December 9, 2019
Diabetic Ketoacidosis (DKA) Explained Clearly – Diabetes Complications

Diabetic Ketoacidosis (DKA) Explained Clearly – Diabetes Complications


welcome to another MedCram
lecture we’re going to talk about diabetic ketoacidosis
DKA now DKA is a pretty significant illness that accounts for about a
hundred and thirty-five thousand hospital admissions every year in the
United States and it has an estimated cost of about 2.4 billion u.s. dollars
every year so pretty sizable chunk of cash is used to treat these patients and
so it behooves us to understand a little bit more about what is DKA how does it
present and how to treat it first I want to kind of take
you to the cellular level so over here I will show you our cell wall and on it
it’s got a insulin receptor also inside the cell you’ll recall that we have
mitochondria and you’ll recall that there is a inter membrane space along
with the matrix the matrix is that inner part now remember where things are
you’ve got glucose outside the cell that wants to move inside and you’ve got
fatty acids as well will draw a fatty acid here you’ll recall this is where Krebs cycle
occurs I’ll abbreviate that as KC and this is where you have beta-oxidation
remember these a fatty acids move inside the cell you’ll also recall that glucose
once it gets inside the cell is going to undergo glycolysis and that it will also
go inside the cell in the form of pyruvate which will eventually get
broken down to the same product and enter Krebs cycle as acetyl coA so in the normal situation
you’ve got insulin insulin binds to its receptor and insulin also prevents for
the most part fatty acids from moving on into the cell for a process of beta
oxidation so in the normal situation what you have is you’ve got insulin
hitting receptor causing glucose to go into the cell glycolysis is occurring
which the end result is pyruvate pyruvate then moves into the
mitochondria Krebs cycle occurs and you get boom ATP great in the situation with
diabetes mellitus type 1 where you have no insulin being secreted or in the case
of diabetes type 2 where you have a very strenuous state high glucagon levels
high epinephrine low insulin levels what you have then is in either of these
cases no insulin secretion or insulin resistance in which case and here’s the
key point here glucose can no longer come into the cell there is no
glycolysis there is no pyruvate then
mode of energy source is cut off similarly insulin is no longer available
to prevent beta oxidation and so what you get at that point is you get quite a
lot of palmitoyl CoA through the enzyme palmitoyl CoA
transferase now no longer being inhibited or being disinhibited and
allowing quite a lot of these palmitoyl CoAs to go inside the cell
and of course what happens there is that they are chopped up into two carbon
units so that’s called beta oxidation so chop chop chop chop chop chop and so
you’re getting quite a bit of two carbon units in here and this these high two
carbon units can be used as you know Acetyl CoA in Krebs cycle to make
energy it’s not the best way of making energy but they can make energy and
those ketone bodies are acetone which looks like this as you might recall
acetoacetate which looks like this and something called
beta-hydroxybutyrate which looks like this as you can see these are a result of
these two carbon units coming together and the breaking up of ketone bodies and
so all of these actually are ketone bodies acetone is very volatile and so
it can turn into a gas and this is what you smell on the breath of somebody who
is in ketoacidosis you get this acetone smell but particularly the thing I want
you to pay attention to here is this carboxylic acid chain and this is the
whole carboxylic acid group right here but particularly this OH group because
this proton comes off very nicely and when it does what you have left behind
is the conjugate base which is negatively charged which is what’s going
to account for your anion gap and if you want more information on the anion gap
please see our lectures on ABG interpretations and medical acid-base so
I think I want to review that and tell you exactly what I’m thinking they’re
number one in DKA we have a lack of insulin and as a result of that we see
blood sugars go up yes but I think the biggest thing that you ought to pick up
from that is number two is that there is no inhibition of fatty acid transport into matrix of mitochondria that’s
important because this means that fatty acids are pouring into the matrix of the
mitochondria as we showed you on the last slide that means beta oxidation is
occurring which as you as you recall beta oxidation is simply when you have
these long chain fatty acids getting chopped up into two carbon units these
two carbon units are then being fed into the krebs cycle but because there’s so
many of them they start combining and forming these ketone bodies and these
ketone bodies are acidic so where’s the acid coming from the acid is coming from
the ketone bodies which are coming from the acid coa which are coming from the
fatty acids which are coming from the outside which are being transported
because there is no insulin that’s very important okay so let’s review that
number one what we’re going to see here is low insulin and as a result of that
this is what we’re going to see low insulin leads to ketone bodies which is
going to lead to acidosis specifically an an ion gap acidosis which is going to
lead to increased potassium now why does that potassium go up in this case it
goes up in this case because there is a proton potassium exchange mechanism
between the cells and so as protons are being increased in the serum and they go
into the cells potassium have to leave the cells and go
into the serum to replace them so you’ll see an increased potassium level at
least initially now decreased insulin also leads to
high glucose high glucose is going to lead to dehydration and why is it going
to do that well because the glucose levels become so high that they exceed
the reabsorption threshold and the kidneys and so what you get then is a
osmotic diuresis that simply means that there’s too many particles in the urine
because of the excess glucose that the kidney can’t reabsorb at all and that
excess osmotic pressure causes fluid to go with it and that causes dehydration
that dehydration is going to do a couple of things it’s going to make all your
potassium shift out of your cells and get dumped and so this kind of then
leads back into this but then as well you get a total body potassium depletion
even though your potassium level in your serum is high you’re being depleted of
your total body potassium so what have we seen here we’ve seen ketone bodies
we’ve seen hyperglycemia we’ve seen acidosis we’ve seen dehydration we’ve
seen osmotic diuresis and we’ve seen total body potassium depletion and along
that you can also put total body phosphate depletion as well
now the dehydration can lead to increased creatinine because of renal
failure and so this is what you typically see in
a patient who comes in with DKA they are at risk because they have low insulin
you can test their blood by checking for ketone bodies and because of this you’ll
see an anion gap metabolic acidosis again look at our lecture on acid-base
but what ketone body show up is is the anion gap metabolic acidosis what that
means is the anion gap which is if you look at the chem 7
sodium subtracted the chloride and the bicarb will be greater than 12 and
that’s usually the first sign you’ll have so you’ll have an anion gap
metabolic acidosis and that anion gap metabolic acidosis is kind of a
surrogate for how big the ketone bodies are but you can actually measure ketone
body some hospitals measure serum ketones okay and some also measure
something called beta hydroxybutyrate you get the acidosis as mentioned
sometimes you’ll see a high potassium usually you’ll see a high potassium but
again the total body potassium is depleted because a lot of those a lot of
the body’s potassium has been depleted outside of the cells and into the serum
you see these patients very dehydrated with maybe sometimes hypotension and
tachycardia because of the osmotic diuresis you’ll see an increased
creatinine because of dehydration and of course you’ll see a high glucose which
is one of the things that we all look for but may not be there we also see
sometimes a low phosphorus sometimes a normal phosphorus so this is the
hallmarks of somebody presenting with DKA let’s talk about how we treat that
coming up here next

