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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
What are the incretin hormones?
- GIP = glucose-dependent insulinotropic peptide | - GLP-1 = glucagon like peptide-1
26
GLP-1 properties
- short half life | - degraded by dipeptidyl peptidase IV; cleaves off 2 AA
27
How are incretin mimetics administered?
subQ
28
incretin mimetics effects
* 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
Mechanism of action for DPP-IV inhibitors
bind to DDP4 enzyme and inhibit it -> more GLP1 -> GLP1 effects
30
Mechanism of action for α-Glucosidase inhibitors
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
Mechanism of action for SGLT2-inhibitors
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
What does alpha glucosidase usually do in the body?
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
What does SGLT2 usually do in the body?
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
What is a side effect for SGLT2-inhibitors?
Major concern from increased glucose in urine -> increased urinary tract infections
35
Mechanism of action for Dopamine Agonist
not known
36
Mechanism of action for Bile Acid Sequestrants
- 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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