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Pharmacology 2 > Exam 3: Antidiabetic > Flashcards

Exam 3: Antidiabetic Flashcards

1
Q

What are the 4 rapid acting insulins?

A

Insulin lispro, insulin aspart, insulin glulisine, and insulin inhaled

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2
Q

What is the short acting insulin?

A

Regular insulin

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3
Q

What is the intermediate acting insulin?

A

NPH insulin

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4
Q

What are the 3 long acting insulins?

A

Insulin glargine, insulin detemir, insulin degludec

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5
Q

What are the anabolic effects of insulin?

A

Decreased gluconeogenesis and increased glycogen synthesis in the liver. Increased glucose uptake in muscle and adipose

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6
Q

Where is GLUT1 found?

A

All tissues, especially red cells and the brain

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7
Q

Where is GLUT2 found?

A

B cells of the pancreas, liver, kidney, and gut

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8
Q

Where is GLUT3 found?

A

Brain, kidney, and placenta

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9
Q

Where is GLUT4 found?

A

Muscle and adipose

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10
Q

What are the adverse effects of insulin?

A
  • Hypoglycemia (tachycardia, confusion, sweats)

- Weight gain

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11
Q

How can hyperinsulinism cause hypoglycemia?

A
  • inadvertent administration of too much insulin
  • Change in type of preparation
  • failure to eat
  • vigorous exercise
  • spontaneous decrease in insulin requirement
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12
Q

What kind of insulin is used in insulin pumps?

A

Rapid acting

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13
Q

What type of insulin is first used in T2D?

A

Long acting

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14
Q

What is the MOA of glucagon?

A
  • Increased blood glucose level by mobilizing hepatic glycogen when available
  • regulates glucose, amino acids, and possible free fatty acid homeostasis
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15
Q

What are the therapeutic effects of glucagon?

A
  • Potent inotropic and chronotropic effects on the heart (used in B blocker overdose)
  • produces profound relaxation of the intestine
  • not very effective in patients with reduced glycogen stores and juveniles respond less than adults
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16
Q

How is glucagon administered?

A

Parenterally (SC, IM, IV)

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17
Q

What kind of drug is Diazoxide?

A

A non diuretic thiazide, vasodilator, and hyperglycemic drug

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18
Q

What is the MOA of Diazoxide?

A

Promotes hyperglycemia by directly inhibiting insulin secretion, decreasing peripheral glucose utilization, or stimulating hepatic glucose production

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19
Q

When in Diazoxide used?

A

In patients with insulinoma

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20
Q

How is Diazoxide administered?

A

Orally, long duration of action

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21
Q

What does Metformin do?

A

Decrease glucose levels in a predominately insulin-independent manner

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22
Q

What is the initial DOC for Type 2 DM if A1C is <10%?

A

Metformin

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23
Q

What are the glycemic effects of Metformin?

A

Promotes a euglycemic state, but glucose is not lowered in non diabetics

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24
Q

What are the cardiovascular effects of Metformin?

Any other effects?

A
  • Decrease macrovascular events and decreased TGs
  • decrease all cause mortality events
  • weight neutral
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25
Q

What is the best pharmacologic therapy for diabetes prevention?

A

Metformin

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26
Q

How is Metformin administered and excreted?

A

Oral administration

Renal excretion

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27
Q

What are the adverse effects of Metformin?

A
  • Hypoglycemia (rare)
  • Diarrhea (most common)
  • Lactic acidosis (most dangerous, dose dependent)
  • Reversible vitamin B12 deficiency
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28
Q

What are the contraindications to Metformin?

A

Lactic acidosis conditions

  • Kidney disease: C/I in renal failure or severe renal impairment (GFR <30)
  • hepatic Disease
  • alcoholism
  • diseases predisposing to tissue hypoxia
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29
Q

Oral glucose stimulates the release of what?

A

Incretins: GLP1 and glucose dependent insulinotropic peptide (GIP)

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30
Q

GLP1 and GIP increase the release of what?

A

Insulin

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31
Q

GLP1 inhibits the release of what?

A

Glucagon

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32
Q

What are the 3 GLP receptor agonists?

A

Exenatide, liraglutide, and semaglutide

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33
Q

What is the MOA of the GLP1 receptor agonists?

A

GLP1 agonists that are resistant to DPP4 degradation

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34
Q

How are GLP1 receptor agonists administered? What is the exception to this?

A

S.C injections either twice a day, or once weekly

Semaglutide is oral

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35
Q

What is the compelling indication of Liraglutide?