54 thoughts on “Diabetic Ketoacidosis (DKA) Explained Clearly – Diabetes Complications

  1. just wondering how this can cause hypotension as mentioned at the end of the video if it increases the amount of ions and substances in the blood?

  2. had a UWORLD question about a DKA patient, who comes into the ER after 2 days, and it says that INTRACELLULAR K+ is Decreased, but EXTRACELLULAR is INCREASED due to two mechanisms:
    1. loss of intercellular free water caused by increase plasma osml which leads to extracellular movement of K+ secondary to increasing [K+]
    and 2. Lack of insulin causes extracellular shifting of K+ ( insulin promotes K+ uptake)

    can any one explain WHY the serum [K+] is high ? isn't the body getting rid of K+ via aldosterone being activated ?

  3. Can you please explain how DKA becomes fatal? My 25 year old son with type 1 died from it according to the medical examiner. I need to understand it, in order to move forward.I was not there when he died,so I didn't see what happened,did he suffer,or would it render him unconscious?

  4. wait so the ketone bodies are produced in the mitochondria when too much acetly-coa builds up, and then they diffuse out to the cytosol and ultimately to the blood?
    is the lack of insulin ultimately causing the carnitine shuttle to work because: lack of insulin isnt activating PP2A which then isnt uninhibiting cytosolic ACC, which then wont create malonyl-coa, which will drop in concentration until it no longer inhibits the carnitine shuttle?

