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Question 1

What is DKA

Answer 1

crisis that occurs as an acute metabolic complication of DM

Question 2

What is HHS

Answer 2

crisis that occurs of DM w/o ketoacidosis

Question 3

Who is DKA more common in

Answer 3

under 65

Type 1 DM

Question 4

Who is HHS more common in

Answer 4

Over 65

Type 2 DM

Question 5

Can DKA happen in type 2 DM

Answer 5

Yes, it can happen in acute situations such as infection, trauma, cardio emergency

Question 6

What are the 2 regulators of the extracellular concentration of glucose

Answer 6

insulin

glucagon

Question 7

what happens in the pancreas when glucose rises

Answer 7

glucose enters pancreas initiating insulin to release

Question 8

What does insulin do and how is it accomplished

Answer 8

restores normal glycemic levels by:

decreasing glycogenolysis and gluconeogenesis

increasing glucose uptake by skeletal muscle and adipose tissue

Question 9

What are the underlying defects in DKA/HHS

Answer 9

1. reduce net effective action of circulating insulin.
2. elevate levels of counter regulatory hormones, glucagon in excess, catecholamines, cortisol, and growth hormone
3. dehydration and electrolyte abnormalities

Question 10

Glucose levels in HHS

Answer 10

can exceed 1000

Question 11

glucose levels in DKA

Answer 11

generally below 800

often 350-450

Question 12

what does it mean when we have insulin deficiency and resistance

Answer 12

Glucose can’t get into cells so body uses fat for energy

Question 13

what organ activates the fatty acids

Answer 13

liver

Question 14

what is an anion gap

Answer 14

difference between negatively charged and positively charged electrolytes

Question 15

what is beta-hydroxybutyrate

Answer 15

main metabolic product in ketoacidosis

Question 16

higher the glucose = ? osmolality

Answer 16

higher

Question 17

what are activated fatty acids converted to

Answer 17

acetyl-CoA and enter ketogenic metabolic pathway forming “ketone bodies”

Question 18

accumulation of ketone bodies causes what

Answer 18

drop in pH (metabolic acidosis)

Question 19

severity of acidosis and increase of anion gap factors

Answer 19

Rate and duration of ketoacid production

Rate of metabolism of ketoacids

Rate of loss of ketoacid anions in urine

Question 20

how does hyperglycemia cause dilutional hyponatrmeia

Answer 20

Hyperglycemia pulls water out of cells, expands ECF, reducing plasma sodium (dilutional hyponatremia)

Question 21

what does glucosuria cause

Answer 21

osmotic diuresis leading to excretion of sodium, potassium, and water

Question 22

potassium in DKA/HHS

Answer 22

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

Question 23

cell compensation in dka

Answer 23

•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+

Question 24

precipitating factors

Answer 24

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

Question 25

DKA presentation

Answer 25

``` 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 ```

Question 26

HHS clinical presention

Answer 26

``` Insidious (several days) Polyuria Polydipsia Weight loss As glucose continues to increase Lethargy, obtunded, coma Signs of volume depletion similar to DKA ```

Question 27

Treatment of DKA and HHS

Answer 27

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)

Question 28

resolved in dka/hhs

Answer 28

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

Question 29

key dka points

Answer 29

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

Question 30

key hhs points

Answer 30

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 as pneumonia and UTIs, insulin deficiency, inflammatory conditions, MI, Stroke, severe dehydration, or the use of some drugs can lead to HHS. Treat volume depletion rapidly with NS, IV insulin, correct electrolyte imbalances