Diabetic Ketoacidosis (DKA) Flashcards Preview

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Flashcards in Diabetic Ketoacidosis (DKA) Deck (21)
1

Describe the major metabolic disturbances in DKA (4):

1. Elevated blood sugar (hyperglycemia >200 mg/dL)
2. Acidosis (high H+, low HCO3-)
3. Potassium derangements (may be high or low)
4. Dehydration

2

What is Cushing's Triad?

Classic signs of increasing intercranial pressure.

1. Hypertension (progressively increasing systolic blood pressure)
2. Bradycardia
3. Irregular respirations (internet says "widening pulse pressure" - difference btwn sys/dia bp increases over time. perhaps these two are related)

3

What are the late signs of cerebral edema?

1. Cushing's triad (particularly hypertension and bradycardia)
2. Fixed, dilated pupils (compression on occulomotor)
3. Mental status changes
4. Headache

4

What is the frequency of cerebral edema in patients treated for DKA?

Cerebral edema, occurring in about 0.15-0.3% of all cases of pediatric DKA, is the leading cause of morbidity and mortality, with a death rate ~24%. A further 20% of patients with cerebral edema suffer long term neurologic outcomes.

5

Be able to identify straightforward DKA (7)

1. Ill appearance (afebrile)
2. tachypneia (rapid breathing)
3. nausea/vomiting/belly pain
4. dehydration
5. Hyperglycemia
6. Ketones in blood/urine
7. acidosis (low pH and HCO3-)

6

Describe the stimulus for insulin release:

Glucose enters the beta cells in the pancreas --> increased ATP/ADP ratio --> closes a channel to cause rising intracellular potassium --> increasing intracellular potassium depolarizes the membrane --> Calcium ions influx --> leads to insulin exocytosis

7

Describe at least three target-site actions of insulin.

1. Liver – store glucose (as glycogen) and lipid, stop lipid and glycogen breakdown
2. Muscle – store glucose, make protein
3. Adipose – store glucose and triglyceride (incorporated into chains of fats)

8

Describe the risk for cerebral edema in DKA.

Cerebral edema is the major cause of morbidity and mortality in DKA. May be present even before treatment starts, but some treatment factors can cause/exacerbate it:
Rapid drops in glucose and sodium from too much or too hypotonic IV fluid

9

What is the treatment for cerebral edema (3)?

1. Mannitol does not cross the blood/brain barrier and is not metabolized. Therefore, it serves to raise the effective osmolality of the blood and pull water back from the brain in order to decrease swelling.
2. elevating the head of the bed,
3. hyperventilating the patient (if intubated) [N.B. Rapid decrease in serum CO2 constricts cerebral arteries and therefore decreases cerebral blood flow]

10

DKA mnemonic?

D (diabetes, defined as abnormally high blood sugar),
K (ketones in the blood and urine)
A (acidosis)

11

In simplified terms, to what are the ketones and acidosis linked?

for now suffice it to say that the ketone production is the source of the acid. It causes a drop in pH and quenches the HCO3- buffer, leading to lower levels.

12

What is the half-life of insulin? What is the clinical significance of knowing this?

5 minutes. Can finely calibrate minute-by-minute insulin levels.

13

Insulin action can be summed up (and more easily remembered) by thinking of it as a signal to “lock up” energy. What is its action in the liver?

+ glucose uptake, glycogen synthesis
- gluconeogenesis
- ketogenesis
+ lipogenesis

14

Insulin action can be summed up (and more easily remembered) by thinking of it as a signal to “lock up” energy. What is its action in muscle?

+ glucose uptake, glycogen synthesis
+ protein synthesis

15

Insulin action can be summed up (and more easily remembered) by thinking of it as a signal to “lock up” energy. What is its action in adipose tissue?

+ glucose uptake
+ triglyceride uptake
+ lipid synthesis

16

What is the dual purpose of IV insulin?

1. Stop ketoacid production
2. increase glucose uptake allowing the patient to stop beta-oxidation of fatty acids (the process that causes metabolic acidosis. see #1)

17

Why give patients dextrose after starting insulin?

The insulin you are giving the patient is going to cause the serum glucose to decrease. Give glucose to prevent hypoglycemia as we continue to give insulin.

18

What are the two cardinal sins in treating DKA?

1. prematurely stopping the insulin infusion
2. failing to use enough dextrose to bring the blood glucose slowly into the target range

19

What name is given to the deep and rapid respirations associated with DKA? What is physiologic process does this breathing pattern attempt to correct?

Kussmal respirations. Kussmal for Ketoacidosis. Increased CO2 expiration helps absorb the excess H+ in the blood.

20

To what is the dehydration due?

The dehydration seen in DKA is largely the result of the osmotic diuresis secondary to hyperglycemia. As blood glucose rises, the collecting duct in the kidney cannot absorb all the glucose. The high osmolarity pulls water into the collecting duct where it is excreted.

Large volumes of water are lost in the urine, even in the setting of dehydration. Meanwhile, as the blood ketoacid concentration rises, the patient experiences nausea and vomiting, making it even more difficult for oral intake to keep up with urine volume loss, resulting in dehydration.

21

The process K+ regulation and the mechanisms by which potassium dysregulation occurs are very complicated. What is the important thing to remember?

A patient in DKA may present with hyperkalemia but will manifest greater potassium needs than most other patients you encounter. Therefore, as you treat this patient, you must continue to watch serum potassium levels and be prepared to make adjustments to the potassium content of IV fluids in order to prevent severe hyperkalemia and severe hypokalemia, both of which can lead to death.