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Therapeutics 2 - Exam 2 > T2DM pt 1 > Flashcards

T2DM pt 1 Flashcards

1
Q

cause of T2DM

A

insulin resistance and reduced insulin secretion

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2
Q

drugs that increase insulin secretion

A

sulfonylureas
meglitinides
incretins

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3
Q

sulfonylurea drugs

A

tolbutamide
tolazamide
chlorpropamide
glyburide
glipizide
glimeperide

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4
Q

meglitinide drugs

A

nateglinide
repaglinide

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5
Q

mechanism of glucose-dependent insulin secretion in B-cells (high glucose)

A
  1. small amounts of glucose are transported into the cell via GLUT 2 transporters
  2. glucose is phosphorylated by glucokinase (now it cannot leave the cell)
  3. Glucose undergoes glycolysis and produces ATP
  4. High concentration of ATP causes a swing in equilibrium in favor of ATP
  5. ATP bind K+ channel blocking inflow
  6. the cell depolarizes
  7. Voltage gated Ca channel is activated allowing influx of Ca
  8. High concentration of Ca activate exocytosis of insulin
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6
Q

mechanism of glucose dependent insulin secretion in B-cells (low glucose)

A
  1. small amounts of glucose are transported into the cell via GLUT 2 transporters
  2. glucose is phosphorylated by glucokinase (now it cannot leave the cell)
  3. Glucose undergoes glycolysis and produces ATP
  4. Low concentration of ATP causes a swing in equilibrium in favor of ADP
  5. ADP bind K+ channel opening the channel allowing influx of Ca
  6. the cell hyper polarizes and stabilizes
  7. Voltage gated Ca channel is closed
  8. No exocytosis of insulin occurs at low Ca concentration
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7
Q

Mechanism of Sulfonylureas

A
  1. Bind and close KATP channel to block inflow of K
  2. the cell depolarizes
  3. Voltage gated Ca channel is activated allowing influx of Ca
  4. High concentration of Ca activate exocytosis of insulin
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8
Q

First generation sulfonylurea drugs

A

Tolbutamide (Orinase)
Tolazamide (Tolinase)
Chlorpropamide (Diabinese)

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9
Q

Tolbutamide potency/duration

A

1 / 6 to 12 hours

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10
Q

tolazamide potency/duration

A

5 / 12 to 14 hours

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11
Q

chlorpropamide potency/duration

A

6 / 24 to 72 hours

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12
Q

2nd generation sulfonylurea drugs

A

Glipizide (Glucotrol)
Glyburide or Glibenclamide (Diabeta, Glynase)
Glimepiride (Amaryl)

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13
Q

Glipizide potency/duration

A

100 / 12 to 24 hrs

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14
Q

glyburide potency/duration

A

150 / 24 hours

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15
Q

glimerpiride potency/duration

A

around 150 / 24 hours

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16
Q

Metiglinides “glinides”

A

Repaglinide (Prandin)
Nateglinide (Starlix)

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17
Q

Repaglinide mechanism

A

same mechanism as sulfonylureas

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18
Q

Repaglinide onset/duration

A

quick onset/short duration of action (t1/2 = 1 hr)

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19
Q

Repaglinide dosing

A

tablet taken before each meal (preprandial)

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20
Q

Nateglinide mechanism

A

non-sulfonylurea KATP channel blocker
very specific for KATP channels in the pancreas vs CV tissue

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21
Q

Nateglinide onset/duration

A

quick onset/short duration of action

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22
Q

Nateglinide advantage over repaglinide

A

nateglinide has a shorter t1/2 so there is less risk of hypoglycemia

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23
Q

Sulfonylurea drug interactions

A
  • drugs which may enhance the action of sulfonylureas and increase the risk of hypoglycemia (salicylates, phenylbutazone, sulfonamides, clofibrate_
  • drugs that have their own hypoglycemic effects which may be additive to the sulfonylurea (Alcohol: excessive acute intake, high dose salicylates)
  • drugs which cause hyperglycemia which in turn oppose the action of sulfonylureas and insulin therapy (Oral contraceptives, epinephrine, thiazide diuretics, corticosteroids, thyroid)
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24
Q

drugs that decrease glucagon secretion

A

Incretins
Amylin

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25
Q

Drugs that decrease glucose reabsorption

A

SGLT2 inhibitors

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26
Q

Drugs that control appetite

A

Incretins
Amylin

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27
Q

Drugs that increase uptake and utilization of glucose

A

Thiazolidinediones
Metformin

28
Q

Drugs that decrease hepatic glucose output

A

Metformin
Thiazolidinediones

29
Q

Drugs that work in the GI tract

A

Incretins
a-glucosidase inhibitors
amylin
Bile acid sequestrant

30
Q

Drugs that treat lipotoxicity

A

Thiazolidinediones

31
Q

GLP-1R agonists

A

Exenatide (Exendin 4; Byetta)
Liraglutide (Victoza)
Lixenatide (Adlyxin)
Dulaglutide (Trulicity)
Semaglutide (Ozempic)

