Electrolytes!!!!!!..... Why u no make sense???

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Dark tar

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Hi everyone.

This topic is basically a huge confusion to me. I know the phases of an action potential. I know the heart's action potentials whether nodal and muscular and that's all fine and dandy but when it comes to me being able to logically predict the outcomes of a certain electrolyte imbalance (like for example: hypokalemia results in muscle weakness) it's a mess.
Please help. Let this be the thread in which I finally put this thing to rest.

I want to understand the effects of hypo/hyper (natremia,kalemia,calcemia) on excitable tissue.

United we understand. Unleash your knowledge on me :bang::bang:
 
There's a chart in the renal section of first aid (p 537 in the 2015 version) that lists the effects of various electrolyte disturbances.
 
Ok I read the table. Is there a way to undersatnd it logically?? Or I just memorize by heart or some silly mnemonic???
 
Hi everyone.

This topic is basically a huge confusion to me. I know the phases of an action potential. I know the heart's action potentials whether nodal and muscular and that's all fine and dandy but when it comes to me being able to logically predict the outcomes of a certain electrolyte imbalance (like for example: hypokalemia results in muscle weakness) it's a mess.
Please help. Let this be the thread in which I finally put this thing to rest.

I want to understand the effects of hypo/hyper (natremia,kalemia,calcemia) on excitable tissue.

United we understand. Unleash your knowledge on me :bang::bang:
I wouldn't say I know it particularly well or in depth, but my simple system is:

Sodium- osmolality issues. Hyper= altered mental status. Hypo= altered mental status (remember to not correct either too rapidly!)
Potassium- arrhythmias, QT abnormalities
Calcium- low = tetany, high = hypercalcemia (stones, moans, groans, bones).

K.I.S.S. I haven't had any trouble logic-ing through UWorld Q's with only the above. Even if others add onto this (and hopefully they will), I would make sure you have the absolute basics down pat before going into detail.
 
I wouldn't say I know it particularly well or in depth, but my simple system is:

Sodium- osmolality issues. Hyper= altered mental status. Hypo= altered mental status (remember to not correct either too rapidly!)
Potassium- arrhythmias, QT abnormalities
Calcium- low = tetany, high = hypercalcemia (stones, moans, groans, bones).

K.I.S.S. I haven't had any trouble logic-ing through UWorld Q's with only the above. Even if others add onto this (and hopefully they will), I would make sure you have the absolute basics down pat before going into detail.

This is pretty good.

The way I was taught and usually think about this is:

The body has various ways of regulating total body sodium in a way that total body sodium usually doesn't change much. Low serum concentration of sodium usually indicates a solvent (water) problem more than a solute problem. Hyponatremia usually means you're holding on to too much water (SIADH, etc.) Too much water leads to cerebral edema and its consequences-lethargy, confusion, coma, seizures, etc. Too high a sodium concentration is also usually a water problem (elderly bedridden person can't drink water, DI, etc.) and can disrupt electrolyte balance and lead to some similar issues. Correcting too fast high to low can give you cerebral edema. Correcting low to high can give you central pontine myelinolysis.

Potassium is part of the cocktail they give in lethal injection. High K+ stops the heart because it interferes in the outward K+ channel flow by decreasing its membrane potential. You will get problems with repolarization (prolonged-->QT prolongation; issues with repolarization-->hyperacute T waves)

Hypokalemia usually results in problems with repolarizing after muscle contraction. You get muscle cramping and stuff.

Insulin can cause potassium uptake by cells.

Calcium is important for a few main things: muscle contraction (tetany in hypocalcemia), neurotransmitter release (psychic moans), bone formation (bones). Calcium deposits with oxalate in kidneys to form stones (calcium citrate is more soluble than calcium oxalate, so citrate is also involved). I'm not exactly sure about the reason for abdominal pain (groans) but here's my hypothesis: high calcium interferes with serotonin release from synaptic vesicles. In the brain this could lead to depression (psychic moans). The enteric nervous system is mostly serotonergic. Disturbances in this could cause dysfunctions in motility and dysfunctions in the pathways that normally perceive pain and insults to the gut. Remember how we use odansetron for hyperemesis of pregnancy, chemo nausea, etc. and how we use SSRIs for IBS? I'm not sure if this is the reason, but it's the way I imagined it.

Obviously don't get mad if everything here is not totally 100% accurate, but it's just how I think about it.

Hope this helped.
 
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The body has various ways of regulating total body sodium in a way that total body sodium usually doesn't change much. Low serum concentration of sodium usually indicates a solvent (water) problem more than a solute problem. Hyponatremia usually means you're holding on to too much water (SIADH, etc.) Too much water leads to hydrocephalus and its consequences-lethargy, confusion, coma, seizures, etc. Too high a sodium concentration is also usually a water problem (elderly bedridden person can't drink water, DI, etc.) and can disrupt electrolyte balance and lead to some similar issues. Correcting too fast high to low can give you hydrocephalus. Correcting low to high can give you central pontine myelinolysis.

Change "hydrocephalus" to "cerebral edema" and this paragraph is on point. Good post.

Hypokalemia usually results in problems with repolarizing after muscle contraction. You get muscle cramping and stuff.
Now this is my kind of explanation 👍
 
Change "hydrocephalus" to "cerebral edema" and this paragraph is on point. Good post.


Now this is my kind of explanation 👍

Yeah, you're right. That should be cerebral edema. I don't know why I kept putting hydrocephalus. I've corrected the error.

Thanks!
 
Sc24, sloop and all of you guys thanks alot for contributing to this post. every help is very appreciated.
 
Calcium's effect on excitable tissue is due to it's small affinity for the ion pore of sodium channels. With hypercalcemia, calcium competes with sodium, which makes the membranes less likely to depolarize. So it doesn't directly influence the release of serotonin as stated earlier, but it would decrease the release of all neurotransmitters dependent on this mechanism.
 
Calcium's effect on excitable tissue is due to it's small affinity for the ion pore of sodium channels. With hypercalcemia, calcium competes with sodium, which makes the membranes less likely to depolarize. So it doesn't directly influence the release of serotonin as stated earlier, but it would decrease the release of all neurotransmitters dependent on this mechanism.

That explaines the tetanus in hypocalcemia. Sodium in having a good day.
 
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