A

It decreased macrovascular events

-FDA approved to reduce risk of major CV events in T2D

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36
Q

What are the effects of GLP-1 receptor agonists?

A
  • Slows gastric emptying so patient eats less
  • Weight loss (compelling indication, only liraglutide)
  • Potential increased B cell number and function
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37
Q

What are the adverse effects of GLP1 RA?

A
  • Hypoglycemia (low risk)
  • GI disturbance
  • acute pancreatitis
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38
Q

What are the contraindications for GLP1 RA?

A
  • History of, or acute, pancreatitis
  • Thyroid cancer (can increase incident of thyroid CA)
  • GI disease
  • renal impairment
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39
Q

What are the two Dipeptidyl-peptidase-4 (DPP-4) inhibitors?

A

Sitagliptan and Linagliptan

40
Q

What is the MOA of the DPP-4 inhibitors?

A

-Potentiates the effects of endogenous incretin hormones by inhibiting their breakdown by DPP4

41
Q

How are DPP-4 inhibitors administered?

How are they excreted and what is the exception to this?

A
  • Oral administration

- Eliminated by the kidney, except Linagliptan is liver/GI

42
Q

What are the therapeutic effects of DPP-4 inhibitors?

A

Cardiovascular: neutral

-Weight neutral

43
Q

What are the adverse effects of DPP-4 inhibitors?

A
  • Hypoglycemia (low risk)
  • Associated with acute pancreatitis
  • joint pain
44
Q

What are the contraindications of GPP-4 inhibitors?

A
  • Renal impairment (except linagliptan)
  • History of, or acute, pancreatitis
  • Slow GI problems
45
Q

What are the 3 SGLT inhibitors?

A

Canagliflozin, Dapagliflozin, and Empagliflozin

46
Q

What is the MOA of SGLT2 inhibitors?

A

Inhibits the sodium-glucose co-transporter 2 (SGLT2) in the kidney, so more glucose is lost in the urine

47
Q

How are SGLT2 inhibitors administered?

48
Q

Which SGLT2 inhibitors are FDA approved to decreased CV events in T2D?

A

Empagliflozin and Canagliflozin

49
Q

Which SGLT2 inhibitor decreases CKD progression?

A

Canagliflozin

50
Q

Which SGLT2 inhibitors decrease the amount of HF hospitalizations?

A

Canagliflozin and Dapagliflozin

*** all can lower BP and promote weight loss

51
Q

What are the adverse effects of SGLT2 inhibitors?

A
  • Hypoglycemia (rare)
  • female genital mycotic infections, UTI, and increased urinary frequency
  • increased serum creatinine, decreased GFR, and rarely renal impairment and AKI
  • increased LDL
  • Increased bone fractures
52
Q

What are the contraindications to SGLT2 inhibitors?

A
  • Severe real impairment or dialysis

- prone to UTIs are other GI infections

53
Q

What are the two Thiazolidinediones (TZDs)?

A

Pioglitazone and Rosiglitazone

54
Q

What is the MOA of TZDs?

A

Ligands to the nuclear PPAR-gamma receptor which can cause post-receptor insulin mimetic action

  • increased glucose transport synthesis in adipose
  • decrease hepatic glucose production
55
Q

How are TZDs administered?

56
Q

What are the therpeutic effects of TZDs?

A

Cardiovascular: decrease TGs, slight HDL increase

  • Lower insulin resistance
  • Potential benefit in reducing the development of T2D, but not as effective as Metformin
57
Q

What are the adverse effects of TZDs?

A
  • Hypoglycemia (rare)
  • weight gain (possibly edema)
  • edema (dont give in HF)
  • increased bone fracture risk
58
Q

What are the contraindications of TZDs?

A
  • Hepatic disease (Troglitazone is hepatotoxic)

- HF

59
Q

What are the two Alpha-glucosidase inhibitors?

A

Acarbose and miglitol

60
Q

What is unique about Alpha-glucosidase inhibitors?

A

They are used for both Type1 and 2 DM

61
Q

What is the MOA of Alpha-glucosidase inhibitors (AGi)?

A

Inhibit alpha-glucosidase in the small intestine, leading to delayed carb digestion and absorption

62
Q

How are a AGis administered?

A

Orally, pre prandially

63
Q

What are the therapeutic effects of AGis?

A
  • Decrease postprandial glucose only

- weight neutral

64
Q

What are the adverse effects of AGis?

A
  • Hypoglycemia (rare)
  • frequent GI effects, flatulence
  • elevated hepatic enzymes
65
Q

What are the C/I of AGis?

