Type 1 Diabetes Lecture Powerpoint Flashcards
Complications of diabetes (5)
- Cardiovascular disease (2-4x higher risk)
- Diabetic nephropathy
- Diabetic retinopathy (leading cause of blindness)
- Diabetic neuropathy
- Amputations (leading cause of non traumatic amputation)
What is the leading cause of end stage renal disease?
Diabetic nephropathy
DCCT study
Done in the early 90’s for type 1 insulin dependent diabetic patients that demonstrated that by reducing A1C by 1% sees a drastic drop in risk of retinopathy, nephropathy, and neuropathy (microvascular diseases)
UKPDS study
Study for type 2 diabetic patients that demonstrated that by reducing A1C by 1% sees a drop in risk for both microvascular complications and macrovascular as well
Criteria for diagnosis of diabetes mellitus (4 options)
- Fasting blood glucose >126 mg/dL
- symptoms of diabetes and casual plasma glucose >200mg/dL
- 2 hour plasma glucose >200mg/dL during oral glucose tolerance test
- Hemoglobin A1C 6.5% or greater
Pre-diabetes hemoglbin A1C range
5.7-6.4%
Blood glucose control guidelines by the ADA (preprandial blood glucose, post, and A1C)
- 90-130mg/dL
- <180 mg/dL
- <7%
Characteristics of type 1 diabetes (6)
- Autoantibodies presence against B cells of pancreas
- Absolute insulin deficiency requiring supplementation
- Most common in youth
- acute onset
- Ketosis prone
- Genetic predisposition
Physiological serum insulin secretion profile
- Spikes after each meal before quickly lowering to low poinr (50% of insulin content)
- In the night time, see drop to low amount but never to zero because of glycogen breakdown and gluconeogenesis from the liver AND kidney** that occur during sleep causes need to keep some insulin up at all times (50% of insulin content)
Between meal and overnight (long acting) insulin options (peakless baseline, 1 shot a day) (5)
- levemir
- lantus
- tresiba
- toujeo
- basaglar
These are incredibly expensive, all made by bacteria and e coli from recombinant human insulin analog modified to be long acting
NPH insulin analog function
Given once every 12 hours (twice a day) to maintain closest to baseline, but does see a peak about 5-6 hours after administration, very cheap and affordable
Quick acting insulin analogue (normal insulin) function
-starts working in about half an hour (take about that amount of time before a meal), peaks within 2 hours, and then quickly drops off, concern if taken without a meal following shortly after
Immediate acting insulin analogues (3) and function
- aspart, glulisine, lispro
- Act almost immediately after taking, most closely mimics the body’s insulin, so fast acting can be given after 10-15 min post meal and dosed corresponding to what percent of meal they ate (good to prevent giving before and then they don’t eat and then we are screwed)
Typical starting dose for between meal and overnight insulin (long acting)
.3 u/kg
Titration of long acting insulin delivery should be dosed to make adjustments based on what patient measurement?
Fasting blood glucose
Need to lower basal analog dosage for long acting insulin if the patient has one of these 2 conditions
-liver cirrhosis
-kidney failure
(both of these are vital to gluconeogenesis and thus must be accounted for to not make hypoglycemic
Continuous glucose monitoring systems
-New devices that are semi-implanted in subQ tissue that can measure blood glucose every 5-10 minutes, useful for patients who are unaware of when they are hypoglycemic (asymptomatic) or in conjugation with an insulin pump
Advantages of continuous subcutaneous insulin infusion (4) and disadvantages (2)
- Programmable for meals and overnight
- greater flexibility of lifestyle
- fewer injections
- control as good as multiple daily injections if not better
- risk of ketosis from interruption
- complexity
Should a continuous subQ insulin infusion fail, patient needs to have what waiting at home?
-long acting insulin refrigerated (allows patient to get it in case of failure of pump, can then just inject pump manually to simulate for meals)
Sliding scale insulin regimens
-Chart that allows for blood glucose level to directly determine amount of insulin to be delivered to patient
Shortcomings of sliding scale insulin regimens
- Reacting to a number opposed to a meal (places at risks for large fluctuations of blood glucose levels)
- does not provide basal insulin coverage
Adjusting bolus and correction doses
(insulin to carbohydrate ratio ICR) 3 questions
1) how much carbohydrate am i going to eat?
2) what is my insulin dose for this amount of carbohydrate
3) should I lower the dose because I plan to be very active or have recently been active?
Hospitalization related causes of hyperglycemia
-Hospitalization and illness related stress can induce uncontrolled hyperglycemia (may relate to pharmacotherapuetic agents, parenteral nutrition, or glucocorticoid therapy) and letting this go unchecked is very bad for outcomes
NICE SUGAR study
6000 critically ill hyperglycemic (hospitalization induced) patients were randomized to tight sugar regulation and loose regulation that found more mortality in tightly controlled group (as they were leaning towards hypoglycemia which increases mortality)
Glycemic control in a hospital patient target range
144-180mg/dL
Switching from IV to subQ insulin
- Timing of administration of long acting subQ must occur before discontinuation of IV insulin which has a very short half life of <10 min (overlap principle)
- After a couple of hours (depending on if its a short acting or intermediate acting insulin) then stop drip to let subQ take over
- look at 24 hr IV requirements for total daily dose
- Because 50% of insulin is basal component and prandial component is 50% divided by 3 for each meal, we can calculate from there
- give 50% of 24 hr requirement subQ long acting
- then divide remaining 50% by meal and administer correspondingly after meal
Glucocorticoid therapy and blood sugar
-Increases insulin resistance and can exacerbate existing hyperglycemia, cause new onset hyperglycemia, and cause potential decrease or loss of insulin sensitivity, fasting plasma glucose is minimally affected but postprandial plasma glucose can increase rapidly
Glucocorticoid therapy blood sugar management option of choice
NPH
Presentation of diabetic ketoacidosis (3)
- Nausea, vomiting
- Altered mental status
- kussmaul respiration
Diabetic ketoacidosis lab values (glucose, pH, serum bicarb)
- > 250 mg/dL
- pH <7.3
- <15meq/L
Diabetic ketoacidosis treatment options (4)
- restoration of volume
- correct acidosis (slower to correct than hyperglycemia)
- replenish K+
- correction of hyperglycemia
Diabetic ketoacidosis treatment steps
- Replenish with normal saline with K+
- once glucose <250 via insulin drip with bolus and infusion
- add D5 (more sugar) until acidosis is clear (bicarb >20 for hours)
Hyperglycemic hyperosmolar nonketotic syndrome differences from diabetic ketoacidosis (3)
- insulin at lower doses as to not correct the acidosis
- administration of fluids (normal or hypotonic fluids)
- replenish K+ if necessary
For type I diabetics, TPN can cause ____ requiring increased ___ to compensate. For type 2 on TPN, might not normally be on ___ but might have to initiate.
hyperglycemia, insulin, insulin
