DKA & HHS Flashcards
(68 cards)
what is DKA caused by?
caused by absence or a markedly inadequate amount of insulin that results in disorders in the metabolism of carbs, proteins, and fats
what are 3 main clinical features of DKA
- hyperglycemia
- dehydration & electrolyte loss
- acidosis
describe short patho of DKA
- no insulin so the amount of glucose that goes into cells is reduced
- because there’s a decrease in glucose, the liver will increase glucose production
- then in order to rid body of excess glucose, kidneys will excrete it (with water and electrolytes)
- osmotic diuresis (polyuria) leads to dehydration and electrolyte loss
- lipolysis converts into free fatty acids and glycerol
- free fatty acids are converted into ketone bodies by the liver
- insulin would normally prevent ketones from occurring but because people with DKA have no insulin
are ketones acids or bases?
ketones are acids! with accumulation of acids it leads to metabolic acidosis
what are 3 main causes of DKA
- decreased or missed dose of insulin
- Illness or infection
- undiagonosed/untreated DM
which hormones promote glucose production?
glucagon, epinephrine, norepinephrine, cortisol and growth hormone
how do the hormones interfere with glucose utilization?
normally hormones enhance break down of triglycerides into free fatty acids and gluconeogenesis (leading to increased glucose and ketones)
list mnfts of DKA
- hyperglycemia –> polyuria/polydipsia
- orthostatic hypotension from intravascular volume depletion
- ketosis and acidosis (GI symptoms will present)
- kussmaul respirations
what BG level range could you find with someone with DKA?
16.6-44.4mmol/L
what lab value shows evidence of ketoacidosis?
low serum bicarbonate (0-15mmol/L) and low pH (6.8-7.3)
would you have low or high PCO2 and why?
you would have low PCO2 (respiratory compensation) which are kussmaul respirations to compensate for metabolic acidosis (short, deeper breathing), blowing off more CO2
in addition to treating hyperglycemia, what is management aimed at?
correcting dehydration, electrolyte loss, and acidosis
why is rehydration important?
- maintains tissue perfusion
- fluid enhancement increases glucose secretion by kidneys
- monitor for FVE in elderly and those with renal/HF
what is the main electrolyte of concern with DKA?
potassium
what are factors of DKA that reduce serum K+ concentration?
- rehydration (leads to increased plasma volume with subsequent decreases in K and increased excretion)
- insulin admin which enhances movement of K from the ECF into cells
why must potassium be infused even if levels are normal?
because extracellular potassium drops during DKA
when would replacement of K be held?
only if hyperkalemia is present or if pt is not urinating
ketones accumulate in body as a result of what?
result of fat breakdown
how does insulin help with acidosis?
acidosis is reversed with insulin which inhibits fat breakdown, which stops acid buildup
when is the cue to stop IV insulin?
when the ketosis is resolved (you know this by having a normal anion gap)
at what BG level should IV dextrose be administered and why?
once its at 14mmol/L to avoid hypoglycemia
why is it crucial to flush the insulin solution through the entire IV infusion set and discard first 50ml?
because insulin molecules adhere to inner surface of IV infusion sets and can cause the initial fluid to cause a decreased concentration of insulin
what is monitored before potassium is administered?
urine output is monitored to prevent hyperkalemia
as DKA resolves and K+ replacement is decreased, what does the nurse ensure?
- that there are no signs of hyperkalemia in ECG
- lab values of K are normal or low
- patient is urinating
