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MS 2 - Unit 5 > "Pharmacology Oral Glycemics I & II Ruth Weinstock" > Flashcards

"Pharmacology Oral Glycemics I & II Ruth Weinstock" Flashcards

1
Q

What causes type 1 DM?

A

Autoimmune destruction of insulin- producing pancreatic beta cells
Insulin therapy is required

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2
Q

How does a healthy pancreas work in the islets of Langerhans?

A

α-cells secrete glucagon • β-cells secrete insulin

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3
Q

How do the islets of Langerhans work in a person with T2DM?

A

α-cells dysfunction: secrete inappropriately high levels of glucagon

Fewer β-cells: secrete insufficient levels of insulin

β-cell mass declines over time

T2DM Is Marked by Blunted Insulin Response and Inadequate Glucagon Suppression After Meals

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4
Q

What are the functions of glucagon-like hormone (GLP-1)?

A
  • Enhances glucose-dependent insulin secretion
  • Slows gastric emptying
  • Suppresses glucagon secretion
  • Promotes satiety
  • Receptors in the islet cells, CNS, elsewhere
  • Metabolized rapidly (half-life 2-3 min) by DPP-4 (dipepetidyl peptidase-4)
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5
Q

T/F: GLP-1 release is reduced in T2DM?

A

True

Without insulin, effect of eating produces hyperglycemia

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6
Q

What is the first line pharmacological therapy for T2DM?

A

At the time of type 2 diabetes diagnosis, initiate metformin therapy along with lifestyle interventions, unless metformin is contraindicated

In newly diagnosed type 2 diabetes patients with markedly symptomatic and/ or elevated blood glucose levels or A1C, consider insulin therapy, with or without additional agents, from the
outset

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7
Q

If noninsulin monotherapy is unsuccessful in the treatment of T2DM, what is the next step?

A

add a second oral agent, a GLP-1 receptor agonist, or insulin

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8
Q

Class: Metformin

*Tx of Hyperglycemia in T2DM

A

Biguanide

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9
Q

MOA: Metformin

*Tx of Hyperglycemia in T2DM

A

Reduces hepatic glucose production by Activating AMP-kinase and inhibits mitochondrial isoform of glycerophosphate dehydrogenase

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10
Q

What are the advantages of metformin?

*Tx of Hyperglycemia in T2DM

A

No weight gain (weight neutral)
• No hypoglycemia
• Reduction in cardiovascular events and mortality
• Possibly less cancer

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11
Q

What are the disadvantages of metformin?

*Tx of Hyperglycemia in T2DM

A

Gastrointestinal side effects (diarrhea, abdominal cramping, anorexia)
• Lactic acidosis (rare)
• Vitamin B12 deficiency

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12
Q

In what patient population is metformin contraindicated?

*Tx of Hyperglycemia in T2DM

A

In patients with reduced kidney function

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13
Q

Class: Glibenclamide/Glyburide

*Tx of Hyperglycemia in T2DM

A

Sulfonylureas (2nd generation)

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14
Q

Class: Glipizide

*Tx of Hyperglycemia in T2DM

A

Sulfonylureas (2nd generation)

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15
Q

Class: Gliclazide

*Tx of Hyperglycemia in T2DM

A

Sulfonylureas (2nd generation)

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16
Q

Class: Glimepiride

*Tx of Hyperglycemia in T2DM

A

Sulfonylureas (2nd generation)

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17
Q 
What is the MOA of the sulfonylureas drugs?
•  Glibenclamide/Glyburide 
•  Glipizide
•  Gliclazide
•  Glimepiride

*Tx of Hyperglycemia in T2DM

A

Closes K-ATP channels on beta cell plasma membranes to increase insulin secretion

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18
Q

T/F: The sulfonylureas drugs are well tolerated.

*Tx of Hyperglycemia in T2DM

A 
True
•  Glibenclamide/Glyburide 
•  Glipizide
•  Gliclazide
•  Glimepiride
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19
Q

What are the disadvantages of the sulfonylureas drugs?