  5. Very good info, and yes.. who gives thumbs DOWN? My 6 yr old Son had tonsils and adenoids removed. Been a challenging few days. These vids help immensely in keeping ketones, which were spiking, down. Choosing the perfect diet, then maintaining a consistent neutral while also making sure to administer a minimum of " 1 unit incilin/carb every 3 hours". Was no walk in the park. Especially when your child's miserable in pain, running a fever and not wanting to eat or drink. Day 5 and looks like we're on our way to a speedy recovery.

  6. In bed with DKA, you fail to mention that it EFFING HURTS! no but really, thank you for the explanation, although I can’t say it makes me feel any better( WAIT THATS HAPPENING INSIDE ME WTH?) it’s nice to understand.

  7. If medical people are so smart why can’t they cure cancer or Alzheimer’s there is more unknown in Medicine than we know, millions of unanswered questions, god isn’t meant to be understood

  8. Excellent video! I am an RN but I like to know the how and why of everything in life, sometimes it is just too much information but you have a way of sorting out the tangle and presenting it with the how and why, love that. Thank you!

  9. Great video, however you clearly showed FA and ACA going into your mitochondria, and you repeatedly said 'moving into the cell, when they were already in the cell in your diagram?  again, nice video

  10. I'm type 1 diabetic and a Highschool AP biology student. I came here with the question why if both hyper and hypoglycemia prevent glucose from entering the cells why are they diffrent. I knew that your body turns fat into energy in situations with high bloodsugar, but I didn't realize that insulin keeps the fatty acids from entering the mitochondria. So that's why! To much insulin = lack of both glucose and ketosis.

  11. So this is explicitly about someone who is not doing a ketogenic diet? You get the high blood glucose levels by absorbing dietary carbohydrates in the absence of insulin or functional insulin receptors.

  12. the reason there is an increase in potassium is because of its competition with hydrogen on albumin. the more hydrogen, the more it binds to albumin, and the more potassium is released into the blood.

  13. This was great, I've been looking for "patient information diabetes type 2" for a while now, and I think this has helped. Have you heard people talk about – Laniley Kansabella Magic – (Have a quick look on google cant remember the place now ) ? Ive heard some decent things about it and my brother in law got amazing results with it.

  14. Thanks for your great video. Ketogenic diet along with intermittent fasting is getting very popular. Can you please give us an analysis of this diet in relation to the belief that the cells will switch from using glucose to ketones for energy?

    And if this is true, how easy is that source of energy is available in case of an emergency, like for example running to catch a bus?

    If you can provide an in depth analysis, that would be so appreciated.

    I really hope you cover this topic.

    Thanks in advance

    Cheers

  15. I love this videos. Should the phosphate level be high prior to giving insulin for a patient with DKA? Phosphate is needed for glycolysis and there's a lack of insulin or inability of the cell to respond to insulin in DKA, therefore, phosphate can't go in the cell to help metabolize the glucose.

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  17. Great lecture. In case anyone is curious, the reason why the Acetyl COA (ACA) made from B-oxidation doesn't go through the Krebs cycle here is because in diabetes there is also a lack of Oxaloacetate (OAA). OAA gets depleted for gluconeogenesis to provide glucose for the brain. (In Krebs Cycle, the first step is combination of ACA and OAA to make citrate.)

  18. If someone that's type 1 diabetic fasts for 3 weeks and 1 week in they only need 2.1 units per day to keep sugars in the range of 65 to 120… Drinking 2 liters of water each day.. Half of which has potassium, sodium and baking soda.. 3/4 of a teaspoon per 750 mL of water.. Is this a recipe for DKA because how little insulin is being used?

  19. I have question.
    Patient known case of DM type 2
    On sc Insulatard 16 units on Night and sc actrapid 10 units TDS.
    Suddenly noted after sc insulatard 16 units admission One hour later , glucose levels at blood 30.
    But no symptoms of DKA.
    Patient no polydipsia or poly uria..no fast breathing. He is totally well.
    After another hour later HGT 26
    After another Hour later 18
    Do we need to work out DKA ??

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