Hyperglycemic Diabetic Emergencies

Question 1

metabolic effects of insulin on muscle cells

Answer 1

1. glut receptor activation and glucose enters cells
2. glucose storage/glycogen synthesis
3. increased uptake of amino acids
4. protein syntehsis

Question 2

metabolic effects of insulin on the liver

Answer 2

1. stops glycogenolysis/break down of glucose stores
2. promotes glycogen formation
3. inhibits AA breakdown
4. inhibits FFA breakdown

Question 3

metabolic effects of insulin on adipose tissue

Answer 3

1. reduction in FFA release/lipase inhibition
2. increase storge of triglycerides

Question 4

3 things that make up the DKA triad

Answer 4

1. hyperglycemia
2. ketosis
3. acidosis

Question 5

 Type 1 DM- __ more common

 Type 2 DM- __ more common
 But both can present in Type 1 and Type 2 DM

Answer 5

 Type 1 DM- DKA more common

 Type 2 DM- HHS more common
 But both can present in Type 1 and Type 2 DM

Question 6

compare DKA and HHS in terms of its onset, presence of acidosis, and amount of insulin that is lacking

Answer 6

DKA: SEVERE acidosis, SEVERE lack of insulin, and FAST onset.

HHS: Mild acidosis, mild lack of insulin, more insideous onset.

Question 7

A 78 year old man has a history of type 2 diabetes and
renal failure. He appears severely dehydrated. His lab
work shows hyperglycemia, hypernatremia but no
acidosis and no ketosis. This indicates NO evidence of:
 A. Gluconeogenesis
 B. Glycogenolysis
 C. Osmotic diuresis
 D. Lipolysis

Answer 7

D: liposis does not occur in HHS
hallmark symptom in HHS is hypernatremia and dehydration. The hallmark symptom of DKA is acidosis

Question 8

pathogenesis of DKA

Answer 8

1. insulin deficiency
   - results in hyperglycemia, then osmotic diuresis (peeing out excess glucose), which leads to dehydration since it’ll pull water out with it. You will get electrolyte depletion
2. glycogenolysis occurs because cells think there isn’t enough glucose. you will also get lipolysis, release of FFA–> makes KETONE BODIES

Question 9

pathogenesis of HHS

Answer 9

• lack of ketosis; insulin levels high enough to prevent lipolysis and ketogenesis, but not high enough to prevent hyperglycemia.
• you do not have ketons, but you are extremely hyperglycemic. Co-existence of decreased renal function
• severe dehydration.

Question 10

4 hormones that inhibit insulin-mediated glucose uptake by muscles.

Answer 10

glucagon, cortisol, growth hormone, epinephrine.

• incresaed in times of stress
• activates glycogenolysis and gluconeogenesis
• activates lipolysis
• inhibits insulin secretion

Question 13

A 78 year old man living on his own is found in his bed
un-rousable. He has a history of type 2 diabetes and
renal failure. His BG is high on a meter check. He
appears severely dehydrated. Based on this history is he
more likely to have:

Answer 13

HHS. he has type 2 diabetes. he is extremely dehydrated, probably because of extreme hyperglycemia. You are more likely to have neurological presentations in HHS

Question 14

Which emergency is more likely to have Kussmaul respiration? Acetone breath? Neurological presentation? Decreased LOC? Loss of EABV/EABV contraction? Nausea?

Answer 14

Kussmaul: DKA
ACetone: DKA– there are ketones

Neurological Presentation: HHS

Decreased LOC: HHS

EABV contraction: HHS

Nausea: DKA

Question 15

Answer 15

Question 16

causes of DKA

Question 17

causes of HHS

Answer 17

Question 18

special risk factors in children

Answer 18

Question 19

6 ways to suspect DKA

Answer 19

1. positive serum ketones or urine ketones
2. ph7.3– acidosis
3. anion gap >12mmol/L
4. plasma glucose is high (>14 usually)
5. bicarbonate is low <15 mmol
6. precipitating factors (ie/ ran out of insulin, on SGLT2inhibitors or prednisone, MI)

Question 20

Question 21

Question 22

Individuals treated with __ inhibitors with symptoms
of DKA should be assessed for this condition even if
blood glucose not elevated– why?

