Diabetic Ketoacidosis (DKA) Explained Clearly – Diabetes Complications

therefore welcomed another MedCramlecture we’re going to talk about diabetic ketoacidosisDKA now DKA is a moderately substantial illness that accounts for about ahundred and thirty-five thousand hospital admissions each year in theUnited Regime and it has an estimated cost of about 2.4 billion u.s. dollarsevery year so pretty sizable glob of cash is used to treat these patients andso it behooves us to understand a little bit more about what is DKA how does itpresent and how to treat it first I want to kind of takeyou to the cellular level so over here I will show you our cell wall and on itit’s got a insulin receptor also inside the cell you’ll recall that we havemitochondria and you’ll recall that there is a inter membrane space alongwith the matrix the matrix is that inner part now remember where things areyou’ve got glucose outside the cadre that wants to move inside and you’ve gotfatty battery-acids as well will glean a fatty battery-acid now you’ll echo this is where Krebs cycleoccurs I’ll abbreviate that as KC and this is where you have beta-oxidationremember these a fatty acids move inside the cell you’ll also recall that glucoseonce it gets inside the cell is going to undergo glycolysis and that it will alsogo inside the cell in the form of pyruvate which will eventually getbroken down to the same product and enter Krebs cycle as acetyl coA so in the normal situationyou’ve got insulin insulin covers to its receptor and insulin likewise prevents forthe most part fatty acids from moving on into the cell for a process of betaoxidation so in the normal situation what you have is you’ve got insulinhitting receptor inducing glucose to go into the cell glycolysis is occurringwhich the end result is pyruvate pyruvate then moves into themitochondria Krebs cycle results and you get boom ATP great in developments in the situation withdiabetes mellitus nature 1 where you have no insulin being secreted or in the caseof diabetes nature 2 where you have a very strenuous commonwealth high glucagon levelshigh epinephrine low-pitched insulin levels what you have then is in either of thesecases no insulin secretion or insulin opposition in which client and here’s thekey point here glucose can no longer come into the cell there is noglycolysis there is no pyruvate thenmode of energy source is cut off similarly insulin is no longer availableto prevent beta oxidation and so what you get at that point is you get quite alot of palmitoyl CoA through the enzyme palmitoyl CoAtransferase now no longer being inhibited or being disinhibited andallowing quite a lot of these palmitoyl CoAs to go inside the celland of course what happens there is that they are chopped up into two carbonunits so that’s called beta oxidation so chop cut cut chop cut chopper and soyou’re getting quite a bit of two carbon legions in here and this these high twocarbon cells can be used as you know Acetyl CoA in Krebs cycle to makeenergy it’s not the most efficient way of realise power but they can realise exertion andthose ketone forms are acetone which looks like this as you might recallacetoacetate which looks like this and something calledbeta-hydroxybutyrate which looks like this as you can see these are a result ofthese two carbon cells coming together and the broken off of ketone bodies andso all of these actually are ketone forms acetone is very volatile and soit can turn into a gas and this is what you smell on the breather of somebody whois in ketoacidosis you get this acetone smell but specially the thing I wantyou to pay attention to here is this carboxylic battery-acid bond and this is thewhole carboxylic battery-acid radical right here but particularly this OH group becausethis proton comes off very nicely and when it does what you have left behindis the conjugate locate which is negatively charged which is what’s goingto account for your anion divergence and if you want more information on the anion gapplease witnes our lecturings on ABG readings and medical acid-base soI think I want to review that and tell you exactly what I’m thinking they’renumber one in DKA we have a lack of insulin and as a consequence of that we seeblood sugars come near yes but I fantasize the biggest thing that you ought to pick upfrom that is number two is that there is no inhibition of fatty battery-acid delivery into matrix of mitochondria that’simportant because this means that fatty battery-acids are pouring into the matrix of themitochondria as we showed you on the last slide that means beta oxidation isoccurring which as you as you echo beta oxidation is simply when you havethese long bond fatty battery-acids getting chopped up into two carbon parts thesetwo carbon forces are then being fed into the krebs cycle but because there’s somany of them they start combining and forming these ketone bodies and theseketone forms are acidic so where’s the acid coming from the acid is coming fromthe ketone figures which are coming from the acid coa which are coming from thefatty acids which are coming from the outside which are being transportedbecause there is no insulin that’s very important okay so let’s review thatnumber one what we’re going to see here is low insulin and as a consequence of thatthis is what we’re going to see low-spirited insulin leads to ketone organizations which isgoing to lead to acidosis specifically an an ion spread acidosis which is going tolead to increased potassium now why does that potassium go up in this case itgoes up in this case because there is a proton potassium exchange mechanismbetween the cadres and so as protons are being increased in the serum and they gointo the cells potassium have to leave the cadres and gointo the serum to replace them so you’ll realize an increased potassium level atleast initially now decreased insulin likewise leads tohigh glucose high-pitched glucose is going to lead to dehydration and why is it goingto do that well because the glucose grades become so high-pitched that they exceedthe reabsorption doorstep and the kidneys and so what you get then is aosmotic diuresis that simply means that there’s too many specks in the urinebecause of the excess glucose that the kidney can’t reabsorb at all and thatexcess osmotic distres compels fluid to go with it and that begins dehydrationthat dehydration is going to do a couple of things it’s going to make all yourpotassium shift out of your cadres and get dumped and so this kind of thenleads back into this but then as well you get a total form potassium depletioneven though your potassium level in your serum is high you’re being depleted ofyour total mas potassium so what have we seen here we’ve seen ketone bodieswe’ve seen hyperglycemia we’ve seen acidosis we’ve seen dehydration we’veseen osmotic diuresis and we’ve seen total torso potassium reduction and alongthat you can also put total body phosphate depletion as wellnow the dehydration can lead to increased creatinine because of renalfailure and so this is what you typically see ina patient who comes in with DKA they are at risk because they have low-grade insulinyou can test their blood by checking for ketone bodies and because of this you’llsee an anion crack metabolic acidosis again look at our lecturing on acid-basebut what ketone figure show up is is the anion gap metabolic acidosis what thatmeans is the anion gap which is if you look at the chem 7sodium subtracted the chloride and the bicarb will be greater than 12 andthat’s usually the first signaling you’ll have so you’ll have an anion gapmetabolic acidosis and that anion gap metabolic acidosis is kind of asurrogate for how large-hearted the ketone torsoes are but you can actually measure ketonebody some hospitals measuring serum ketones okay and some likewise measuresomething announced beta hydroxybutyrate you get the acidosis as mentionedsometimes you’ll hear a high potassium generally you’ll ascertain a high potassium butagain the full amounts of the figure potassium is depleted because a lot of those a lot ofthe body’s potassium has been expended outside of the cells and into the serumyou receive these patients highly dehydrated with maybe sometimes hypotension andtachycardia because of the osmotic diuresis you’ll verify an increasedcreatinine because of dehydration and of course you’ll check a high glucose whichis one of the things that we all look for but may not be there we too seesometimes a low phosphorus sometimes a normal phosphorus so this is thehallmarks of somebody presenting with DKA let’s talk about how we treat thatcoming up here next

Learn More…

Keto Breads

Traditional Bread is the #1 Health Danger In Your Diet and Contains a Hidden Compound that Makes it Nearly IMPOSSIBLE to Burn Fat & Lose Weight!

You May Also Like