*Tx of Hyperglycemia in T2DM

A
  • Relatively glucose-independent stimulation of insulin secretion: Hypoglycemia, including episodes necessitating hospital admission and causing death
  • Weight gain
  • May blunt myocardial ischemic preconditioning
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20
Q

Class: Repaglinide

*Tx of Hyperglycemia in T2DM

A

Meglitinides

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21
Q

Class: Nateglinide

*Tx of Hyperglycemia in T2DM

A

Meglitinides

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22
Q

MOA: Meglitinides (Repaglinide, Nateglinide)

*Tx of Hyperglycemia in T2DM

A

Same as the sulfonylureas: Closes KATP channels on β-cell plasma membranes to increase insulin secretion

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23
Q

What are the advantages of the Meglitinides (Repaglinide and Nateglinide) over the sufonylureas drugs?

*Tx of Hyperglycemia in T2DM

A

Accentuated effects around meal ingestion (short- acting)

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24
Q

What are the side effects of the Meglitinides (Repaglinide and Nateglinide)?

*Tx of Hyperglycemia in T2DM

A
  • Hypoglycemia
  • Weight gain
  • May blunt myocardial ischemic preconditioning
  • Dosing frequency (before each meal)
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25
Q

Class: Pioglitazone

*Tx of Hyperglycemia in T2DM

A

Thiazolidinediones (Glitazones)

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26
Q

MOA: Pioglitazone

*Tx of Hyperglycemia in T2DM

A

Activates the nuclear transcription factor PPAR-γ to increase peripheral insulin sensitivity

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27
Q

What are the advantages of Pioglitazone?

*Tx of Hyperglycemia in T2DM

A
  • No hypoglycemia
  • HDL cholesterol ↑
  • Triglycerides ↓
  • Possible reduction in myocardial infarctions
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28
Q

What are the disadvantages of Pioglitazone?

*Tx of Hyperglycemia in T2DM

A
  • Weight gain
  • Edema
  • Heart failure
  • Bone fractures
  • Increased bladder cancer risk
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29
Q

Class: Rosiglitazone

*Tx of Hyperglycemia in T2DM

A

Thiazolidinediones (Glitazones)

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30
Q

Rosiglitazone is similar to pioglitazone in its MOA, but has different disadvantages. What are they?

*Tx of Hyperglycemia in T2DM

A 
•  LDL cholesterol ↑ 
•  Weight gain
•  Edema
•  Heart failure
•  Bone fractures
•  Increased cardiovascular events (mixed
evidence)
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31
Q

Rosiglitazone is contraindicated in patients with what condition?

*Tx of Hyperglycemia in T2DM

A

Heart disease

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32
Q

Class: Acarbose

*Tx of Hyperglycemia in T2DM

A

α-Glucosidase inhibitors

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33
Q

Class: Miglitol

*Tx of Hyperglycemia in T2DM

A

α-Glucosidase inhibitors

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34
Q

MOA: α-Glucosidase inhibitors (Acarbose and Miglitol)

*Tx of Hyperglycemia in T2DM

A

Inhibits intestinal alpha-glucosidase in order to slow intestinal carbohydrate digestion and thus glucose absorption

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35
Q

What are the advantages of the α-Glucosidase inhibitors (Acarbose and Miglitol)?

*Tx of Hyperglycemia in T2DM

A
  • Nonsystemic medication
  • Postprandial glucose ↓
  • Weight neutral
  • No hypoglycemia
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36
Q

What are the disadvantages of the α-Glucosidase inhibitors (Acarbose and Miglitol)?

*Tx of Hyperglycemia in T2DM

A
  • Gastrointestinal side effects (gas, flatulence, diarrhea, abdominal fullness and discomfort)
  • Dosing frequency
  • Modest reduction in A1c
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37
Q

Class: Exenatide

*Tx of Hyperglycemia in T2DM

A

GLP-1 receptor agonists (incretin mimetics)

Dose Exenatide twice daily or weekly - injectible

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38
Q

Class: Liraglutide

*Tx of Hyperglycemia in T2DM

A

GLP-1 receptor agonists (incretin mimetics)

Dose Liraglutide daily - injectible

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39
Q

Class: Albiglutide

*Tx of Hyperglycemia in T2DM

A

GLP-1 receptor agonists (incretin mimetics)

Dose Albiglutide weekly - injectible

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40
Q

Class: Dulaglutide

*Tx of Hyperglycemia in T2DM

A

GLP-1 receptor agonists (incretin mimetics)