Answer 22

Individuals treated with SGLT2 inhibitors with symptoms
of DKA should be assessed for this condition even if
blood glucose not elevated– because SGLT2 inhibitors may lower threshold for developing
DKA

Question 23

Answer 23

Question 24

investigations when someone has DKA

Answer 24

Electrolytes, anion gap, osmolality, glucose, gas

Question 25

general treatment of both DKA and HHAs

Answer 25

not insulin immediately

Question 26

Principles of Treatment for Adult DKA

Answer 26

gotta avoid hypokalemia because you have no supply of it to begin with– you have an artificlaly high amount.

• when you have DKA, you have osmotic diuresis. You pee out glucose, but you also pee out Na+ and K+. your body senses the fall in K+, and your cells secrete K+ out, leaving less in your cells. ON lab values, your K+ might be normal, but your cells are truly hypokalemic. If you were to give fluid, say, saline with no added KCl, you will address their low water status but you will dilute whatever potassium they have left even more. When you add insulin, even mre osmlality will drop– gotta watch out.

Question 27

principles of treatment for adult HHS

Answer 27

Question 28

note: principles of treatment for pediatric DKA

Question 29

memorize this treatment protocol

Answer 29

correct K+ deficiency before giving insulin

Question 30

DKA: Fluids, Potassium, Acidosis are the cornerstone treatment.

• replace fluids with IV ___ saline until euvolemic (since they originally will be dehydrated/low EABV)
• once euvolemic, consider plasma __ and glucose to determine the IV fluid type. If Na is normal or high, can give __ saline. If Na+ is low, then give __ saline.
• once plasma glucose reaches ___, add __ to IV fluids to maintain plasma glucose at a __ to __ mmol range.

Answer 30

• replace fluids with IV .9 saline until euvolemic (since they originally will be dehydrated/low EABV)
• once euvolemic, consider plasma Na and glucose to determine the IV fluid type. If Na is normal or high, can give .45 saline. If Na+ is low, then give .9 saline.
• once plasma glucose reaches 14, add d5 w to IV fluids to maintain plasma glucose at a 12 to 14 mmol range

Question 31

Replace Potassium: Hypokalemia is an avoidable cause of death in DKA.

is K+ is below ___< give ___ mmol of KCl and NO INSULIN.

if K+ is above that limit, give less KCl

Answer 31

is K+ is below 3.3< give 40 mmol of KCl and NO INSULIN.

if K+ is above that limit, give less KCl

Question 32

DKA: Management of Acidosis with Insulin

• Fixed dose IV insulin at___U/kg/hour
• Insulin is used to suppress ketogenesis and treat the acidosis, not just the glucose!
• Insulin should be maintained until the anion gap normalizes

Answer 32

Fixed dose IV insulin at 0.1 U/kg/hour

• Insulin is used to suppress ketogenesis and treat the acidosis, not just the glucose!
• Insulin should be maintained until the anion gap normalizes

Question 33

T/F you should start someone in DKA with bicarbonate infusion because usually bicarb is really low.

Answer 33

false.DKA requires intravenous insulin administration (0.1 units/kg/h) for
resolution; bicarbonate therapy may be considered only for extreme
acidosis (pH ≤7.0)

Question 34

You are examining a 10 year old girl who was admitted
for new onset type 1 diabetes mellitus with DKA last
night. On exam, she has a new onset right side
hemiparesis. What do you think has happened?
 A. She has developed hypocalcemia
 B. She has developed a thrombotic stroke
 C. She has developed hypophosphatemia

Answer 34

could be cerebral edema since this could be due to a cranial nerve palsie!!

Question 36

0.5 to 1.0% of pediatric cases are complicated by cerebral
edema (CE) which is associated with significant morbidity (21-
35%) and mortality (21-24%)

Management?

Answer 36

Do NOT administer hypotonic fluid rapidly
 Do NOT give IV insulin bolus
 Start IV insulin infusion 1 hour AFTER fluid resuscitation has
begun

Question 37

main ways to prevent DKA and HHS episodes

Answer 37

education!!