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OU Module Endo Fall 2018 > Pharmacology of Oral medications for Type 2 Diabetes Mellitus Exam 2 > Flashcards

Pharmacology of Oral medications for Type 2 Diabetes Mellitus Exam 2 Flashcards

1
Q

What are the insulin secretagogues? (drug classes)

A
  • Sulfonylureas

- Meglitinides (Glinides)

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2
Q

What are the Sulfonylureas?

A

only need to know second generation:

  • Glimepride (Amaryl)
  • Glipizide (Glucotrol XL)
  • Glyburide / Glibenclamide (Diabeta, Glynase, Micronase)
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3
Q

What are the Meglitinides (Glinides)?

A
  • Repaglinide (Prandin)

- Nateglinide (Starlix)

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4
Q

What are the insulin sensitizers? (classes only)

A
  • Biguanides

- Thiazolidinediones

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5
Q

What are the Biguanides?

A

Metformin (Glucophage, Glucophage XR, Glumetza, Fortamet, Riomet)

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6
Q

What are the Thiazolidinediones?

A
  • Pioglitazone (Actos)

- Rosiglitazone (Avandia)

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7
Q

What are the gut or incretin-related drugs? (classes only)

A
  • Incretin mimetics
  • Dipeptidyl peptidase IV (DPP-IV) inhibitors
  • Alpha-glucosidase inhibitors
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8
Q

What are the incretin mimetics?

A
  • Exenatide (Byetta, Bydureon)

- Liraglutide (Victoza)

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9
Q

What are the Dipeptidyl peptidase IV (DPP-IV) inhibitors?

A
  • Sitagliptin (Januvia)

- Saxagliptin (Onglyza)

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10
Q

What are the Alpha-glucosidase inhibitors?

A
  • Acarbose (Precose)

- Miglitol (Glyset)

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11
Q

What are the classes of drugs for oral DM medications?

A
  • Insulin Secretagogues
  • Insulin Sensitizers
  • Gut or Incretin-related drugs
  • Sodium Glucose Transporter 2 (SGLT2) inhibitor
  • Dopamine Agonist
  • Bile Acid Sequestrant
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12
Q

What are the Sodium Glucose Transporter 2 (SGLT2) inhibitors?

A
  • Canagliflozin (Invokana)

- Dapagliflozin (Farxiga)

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13
Q

What are the Dopamine Agonists?

A

Bromocriptine (Cycloset)

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14
Q

What are the Bile Acid Sequestrants?

A

Colesevelam hydrochloride (WelCHOL)

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15
Q

Mechanism of action for Sulfonylureas

A

Sulfonylureas bind to the sulfonylurea portion on the ATP/K channel -> closes it -> membrane potential changes -> Ca++ channel opens -> exocytosis of insulin granules

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16
Q

What is the difference between the first and generation Sulfonylureas?

A
  • First generation: Lower binding affinity to the SUR1 -> give higher doses -> Higher side effects
  • Second generation: Higher binding affinity to the SUR1; more potent -> give lower doses -> Lesser side effects
17
Q

Mechanism of action for Glinides or Meglitinides

A

bind to different subunit (than sulfonylureas) on the sulfonylurea portion on the ATP/K channel -> closes it -> membrane potential changes -> Ca++ channel opens -> exocytosis of insulin granules

18
Q

Properties of Glinides or Meglitinides

A
  • Very rapid onset and short duration of action
  • first-phase insulin release is stimulated in a glucose-sensitive manner
  • if pts are allergic to sulfa, they can be on this med
19
Q

Mechanism of action for Biguanides

A

goes into liver cell through OCT1 -> inhibits mitochondrial respiration via complex 1 -> decreases ATP -> more AMP -> AMPK gets activated which decreases lipid / cholesterol synthesis + affect gene expression + affect FBPase (which would decrease gluconeogenesis)

20
Q

Effects of Biguanides

A
  • less lipid / cholesterol synthesis
  • less weight gain
  • less glucose production from liver
  • less hyperglycemia
  • decreased glucagon receptor activity
21
Q

What are the various mechanism of metformin?

A
  • Anti-cancer agent: decrease energy levels -> increase AMP -> activate AMP -> becomes cytotoxic to cancer cells
  • Insulin sensitizer: increases Adiponectin released from adipose tissues -> increase insulin sensitivity and helps body utilize glucose
22
Q

Mechanism of action for Thiazolidinediones (Glitazones)

A

binds to PPARγ -> forms drug receptor complex -> change conformation -> go into nucleus -> bind to DNA for gene transcription -> overall effects are less glucose production and more insulin sensitivity

23
Q

Effects if Thiazolidinediones (Glitazones)

A
  • less glucose production

- increased insulin sensitivity

24
Q

Mechanism of action for GLP1 agonist

A

binds to GLP1 receptor in beta cells -> activate cascade / adenylyl cyclase -> increase ATP -> closes ATP/K channel -> changes membrane potential -> Ca++ channels open -> Ca++ comes into cell -> exocytosis release of insulin

25
Q

What are the incretin hormones?

A
  • GIP = glucose-dependent insulinotropic peptide

- GLP-1 = glucagon like peptide-1

26
Q

GLP-1 properties

A
  • short half life

- degraded by dipeptidyl peptidase IV; cleaves off 2 AA

27
Q

How are incretin mimetics administered?

A

subQ

28
Q

incretin mimetics effects

A
  • Improve glucose-dependent insulin secretion
  • Slows rate of gastric emptying
  • Decrease food intake (↓ rate of gastric emptying, ↑ weight loss)
  • Decrease postprandial glucagon secretion
  • Promote β-cell proliferation
  • Byetta has insulin sensitizing effect
29
Q

Mechanism of action for DPP-IV inhibitors

A

bind to DDP4 enzyme and inhibit it -> more GLP1 -> GLP1 effects

30
Q

Mechanism of action for α-Glucosidase inhibitors

A

decreases the amount of glucose in the blood -> when inhibited, does not break down polysaccharides into glucose -> they get excreted since we do not absorb polysacc (only monosacc) -> less sugar absorbed -> less hyperglycemia

31
Q

Mechanism of action for SGLT2-inhibitors

A

glucose gets excretes into urine because the SGLT2 is not able to reabsorb the glucose in the kidney -> more glucose gets excreted into the urine and less glucose gets back into the blood stream

32
Q

What does alpha glucosidase usually do in the body?

A

alpha glucosidase enzymes in small intestines -> break down complex sugars into glucose -> can be absorbed into blood stream -> glucose gets picked up from glucose transporters -> can use glucose in all of our tissues

33
Q

What does SGLT2 usually do in the body?

A

after we digest our food, the kidney reabsorbs the glucose; SGLT1 is the glucose transporter that sits on the lumen on the proximal tubules (glucose gets reabsorbed from this transporter) -> goes through the cell and to the GLUT2 transporter and brings it back into our blood

34
Q

What is a side effect for SGLT2-inhibitors?

A

Major concern from increased glucose in urine -> increased urinary tract infections

35
Q

Mechanism of action for Dopamine Agonist

A

not known

36
Q

Mechanism of action for Bile Acid Sequestrants

A
  • bind to the negatively charged end of the bile acid -> the liver uses cholesterol to make bile -> drugs goes through intestine and binds to bile acid -> takes it out of system -> body has to make more bile acid which increases CYP7A1 activation -> the more bile acid we make, the more cholesterol we need to utilize -> getting rid of cholesterol in the system -> reduce weight loss and free fatty acids
  • also reduced bile acids = reduced FXR = reduced glucose production

OU Module Endo Fall 2018 (27 decks)

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