Dose Dulaglutide weekly - injectible

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41
Q 
MOA: GLP-1 receptor agonists (incretin mimetics):
•  Exenatide
•  Liraglutide
•  Albiglutide
•  Dulaglutide

*Tx of Hyperglycemia in T2DM

A

Activates GLP-1 receptors to:
• Insulin secretion ↑ (glucose-dependent)
• Glucagon secretion ↓ (glucose-dependent)
• Slowsgastricemptying
• Satiety ↑

42
Q 
What are the advantages of the GLP-1 receptor agonists (incretin mimetics)?
•  Exenatide
•  Liraglutide
•  Albiglutide
•  Dulaglutide

*Tx of Hyperglycemia in T2DM

A

Weight reduction;

Potention for improved beta-cell mass/function

43
Q 
What are the disadtantages of the GLP-1 receptor antagonists (incretin mimetics)?
•  Exenatide
•  Liraglutide
•  Albiglutide
•  Dulaglutide

*Tx of Hyperglycemia in T2DM

A

• Gastrointestinal side effects (nausea, vomiting, diarrhea) • Cases of acute pancreatitis observed
• Hypoglycemia(less than sulfonylureas)
• Caution with renal insufficiency
• C-cellhyperplasia/medullary thyroid tumors in animals (liraglutide)
• Injectable
• Long-term safety unknown-
–increased pancreatic cancer

44
Q

Class: Sitagliptin

*Tx of Hyperglycemia in T2DM

A

DPP-4 inhibitors (incretin enhancers)

45
Q

Class: Alogliptin

*Tx of Hyperglycemia in T2DM

A

DPP-4 inhibitors (incretin enhancers)

46
Q

Class: Saxagiptin

*Tx of Hyperglycemia in T2DM

A

DPP-4 inhibitors (incretin enhancers)

47
Q

Class: Linagliptin

*Tx of Hyperglycemia in T2DM

A

DPP-4 inhibitors (incretin enhancers)

48
Q

MOA: DDP-4 inhibitors (incretin enhancers) (the gliptins)

*Tx of Hyperglycemia in T2DM

A 
Inhibit DDP-4 activity to:
•  Active GLP-1 concentration ↑ and 
Active GIP concentration ↑
•  Insulin secretion ↑
•  Glucagon secretion ↓
49
Q 
What are the advantages of DDP-4 inhibitors?
•  Sitagliptin
•  Alogliptin
•  Saxagliptin
•  Linagliptin

*Tx of Hyperglycemia in T2DM

A

No hypoglycemia;

Weight neutral

50
Q 
What are the disadvantages of the DDP-4 inhibitors?
•  Sitagliptin
•  Alogliptin
•  Saxagliptin
•  Linagliptin

*Tx of Hyperglycemia in T2DM

A
  • Occasional reports of urticaria/angioedema; URIs, headache, arthralgias
  • Cases of pancreatitis observed
  • Long-term safety unknown
51
Q

Class: Canaglifozin

*Tx of Hyperglycemia in T2DM

A

SGLT2 (sodium glucose cotransporter 2) inhibitor

52
Q

Class: Dapaglifozin

*Tx of Hyperglycemia in T2DM

A

SGLT2 (sodium glucose cotransporter 2) inhibitor

53
Q

Class: Empaglifozin

*Tx of Hyperglycemia in T2DM

A

SGLT2 (sodium glucose cotransporter 2) inhibitor

54
Q

MOA: SGLT2 (sodium glucose cotransporter 2) inhibitor
• Canagliflozin
• Dapagliflozin
• Empagliflozin

*Tx of Hyperglycemia in T2DM

A

Reduces glucose resorption in the kidney; α cell agonist in order to increase urinary glucos excretion and increase glucagon secretion

55
Q 
What are the advantages of 
•  Canagliflozin 
•  Dapagliflozin 
•  Empagliflozin
?

*Tx of Hyperglycemia in T2DM

A

Ho hypoglycemia;

Weight loss possible

56
Q 
What are the disadvantages of
•  Canagliflozin 
•  Dapagliflozin 
•  Empagliflozin
?

*Tx of Hyperglycemia in T2DM

A
  • Volume depletion (hypotension, renal impairment); hyperkalemia; ketoacidosis
  • Genital mycotic infections; UTIs
  • Hypersensitivity; increased LDL-chol
  • Reduced bone density, increased bone fracture risk
  • Long-term safety unknown; avoid in renal insufficiency
57
Q

Class: Colesevelam

*Tx of Hyperglycemia in T2DM

A

bile acid sequestrant

58
Q

MOA: Colesevelam

*Tx of Hyperglycemia in T2DM

A

Reduces hepatic glucose production

59
Q

What are the advantages of Colesevelam?

