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Endo > Diabetes Meds > Flashcards

Diabetes Meds Flashcards

1
Q

Differentiate when readings are high in postprandial vs. fasting hyperglycemia

A

Fasting hyperglycemics have high blood sugar upon waking

Postprandial hyperglycemia is when glucose spikes abnormally high after a meal, then takes longer to decline

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2
Q

What injection may be used as an adjunct to insulin in a type I diabetic?

A

Amylin anaolg = Symlin

-amylin - hormone that peaks (and is released from beta-cells) w/ insulin

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3
Q

Describe injections vs. pump for type I diabetics

A

Frequency of injection

Injections you have to give at least 4 separate shots a day of insulin: one at each meal and one basal dose in morning

While pump you change injection site about every 3 days- then it monitors blood glucose rather continuously and will count the units of insulin for you if you put in grams of carbs

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4
Q

At what percent of beta-cell mass to pts clinically present w/ type I diabetes?

A

When only 10% of beta-cell mass remains

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5
Q

What two antibodies are characteristic of type I diabetes

A

autoICA = auto islet cell antibody

autoGAD = glutamate dehydroxenase = target of autoantibodies in ppl that later develop DM1

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6
Q

What are the two forms of long-acting insulin?

A

Insulin determir = Levemir

Insulin glargine = Lantus

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7
Q

Insulin glargine

a) onset
b) peak
c) duration of action

A

Long acting insulin = Lantus

a) 1-2 hours
b) no pronounced peak
c) 24 hours

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8
Q

Insulin determir

a) onset
b) peak
c) duration of action

A

Long acting insulin = Levamir

a) 1-2 hours
b) relatively flat
c) up to 24 hours

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9
Q

Insulin lispro

a) onset
b) peak
c) duration of action

A

Short-acting insulin

a) 15 min
b) peaks in .5-1.5 hours
c) lasts for 3-5 hours

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10
Q

Insulin aspart

a) onset
b) peak
c) duration of action

A

Short-acting insulin

a) starts effect in 15 minutes
b) peaks in .5-1.5 hours
c) lasts 3-5 hours

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11
Q

Insulin glulisine

a) onset
b) peak
c) duration of action

A

Short-acting insulin

a) starts w/in 15 minutes
b) peaks in .5-1.5 hours
c) lasts 3-5 hours

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12
Q

Insulin glargine vs. insulin glulisine

A

Glargine = long acting = lantus

Glulisine = short acting

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13
Q

Describe the activity profile of long acting insulin

A

Pretty steady (doesn’t have a distinct peak) and lasts about 24 hours

-structure modified to delay the disintegration of the alpha and beta chains of insulin

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14
Q

Describe the activity profile of short acting insulin

A

Peaks quickly and lasts shorter than regular human insulin

-specific properties (modified structure) to have the alpha and beta chains disintegrate faster => even more rapid-acting than regular human insulin

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15
Q

Regular human insulin

a) onset
b) peak
c) duration of action

A

Considered short acting (btwn rapid and long-acting)

a) starts in 30-60 minutes
b) peaks in 2-4 hours
c) lasts for 5-8 hours

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16
Q

Human NPH insulin

a) onset
b) peak
c) duration of action

A

Intermediate-acting insulin: longer-lasting than regular human insulin, yet less preferred compared to long-acting insulin

a) starts in 1-3 hours
b) peaks in 6-12 hours
c) lasts 12-24 hours

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17
Q

What are pre-mixed insulin analogs?

Why are they not preferred to basal + bolus method?

A

Pre-mixed insulin analogs are a mix of intermediate and rapidly acting insulin

ex: novolog, humalog, novolin, humulin

  • have to take w/ meals b/c of the rapid insulin part
  • really used for pts who won’t comply w/ the 4+ injections per day, so give this w/ meals BID
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18
Q

Novolg

A

Pre-mixed insulin analog

-contains both intermediate and rapid acting insulin

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19
Q

Humalog

A

Pre-mixed insulin analog

-contains both intermediate and rapid acting insulin

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20
Q

Give two reasons why a person may need a higher starting dose of insulin

A

(1) obesity

(2) taking steroids

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21
Q

Who typically requires a higher starting dose of insulin: type I or type II diabetics?

A

Type II b/c they have insulin resistance => need a larger dose of insulin to have the achieve effect

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22
Q

Is the initial insulin requirement usually higher or lower than the pt’s ultimate needs?