A
  • GI disease, obstruction, ileus, IBD, hiatal hernia
  • Hepatic disease
  • renal impairment
66
Q

What is the MOA of Sulfonylureas (SU)?

A

Binding to and blocking ATP sensitive K channels to cause membrane depolarization and increased Ca influx on B cells, leading to insulin release

***these are not commonly used

67
Q

What are the therapeutic effects of SUs?

A
  • Decreased risk of MI and microvascular disease in long term therapy
  • Decrease all-cause mortality
  • decrease serum glucagon
68
Q

How are SUs administered?

69
Q

What are the adverse effects of SUs?

A
  • Hypoglycemia, highest risk of any non-insulin therapy and why they are not used often
  • weight gain
  • GI side effects
70
Q

What are the contraindications of SUs?

A
  • patients with allergies to sulfas

- Caution in patients with severe renal disease or hepatic dysfunction

71
Q

What are the 3 second generation SUs?

A
  • Glyburide
  • Glipizide
  • Glimepiride
72
Q

Out of the 3 second generation SUs, which causes the worst hypoglycemia? Which causes the least?

A

Worst: Glyburide
Least: Glipizide

73
Q

What kind of drug is Repaglinide?

A

Metaglitinide (GLN)

74
Q

What is the MOA of GLNs?

A

Same as SUs

75
Q

What are the important pharmacokinetics of GLNs?

A
  • Rapid action and short half life (mimics insulin)
  • administered orally, preprandially
  • Metabolized in the liver by CYP3A4
76
Q

What are the therapeutic effects of GLNs?

A
  • Decrease postprandial glucose only

- weight neutral

77
Q

What are the adverse effects of GLNs?

A

-Repaglinide can cause moderate hypoglycemia (less than 2nd generation SUs)

78
Q

What are the contraindications to GLNs?

A
  • Don’t combine with SUs

- caution in liver impairment

79
Q

What kind of drug is Colesevelam?

A

Bile acid binding resin

-Glycemic effect MOA is unknown

80
Q

What are the therapeutic effects of Colesevelam?

A
  • combo with other anti diabetic drugs can decrease basal plasma glucose
  • reduces LDL
  • weight neutral
81
Q

What are the most common adverse effects of Colesevelam?

A

Constipation and bloating

82
Q

What is the MOA of Bromocriptine?

A

Dopamine agonist that augments low hypothalamic dopamine levels, which inhibits excessive sympathetic tone within the CNS, which decreases postmeal plasma glucose levels due to enhance suppression of hepatic glucose production

83
Q

What are the important pharmacokinetics of Bromocriptine?

A

Orally administered within 2 hours of awakening

-metabolized by CYP3A4

84
Q

What are the therapeutic effects of Bromocriptine?

A
  • Decrease postprandial glucose levels
  • decreased FFA and TGs
  • decreased CV end point problems
  • weight neutral
85
Q

What are the contraindications to Bromocriptine?

A

Caution with CYP3A4 inhibitors, inducers, or substrates

86
Q

What kind of drug is Pramlintide?

A

Amylin-like peptide

87
Q

When is pramlintide use?

A

Only as an adjunct to insulin therapy in Type 1 and 2 DM

88
Q

What is the MOA of Pramlintide?

A

-works with insulin to regulate postprandial glucose by decreases gastric emptying, supression of postprandial glucose secretion,and modulation of appetite to decrease calorie intake

89
Q

How is Pramlintide administered?

A

S.C injection 3x per day

90
Q

What are the therapeutic effects of pramlintide?

A
  • In combo with insulin, decrease postprandial glucose

- weight loss

91
Q

What are the adverse effects of pramlintide?

A

Hypoglycemia (only with insulin)

-GI disturbance

92
Q

What is the contraindication to Pramlintide?

A

Slow GI problems (gastroparesis)

93
Q

Which two insulin types can be used IV?

A

Rapid acting and short acting

94
Q

Why is rapid acting insulin preferred over regular insulin?

A

Rapid acting causes less hypoglycemia

95
Q

What are the 3 drugs approved fro ASCVD and DM?

A

Liraglutide, Empagliflozin, and canagliflozin

96
Q

Whatclasses of anti diabetic drugs cause weight gain?

A

Insulin, SUs, and TZDs

97
Q

What 3 classes of antidiabetic drugs cause weight loss?

A

GLP-1 RA, Pramlintide, and SGLT2 inhibitors

Pharmacology 2 (12 decks)

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