Diabetic Ketoacidosis Flashcards
Name at least 5 important signs and symptoms of diabetes
Rapid deep breathing (elevated heart rate) Fruity odor to breath diffuse TTP on abdomen Cool hands and fee, cap refill of +4sec Polyuria/ noctiuria \+N/V elevated BS Glucose in urine unintentional weight loss
What pancreas cells release insulin
Beta cells
Type 1 DM is autoimmune process that destroys these cells
51 amino acid protein
4-6 minute half life
Describe the path/ effect of glucose on cells
Glucose enters @ GLUT2 transporter -> glycolysis -> increase [ATP] v [ADP] -> ATP sensitive K+ channel closes -> intracellular increase in K+ -> membrane depolarization -> voltage gated Ca channel activated -> Ca influx -> exocytosis of insulin containing secretory granules
Describe the basic function of insulin
“locks up” energy
- Glucose and triglyceride uptake
- Synthsis of fats, proteins and glycogen (inhibiting their breakdown)
Name 3 tissues where insulin acts
Liver
muscle
adipose
What is insulin’ action on the liver
\+ glucose uptake \+ glycogen synthesis - ketigenesis - gluconeogenesis \+lipogenesis
What is insulin’s action on muscle?
+ glucose uptake
+ glycogen synthesis
+ protein synthesis
What is insulin’s action on adipose?
+ glucose uptake
+ triglyceride uptake
+ lipid synthesis
What is the cause of and treatment for elevated blood sugar in diabetic ketoacidosis?
cause: insulin usually signals uptake of sugar, w/ destruction of B cells, no longer happens -> extracellular glucose builds up
Tx:
1) IV insulin (decrease BS, halting ketoacid production)
- Because it takes longer to resolve ketoacidosis:
2) IV dextrose hrs before stopping insulin
2 cardinal signs in DKA management: prematurely stopping insulin
or failing to use enough dextrose
What causes acidosis in DKA patients? What is its effect?
Cause: result of beta oxidation of fatty acids -> produces H+ ions and ketone bodies
Result/ compensation: Increase in respiratory volume (hasten elimination of CO2)
What is the equilibrium equation for carbon dioxide and bicarbonate?
H+ + HCO3- H2CO3 H2O + CO2
What causes the dehydration seen in DKA patients?
osmotic diuresis 2/2 hyperglycemia:
- usually blood filtered in kidney and glucose reabsorbed
_ in DKA glucose is too high to be reabsorbed -> glucose lost in urine - Elevated concentration of urine -> increased osmolarity-> decrease in water reabsorption
Ultimately leads to nausea and vomiting
as blood concentration of glucose increases, sipral worsens
=> best Tx = iv fluids
Explain the potassium derangement seen in DKA patients
patients fight dehydration by holding Na more tightly -> in kidney Na retained at expense of K
K lost in urine
tricky because this can cause overall hyperkalemia (outside cells) despite shortage
Explain cerebral edema in DKA
incompletely understood
Due to acidosis -> disregulated cerebral blood flow (disruption of BBB?)
= Iatrogenic: must rehydrate slowly => Cerebral edema
What are they symptoms of cerebral edema?
mental status change
cushing’s triad (HTN, Bradycardia, irregular respirations)
Fixed, dilated pupils