A

Initial requirements often overestimate ultimate needs

-once pt breaks the ‘glucose toxicity’ w/ their initial insulin treatment they often settle at a lower insulin level

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23
Q

What is the TIDM average TDD?

A

TDD = total daily dose

TDD for a TIDM is typically .4 units/kg

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24
Q

What is the T2DM average TDD?

A

TDD = total daily dose

TDD for a T2DM is typically .4-1 units/kg

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25
Q

Percent of TDD of insulin that is given as a basal dose

A

TDD = total daily dose (includes both long and rapid acting insulin)

50% of the TDD is given as a basal dose (long acting insulin)

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26
Q

Distinguish basal insulin and bolus insulin by

a) activity profile
b) main function
c) percent of TDD

A

Basal insulin = long acting insulin (glargine, detemir)

a) level remains nearly constant for 24 hrs
b) fxns to control glucose production btwn meals and overnight
c) 50% given in each basal insulin dose

Bolus insulin = short acting insulin

a) immediate risk and sharp peak at one hour post-injection
b) fxn = prevent hyperglycemia after meals
c) 10-20% of TDD given at each meal

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27
Q

2 factors that determine dosage of prandial insulin

A

(i) carbohydrate ratio- takes into account how many grams of carbohydrates were consumed
- estimate how many units of insulin is needed for a certain # of CHO

(ii) correction factor- takes into account insulin resistance/sensitivity
- estimate how much 1 unit of insulin will lower the blood glucose level

28
Q

What is the average carbohydrate ratio?

A

1:15

ex] if you eat two slices of bread (15g CHO in one slice) => inject 2 units of insulin

29
Q

What is the average insulin correction factor?

A

1:50

ex] if wake up and blood sugar is 200 mg/dl, take 2 units of insulin to raise the blood sugar 100 unites

30
Q

Symlin

A

= Amylin

-adjunct antihyperglycemic therapy to mealtime insuln

31
Q

Mechanism of amylin activity

A
  • prolongs gastric emptying
  • reduces the post-prandial rise in plasma glucose
  • decreases caloric intake thru centrally-mediated appetite suppression

Main biggie = can help pts used weight
=> used sometimes in addition to insulin (it is another injection, can be put in the pump)

32
Q

First line treatment for T2DM

A

-start w/ lifestyle and dietary changes, then first line oral meds = Metformin

33
Q

Last resort treatment for T2DM

A

Since T2DM is a progressive disorder (w/ progressive beta-cell dysfunction => progressive worsening of glycemic control) T2DM may eventually need insulin once their beta-cells ‘burn out’

-pancreatic burn out = when the beta-cells in T2DM can no longer secrete higher doses of insulin to compensate for the insulin resistance

34
Q

What are the two main fxns of metformin?

A

(i) insulin sensitizer
- increases sensitivity of peripheral tissues to insulin => takes stress off the beta-cells to secrete extra insulin

(ii) decreases endogenous production of glucose by the liver
- inhibits hepatic gluconeogenesis

35
Q

Metformin

a) cost
b) Hgb A1C reduction
c) risk of weight loss/gain?
d) risk of hypoglycemia

A

Metformin = first line treatment for T2DM

a) very cheap
b) reduction in Hgb A1C by 1.5%
c) weight neutral, in some cases weight loss
d) low risk of hypoglycemia

36
Q

When is metformin contraindicated?

A

Metformin is cleared renally => contraindicated in pts w/ renal insufficiency

37
Q

In what stage of diabetes progression is lifestyle modifications really helpful?

A

Prevention
-a 5-10% weight loss can decrease risk of developing diabetes by 58% in pts w/ IGT

-also helps improve control in ppl w/ diabetes

38
Q

Mechanism of Sulfonylureas

A

Binds to sulgonyulrea receptor on beta-cells to stimulate insulin secretion

(inhibits ATP-activates K+ channel which depolarizes the cell => opens Ca2+ channels => Ca2+ rushes in and causes exocystosis of pre-made vesicles storing insulin)

39
Q

Which T2DM drug can improve microvascular outcomes?

