DKA/HHS Flashcards
underlying metabolic abnormality of DKA/HHS
absolute or relative insulin deficiency
counterregulatory hormones of DKA
glucagon, catecholamines, cortisol
role of hypercortisolemia in DKA
caused proteolysis (provides amino acid precursors for gluconeogenesis)
what is the effect of catecholamines on insulin sensitivity
decreases insulin sensitivity
mechanism of hyperglycemia in DKA/HHS
low insulin > elevated glucagon > elevated hepatic glucose production > decreased peripheral glucose use
which enzyme is activated in DKA and causes breakdown of triglycerides and release of FFA?
hormone-sensitive lipase
where are FFA converted to ketone bodies
liver
where does beta oxidation of FFA take place within the cell
mitochondria
product of the beta oxidation pathway
acetyl CoA
what ketoacids are made from acetyl CoA
acetoacetate
b hydroxybutyrate
what is acetone converted from
acetoacetic acid
which ketone is measured in the urine
acetoacetic acid
which ketoacids cause the anion gap in DKA?
b hydroxybutyric acid
acetoacetic acid
fluid deficit in DKA
5-7L
fluid deficit in HHS
7-12L
potassium deficit in DKA/HHS
3-6mEq/kg
70kg = 300-500 mEq
fastest rate of peripheral IV potassium replacement
10 mEq/hr
fastest central line potassium replacement
20 mEq/hr
definition of HHS
serum osm > 320, pH > 7.30
treatment of DKA/HHS
fluids
potassium
insulin
fluid deficit should be corrected within how many hours
24
insulin should be withheld if potassium drops below what value
3.3
potassium should be replaced once level drops below what value in DKA
5.0
role of bicarbonate therapy in DKA
if pH < 7.0
role of phosphate replacement in DKA
theoretical benefit
mechanism of cerebral edema in DKA treatment
idiogenic osmoles take time to dissapate; rapid fluid correction; insulin therapy leads to entry of osmotically active particles into the cell
