swelling of neurons.
B. PotassiumLoss at kidneys is affected by: aldosterone (see above) and simple blood
K+ concentration; when it is high, secretion increases and vice versa (simply as a
result of more "bumping into" channels that will transport it out).
Hyperkalemia (caused by renal failure) and hypokalemia (excess
aldosterone or dietary deficiency) both associated with neuromuscular problems,
particularly cardiac muscle.
C. Calcium- Most calcium is reabsorbed at the kidneys, any excess exceeds
transport max and is urinated. However, reabsorption will increase in response to
PTH and calcitriol.
Hypocalcemia (caused by a dietary deficiency of Ca2+ or vitamin D and
hypoparathyroidism) and hypercalcemia (caused by oversupplementation of
vitamin D and Ca2+ or hyperparathyroidism) are both associated with
neuromuscular problems in addition to other potential symptoms.
IV. Acid-Base Balance (Focusing on plasma and acidosis).
A. Where do H+ come from? Cellular metabolism. Some common acids:
H2CO3 (this is only a buffer if its H+ is taken out of solution and HCO3- is left in
solution to pick up OTHER H+)
Lactic Acid
Ketone bodies
Sulfuric and Phosphoric Acids (biproducts of amino acid and nucleic acid
breakdown)
B. Getting rid of excess H+: Buffers can bind H+ and take them out of solution,
but if you keep on producing more (and cells do), pretty soon all the buffers will
be saturated and won't be able to bind any more H+. So, in addition to buffers
(which temporarily take excess H+ out of solution), we need to be able to get rid
of H+ completely. To do this, we can either tie H+ up into a covalent bond in
water or we can just excrete the H+.
1. Temporary fixes: buffers. The two most important plasma buffers are
proteins and HCO3-. You know how HCO3- is generated and how it
works. In addition, cells of the collecting ducts of the kidneys generate
HCO3- (guess how!) and simply dump the H+ into the urine. Proteins can
also reversibly bind H+. For example, you know that Hb binds H+ in
tissues and then lets go of it in the lungs.
2. Permanent Fix #1: Tie H+ up in a covalent bond (respiratory
compensation). Remember, in the lungs: HCO3- + H+ --> H2CO3 --> CO2 +
H2O. In this way, H+ get stuck into water, and CO2 is removed completely.
When cells are very active, lots of CO2 gets produced in tissues (therefore
lots of H+, right? what happens in tissues, again?). Respiration increases to rid the
blood of excess CO2 (and thereby, excess H+).
-Problems with respiratory compensation (not breathing the right amount
for the amount of CO2 being produced by cells):
Hypoventilation- in this case, you're not getting rid of enough
CO2, therefore you are not tying up enough H+ in H2O. Acidosis can
result.
Hyperventilation- in this case, you're getting rid of too much CO2
and taking too many H+ out of solution. Alkalosis can result. Putting a
paper bag over someone's nose when they hyperventilate helps them to
recover their CO2 (and therefore H+).
3. Permanent Fix #2: Excrete H+ (renal compensation). When pH drops,
the kidneys increase secretion of H+ into urine.
(see above, temporary fix, to see where the following fits in) The kidneys
also help to regulate blood pH because tubule cells contain carbonic anhydrase.
When pH drops, the cells generate HCO3- and H+ (how, again?). The H+ are
excreted, and the HCO3- are sent to the blood, in exchange for a Cl-.