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Endocrine II - Exam 2 > Pharm of type 1 and 2 DM - SRS > Flashcards

Pharm of type 1 and 2 DM - SRS Flashcards

1
Q

What are the rapid acting insulin agents we must know?

3 bold

A
  1. Lispro
  2. Aspart
  3. Glulisine
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2
Q

What are the short acting drugs we must know?

A

Regular insulin

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3
Q

What are the intermediate insulins we must know?

2 bold

A
  1. NPH
  2. NPL
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4
Q

What are the ultra-long acting insulins?

2 bold

A
  1. Glargine insulin
  2. Insulin Detemir
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5
Q

What are the fixed - mix insulins?

A
  1. NPH / Regular (50%/50%)
  2. NPH / Regular (70%/30%)
  3. NPL / Lispro (75%/25%)
  4. NPL/ Lispro (50%/50%)
  5. Aspart protamine/aspart (70%/30%)
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6
Q

What are the categories of hypoglycemic agents we need to know?

9 - all bold, sorry

A
  1. Biguanides
  2. Sufonylureas
  3. Meglitinides
  4. alpha-Glucosidase Inhibitors
  5. TZDs
  6. Glucagon-like Peptide-1 (GLP-1) Agonists
  7. Dipeptidyl-Peptidase-4 (DPP-4) Inhibitors
  8. Amylin analog
  9. Sodium-Glucose Co-transporter 2 (SGLT2) Inhibitors
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7
Q

What is the biguanide we must know?

A

metformin

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8
Q

What are three sufonylureas we must know?

A
  1. Glipizide
  2. Glyburide
  3. Glimepiride
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9
Q

What are two meglitinides we must know?

A
  1. Repaglinide
  2. Nateglinide
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10
Q

What are two alpha-clucosidase inhibitors?

A
  1. Acarbose
  2. Miglitol
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11
Q

What are two (one bold) TZDs we need to know?

A
  1. Rosiglitazone
  2. Pioglitazone
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12
Q

What is an example of a Glucagon-like Peptide-1 (GLP-1) Agonist?

A

Exenatide

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13
Q

What is the by far most important hypoglycemic drug?

A

Metformin

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14
Q

What is the shared suffix of the DPP-4 inhibitors?

A

Gliptins

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15
Q

What is an example of an amylin analogue?

A

Pramlintide

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16
Q

What is an example of a Sodium-Glucose Co-transporter 2 (SGLT2) Inhibitor?

A

Flozins

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17
Q

beta cells of pancreatic islet synthesize insulin from preproinsulin to proinsulin to insulin. What are the chains and peptides?

A

A and B chains

C peptide

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18
Q

What forms will insulin be found in?

What coordinates the more complex forms?

A

Monomers, dimers, hexamers

Zinc 2+

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19
Q

The secretion of insulin is tightly regulated by the interplay of what 4 things?

(techically a lot more than four but there are some serious generalizations here)

A
  1. nutrients, especially glucose
  2. GI hormones
  3. pancreatic hormones
  4. autonomic neurotransmission
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20
Q

What is the principle stimulus for insulin secretion?

A

Glucose

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21
Q

What is the glucose transporter found in the Beta islet cell?

A

Glut2

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22
Q

How many phases of insulin secretion does a normal person have in response to a meal?

What are they?

A

2 phases

  • Phase I - rapid rise and fall
  • Phase II - slower, more gradual increase
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23
Q

How many phases of insulin secretion does a type I diabetic have post prandial?

A

None, no insulin secretion

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24
Q

initially, Type 2 DM patient may have elevated plasma insulin levels and tissue insulin resistance, but often one phase of insulin release is dysregulated, which one?

What happens years later?

A

First phase

Years later, beta cells fail and insulin levels are constitutively low

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25
Q

Identify the patient type shown based on the graph of post prandial insulin secretion.

A
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26
Q

Insulin circulates as what?

A

A free monomer

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27
Q

Where is insulin degraded?

A

Liver and Kidney

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28
Q

What is the half life of insulin?

A

5 - 15 minutes

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29
Q

All cells have insulin receptors, when bound what do they do in the fist step of the signaling cascade?

A

Insulin receptor is a tyrosine kinase that stimulates phosphorylation or dephosphorylation of cell-specific intracellular signal transduction proteins.

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30
Q

Glucose is transported into cells by facilitated diffusion by means of Glucose Transporters (GLUT). What are the types and where are they found?

A

GLUT-1: all cells

GLUT-2: pancreas, liver

GLUT-3: Brain

GLUT-4: muscle and fat cells

31
Q

What are two things that insulin stimulates regarding glucose?

