final Flashcards
What is DKA
crisis that occurs as an acute metabolic complication of DM
What is HHS
crisis that occurs of DM w/o ketoacidosis
Who is DKA more common in
under 65
Type 1 DM
Who is HHS more common in
Over 65
Type 2 DM
Can DKA happen in type 2 DM
Yes, it can happen in acute situations such as infection, trauma, cardio emergency
What are the 2 regulators of the extracellular concentration of glucose
insulin
glucagon
what happens in the pancreas when glucose rises
glucose enters pancreas initiating insulin to release
What does insulin do and how is it accomplished
restores normal glycemic levels by:
decreasing glycogenolysis and gluconeogenesis
increasing glucose uptake by skeletal muscle and adipose tissue
What are the underlying defects in DKA/HHS
- reduce net effective action of circulating insulin.
- elevate levels of counter regulatory hormones, glucagon in excess, catecholamines, cortisol, and growth hormone
- dehydration and electrolyte abnormalities
Glucose levels in HHS
can exceed 1000
glucose levels in DKA
generally below 800
often 350-450
what does it mean when we have insulin deficiency and resistance
Glucose can’t get into cells so body uses fat for energy
what organ activates the fatty acids
liver
what is an anion gap
difference between negatively charged and positively charged electrolytes
what is beta-hydroxybutyrate
main metabolic product in ketoacidosis
higher the glucose = ? osmolality
higher
what are activated fatty acids converted to
acetyl-CoA and enter ketogenic metabolic pathway forming “ketone bodies”
accumulation of ketone bodies causes what
drop in pH (metabolic acidosis)
severity of acidosis and increase of anion gap factors
Rate and duration of ketoacid production
Rate of metabolism of ketoacids
Rate of loss of ketoacid anions in urine
how does hyperglycemia cause dilutional hyponatrmeia
Hyperglycemia pulls water out of cells, expands ECF, reducing plasma sodium (dilutional hyponatremia)
what does glucosuria cause
osmotic diuresis leading to excretion of sodium, potassium, and water
potassium in DKA/HHS
Both DKA and HHS present with total decreased potassium levels
Increased urinary loss (with normal kidney function)
GI losses
Serum potassium is normal to high due to hyperosmolality and insulin deficiency
plasma osmolality causes water to move out of the cells and potassium also moves into ECF
Insulin normally promotes potassium uptake by the cells. Lack of insulin contributes to increased levels
cell compensation in dka
•Increase in [H+] (concentration) seen with acidosis
H+ move into the cell
More positively charged ions in the cell
K+ moves out of the cell
Electrical neutrality is restored inside the cell
A temporary correction of the pH
•Process will reverse as the pH returns to normal
•HOWEVER, if the kidneys are working, they will excrete the excess K+
•Body can have a depletion of K+
precipitating factors
Infection (pneumonia or UTI) without insulin adjustment
Acute major illness or inflammatory process (MI, CVA, Sepsis, Pancreatitis)
New onset type 1 diabetes, DKA is a common presentation
Drugs that affect carbohydrate metabolism (glucocorticoids, thiazide diuretics)
Use of SGLT2 inhibitors (treatment in type 2 diabetes, but also used in type 1) (DKA)
Cocaine use (DKA)
Poor compliance with insulin regimen or faulty sub-q insulin infusion devices
DKA presentation
Rapid onset (over 24 hours) Polyuria, polydipsia GI effects (nausea, vomiting, abdominal pain) May have neurologic effects Volume depletion decrease skin turgor Dry oral mucosa Tachycardia Hypotension Fruity odor of breath Kussmaul respirations
HHS clinical presention
Insidious (several days) Polyuria Polydipsia Weight loss As glucose continues to increase Lethargy, obtunded, coma Signs of volume depletion similar to DKA
Treatment of DKA and HHS
Fluid replacement
Correction of electrolyte imbalances
Administration of insulin by infusion
Sodium bicarbonate (DKA with metabolic acidosis, pH < 7.2 [7.1])
Dextrose may be added to saline solution when serum glucose falls to 200 mg/dL (DKA) if the patient still has an anion gap (while still on a continuous insulin infusion)
resolved in dka/hhs
The hyperglycemic crisis is resolved with the following goals
With DKA - Ketoacidosis has resolved (the anion gap has closed)
With HHS – Patient is mentally alert and plasma osmolality has dropped to 315 mOsmol/kg
Patient is able to eat and can transition back to SQ insulin
key dka points
DKA is a condition of ketones in the blood, metabolic acidosis leading to anion gap, and (usually) hyperglycemia associated with insulin deficiency.
Mostly affects patients with type 1 diabetes.
Lack of adherence to insulin doses and/or physiologic stressors (infection,myocardial infarction) are common causes of DKA
Treat volume depletion rapidly with 0.9% normal saline. Supplement potassium as needed,IV infusion of insulin
Monitor glucose, electrolyte levels, anion gap
key hhs points
Marked hyperglycemia, dehydration, electrolyte imbalance, and hyperosmolality
Mostly affects patients with type 2 diabetes.
Has a higher mortality rate than DKA
Symptoms of illnesses such aspneumonia and UTIs, insulindeficiency, inflammatory conditions, MI, Stroke, severe dehydration,or the use of some drugscan lead to HHS.
Treat volume depletionrapidly with NS, IV insulin, correct electrolyte imbalances
