DKA vignette

Question 1

Insulin is a

Answer 1

hormone that is central to regulating carbohydrate and fat metabolism in the body.

Question 2

Insulin function

Answer 2

1. Promotes glucose uptake in the muscle
2. Promote storage of carbohydrate as glycogen
3. Decrease formation of glucose in the liver (gluconeogenesis)
4. Promotes storage of fatty acids as triglycerides and decreases the formation of ketone bodies

Question 3

____ in the ____ release insulin in two phases.

Answer 3

Beta cells

slets of Langerhans

Question 4

The first phase insulin release is

Answer 4

rapidly triggered in response to increased blood glucose levels.

Question 5

The second phase is a

Answer 5

sustained, slow release of newly formed vesicles that are triggered independently of sugar.

Question 6

description of the first phase

Answer 6

Glucose enters the beta cells through the glucose transporter GLUT2
• Glucose goes into glycolysis and the respiratory cycle where multiple high-energy ATP
molecules are produced by oxidation
• Dependent on the ATP:ADP ratio, and hence blood glucose levels, the ATP-dependent
potassium channels (K+) close and the cell membrane depolarizes
• On depolarization, voltage controlled calcium channels (Ca2+) open and calcium flows into the
cells
• Significantly increased amounts of calcium in the cells causes release of previously synthesized
insulin, which had been stored in secretory vesicles.

Question 7

DKA results from a _____; in response the body _______

Answer 7

shortage of insulin

switches to burning fatty acids and producing acidic ketone bodies

Question 8

the cause most of the symptoms and complications

Answer 8

the body switching to burning fatty acids and producing acidic ketone bodies

Question 9

the body switching to producing ketone bodies causes

o This drives the reaction:

Answer 9

Ketones accumulate in the blood as an acid resulting in excess H+ (turn the blood acidic)

Excess CO2 is eliminated through the lungs: Kussmaul respirations (labored breathing pattern – form of hyperventilation)

Question 10

Ketones also participate in

Answer 10

osmotic diuresis and lead to further electrolyte losses

o Accompanying this is the release of various counterregulatory hormones such as glucagon and adrenaline, as well as cytokines

Question 11

o Cytokines lead to increased markers of

Answer 11

inflammation, even in the absence of infection

Question 12

Prior to treatment, the patient’s potassium levels change:

Answer 12

o The majority of the K+ is intracellular
o In acidosis, H+ extracellular is exchanged for K+ intracellular
o K+ is lost in the urine
o The net result is total body K+ depletion in the face of normal or high normal K+ level in the blood

Question 13

The most dangerous DKA complication is ____

Answer 13

cerebral edema;

Question 14

_____ is the main cause of death in children with DKA.

Answer 14

cerebral edema

Question 15

cerebral edema causes

Answer 15

Some maintain that it is the result from overvigorous fluid replacement, but the complication may develop before treatment has been commenced.

Question 16

Risk factors for cerebral edema:

Answer 16

Risk factors for cerebral edema: o Severe DKA
o High BUN
o More severe acidosis o Lower pCO2
o Higher [K+]
o Patients with their first episode of DKA 
o Young (less than 5 years of age)
o Longer duration of symptoms
o Dehydration
o Increased inflammation and coagulation

Question 17

Treatment complications:

that can increase cerebral edema risk

Answer 17

Treatment complications:
o Lesser rise in [Na+] during treatment
o Insulin within the first hour of fluid therapy
o Bicarbonate administration
o High volume of fluid administered over first 4 hrs o Early ↓ in effective plasma osmolality

Question 18

What causes death in cerebral edema?

Answer 18

The swelling of brain tissue leads to raised intracranial
pressure, ultimately leading to death.
1. permeability of capillaries in brain is hitherto water than glucose
2. free water travels down the osmotic gradient into the brain causing swelling in the closed box of the skull

Question 19

The first signs of cerebral edema are

Answer 19

often subtle changes in mental status. Patients may become newly combative, or complain of onset of a new headache.

Question 20

Cerebral edema can be avoided with

Answer 20

careful and slow decrease in blood glucose levels and slow fluid replacement.

Question 21

Insulin is a ______ released by the _____

Answer 21

51 amino acid protein released by the beta cells of the pancreas.

Question 22

glucose enters the cell through the

Answer 22

GLUT2 transporter

undergoes glycolysis, leading to an increase in the intracellular ATP to ADP ratio.

Question 23

The increase in intracellular ATP closes the ATP-sensitive potassium channel, preventing

Answer 23

outward leak of potassium ions.

Question 24

The resultant buildup of intracellular potassium, causes

Answer 24

depolarizes the membrane, activating a voltage-gated calcium channel and leading to calcium influx.

Question 25

The increased intracellular calcium ion concentration leads to

Answer 25

exocytosis of preformed insulin-containing secretory granules.

Question 26

Once released from the beta cell into the bloodstream, human insulin has a half-life of about_____

Answer 26

5 minutes, allowing for minute-by-minute fine control of blood sugar.

Question 27

Insulin actions: Liver

Answer 27

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

Question 28

insulin actions in muscles

Answer 28

+ glucose uptake, glyocgen sythesis

+ protein synthesis

Question 29

insulin actions in adipose

Answer 29

+ glucose uptake
+ triglyceride uptake
+ lipid synthesis

Question 30

The intravenous insulin serves two purposes:

Answer 30

decreasing the blood glucose concentration and halting ketoacid production.

Question 31

However, it invariably takes a longer time to resolve the _____than to ____

Answer 31

ketoacidosis

decrease the glucose to normal levels.

Therefore, you will paradoxically need to start an intravenous infusion of dextrose hours
before stopping the intravenous insulin.

Question 32

Two cardinal sins in DKA management are

Answer 32

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

Question 33

The acidosis seen in DKA is a result of

Answer 33

beta oxidation of fatty acids

Question 34

Cerebral edema, occurring in about _____ of all cases of pediatric DKA, is the leading cause of morbidity and mortality, with a death rate

Answer 34

0.15-0.3%

~24%.

Question 35

identify straightforward DKA

Answer 35

1. Ill appearance, rapid breathing, nausea/vomiting/belly pain, dehydration
2. Hyperglycemia, Ketones in blood/urine, acidosis (low pH and HCO3-)

Question 36

the major metabolic disturbances in DKA

Answer 36

o High blood sugar (>200 mg/dL)
o Acidosis (low pH and HCO3-)
o Potassium may be high or low (typically normal to elevated blood levels
early on, but with risk of falling potassium during treatment)
o Dehydration

Question 37

stimulus for insulin release:

Answer 37

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

Question 38

Describe at least three target-site actions of insulin.

Answer 38

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)

Question 39

treatment factors

can cause/exacerbate Cerebral edema

Answer 39

Rapid drops in glucose and sodium from too much or too hypotonic

IV fluid

Question 40

Cerebral edema Presents with

Answer 40

mental status changes, headache, Cushing’s triad,

fixed/dilated pupils.

Question 41

Cerebral edema treatment

Answer 41

raise the osmolality of the blood.