DKA & HHS (Final Exam)

Question 1

DKA involves __________ and hyperglycemia

Answer 1

ketoacidosis

Question 2

HHS involves more severe hyperglycemia without __________

Answer 2

Ketoacidosis

Question 3

In what age group is DKA more common in?

Answer 3

People under 65 years of age

Question 4

Which one is mostly associated with type 1 DM

Answer 4

DKA

Question 5

Can DKA ever occur in type 2 DM?

Answer 5

Yes under extreme conditions

-Stress
-Trauma
-Serious infections

Question 6

HHS is mostly common with which type of DM?

Answer 6

Type 2

Question 7

HHS is more common in pepole

Answer 7

over 65 years of age

Question 8

Why is there not acidosis in HHS

Answer 8

Type 2 diabetics still make insulin so there is enough breakdown of the fat

Question 9

Normal Response to Hyperglycemia

Answer 9

Extracellular concentration of glucose is regulated by insulin and glucagon

When serum glucose rises, glucose enters pancreas initiating insulin release

Insulin restores normal glycemic levels

Question 10

Once released, how does insulin restore normal glycemic levels?

Answer 10

-Diminishing hepatic glucose production (Decrease glycogenolysis and gluconeogenesis)

-Increase glucose uptake by skeletal muscles and adipose tissue

Question 11

Insulin with DKA

Answer 11

No insulin production

Question 12

Insulin with HHS

Answer 12

Ineffective action of insulin

Question 13

DKA early S/S

Answer 13

R/T ketoacidosis

-SOB
-ADB pain
-Nausea
-Vomiting

Question 14

Why do patients with DKA have a lower blood glucose compared to HHS

Answer 14

They have symptoms of ketoacidosis which requires them to seek treatment earlier

They tend to be younger and have a better GFR so they can secrete some of the glucose

Question 15

Normal serum glucose in HHS

Answer 15

Can exceed 1000 mg/dL

Question 16

Normal serum glucose in DKA

Answer 16

Typically below 800

Often (350-450)

Question 17

Ketone Production (DKA)

Answer 17

Insulin deficiency / resistance — glucose can’t get into the cell

The cells have no energy so the body begins to break down LIPOLYSIS of peripheral fat stores and releases free fatty acid / glycerol

Fatty acids are transported to liver and become activated

Activated fatty acids are then converted to acetyl-CoA and form KETONE BODIES

KETONE BODIES accumulate causing drop in pH (acidosis)

Question 18

Why does ketone production not happen in HHS

Answer 18

-There is still sufficient insulin activity to minimize lipolysis and therefore minimize ketone formation

Question 19

DKA typically presents with an elevated

Answer 19

Anion gap metabolic acidosis

Question 20

What is anion gap?

Answer 20

The differences between positively charged vs negatively charged electrolytes

Sodium + Chloride - Bicarb

Question 21

What is the main ketone we monitor in DKA?

Answer 21

Beta-hydroxybutyrate

Question 22

Plasma osmolality in DKA and HHS is elevated because of

Answer 22

Hyperglycemia (high glucose levels)

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

Question 23

Why do we not treat hyponatremia in DKA or HHS

Answer 23

This level is related to there being a increase plasma osmolality s/t increase in glucose

So the sodium level should correct when we treat the hyperglycemia

Question 24

Glucosuria causes osmotic diuresis leading to excretion of

Answer 24

Sodium

Potassium

Water

Question 25

The majority of body's potassium is found in the cells, so with metabolic acidosis

Answer 25

The Hydrogen ions and exchanged with potassium ions at the cellular level Potassium comes out of the cell HYPERKALEMIA As pH starts to correct the potassium will go back into the cells This is why we do not treat hyperkalemia unless the patient is symptomatic

Question 26

Metabolic acidosis causes hyperkalemia but why can both DKA and HHS present with decreased WHOLE BODY potassium levels?

Answer 26

Increase urinary loss (with normal kidney function) GI losses

Question 27

Patient can be originally hyperkalemic but have a

Answer 27

total whole body hypokalemia

Question 28

Cellular Compensation - DKA

Answer 28

Increase H+ concentration with acidosis H+ moves into cell K+ moves out of cell Electrical neutrality is restored inside the cell Temporary correction in pH is achieved 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 29

DO NOT BRING POTASSIUM LEVEL DOWN UNLESS THE POTASSIUM IS CAUSING PROBLEMS

Question 30

DKA / HHS: Precipitating Events

Answer 30

Infection without insulin adjustment Acute major illness or inflammatory process New onset type 1 diabetes (DKA is a common presentation) Glucocorticoids / Thiazide diuretics (drugs that affect carbohydrate metabolism) SLGT2 inhibitors Cocaine use or substance abuse Poor compliance with insulin regimen or faulty sub-1 insulin devices

Question 31

DKA onest

Answer 31

Very rapid (within 24 hours)

Question 32

DKA: Clinical Manifestations

Answer 32

Polyuria - Polydipsia Dehydration GI effects Neurologic effects (drunk / obtunded) Fruity odor breath Kussmaul respirations Tachycardia VOLUME DEPLETION

Question 33

DKA / HHS: Volume depletion manifestations

Answer 33

-Decrease skin turgor -Dry oral mucosa -Tachycardia -Hypotension

Question 34

HHS: Clinical Manifestations

Answer 34

Polyuria Polydipsia Weight Loss AS GLUCOSE RISES -lethargy-obtunded-coma Volume depletion

Question 35

Treatment of DKA and HHS

Answer 35

1. Fluid replacements (stabilize) 2. Correct electrolyte imbalances 3. Administration of insulin by infusion 4. Sodium bicarbonate if pH <7.2 5. Dextrose my be added to saline solution when serum glucose falls to 200 mg/dL (still continue with insulin) REQUIRES VERY FREQUENT MONITORING

Question 36

How do we know DKA has resolved?

Answer 36

Ketoacidos has resolved with the anion gap has closed (beta-hydroxy)

Question 37

How do we know hyperglycemia has resolved with HHS

Answer 37

Patient is mentally alert and plasma osmolality has drop to 315 mOsmol/kg Patient is able to eat and can transition back to SQ insulin

Question 38

DKA KEY POINTS

Answer 38

DKA is ketones in the blood --- metabolic acidosis leading to anion gap and (usually) hyperglycemia Most affects patients with type 1 Lack of adherence to insulin doses and stressors are common causes Treat volume depletion rapidly with 0.9 NS. Supplement potassium as needed, IV infusion of insulin

Question 39

HHS KEY POINTS

Answer 39

Hyperglycemia - dehydration - electrolyte imbalance - hyperosmolarity Type 2 DM Higher mortality rate than DKA Treat volume depletion rapidly with NS -- IV insulin -- correct electrolyte imbalances