Diabetes Flashcards
Explain blood glucose homeostasis with insulin and glucagon
low glucose –> alpha cells of pancreas secrete glucagon –> increased gluconeogenesis, glycogenolysis, decreased glycogeneis, lipogenesis, proteogenesis –> increased glucose until homeostasis
High glucose –> beta cells of pancreas secrete insulin –> increased glucose uptake into cells, decreased glycogenolysis and gluconeogenesis –> decreased glucose until homeostasis
Difference between diagnosis of DM with adults vs. children
2 or more readings: fasting blood glucose > 7.0 mmol/L, or random blood glucose > 11.1 mmol/L, or oral glucose tolerance test > 11.1 mmol/L (2 hours post)
Children: if symptomatic or > 11 mmol/L
Gestational DM if > 10.3 mmol/L for OGTT
Explain HbA1C and weakness of it
% of Hgb in which glucose has been incorporated due to high blood glucose over the life of the RBC (120 days)
> 7% is positive diagnosis of DM
Weaknesses: gives average so does not indicate highs and lows
Also, because it is related to Hgb, conditions that affect RBC and Hgb will affect readings e.g. if anemic, then falsely low reading, even if blood glucose was high
3 contributing factors to long-term complications in DM
1) Abnormal glycoproteins in basement membrane, vessel walls, macrophages –> structural defects
2) Increased activation of sorbitol pathway:
Glucose –> sorbitol –> fructose (normal)
but when glucose is high, sorbitol conversion to fructose is inhibited, so there is high sorbitol, which is hyperosmolar, causing increased intracellular fluid, and decreased Na/K pump activity –> peripheral neuropathy
3) chronic tissue hypoxia due to high affinity of HgbA1c to O2 –> therefore, O2 not released to tissues
Describe the pathophysiology of DKA in Type 1 DM
NO insulin –> increase in blood glucose –> hyperosmolar diuresis –> dehydration and decreased blood volume –> hypotension –> shock/coma/death
also: no insulin –> proteolysis for gluconeogenesis (GNG) –> increased glucose and urea –> hyperglycemia and negative nitrogen balance –> death
also: no insulin –> lipolysis for GNG –> ketogenesis –> ketonuria causes loss of K+, Na+, phosphates –> electrolyte imbalance –> shock, coma, death
ketones also in blood –> lowers pH (acidic) –> ketoacidosis –> Kussmaul’s respirations to compensate and shock, coma, death
Describe the pathogenesis of HHNS in Type 2 DM
Low insulin –> hyperglycemia –> osmotic diuresis –> dehydration and decreased blood volume –> decreased renal perfusion –> renal failure –> seizures, coma, death
osmotic diuresis and dehydration causes hemoconcentration which increases risk for thrombosis
decreased tissue perfusion causes increased anaerobic metabolism –> lactic acid (metabolic acidosis) –> CNS depression
osmotic diuresis causes hypokalemia and cardiac dysrhythmias, fluid/electrolyte imbalance which causes CNS changes
renal failure causes increased BUN and creatinine, which also contributes to metabolic acidosis
Proteolysis –> negative nitrogen balance
3 classic manifestations of DM
polyuria, polydipsia, polyphagia
more pronounced in type 1 than 2
polyuria due to glucosuria - high osmotic pressure
polydipsia due to diuresis
polyphagia due to protein breakdown –> hunger
Type 1 or 2 DM more likely to have weight loss? Weight gain?
Type 1: weight loss
Type 2: weight gain
Type 1 or 2 DM more likely to have ketonuria?
Type 1 only because enough insulin in type 2 to not break down fats for GNG
Type 1 or 2 DM more likely to have blurred vision?
Type 2 > Type 1 because of chronic exposure of lense and retina to hyperosmolar fluids - changes shape and qualities of lens
Type 1 or 2 DM more likely to have recurrent infection?
Type 2 > Type 1 because defect in inflammatory cells and impairment of WBC phagocytosis
Type 1 or 2 DM more likely to have weakness and fatigue?
Type 1 < Type 2
Due to potassium loss in urine and protein catabolism
Explain the difference between Somogyi effect and Dawn phenomenon
Both have hyperglycemia in am (waking)
Somogyi due to counterregulatory hormones producing glucose due to EXCESS insulin administered hs vs. Dawn phenomenon as a result of hs insulin wearing off too early (decreasing duration of medication)
Somogyi effect in Type 1 DM only
Dawn phenomenon works in both Type 1 and 2
Treatment for Somogyi is decrease in insulin dose; treat Dawn phenomenon with longer acting insulin
Emergency treatment for DKA or HHNS
1) IV fluids to treat dehydration (due to diuresis) until kidney perfusion at least 60 mL/hr
2) insulin bolus followed by insulin infusion with Dextrose (to prevent hypoglycemia)
3) treat electrolyte imbalances
4) when glucose stabilized, and able to tolerate PO, then go to sliding scale
What is the onset/peak/duration of rapid-acting insulins (Lispro, Aspart, Glulisine)?
O: 10-15 min
P: 60-90 min
D: 3-5 hr