DKA Vignette

Question 1

What does DKA stand for?

Answer 1

1. diabetes: hyperglycemia
2. ketones: in blood and urine (ketonemia/ketonuria)
3. acidosis: drop of pH in blood <7.3

Question 2

Symptoms/clinical presentations of DKA

Answer 2

the ‘polys’ and weight loss

• polyuria
• polydipsia
• rapid breathing
• dehydration
• stomach pains (but not diarrhea)

Question 3

4 metabolic disturbances in DKA

Answer 3

1. hyperglycemia (high blood sugar bc no insulin)
2. acidosis
3. potassium derrangements
4. dehydration

Question 4

What cells secrete insulin?

Answer 4

beta cells of pancreas (senses glucose levels)

Question 5

describe the process of insulin release by beta cells

Answer 5

1. glucose enters cell via GLUT2 transporter and undergoes glycolysis (increase in intercellular ATP/ADP)
2. causes closure of ATP-sensitive potassium channel, preventing outward leak of K+
3. build up of intracelluar potassium –> depolarizes the membrane –> activates VG Calcium channels –> Calcium influx
4. increase in [Ca2+] leads to exocytosis of preformed insulin containing secretory granules

-once released from beta cell, insulin has half life of ~5 min

Question 6

Insulin action

Answer 6

“locks up” / store E

stimulates uptake of glucose and triglycerides, while promoting synthesis of fats, proteins, glycogens.

Question 7

Where is glucose stored?

Answer 7

1. liver
2. muscle
3. adipose tissue

Question 8

Insulin action on glucose in…

1. Liver
2. muscle
3. adipose

Answer 8

1. liver: 
    \+ glucose uptake/synthesis
    \+ lipogenesis
    - gluconeogenesis
    - ketogenesis

2. muscle:
   + glucose uptake
   + glycogenssynthesis
   + Protein synthesis
3. adipose:
   + glucose uptake
   + triglyceride uptake
   + lipid synthesis

Question 9

how does the body compensate for acidosis?

Answer 9

increasing respiratory volume to rid CO2.

Question 10

deep/rapid respiration in DKA is known as what?

Answer 10

Kussmaul respiration 
(K for ketoacidosis)

Question 11

why do DKA pts get dehydrated?

Answer 11

body tries to hold onto resources

1. glucose reabsorption normally occurs in proximal kidney tubules
2. high glucose [ ] –> carrier proteins cant handle it = glucose runs into urine
3. water gets pulled with it (high osmol)

Question 12

describe two causes of K+ derangements in DKA

Answer 12

K loss due to dehydration

1. as pts fight dehydration, body compensates by holding onto sodium
2. stimulates an antiport mechanism where sodium is retained at expense of K+ loss in urine

K is also lost due to acidosis
1. acidosis leads to influx of H+ into cells
2. results in charge neutral efflux of K+ out of cell and into urine.
(resulting in excess extracellular K - hyperkalemia despite loss in K levels intra)

Question 13

What is the leading cause of death in Pts with DKA?

Answer 13

cerebral edema (very rare, but very fatal) ~25% die

Question 14

What are the later signs of cerebral edema?!

Answer 14

hypertension
bradycardia
fixed, dilated pupils

Question 15

cerebral edema therapy

Answer 15

mannitol: dumps osmols in blood, and water flows out of brain into blood.