Treatment of Type 2 Diabetes: Oral Agents Flashcards Preview

DEMS: Unit II > Treatment of Type 2 Diabetes: Oral Agents > Flashcards

Flashcards in Treatment of Type 2 Diabetes: Oral Agents Deck (19)
Loading flashcards...
1
Q

Organ systems targeted by glucose-lowering therapies + role in regulating glucose homeostasis

A
  • Pancreas
    • Secretes insulin and glucagon
  • Liver
    • Major player in gluconeogenesis, glycogen synthesis, etc
  • Muscle
    • Stores glycogen, undergoes glycogenolysis, takes up glucose when insulin is high
  • Adipose tissue
    • Takes up glucose when insulin is high
  • GI
    • Secretes incretin enhancers which assist insulin-mediated reduction of glucose levels
2
Q

Main classes of non-insulin medications

A
  • Sulfonylureas
    • ex. glipizide, glyburide
  • Biguanide
    • ex. Metformin
  • Thiazolidinediones
    • ex. Pioglitazone, rosiglitazone
  • Incretin enhancers (GIP, GLP, DDP)
  • GLP-1 Agonists
    • ex. exenatide, liraglutide
  • DPP4 inhibitors
    • ex. sitagliptin
  • Amylin analogue
    • ex. pramlintide
3
Q

Sulfonylureas: examples

A

ex. glipizide, glyburide

4
Q

Sulfonylureas: MOA

A
  • MOA: Increase endogenous insulin secretion by closing ATP sensitive K+ channels → depolarization → Voltage gated Ca2+ channels → exocytosis of insulin
  • SOA: Pancreas
5
Q

Biguanide: examples, MOA

A
  • ex. Metformin
  • MOA: Acts at the liver to potentiate suppressive effects of insulin on hepatic glucose production
  • SOA: Liver
6
Q

Thiazolidinediones: examples

A

ex. Pioglitazone, rosiglitazone

7
Q

Thiazolidinediones: MOA

A
  • Insulin sensitizing → activates PPAR ɣ receptor ==> increases insulin action ==> transcription of genes involved in adipocyte differentiation, glucose & lipid metabolism amongst other.
  • SOA:
    • Mainly skeletal muscle & adipose tissue
    • (liver - decreases gluconeogensis)
8
Q

Incretin enhancers (GIP,GLP, DDP): MOA

A
  • MOA: Incretins contribute to the control of postprandial glycemia by ↑ insulin
  • SOA:
    • GI
    • pancreas
9
Q

GLP-1 Agonists: exmaples

A

ex. exenatide, liraglutide

10
Q

GLP-1 Agonists: MOA

A
  • MOA: GLP-1 amplifies glucose stimulated insulin secretion, inhibits glucagon secretion, slows gastric emptying, and increases satiety in the CNS
  • SOA:
    • GI
    • pancreas
11
Q

DPP4 inhibitors: examples

A

sitagliptin

12
Q

DPP4 inhibitors: MOA

A
  • MOA: DPP4 inhibition prevents GLP-1 degradation ==> Enhance pancreatic insulin secretion and suppress glucagon, no effect on appetite or gastric emptying
  • SOA:
    • GI
    • pancreas
13
Q

Amylin analogue: examples

A

pramlintide

14
Q

Amylin analogue: MOA

A
  • MOA: Amylin is a peptide co-secreted with insulin, and inhibits gastric emptying and glucagon secretion acutely, leading to reduced food intake and weight loss
  • SOA:
    • GI
    • pancreas
15
Q

Blood glucose and HbA1c goals for adults w/DM

A
  • Hemoglobin A1c (HbA1c or A1c)
    • < 7% (general), 6% (individual)*
    • without significant hypoglycemia
  • Fasting glucose
    • 70-130 mg/dL
  • 2 hour postprandial glucose
    • < 180 mg/dL
16
Q

Routine monitoring for adults with diabetes

A
  • home blood glucose monitoring
    • check fingerstick blood glucoses at least twice per day at specific timepoints:
    • fasting, before lunch, before dinner, and at bedtime
  • record: glucose results, insulin admin, diet, physical activity
17
Q

Characteristics of incretin enhancers

A
  • Incretin enhancers are GI mediated molecules that assist insulin-mediated glucose reduction post-prandium
  • serum insulin levels increase significantly more upon oral dosage of glucose vs. IV due to incretin enhancers
  • main incretin enhancers: GLP-1 & GIP
    • GLP-1 = glucagon-like peptide-1
    • GIP = glucose-dependent insulinotropic polypeptide
18
Q

GLP-1 and T2D

A

Type 2 diabetics have normal or elevated levels of GLP-1 but are resistant to its insulin stimulatory actions

19
Q

Fxn of DPP-4 (dipeptidyl peptidase-IV)

A

an enzyme that rapidly inactivates (within minutes) GLP-1 & GIP