A

Insulin stimulates glucose uptake

Insulin stimulates glucose storage and utilization

32
Q

What are two things glucose inhibits regarding glucose?

A

Insulin inhibits glycogen breakdown (glycogenolysis)

Insulin inhibits glucose synthesis (gluconeogenesis)

33
Q

What are the actions of insulin on liver cells?

A

Decreased…

  • gluconeogenesis
  • glycogenolysis
  • lipolysis
  • protein breakdown

Increased

  • Glycolysis
  • glycogenesis
  • lipogenesis
34
Q

What are the actions of insulin on fat cells?

A

Decrease

  • lipolysis

Increase

  • synthesis of triglycerides
  • glucose uptake
  • glycerol synthesis
  • fatty acid synthesis
35
Q

What are the actions of insulin on muscle tissue?

A

Increase

  • glucose uptake
  • glycolysis
  • glycogenesis
  • AA uptake
  • protein synthesis

No decreases

36
Q

Compare and contrast the following for DM I vs II.

  • Age of onset
  • Nutritional status at onset
  • prevalence
  • genetic predisposition
  • defect or deficiency
A
37
Q

What did the ACCORD trial of over 10K patients with DM II and either with or at risk for cardiovascular disease find?

A

Treating patients intensively to an A1C target of <6.0% did not significantly reduce the incidence of major CV events and was associated with increased all-cause mortality compared to patients treated to a target A1C of 7.0-7.9%

38
Q

The Diabetes Control and Complications Trial (DCCT) yielded what conclusion regarding the treatment of DM?

A

Intensive therapy to attain euglycemia dramatically reduces the incidence of and severity of long-term complications.

39
Q

So, nIntensive therapy to attain euglycemia dramatically reduces the incidence of and severity of long-term complications. Thats great!

  • What is the major problem with this?
  • What else makes this a difficult task to accomplish?
A
  • Hypoglycemia - The more intense the attempt to maintain “normal” glucose levels, the greater the risk of hypoglycemia
  • Maintenance of Intensive Insulin Therapy requires educated, motivated patient
40
Q

Hemoglobin A1c is glycosylated hemoglobin and is a convenient index of long-term exposure to elevated glucose. The T1/2 is 120 days. This is used to monitor therapeutic goals. What is the recommendation for the HbA1c level?

A

Recommendation: Hemoglobin A1c < 6.5% - 7.0%

41
Q

Identify the insulins shown on the graph, based on their time course.

A
42
Q

Describe the typical thirds approach to the insulin regimen based on a 30 unit per day amount.

A

2/3 total dose before breakfast

  • 2/3 NPH (14U)
  • 1/3 Regular (6U)

1/3 total dose in the evening

  • 1/3 Regular before dinner (3U)
  • 2/3 NPH at bedtime (7U)
43
Q

Hypoglycemia is an important and dangerous ADR to insulin therapy. What are four causes of this?

A
  • inappropriate dose
  • mismatch of time of injection versus food intake
  • exercise-induced glucose demand
  • increase need for insulin
44
Q

List as many ssx as you can for hypoglycemia.

A
  1. sweating
  2. hunger
  3. paresthesias
  4. palpitations
  5. tremor
  6. anxiety
  7. confusion
  8. weakness
  9. drowsiness
  10. blurred vision
  11. loss of consciousness
45
Q

What are two treatment options we can use to combat Insulin derived hypoglycemia?

A
  1. Glucose
  2. Glucagon
46
Q

As we have discussed, DM II has features of diminished insulin secretion, tissue resistance to insulin and obesity.

What are two other characteristics of DM II that are “enhanced”?

A
  1. Enhanced glucagon
  2. Enhanced gluconeogenesis
47
Q

Metformin has antihyperglycemic actions, what specific processes are influenced by this drug?

Are they increased or decreased? 6, 3 each with 2 bolds

A

Increased

  • Insulin action
  • glycolysis
  • uptake and utilization by muscle

Decreased

  • Gluconeogenesis
  • hepatic glucose output
  • intestinal absorption of glucose
48
Q

Metformin may be given in monotherapy or added to any of what five other drug types?

A
  • GLP-1 agonist
  • DPP-4 inhibitor
  • glinide
  • sulfonylurea
  • TZD
49
Q

What are three advantages of Metformin therapy?

!! Test Question for sure !!

A
  1. No weight gain
  2. No hypoglycemia
  3. Favorable lipid profile
50
Q

Diet can make a huge impact on type II DM, what percentage of patients is this approach going to fail in?

A

99%, most people cannot make the change

51
Q

Metformin has advantages over CUs and Insulin in some obese, insulin resistant patients. Lactic acidosis is a rare complication of therapy, especially in patients with? 3

A
  1. Renal insufficiency
  2. Hepatic insufficiency
  3. Cardiovascular disease
52
Q

What are some common side effects of metformin?