*Tx of Hyperglycemia in T2DM

A
  • No hypoglycemia

* LDL cholesterol ↓

60
Q

What are the disadvatages of colesevalem?

*Tx of Hyperglycemia in T2DM

A 
•  Constipation
•  Triglycerides ↑
•  May interfere with absorption of other
medications
•  Modest reduction in A1c
61
Q

Hypoglycemia is most common when taking what medication?

A
  • Most common with treatment with sulfonylurea drugs and insulin
  • More common in type 1 vs. type 2 diabetes
  • Increased risk if over 60 years old, impaired renal function, poor nutrition, liver disease, increased physical activity, longer duration of diabetes
62
Q

What is the preferred treatment for hypoglycemia?

A
  • Glucose (15–20 g) preferred treatment for conscious individual with hypoglycemia
  • Glucagon should be prescribed for all individuals at significant risk of severe hypoglycemia and caregivers/family members instructed in administration
63
Q

When is glucagon therapy indicated for hypoglycemia?

A
  • Given only if unconscious or unable to swallow - patient never gives to self
  • Turn on side - nausea, vomiting, call 911
  • type 1 should always have prescription
  • type 2 with previous severe low blood sugar
64
Q

How is severe hypoglycemia treated in a hospital setting?

A

IV dextrose

65
Q

What are some causes of oral therapy inadequacy in diabetes mgmt?

A 
Dietary noncompliance;
Physical inactivity;
Stress;
Insulin resistance;
Simultaneous use of diabetogenic drugs;
Progressive beta-cell dysfunction (insulin deficiency)
66
Q

T/F: A1C can still rise 0.2-0.3% yearly with stable oral monotherapy

A

True

This rate is the same as for diet alone, sulfonylureas, and metformin treatment

67
Q

Amylin is a protein released with insulin from beta cells in response to eating. It is deficient in T1DM with variable levels in T2DM. What is its action?

A

– Slows gastric emptying
– Suppresses postprandial glucagon secretion
– May reduce appetite

68
Q

Class: Pramlintide

A

Amylin analog

69
Q

MOA: Pramlintide

A
  • Reduces post-prandial glucose levels (inhibits glucagon production, slows gastric emptying)
  • Use with short/rapidly acting insulin
70
Q

In what patient population if Pramlintide indicated?

A

For use in adults with insulin-requiring diabetes

71
Q

What is a major side effect of Pramlintide?

A

Significant risk of hypoglycemia

72
Q

What are the side effects of Pramlintide?

A

GI side effects, especially nausea;

Significant risk of hypoglycemia

73
Q

What are the advantages of Pramlintide?

A

May reduce appetite and promote weight loss

74
Q

When is insulin therapy indicated in patients?

A

All patients with T1DM;
T2DM with:
- Glucose toxicity
- Insufficient endogenous insulin production
- Contraindication to oral therapy
– Significant hyperglycemia at presentation
– Hyperglycemia on maximal doses of oral agents
Decompensation ie
– Acute injury, stress, infection, myocardial ischemia
– Severe hyperglycemia with ketonemia and/or ketonuria
– Uncontrolled weight loss
– Use of diabetogenic medications (eg, corticosteroids)
– Surgery
– Pregnancy
– Serious renal or hepatic disease

75
Q

Intermediate-acting insulin is also known as:

A

– NPH (N= neutral pH, P= protamine zinc,

H=origin in Hagedorn’s laboratory)

76
Q

Class:
Lispro insulin;
Aspart insulin;
Glulisine insulin

A

rapid-acting insulin analogs

amino acid changes speed absorption

77
Q

Class:
Detemir insulin (rDNA origin);
Neutral protamine insulin (NPL);
Neutral protamine aspart (NPA)

A

Intermediate-acting insulin analogs

78
Q

Class: Glargine insulin

A

Long-acting insulin analog (basal insulin)

79
Q

Class: Degludec insulin

A

Ultra-long acting basal insulin analog

Low 24 hour variability

80
Q

What is an advantage of degludec/aspart 70/30?

