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Endrocrine Exam 2 > Pharmacology: Diabetews > Flashcards

Pharmacology: Diabetews Flashcards

1
Q

What are the 4 ADA diagnostic criteria for diabetes?

A
  1. FBS > 126 mg/dL on more than 1 occasion
  2. Random glucose over 200 mg/dL (with symptoms)
  3. Abnormal GTT
  4. A1C > 6.5%
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2
Q

What are 4 actions of insulin?

A
  1. Induces LPL on adipose tissue capillary
  2. Inhibits intracellular hormone sensitive lipase
  3. Stimulates glycogenisis, suppresses gluconeogenesis
  4. Stimulates protein synthesis
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3
Q

What hydrolyzes TG in blood so free FAs can enter adipose?

A

LPL

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4
Q

What hydrolyzes TG in adipose cell to break down fat and release FFAs into blood, stimulated by glucagon?

A

HSL

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5
Q

What kind of insulin is Lispro and Aspart?

A

Short-acting

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6
Q

When should short acting insulin be taken?

A

Very close to a meal… it has the most rapid onset of action

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7
Q

What type of insulin is NPH?

A

Intermediate acting

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8
Q

What is a long acting insulin?

A

Glargine

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9
Q

In conventional insulin therapy, when is insulin given?

A

Before breakfast and before the evening meal

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10
Q

What is in conventional insulin therapy?

A

Combination of short and intermediate acting insulins

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11
Q

What is honeymoon phase with conventional insulin therapy?

A

After 1-3 weeks of treatment, insulin requirements decrease…temporarily regain own insulin secretory capacity… this may last weeks to months

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12
Q

How is intensive insulin therapy given?

A

Long acting in AM and then 3 doses of regular or lispro insulin at the 3 main meals

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13
Q

What are the 4 actions of drugs for Type 2 DM?

A
  1. Decrease glucose production
  2. Increase insulin secretion
  3. Increase insulin sensitivity
  4. Decrease glucose absorption
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14
Q

What are the 2 actions of metformin?

A
  1. Decreases hepatic glucose production (gluconeogenesis)

2. Increases insulin sensitivity- Increases peripheral glucose uptake and utilization

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15
Q

What type of drug is metformin?

A

Biguanide

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16
Q

What are 2 advantages of metformin over other type 2 DM drugs?

A
  1. Doesn’t produce hyperinsulinemia

2. Doesn’t produce hypoglycemia

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17
Q

Glucose is taken up into the cell by what transporter?

A

GLUT 2

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18
Q

What traps glucose in the cell?

A

Glucokinase

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19
Q

What is glucose metabolized to once in the cell?

A

ATP

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20
Q

When ATP is produced, it closes what channels leading to depolarizaton?

A

K

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21
Q

What does depolarization do?

A

Opens the voltage gated Ca channels

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22
Q

What does Ca do?

A

Stimulates the fusion of the synaptic vesicle with the cell membrane and releases insulin

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23
Q

What do sulfonylureas do?

A

Block the K channel…this makes the cell look like there is an influx of glucose (depolarizes the cell), which will increase the release of insulin

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24
Q

What are 2 AE of sulfonylureas?

A
  1. Disulfram reactions

2. Hypoglycemia

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25
Q

What are the 3 actions of thiazolidinediones?

A
  1. Increase insulin sensitivity
  2. Increase glucose uptake
  3. Decrease hepatic glucose production (gluconeogenesis)
26
Q

What is a complex oligosaccharide that decreases digestion of ingest carbs?

A

Alpha glucosidase inhibitors

27
Q

How do alpha-glucosidase inhibitors work?

A

Competitive, reversible inhibition of intestinal brush border enzymes

28
Q

What is the primary effect of alpha glucosidase inhibitors?

A

Affects postprandial blood glucose… decreases by 40-60 mg/dL

29
Q

What is 1 advantage of rDNA-produced insulin over bovine insulin?

A

It is less antigenic….bovine insulin causes allergic reactions to impurities and to insulin molecule itself

30
Q

What is the Somogyi Phenomenon?

A

Early morning hyperglycemia (7am) secondary to late evening (2am) hypoglycemia

31
Q

What causes 2AM hypoglycemia and what does this cause?