A

GI mostly

  1. Anorexia
  2. nausea
  3. abdominal discomfort
  4. diarrhea
53
Q

The first generation sulfonylureas are no longer used. What are the second and third generation SUs?

A

Second Generation

  • Glipizide
  • Glyburide

“Third” Generation

  • Glimeperide
54
Q

Describe the MOA for the SUs.

A
  1. Block ATP-sensitive K+ channel
  2. Leads to depolarization and influx of Ca++
  3. Results in insulin secretion
55
Q

What are the ADRs of the SU drugs?

A
  1. Weight gain
  2. Hypoglycemia
56
Q

SUs are only useful in what patients?

A

Type II diabetics that still have functional Beta cells.

57
Q

Chorpropamide is a first generation SU that has a very long T1/2, weakly active metabolites, and is the longest acting SU.

Why don’t we use these now?

A

Highest frequency of side effects.

58
Q

Which of the SU drugs appears to produce less weight gain in patients than the others?

A

Glimepiride

59
Q

What are the contraindications for glimepiride? 7

A
  1. Sulfa allergy
  2. pregnancy
  3. type 1 DM
  4. Ketoacidosis
  5. renal failure
  6. hepatic failure
  7. major surgery
60
Q

Which of the SUs has greater incidence of severe prolonged hypoglycemia?

A

Glyburide

61
Q

What is the MOA for the meglitinides?

A
  1. Non-sulfonylurea insulin releasing agents
  2. Blocks ATP-sensitive K+ channel
  3. Binds at different site than sulfonylureas
62
Q

What is the MOA of alpha-glucosidase inhibitors?

A

Inhibit digestion of complex sugars, with decreased sugar uptake after a meal.

63
Q

What are the problems we run into with alpha-glucosidase inhibitors?

A

Extreme flatulence and GI upset (poor compliance)

Hypoglycemia when combined with insulin or SUs

64
Q

GLP-1 agonists cause glucose dependent enhancement of insulin secretion, inhibits glucagon secretion, suppresses appetite and induces satiety, reduces gastric emptying and stimulates islet cell growth/differentiation/regen.

What are the benefits of this class?

A
  1. Decreased HbA1c
  2. Decreased post prandial glucose
  3. weight loss
  4. Little hypoglycemia
65
Q

ADRs for GLP-1 agonist?

A

GI upset

Pancreatitis

66
Q

GLP-1 agonists can be used as monotherapy or in combination with:

Metformin (in dual therapy)

Metformin + TZD (triple therapy)

Metformin + Sulfonylurea (triple therapy)

What is it specifically not approved for use with?

A

Insulin

67
Q

Dipeptidyl Peptidase-4 Inhibitors (DPP-4 Inhibitors) can be used in monotherapy or combo with what other drugs?

A

Metformin

SUs

TZD

68
Q

What is the MOA of pioglitazone and rosiglitazone?

A

Insulin sensitization

69
Q

nPramlintide is a synthetic analog of amylin, a peptide co-secreted with insulin from pancreatic b-cells and is used in Type 1 or type 2 diabetics already using insulin, especially those with insulin resistance requiring large doses of insulin. How must this be administered?

What can it not be mixed intosolution with?

A

SQ injection before meals.

Do not mix with insulin.

70
Q

What is the MOA of Pioglitazone & Rosiglitazone?

A

Bind to nuclear transcription factors involved in insulin action, causing…

  • decreased insulin resistance
  • increased peripheral action of insulin
  • increased glucose uptake, ­GLUT-1 & GLUT-4
  • decreased hepatic glucose output
71
Q

Pioglitazone & Rosiglitazone take several weeks to develop clinical effect, and is useful d/t most DM II’s being insulin resistant. What are the long term risks of these drugs?

6

A
  1. Increased risk MI
  2. Weight gain
  3. Bladder cancer
  4. Fluid retention
  5. CHF
  6. Fractures
72
Q

What is the MOA forCanagliflozin, Dapagliflozin, Empagliflozin?

A

Inhibition of SGLT2

SGLT2 is a membrane protein expressed mainly in the kidney. It transports filtered glucose from the proximal renal tubule into tubular epithelial cells. By inhibiting SGLT2, canagliflozin decreases glucose reabsorption, increases urinary glucose excretion, and lowers blood glucose levels.

73
Q

The long term safety of SGLT2 inhibitors is still unknown. What ADR happens that we are aware of?

A

Genital mycotic infections can occur in both men and women; long-term safety still unknown.

74
Q
A

Endocrine II - Exam 2 (16 decks)

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