3. Diabetic Ketoacidosis Flashcards
very generally, what is the function of insulin?
to allow storage of calories in the form of glycogen, proteins, TAGs
carbohydrates: circulating form? storage form?
circ: glucose.
storage: glycogen
fats: circulating form? storage form?
circ forms: triglycerides, lipoapoproteins
storage forms: triglyceride fat droplets, membranes
proteins: circulating form? storage form?
circ: amino acids.
storage: cellular proteins
what are the first few events that lead towards diabetic ketoacidosis?
insulin stops for some reason (usually pt stops taking it). glucose rises, and leads to osmotic diuresis.
at what serum level can kidney no longer recapture all glucose? what is the result?
at a BG of about 200, kidney cannot recapture glucose. result = osmotic diuresis and hypovolemia
when circ volume falls as a result of osmotic diuresis, what is response of arteries?
sympathetic response = release of epinephrine, cortisol, growth hormone. effect is vasoconstriction and attempt to maintain pressure, also lessened response to insulin
what is the balance of insulin and glucagon once someone stops taking insulin? what is the effect?
relatively greater glucagon. effect is overall a catabolic state (as opposed to anabolic)
what is the effect of low insulin on the liver? what enzymes incr and which decr?
liver:
- reduced storage of glucose via decr activity of glycogen synthase, incr activity of PFK, incr activity of pyruvate kinase
- increased glucose production via decr activity of glucose-6P
what is the effect of low insulin on the fat? what enzymes incr and which decr?
release of free fatty acids into circulation
increased hormone sensitive lipase activity -> lipolysis & release of FFA
what is the effect of low insulin on muscle?
protein breakdown, release of alanine into circulation. less uptake of glucose because GLUT4 transporter requires insulin to import
very generally: what do the liver, fat, and muscle tissues do in the absence of insulin? (what processes/what do they release)
Liver: gluconeogenesis, releases glucose
Fat: lipolysis, releases FFA, glycerol
Muscle: proteolysis, releases alanine
if you see a patient in a state of DKA, you can be 99% sure he has what type of DM? why?
T1DM. because T2DM pts make a tiny amount of insulin, which is sufficient to prevent acidosis
T1DM patient: is there ever reason to withhold insulin? what about T2DM?
T1DM: never stop giving insulin. they need enough to replete their basal level of glucose, even if they are not eating/going for a surg procedure
T2DM: may hold insulin (or cut in half) if not eating or going for surg.
why does someone start making ketones?
if the pathway from FFA –> Acetyl-CoA –> krebs cycle is saturated (requires NAD, which can be used up), then the other option is for the Acetyl-CoA to turn into ketones.
under what scenarios will someone create ketone bodies?
- complete lack of insulin (DKA)
- complete lack of glucose (starvation)
what will be the fate of FFA in the liver if insulin > glucagon? what if glucagon > insulin?
more insulin: triglyceride synthesis, TCA
more glucagon: keton bodies
what are the names of the two ketone bodies?
Beta-hydroxybutyrate, Acetoacetate
someone in DKA will have what kind of breathing?
deep and rapid: Kussmaul. breath will be fruity because he is trying to blow off acid via beta-hydroxybutyrate
what is the first line of treatment for someone in DKA?
volume repletion.
what is the status of potassium levels in DKA?
high serum K levels, but low intracellular levels. reason: acidic blood has been buffered by cell trading K+ for H+. Potassium has been drawn out of cells
what will happen if you re-hydrate someone in DKA without replacing their potassium?
once the acidosis corrects, they will become dangerously low in serum K and may have a heart attack.
which electrolytes are low in someone with DKA? what processes cause them to be low?
potassium (due to acid buffering), sodium (due to osmotic diuresis) and phosphate (also due to diuresis)
what is the reason why we replete volume in DKA before we give insulin?
since pt is so hypovolemic, sympathetic system has tried to vasoconstrict. Lots of epinephrine/cortisol in system which will antagonize insulin if insulin is given before sympathetic system calms down.
