Diabetic Ketoacidosis (DKA) Explained Clearly – Diabetes Complications

therefore welcomed another MedCramlecture we’re going to talk about diabetic ketoacidosisDKA now DKA is a pretty significant illness that accounts for about ahundred and thirty-five thousand hospital admissions every year in theUnited Country and it has an estimated cost of about 2.4 billion u.s. dollarsevery year so pretty sizable chunk 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 goes to show you our cadre 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 cell that wants to move inside and you’ve gotfatty battery-acids as well will suck a fatty acid here you’ll recall this is where Krebs cycleoccurs I’ll abridge that as KC and this is where you have beta-oxidationremember these a fatty battery-acids move inside the cell you’ll likewise 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 recruit Krebs cycle as acetyl coA so in the normal situationyou’ve got insulin insulin covers to its receptor and insulin too 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 compelling 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 the situation withdiabetes mellitus sort 1 where you have no insulin being secreted or in the caseof diabetes kind 2 where you have a terribly strenuous regime high-pitched glucagon levelshigh epinephrine low insulin levels what you have then is in either of thesecases no insulin secretion or insulin resistance in which event and here’s thekey point now 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 chop chopper cut chop chopper and soyou’re getting quite a bit of two carbon legions in here and this these high-pitched twocarbon sections can be used as you know Acetyl CoA in Krebs cycle to makeenergy it’s not the most effective means of originating power but they can move vigor andthose ketone people 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 divisions coming together and the breaking up of ketone bodies andso all of these actually are ketone figures 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 particularly the thing I wantyou to pay attention to here is this carboxylic acid bond and this is thewhole carboxylic acid group right here but especially this OH group becausethis proton comes off very nicely and where reference is does what you have left behindis the conjugated base which is negatively charged which is what’s goingto account for your anion crack and if you demand more information on the anion gapplease recognize our lecturings on ABG versions 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 result of that we seeblood sugars come near yes but I judge the biggest thing that you ought to pick upfrom that is number two is that there is no inhibition of fatty acid shipping into matrix of mitochondria that’simportant because this means that fatty acids are pouring into the matrix of themitochondria as we indicated you on the last slide that symbolizes beta oxidation isoccurring which as you as you recall beta oxidation is simply when you havethese long series fatty battery-acids coming chopped up into two carbon sections thesetwo carbon sections 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 torsoes are acidic so where’s the acid coming from the acid is coming fromthe ketone bodies 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 result of thatthis is what we’re going to see low-toned insulin leads to ketone mass 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 cells and gointo the serum to replace them so you’ll view an increased potassium level atleast initially now decreased insulin likewise leads tohigh glucose high glucose is going to lead to dehydration and why is it goingto do that well because the glucose tiers become so high 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 pressing compels fluid to go with it and that motives dehydrationthat dehydration is going to do a couple of things it’s going to make all yourpotassium shift out of your cadres and get dropped 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 form 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 figure potassium exhaustion 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-pitched insulinyou can test their blood by checking for ketone bodies and because of this you’llsee an anion breach metabolic acidosis again look at our castigate on acid-basebut what ketone form 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-scale the ketone bodies are but you can actually measure ketonebody some hospitals appraise serum ketones okay and some also measuresomething called beta hydroxybutyrate you get the acidosis as mentionedsometimes you’ll identify a high potassium typically you’ll read a high potassium butagain the full amounts of the mas potassium is sapped because a great deal of those a lot ofthe body’s potassium has been depleted outside of the cadres and into the serumyou watch these patients exceedingly dehydrated with maybe sometimes hypotension andtachycardia because of the osmotic diuresis you’ll realise an increasedcreatinine because of dehydration and of course you’ll meet 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 ordinary phosphorus so this is thehallmarks of somebody displaying with DKA let’s talk about how we treat thatcoming up here next

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