Therapeutics 2 - Exam 2 > T2DM pt 1 > Flashcards

T2DM pt 1 Flashcards

(66 cards)

Study These Flashcards
1
Q

cause of T2DM

A

insulin resistance and reduced insulin secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

drugs that increase insulin secretion

A

sulfonylureas
meglitinides
incretins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

sulfonylurea drugs

A

tolbutamide
tolazamide
chlorpropamide
glyburide
glipizide
glimeperide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

meglitinide drugs

A

nateglinide
repaglinide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

First generation sulfonylurea drugs

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Tolbutamide potency/duration

A

1 / 6 to 12 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

tolazamide potency/duration

A

5 / 12 to 14 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

chlorpropamide potency/duration

A

6 / 24 to 72 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

2nd generation sulfonylurea drugs

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Glipizide potency/duration

A

100 / 12 to 24 hrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

glyburide potency/duration

A

150 / 24 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

glimerpiride potency/duration

A

around 150 / 24 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Metiglinides “glinides”

A

Repaglinide (Prandin)
Nateglinide (Starlix)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Repaglinide mechanism

A

same mechanism as sulfonylureas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Repaglinide onset/duration

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Repaglinide dosing

A

tablet taken before each meal (preprandial)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Nateglinide mechanism

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Nateglinide onset/duration

A

quick onset/short duration of action

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Nateglinide advantage over repaglinide

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

drugs that decrease glucagon secretion

A

Incretins
Amylin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Drugs that decrease glucose reabsorption
SGLT2 inhibitors
26
Drugs that control appetite
Incretins Amylin
27
Drugs that increase uptake and utilization of glucose
Thiazolidinediones Metformin
28
Drugs that decrease hepatic glucose output
Metformin Thiazolidinediones
29
Drugs that work in the GI tract
Incretins a-glucosidase inhibitors amylin Bile acid sequestrant
30
Drugs that treat lipotoxicity
Thiazolidinediones
31
GLP-1R agonists
Exenatide (Exendin 4; Byetta) Liraglutide (Victoza) Lixenatide (Adlyxin) Dulaglutide (Trulicity) Semaglutide (Ozempic)
32
Drugs that increase the incretin effect
GLP-1R agonists GLP-1 & GIP dual agonist DPP-IV inhibitors Amylin Analogs
32
GLP-1 & GIP dual agonists
Tirzepatide (Mounjaro, Zepbound)
33
DPP-4 inhibitor drugs
Saxagliptin (onglyza) Sitagliptin (Januvia) Linagliptin (Tradjenta) Alogliptin (Nesina)
34
Amylin analog
Pramlintide (Symlin)
35
Incretins
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
GLP-1 functions
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
GLP-1 signaling pathway
Gs and Gq may explain why GLP-1 is more effective
37
Exenatide
GLP-1 analog 39 amino acid peptide from Gila monster saliva
37
GIP signaling pathways
Gs
37
advantages of GLP-1 in treatment of T2DM
reduced hyperglycemia with low risk of hypoglycemia weight loss increased beta cell mass (hard to show in humans but has been seen)
38
strategies of GLP-1 treatment of T2DM
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
GLP-1 agonists AE
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
GLP-1 MOA
activates GLP-1R and enhances 1st phase insulin secretion (postprandial)
41
Exenatide duration of action
longer half life than endogenous GLP-1
42
Exenatide dosing
Twice daily injections once weekly injections (Bydureon) both are co-administered with metformin, TzDs, or sulfonylureas
43
Liraglutide
GLP-1 analog human GLP-1 (hGLP-1) aa 7-37 (cleavage occurs taking away first 6 aa)
44
Liraglutide duration
t1/2 of 13 hours
45
Liraglutide dosing
0.6-3 mg SC daily can be co-administered with metformin, TzDs, and sulfonylureas
46
Dulaglutide
GLP-1R agonist alanine is substituted with a valine
47
Dulaglutide dosing
0.75 or 1.5 mg injected SC once weekly
48
Lixisenatide
GLP-1R agonist 44 aa peptide (extended with a polylysine tail)
49
Lixisenatide dosing
50 or 100 µg injected SC daily before breakfast
50
Semaglutide
GLP-1R agonist 31 aa peptide (alanine is replace with 2-aminoisobutyratye)
51
Semaglutide duration of action
extensively bound to serum albumin t1/2 ~ 1 week
52
Semaglutide (Rybelsus)
orally available GLP-1R agonist oral bioavailability - 0.4-1.0%
53
Semaglutide (Rybelsus) dosing
3, 7, or 14 mg once daily much larger dose, so low availability is counteracted
54
Soliqua
100 U glargine + 33 µg lixisenatide/ml max daily dose 60 U/20 µg
55
dosing Soliqua
injected SC once daily
56
Xultophy
100 U degludec + 3.6 mg liraglutide/ml max daily dose 50 U/1.8 mg
57
Tirzepatide
Full GIP receptor agonist Biased GLP-1R agonist
58
Mechanism of Biased GLP-1R agonist
preferential coupling to cAMP over B-arrestin, which reduces internalization (desensitization) of GLP-1R to maintain GLP-1 effect
59
Coupling of B-arrestin
method by which you desensitize GLP-1 receptors, coupling kicks of internalization of GLP-1 which terminates its activity
60
Tirzepatide dosing
once weekly SC injections
61
Tirzepatide advantages
reduces A1c and body weight more effectively than GLP-1R agonists
62
Dipeptidyl peptidase (DPP) 4
cleave and break down incretins
Therapeutics 2 - Exam 2
flashcards
Decks in class (9)
# Cards
Brainscape helps you reach your goals faster, through stronger study habits.
© 2026 Bold Learning Solutions. Terms and Conditions