A

Reduced hypoglycemia compared with other premixed insulins

81
Q

What are the advantages of premixed insulin?

A

– Convenient
– Potentially longer shelf life – avoids problem of protamine-bound insulin exchanged with lispro/aspart/Regular
– Fewer dosing errors
– Simple (pens)

82
Q

T/F: Premixed insulins are rarely used in T1DM.

83
Q

What are the disadvantages of premixed insulins?

A

– Loss of flexibility in matching to
• Carbohydrate intake
• Physical activity
– Harder to treat short-term hi or low blood glucose levels
– Lack of clinical outcome data – Hypoglycemia risk

84
Q

When not in a hospital setting, insulin is typically administered how?

85
Q

Inhaled insulin is contraindicated in what patient populations?

A

COPD and asthma

may cause FEV decrease;
long term risks unknown

86
Q

What are the regional differences in insulin absorption?

A

– Abdomen > arm > buttocks > thigh
– Rotate sites within region
– Use specific regions for specific times of day

87
Q

What is split-mix insulin therapy?

A

2x a day at breakfast and dinner, can include bedtime dose

Disadvantages
– Not very physiological
– Greater likelihood of nocturnal hypoglycemia given peak of presupper NPH
– Greater chance of fasting hyperglycemia

88
Q

What is the basal/bolus insulin concept?

A

• Basal insulin
– Suppresses glucose production between meals and
overnight
– Usually 40% to 50% of daily needs

• Bolus insulin (mealtime)
– Matched to carbohydrate intake, premeal glucose,
anticipated activity
– Limits hyperglycemia after meals
– Usually 10% to 20% of total daily insulin requirement at each meal

89
Q

What are the side effects of insulin therapy?

A 
Hypoglycemia;
Weight gain;
Allergic rxn (local or systemic);
Liphypertrophy;
Lipoatrophy (atrophy of subcutaneous fat at the injection site)
90
Q

Continuous Subcutaneous Insulin Infusion (CSII) Systems infuse what kind of insulin?

A

rapid-acting

in-dwelling catheter

91
Q

What insulin therapy has shown the greatest reduction in A1C levels in those with the highest starting A1C?

A

Insulin pump therapy

  • Glycemic control as good as with multiple daily injections if not better
  • ↓ severe hypoglycemia, especially if history of severe hypoglycemia
  • Good patient satisfaction
  • Greater QOL and lifestyle flexibility
  • More expensive than injection therapy
92
Q

What is “IOB?”

A

• Insulin-on-board (IOB): amount of insulin from last bolus not yet absorbed

93
Q

Define “stacking.”

A

Insulin bolus when there is IOB

94
Q

Define “sensitivity factor.”

A

Correction factor: amount of glucose lowering expected from one unit of insulin

95
Q

What are the major obstacles to optimal insulin therapy?

A
  • Hypoglycemia
  • Hyperglycemia
  • Glycemic excursions/glucose variability
96
Q

When should patients monitor their glucose?

A

– Prior to meals and snacks
– Occasionally postprandially
– At bedtime
– Prior to exercise
– When they suspect low blood glucose
– After treating low blood glucose until they are normoglycemic
– Prior to critical tasks such as driving

97
Q

T/F: A normal A1C may be the result of hypoglycemic events in uncontrolled DM patients.

A

True - emphasizes the need for continuous BG monitoring

98
Q

What patients are candidates for CGM?

A
  • Repeated hypoglycemia
  • Hypoglycemic unawareness
  • Discrepancies between A1C and SMBG • Pregnancy
  • Unable to achieve goals
99
Q

Summarize treatment goals in T1DM.

A 
•  Diet, physical activity, education 
•  Basal/bolus insulin therapy with:
– Multiple daily injections or
– Insulin pump therapy
•  Sensor-augmented insulin therapy in selected patients
100
Q

Summarize treatment goals in T2DM.

A
  1. Diet, exercise and education
  2. Unless contraindicated, metformin is the optimal 1st line drug
  3. After metformin, combination therapy with 1-2 other oral/injectible agents is reasonable; minimize side effects
  4. Ultimately, many patients will require insulin therapy alone or in combination with other agents to maintain BG control

MS 2 - Unit 5 (21 decks)

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