Type 1 Diabetes Lecture Powerpoint

Question 1

Complications of diabetes (5)

Answer 1

• Cardiovascular disease (2-4x higher risk)
• Diabetic nephropathy
• Diabetic retinopathy (leading cause of blindness)
• Diabetic neuropathy
• Amputations (leading cause of non traumatic amputation)

Question 2

What is the leading cause of end stage renal disease?

Answer 2

Diabetic nephropathy

Question 3

DCCT study

Answer 3

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)

Question 4

UKPDS study

Answer 4

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

Question 5

Criteria for diagnosis of diabetes mellitus (4 options)

Answer 5

• 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

Question 6

Pre-diabetes hemoglbin A1C range

Answer 6

5.7-6.4%

Question 7

Blood glucose control guidelines by the ADA (preprandial blood glucose, post, and A1C)

Answer 7

• 90-130mg/dL
• <180 mg/dL
• <7%

Question 8

Characteristics of type 1 diabetes (6)

Answer 8

• Autoantibodies presence against B cells of pancreas
• Absolute insulin deficiency requiring supplementation
• Most common in youth
• acute onset
• Ketosis prone
• Genetic predisposition

Question 9

Physiological serum insulin secretion profile

Answer 9

• 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)

Question 10

Between meal and overnight (long acting) insulin options (peakless baseline, 1 shot a day) (5)

Answer 10

• 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

Question 11

NPH insulin analog function

Answer 11

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

Question 12

Quick acting insulin analogue (normal insulin) function

Answer 12

-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

Question 13

Immediate acting insulin analogues (3) and function

Answer 13

• 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)

Question 14

Typical starting dose for between meal and overnight insulin (long acting)

Answer 14

.3 u/kg

Question 15

Titration of long acting insulin delivery should be dosed to make adjustments based on what patient measurement?

Answer 15

Fasting blood glucose

Question 16

Need to lower basal analog dosage for long acting insulin if the patient has one of these 2 conditions

Answer 16

-liver cirrhosis
-kidney failure
(both of these are vital to gluconeogenesis and thus must be accounted for to not make hypoglycemic

Question 17

Continuous glucose monitoring systems

Answer 17

-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

Question 18

Advantages of continuous subcutaneous insulin infusion (4) and disadvantages (2)

Answer 18

• 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

Question 19

Should a continuous subQ insulin infusion fail, patient needs to have what waiting at home?

Answer 19

-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)

Question 20

Sliding scale insulin regimens

Answer 20

-Chart that allows for blood glucose level to directly determine amount of insulin to be delivered to patient

Question 21

Shortcomings of sliding scale insulin regimens

Answer 21

• Reacting to a number opposed to a meal (places at risks for large fluctuations of blood glucose levels)
• does not provide basal insulin coverage

Question 22

Adjusting bolus and correction doses

(insulin to carbohydrate ratio ICR) 3 questions

Answer 22

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?

Question 23

Hospitalization related causes of hyperglycemia

Answer 23

-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

Question 24

NICE SUGAR study

Answer 24

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)

Question 25

Glycemic control in a hospital patient target range

Answer 25

144-180mg/dL

Question 26

Switching from IV to subQ insulin

Answer 26

• 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

Question 27

Glucocorticoid therapy and blood sugar

Answer 27

-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

Question 28

Glucocorticoid therapy blood sugar management option of choice

Answer 28

NPH

Question 29

Presentation of diabetic ketoacidosis (3)

Answer 29

• Nausea, vomiting
• Altered mental status
• kussmaul respiration

Question 30

Diabetic ketoacidosis lab values (glucose, pH, serum bicarb)

Answer 30

• > 250 mg/dL
• pH <7.3
• <15meq/L

Question 31

Diabetic ketoacidosis treatment options (4)

Answer 31

• restoration of volume
• correct acidosis (slower to correct than hyperglycemia)
• replenish K+
• correction of hyperglycemia

Question 32

Diabetic ketoacidosis treatment steps

Answer 32

• 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)

Question 33

Hyperglycemic hyperosmolar nonketotic syndrome differences from diabetic ketoacidosis (3)

Answer 33

• insulin at lower doses as to not correct the acidosis
• administration of fluids (normal or hypotonic fluids)
• replenish K+ if necessary

Question 34

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.

Answer 34

hyperglycemia, insulin, insulin