A

Long or intermediate acting insulin- This stimulates counter regulatory (glucagon) hormones to increase blood glucose

32
Q

What needs to be done to compensate Somogyi phenomenon?

A

Decrease long acting insulin

33
Q

What are 3 adverse effects of insulin?

A

Hypoglycemia, weight gain, lipodystrophy

34
Q

What is the most potentially dangerous AE to metformin?

A

Lactic acidosis

35
Q

What increases the risk of lactic acidosis due to metformin?

A

Renal dysfunction and age

36
Q

What does metformin reduce the absorption of?

A

B12

37
Q

What are 2 CI to metformin?

A

Renal failure and CHF

38
Q

What are 2 AE to thiazolidinediones?

A
  1. Exacerbates CHF

2. Check transaminases…heptaic issues

39
Q

What binds to sulfonylurea receptors and closes ATP-sensitive channels, but has a short half life?

A

Glinidines

40
Q

What blocks the K channels making the cell look like there is an influx of glucose, resulting in the increased release of insulin?

A

Sulfonylureas

41
Q

How do dipeptidyl peptisase inhibitor-4 work?

A

Increase incretins by inhibiting DPP-4

42
Q

What is the effect of increasein incretins?

A

Increase glucose mediated insulin secretion and suppress glucagon secretion

43
Q

What inactivates incretins?

A

DDP-4

44
Q

What are 2 incretins?

A

GLP-1 and GIP

45
Q

What should be done until adequate glycemic control is achieved and how long might this take?

A

Increase dose of oral agent or add 2nd agent…4-8 weeks

46
Q

Who should insulin be added for?

A

Newly diagnosed type 2 diabetics with markedly symptomatic and/or elevated blood sugars

47
Q

What can be added to oral antihyperglycemic agent regimen when needed?

A

Insulin

48
Q

What is eventually needed for may patients with type 2 DM because it is a progressive disease?

A

Insulin therapy

49
Q

What is the level of HA1C expected with adequate glycemic control?

A

Under 7%

50
Q

What is the portion of proinsulin that is cut out in processing?

A

C-peptide

-So there is one C-peptide molecule for every pro-insulin

51
Q

What is an indicator of endogenous proinsulin, and thus insulin production?

A

C-peptide

-Synthetic insulin doesn’t contain C-peptide

52
Q

What are the diadvantages of metformin?

A
  1. GI side effects
  2. Risk of lactic acidosis
  3. Can NOT be used in patients with renal dysfunction
  4. Should be held in pts receiving IV contrast or undergoing surgical procedure until stable renal function is established.
53
Q

What are the disadvantages of sulfonylureas?

A
  1. Potential for severe, prolonged hypoglycemia

2. Weight gain

54
Q

What are the disadvantages of thiazolinediones?

A
  1. Weight gain and fluid retention
  2. Contraindicated in NYHC III or IV
  3. Increase fracture risk in women
  4. Some questions about cardiovascular events. There has been recent news concerning Avandia.
  5. Some question linking these to higher incidence of bladder cancer.
55
Q

What are the disadvantages of alpha glucosidase inhibitors?

A

Increased deliverly of CHO to colon results in flatulence and diarrhea

56
Q

What is released from endocrine cells in the small intestinal mucosa primarily in response to oral nutrient ingestion?

A

Incretin hormones

-glucose-dependent insulinotropic peptide (GIP) and glucagon-like peptide-1 (GLP-1)

57
Q

What are the effects most relevant to metabolic dysfucntion of incretin hormones?

A
  1. Stimulation of insulin

2. Suppression of glucagon (resultant reduction in fasting and post-prandial glucose

58
Q

What is impaired in type 2 DM?

A

Incretin secretion and/or action

59
Q

What is the enzyme responsible for the short half-life of endogenous incretins?

A

DDP-4 (dipeptidyl peptidase)

60
Q

What can be done to help with issues with incretin secretion and action in type 2 DM?

A

Adminiter long-acting DDP-4 resistant peptides that bind to and activate the GLP-1 receptor

Endrocrine Exam 2 (7 decks)

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