DKA/HHS Flashcards
DKA
ketones in blood
Metabolic acidosis – anion gap
Hyper glycemia with insulin deficiency
Who is DKA more common in?
under 65 years
Type one diabetes
HHS
Marked hyperglycemia
Dehydration, electrolyte imbalance
Hyper osmolality
No ketoacidosis
Who does HHS occur more in?
over 65
Type two diabetes
response to hyperglycemia
Extracellular concentration of glucose is regulated by insulin and glucagon
When serum insulin increases glucose goes to the pancreas to initiate insulin release
Insulin restores normal glucose by decreasing hepatic production, gluconeogenesis, glycogenolysis
Increased glucose uptake by skeletal muscles and Adipose tissue
Patho of hyperglycemia
Decreased insulin or resistance
Increased catecholamines and cortisol – increased hepatic production
Dehydration and electrolyte abnormalities
hyperglycemia with HHS
Serum glucose greater than 1000
Glucosuria results from osmotic diuresis
hyperglycemia with DKA
Serum glucose less than 800, 350 to 450
Presents earlier with symptoms of ketoacidosis
Tends to be with younger patients with increased GFR
ketone production
Insulin deficiency in resistance – cells. Use fat for energy
Lipolysis of peripheral fat stores, releases free fatty acids and glycerol
free fatty acids go to the liver to become activated
Activated free Fatty acids convert to acetyl coA– ketone bodies
Ketone bodies decrease pH – metabolic acidosis
why doesn’t ketone production occur with HHS?
Patient still can produce some insulin to minimize lipolysis
anion gap
Occurs with DKA
Caused by production and accumulation of ketones
what is the severity of acidosis within anion gap depend on?
Rate and duration of keto acid production
Rate of metabolism of keto acids
Rate of loss of ketoacid anions in urine
is plasma osmolality increased or decreased with elevated glucose?
Increased
Hyperglycemia pulls water out of cells results in decreased plasma, sodium-dilutional hyponatremia
how is plasma osmolality affected by glycosuria?
Decreased from osmotic diuresis
Excretion of sodium, potassium, water
potassium
Decreased with both DKA & HHS
Increased urinary loss, G.I. loss
Cellular compensation
H+ moves into the cell
K+ moves out of the cell
precipitating factors
Infection – pneumonia, UTI
Acute major illness – MI, CVA, sepsis, pancreatitis
New onset type one diabetes, DKA
Drugs – glucocorticoids, thiazide, diuretics
SLG T2, inhibitors
Cocaine/substance use
Poor compliance with insulin regimen
DKA s/sx
rapid, 24 hours
Polyuria, polydipsia
N/V/abdominal pain
Fruity odor breath **
Kussmaul respirations **
Neuro effects
Decrease volume – decrease skin turgor, drymucosa, tachycardia, hypotension
HHS s/sx
insidious – several days
Polyuria, polydipsia
Decreased weight
As glucose increases, – lethargy, obtunded, coma**
s/sx fluid volume deficit
treatment
Fluid replacement, rapid-isotonic saline
correct fluid and electrolyte imbalance
Administer insulin by infusion
Sodium bicarb – DKPH less than 7.2
Dextrose added to fluids, if glucose less than 200 with anion gap
how to know if DKA is resolved
Keto acidosis is gone
Anion gap closed
Monitor fluid and electrolyte, glucose, anion gap
how to know if HHS is resolved
Patient is mentally alert
Plasma osmolality greater than or equal to 315
Patient is able to eat in transition to sub Q insulin
