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EndoRepro 2 Exam 2 > Diabetes drugs - Konorev > Flashcards

Diabetes drugs - Konorev Flashcards

1
Q

what is the diagnostic criteria of diabetes mellitus?

A

increased plasma glucose levels >125 mg/dl

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2
Q

what effect do T3/T4, glucagon, epinephrine and glucocorticoids have on blood glucose levels?

A

they increase blood glucose levels

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3
Q

what happens in diabetes?

A

loss of insulin or insulin responsiveness -> unopposed mobilization of glucose

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4
Q

what does the insulin receptor-PI3K-Akt pathway have effects on?

A

glucose, lipid and protein metabolism, via regulation of enzyme activities or gene expression

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5
Q

what does the insulin receptor-MAP kinase pathway have effects on?

A

regulation of gene transcription and cell proliferation

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6
Q

what are the anabolic effects of insulin on carbohydrate metabolism?

A

promotes intracellular glucose transport and utilization

  • GLUT4 translocation to the cell membrane in skeletal muscle, cardiac myocytes, and adipocytes
  • activation of glycoslysis
  • activation of glycogen syntheses
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7
Q

how does insulin oppose catabolic effects of other hormonal systems?

A
  • inhibits gluconeogenesis

- inhibits glycogenolysis

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8
Q

what drugs class are:

  • sulfonylureas
  • meglitinides
  • GLP-1 agonists
  • dipeptidyl Peptidase-4 (DPP-4) inhibitors
A

insulin secretagogues

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9
Q

what are the rapid-acting insulins? (3)

A
  • aspart (novolog)
  • lispro (humalog)
  • glulisine (apidra)
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10
Q

what is the one short acting insulin

A

regular insulin (Humulin, novolin)

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11
Q

what is the intermediate acting insulin?

A

NPH - neutral protamine hagerdorn

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12
Q

what are the two long-acting insulins?

A
  • detemir (Levemir)

- glargine (Lantus)

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13
Q

what is the standard delivery method for insulin?

A

subcutaneous injection using disposable needles and syringes

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14
Q

what insulin delivery system has

  • continuous glucose sensor
  • controlling device (microchip)
  • insulin pump
A

artificial/bionic pancreas

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15
Q

what is a bi-hormonal bionic pancreas?

A

it delivers both insulin and glucagon

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16
Q

what is the MOA of amylin?

A
  • inhibits glucagon secretion
  • enhances insulin sensitivity
  • decreases gastric emptying (slows the rate of intestinal glucose absorption)
  • causes satiety
17
Q

what is the amylin analog drug?

A

pramlintide (symlin)

18
Q

what are the endogenous factors of insulin secretion regulation? (3)

A
  • glucose
  • GPCR-Gs ligands (B2-adrenergic agonists, GLP-1 agonists)
  • GPCR-Gi ligans (somatostatin, a2-adrenergic agonists)
19
Q

what are the drug targets of insulin?

A
  • resting membrane potential and specifically K-ATP channel
  • voltage-dependent (L-type) calcium channel
  • GPCR-Gs/GPCR-Gi cAMP axis
20
Q

incretin mimetics activate GLP-1 receptor or boost endogenous GLP-1 levels

A

insulin secretagogues

21
Q

these drugs are a group of gastrointestinal hormones that cause a decrease in blood glucose levels

A

incretins

22
Q

this incretin is synthesized by intestinal L-cells, and promotes:

  • b-cell proliferation
  • insulin gene expression
  • glucose-dependent insulin secretion
A

Glucagon-like peptide-1 (GLP-1)

  • inhibits glucagon secretion
  • also causes satiety, inhibits gastric emptying
23
Q

why is GLP-1 not an effective drug?

A

it has a very short half life (1-2 mins)

24
Q

what are the two long-acting GLP-1 receptor agonists?

A
  • exenatide (Byetta)

- liraglutide (Victoza)

25
Q

what are the 4 DPP-4 inhibitors? (gliptins)

A
  • sitagliptin
  • linagliptin
  • saxagliptin
  • alogliptin
26
Q

what is the MOA of DPP-4 inhibitors?

A
  • DPP-4 is a serine protease that degrades GLP-1 and other incretins
  • they increase levels of GLP-1 to enhance its interactions with the cognate receptor
  • effects are similar to those of GLP-1 agonists
27
Q

what are the 3 first generation sulfonylurea K-ATP channel blockers?

A
  • chlorpropamide
  • tolbutamide
  • tolazamide
28
Q

what are the 3 second generation sulfonylurea K-ATP channel blockers?

A
  • glipized
  • glyburide
  • glimepiride
29
Q

what are the 2 non-sulfonylurea K-ATP channel blockers?

A
  • nateglinide

- repaglinide

30
Q

what is the MOA of K-ATP channel blockers?

A
  • they bind to sulfylurea receptor

- blocking K current through Kir6.2 inwardly rectifying potassium channel

31
Q

what is the MOA of metformin (glucophage)

A

activation of AMP-dependent protein kinase

32
Q

what are the 2 thiazolidinediones?

A
  • pioglitazone (actos)

- rosiglitazone (avandia)

33
Q

what is the MOA of thiazolidinediones?

A
  • ligands of peroxisome proliferator-activated receptor-gamma (PPARy)
  • PPARu is a nuclear receptor expressed primarily in fat, muscle, liver tissue, and endothelium
34
Q

thiazolidinediones increase the transcription of what?

A
  • Glut4 in skeletal muscle
  • Glut4 in adipocytes
  • IRS1, IRS2, Pi3K
35
Q

thiazolidinediones decrease the transcription of what?

A
  • PEPCK

- NF-kb, AP-1

36
Q

what are the 3 sodium-glucose cotransporter 2 inhibitors? (gliflozins)

A
  • canagliflozin
  • dapaglifozin
  • empagliflozin
37
Q

what do SGLT2 inhibitors do?

A

they partially block reabsorption of glucose, so more of it is excreted

38
Q

what are the 2 a-glycosidase inhibitors?

A
  • acarbose

- miglitol

39
Q

what is the MOA of a-glycosidase inhibitors?

A
  • only monosaccharides are absorbed from GI into the blood
  • competitive inhibition of a-glycosidases, a family of enzymes on the intestinal epithelium defer digestion and thus absorption of ingested starch and disaccharides
  • lower postprandial hyperglycemia to create an insulin-sparing effect

EndoRepro 2 Exam 2 (10 decks)

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