A

Sulfonylureas

40
Q

Risks of sulfonyulreas

A
  • weight gain
  • hypoglycemia

Sulfonyulreas basically just telling the pancreas to pump out as much insulin as possible all the time => nonspecific and constantly anabolic signal => weight gain and hypoglycemia

41
Q

Difference btwn sulfonylureas and meglitinides

A

Same mechanism of action and risks. Meglitinides are shorter acting and cause a slightly smaller (.5%) reduction in A1C

42
Q

Change in A1C expected on sulfonylureas

A

1-2% reduction

43
Q

Thiazolidinediones (TZD) mechanism and fxn

A

Activates PPAR-gamma activity to increase peripheral insulin sensitivity

44
Q

Benefits of TZDs over sulfonylureas

A

TZDs do not cause hypoglycemia

45
Q

Why are TZDs not commonly used anymore?

A

Risk of heart problems/complications

-MI, heart failure, weight gain

46
Q

What is the difference in insulin stimulus by oral nutrition vs. isoglycemic IV challenge?

A

Something about intaking the glucose into the GI tract that contributes to regulate how much we eat = incretins!

47
Q

What are incretins?

A

Gut-derived hormones that stimulate insulin production by the pancreas

GLP-1 = glucagon-like-peptide 1
GIP = glucose-dependent-insulinotropic peptide
48
Q

Describe incretins effect on the pancreas

A

GLP-1, GIP causes the pancreas to produce and release more insulin

-increases beta-cell proliferation and survival

49
Q

GLP-1’s effect on the brain

A

increased nausea and satiety

decreased food intake => decreased body weight

50
Q

GLP-1’s effect on adipocytes

A

increased lipolysis

increased fatty acid synthesis

51
Q

GLP-1’s effect on the stomach

A

decreases gastric emptying => food stays in stomach longer => feel fuller longer

52
Q

Exenatide

A

= GLP-1 receptor agonists

53
Q

Benefit of GLP-1 receptor agonists over endogenous GLP-1

A

GLP-1 receptor agonists are not degraded by DPP-IV => can have longer lasting effect

54
Q

Which DM2 drugs can cause weight gain?

A
  • Sulfonylureas
  • Meglitinides
  • TZDs
55
Q

Which DM2 drugs can cause weight loss?

A
  • Metformin

- GLP-1 receptor agonists

56
Q

Which DM2 drug increases the pt’s risk of pancreatitis?

A

DPP IV inhibitors

57
Q

Mechanism of DPP IV inhibitors

A

DPP IV is an enzyme that naturally breaks down GLP-1 => if you inhibit DPP IV then more GLP-1 will be around and can exert its incretin effects longer

58
Q

What is SGLT2? Fxn?

A

SGLT2 = sodium glucose transporter 2

-reabsorbs 90% of glucose in the proximal tubule
=> in ppl w/o diabetes (or w/ plasma glucose

59
Q

Fxn of SGLT2 inhibitors

A

Inhibit glucose reabsorption in proximal tubule of kidney => glucose gets filtered out into urine

60
Q

Benefits of SGLT2 inhibitors

A
  • weight loss

- can lose a decent amount of blood sugar in urine

61
Q

Risks of SGLT2 inhibitors

A

Lots of sugar in the urine that can act as substrates for microbes and osmole to draw out water

  • genital candidiasis
  • urinary bacterial infections (UTIs)
  • dehyrdation
62
Q

In step-up therapy for T2DM describe the order of regimens

A

non-insulin regimen –>
basal insulin only –>
basal insulin + 1 rapid-acting insulin injection or pre-mixed insulin twice daily –>
basal insulin + 2 or more rapid-acting insulin injections

63
Q

Benefits of exercise- T1DM or T2DM?

a) mitochondrial abnormalities
b) muscle TG
c) HDL
d) insulin sensitivity

A

Exercise is beneficial in both T1 and T2 (duh, in everyone!)

a) reverses mitochondrial abnormalities in skeletal muscle
b) reduces muscle TG
c) increases HDL
d) improves insulin sensitivity even in the absence of weight loss

64
Q

What is the goal A1C?

A

In general

65
Q

When is blood sugar normally lowest?

A

Upon waking or after exercise

=> can’t just measure blood glucose in the morning and assume you’re ok b/c can be falsely low

66
Q

Two reasons A1C may not be at goal (is too high)?

A

(i) Has the pt been misdiagnosed w/ the wrong type of diabetes?
(ii) Is there a big difference btwn FBG and post-prandial BG?

67
Q

Two reasons Hgb A1C may be falsely low or at goal?

A

(i) Anemia
- if pt doesnt have a lot of Hgb available then not a lot will be glycosylated, a higher percent will be newer reticulocytes that haven’t been around long enough to get glycosylated

(ii) Occasional hypoglycemia states messing up the average?

Endo (4 decks)

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