Ketoacidosis Flashcards
Rapid acting insulin
Lispro
Onset = 15-30 minutes
Peak = 30-90 minutes
Duration = 3-5 hrs
Long acting insulin
Glargine
Onset = 1-1.5 hrs
Duration = 24 hrs
NO PEAKS
Short acting
Regular
Onset = 30-60 min
Peak = 2-5 hrs
Duration = 5-8 hrs
Intermediate
NPH
Onset = 1-2 hrs
Peak = 4-12 hrs
Duration = 18-24 hrs
How does insulin effect menstrual cycle
Insulin stimulates gonadotropin hormone
- so, low insulin –> low gonadotropin hormone –> less FSH and LH –> dysregulation of menstrual period
Type 1 diabetes genetics
HLA-DR3 and DR4 –> 90% of Caucasians with diabetes have those haplotypes
Type IV hypersensitivity –> T cell destruction of pancreatic beta cells –> low insulin –> hyperglycemia
Mechanism of Insulin
Insulin binds to its receptor (tyrosine kinase) → tyrosine phosphorylation of receptor → glycogen, lipid, and protein synthesis as well as increased expression of GLUT-4 receptor for glucose uptake into cells (adipose tissue and skeletal muscle)
K+ Homeostasis
High K+ –> increased ROMK and BK channels in Principal Cells, increased Na/K ATPase activity in all cells
Low K+ –> decreased ROMK and BK channels in Principal Cells, increased K/H ATPase in alpha-intercalated cells
Causes of moving K into cells
Hyperinsulinemia
Increased catecholamines
Metabolic alkalosis
Causes of moving K out of cells
Insulin deficiency
Metabolic acidosis
Tm of glucose
Tm is the maximum amount of glucose the kidney can reabsorb. Once the kidney reaches its maximum, glucose can’t be reabsorbed any further because the channels are saturated –> glucosuria
Respiratory compensation of metabolic acidosis
Kussmaul respirations
rapid shallow breathing –> blow off CO2 –> shift equation toward CO2 and away from H+
Respiratory compensation of metabolic alkalosis
Hypoventilation
- decrease in breathing –> increase CO2 –> shift equation toward H+ and away from CO2
Most common precipitating factor of DKA
Not taking insulin
Stressors effects on precipitating DKA
Stressors cause release of Epi –> blocks insulin action and stimulates glucagon –> decrease utilization of glucose in periphery and increased gluconeogenesis –> severe hyperglycemia –> osmotic diuresis and dehydration