32
Q

Drugs that increase the incretin effect

A

GLP-1R agonists
GLP-1 & GIP dual agonist
DPP-IV inhibitors
Amylin Analogs

32
Q

GLP-1 & GIP dual agonists

A

Tirzepatide (Mounjaro, Zepbound)

33
Q

DPP-4 inhibitor drugs

A

Saxagliptin (onglyza)
Sitagliptin (Januvia)
Linagliptin (Tradjenta)
Alogliptin (Nesina)

34
Q

Amylin analog

A

Pramlintide (Symlin)

35
Q

Incretins

A

a group of hormones produced by the gastrointestinal system in response to glucose absorption that stimulate the release of insulin from the pancreas and help preserve the beta cells
GIP and GLP-1

36
Q

GLP-1 functions

A

stimulate insulin secretion
suppress glucagon secretion
slows gastric emptying
reduces food intake
increases B cell mass and maintains B cell function
improves insulin sensitivity
enhances glucose disposal

37
Q

GLP-1 signaling pathway

A

Gs and Gq
may explain why GLP-1 is more effective

37
Q

Exenatide

A

GLP-1 analog
39 amino acid peptide from Gila monster saliva

37
Q

GIP signaling pathways

A

Gs

37
Q

advantages of GLP-1 in treatment of T2DM

A

reduced hyperglycemia with low risk of hypoglycemia
weight loss
increased beta cell mass (hard to show in humans but has been seen)

38
Q

strategies of GLP-1 treatment of T2DM

A

provide long-lasting GLP-1 analog
prevent degradation of endogenous GLP-1
Positive allosteric modulators for the GLP-1 receptor (allows the body to respond to lower concentrations of GLP-1, going in for approval soon)

39
Q

GLP-1 agonists AE

A

N/V (usually lasts ~ 1 month), pancreatitis, risk of thyroid C-cell tumors - monitor calcitonin levels (contraindicated in pts with a family history of medullary thyroid cancer)

40
Q

GLP-1 MOA

A

activates GLP-1R and enhances 1st phase insulin secretion (postprandial)

41
Q

Exenatide duration of action

A

longer half life than endogenous GLP-1

42
Q

Exenatide dosing

A

Twice daily injections
once weekly injections (Bydureon)
both are co-administered with metformin, TzDs, or sulfonylureas

43
Q

Liraglutide

A

GLP-1 analog
human GLP-1 (hGLP-1) aa 7-37 (cleavage occurs taking away first 6 aa)

44
Q

Liraglutide duration

A

t1/2 of 13 hours

45
Q

Liraglutide dosing

A

0.6-3 mg SC daily
can be co-administered with metformin, TzDs, and sulfonylureas

46
Q

Dulaglutide

A

GLP-1R agonist
alanine is substituted with a valine

47
Q

Dulaglutide dosing

A

0.75 or 1.5 mg injected SC once weekly

48
Q

Lixisenatide

A

GLP-1R agonist
44 aa peptide (extended with a polylysine tail)

49
Q

Lixisenatide dosing

A

50 or 100 µg injected SC daily before breakfast

50
Q

Semaglutide

A

GLP-1R agonist
31 aa peptide (alanine is replace with 2-aminoisobutyratye)

51
Q

Semaglutide duration of action

A

extensively bound to serum albumin
t1/2 ~ 1 week

52
Q

Semaglutide (Rybelsus)

A

orally available GLP-1R agonist
oral bioavailability - 0.4-1.0%

53
Q

Semaglutide (Rybelsus) dosing

A

3, 7, or 14 mg once daily
much larger dose, so low availability is counteracted

54
Q

Soliqua

A

100 U glargine + 33 µg lixisenatide/ml
max daily dose 60 U/20 µg

55
Q

dosing Soliqua

A

injected SC once daily

56
Q

Xultophy

A

100 U degludec + 3.6 mg liraglutide/ml
max daily dose 50 U/1.8 mg

57
Q

Tirzepatide

A

Full GIP receptor agonist
Biased GLP-1R agonist

58
Q

Mechanism of Biased GLP-1R agonist

A

preferential coupling to cAMP over B-arrestin, which reduces internalization (desensitization) of GLP-1R to maintain GLP-1 effect

59
Q

Coupling of B-arrestin

A

method by which you desensitize GLP-1 receptors, coupling kicks of internalization of GLP-1 which terminates its activity

60
Q

Tirzepatide dosing

A

once weekly SC injections

61
Q

Tirzepatide advantages

A

reduces A1c and body weight more effectively than GLP-1R agonists

62
Q

Dipeptidyl peptidase (DPP) 4

A

cleave and break down incretins

Therapeutics 2 - Exam 2 (9 decks)

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