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Endocrine II midterm > Konorev DSA: Drugs for Diabetes > Flashcards

Konorev DSA: Drugs for Diabetes Flashcards

1
Q

Rapid Acting Inulins

A
  • aspart
  • lispro
  • glulisine
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2
Q

short acting insulins

A

-regular insulin

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3
Q

Intermediate acting insulin

A

NPH

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4
Q

Long acting insulin

A
  • Detemir

- Glargine

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5
Q

Amylin analog

A

-Pramlintide

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6
Q

Insulin secretagogues

A
  • incretin memetics

- Katp channel blockers

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7
Q

Incretin Mimetics

A
  • GLP-1 agonists: Exenatide, Liraglutide

- Dipeptidyl peptidase-4 (DPP-4) inhibitors: Sitagliptin, linagliptin, saxagliptin, alogliptin

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8
Q

Katp channel blockers

A
  • sulfonylureas

- Meglitinides

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9
Q

first generation sulfonylureas

A
  • Chorpropamide
  • tolbutamide
  • tolazamide
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10
Q

Second generation Sulfonylureas

A
  • Glipizide
  • Glyburide
  • Glimepride
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11
Q

Meglitinides

A
  • Nateglinide

- Repaglinide

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12
Q

Biguanides

A

Metformin

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13
Q

Thiazolidinediones

A
  • Pioglitazone

- Rosiglitazone

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14
Q

Sodium-glucose co transporter 2 (SGLT2) inhibitors

A
  • Canagliflozin
  • Dapagliflozin
  • Empagliflozin
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15
Q

Inhibitors of alpha-glycosidases

A
  • Acarbose

- Miglitol

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16
Q

What are the end effects of insulin?

A
  • increased glycogen/lipid/protein synthesis
  • decreased lipolysis
  • cell growth and differentiation
  • AKT pathway: regulation of enzyme activities
  • MAP kinases: regulation of gene trascription and cell proliferation
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17
Q

What transcription factor is for cell growth and differentiation and for cell proliferation and increased survival?

A

ELK1

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18
Q

Which TF is for cell growth and differentiation and cell proliferation and apoptosis

A

-AP-1

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19
Q

Which TF will give of decreased glycogenolysis, decreased gluconeogenesis, and escaped the cell cycle arrest and increases proliferation?

A

FoxO1

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20
Q

What happens with GLUT4 when insulin binds IRS?

A

gets translocated to the cell membrane

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21
Q

What are the effects on carb metabolism by Insulin?

A
  • glucose transport (GLUT4)
  • Activation of glycolysis
  • Activation of glycogen synthesis
  • Inhibition of gluconeogenesis
  • Inhibition of glycogenolysis
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22
Q

Is cAMP lowered or elevated by insulin binding?

A

lowered

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23
Q

Insulin effects on lipid metabolism

A
  • inhibition of lipolysis :decreased hormone-sensitive lipase, decreased TG breakdown
  • enhanced lipogenesis: increased expression of FA synthase
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24
Q

Insulin effects on protein metabolism

A
  • increased ptn synth

- increased mTOR,,,, ribosome biogenesis, mRNA translation

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25
Q

Why are the rapid acting insulins so rapid?

A

-mutations fromhuman sequence block assembly of dimers and hexamers… allow for faster absorption

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26
Q

Clinical use of rapid-acting insulins

A

-postprandial hyperglycemia…taken before a meal

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27
Q

What is used for overnight coverage of insulin in the body?

A
  • just regular insulin
  • if for postprandial hyperglycemia, inject 45 min before the meal
  • lasts 10 hrs
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28
Q

What is used for basal insulin maintenance and/or overnight coverage?

A

NPH, the intermediate acting insulin

-lasts 4-12 hrs

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29
Q

What is used for pretty much only basal insulin maintenance?

A

Long acting insulin: Detemir or Glargine

-lasts 24 hrs

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30
Q

Indications for insulin use?

A

Type 1 or 2 diabetes

  • or Severe Hyperkalemia, remember that it also traps all of the K+ in the cell
  • use loop diuretics to eliminate K+ from the body
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31
Q

Adverse effects of Insulin

A
  • hypoglycemia
  • lipodystrophy
  • Resistance: they will develop insulin binding antibodies
  • Allergic rxns (rare)
  • hypokalemia
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32
Q

What is the most common complication of insulin therapy?

A

Hypoglycemia

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33
Q

Common causes of hypoglycemia

A
  • delay of a meal or a missed meal
  • exercise: exercised muscle consumes more glucose
  • overdose of insuin
34
Q

Signs of hypoglycemia

A
  • confusion,m dizarre behavior, seizures, coma
  • sympathetic hyperactivity: tachycardia, palpitations, sweating, tremor
  • Parasympathetic hyperactivity: hunger, nausea
  • Patients on tight glycemic control: “hypoglycemic unawareness”
35
Q

Tx for hypoglycemia

A
  • glucose: juice, candy, etc. if consciou; I.V. glucose if unconscious
  • Diazoxide: stong hyperglycemic agent- Katp channel opener…. also inhibits the release of insulin by beta cells
  • Glucagon
36
Q

MOA of Glucagon

A
  • Gs coupled GPCR
  • activation of AC
  • PKA
  • phosphorylase…. glycogenolysis
  • increased expression of PEPCK and Glu-6-Pase…. gluconeogenesis
37
Q

Effects of Glucagon

A
  • Hepatocytes: increased glucose output, glycogen depletion (non of this nonsense in skeletal m.)
  • Potent inotropic and chronotropic effcet on the heart
  • GI smooth muscle relaxation
  • Increase insulin release by beta-cells
  • increase release of catecholamines by chromaffin cells (contraindicatedin pheochromocytoma patients)
38
Q

Clinical uses of glucagon

A
  • moderate-to severe hypoglycemia
  • beta-blocker overdose
  • Radiology of the bowel
39
Q

Amylin analog

A

Pramlintide

40
Q

What is pramlintide used for?

A

type 1 or 2 diabetes

-injected sc before meals as an adjunct to insulin therapy

41
Q

Adverse effects of pramlintide

A
  • GI: nausea, vomiting, diarrhea, anorexia

- Severe hypoglycemia, especially if used together with insulin… insulin dose should be reduced

42
Q

Drug interactions with Pramlintide

A

-enhances effects of anticholinergic drugs in GI tract

43
Q

What are the long acting GLP-1 receptor agonists?

A
  • Exenatide

- Liraglutide

44
Q

Clinical use of Exenatide or Liraglutide

A
  • release of GLP-1 is diminished post prandially in type 2 diabetes pts
  • approved in type 2 diabetics not adequately controlled by metformin/sulfonylureas/thiazolidinediones
  • doses of other anti-diabetic meds should be reduced to avoid hypoglycemia
45
Q

Adverse effects of GLP-1 receptor antagonists

A
  • Nausea, comiting, diarrhea, anorexia
  • lower risk of hypoglycemia vs. pramlintide
  • linked to cases of acute pancreatitis and pancreatic cancer
  • possible link to thyroid cancer
46
Q

What are the DPP-4 inhibitors?

A
  • the gliptins
  • Sitagliptin
  • Linagliptin
  • Saxagliptin
  • Alogliptin
47
Q

MOA of DPP-4 inhibitors?

A
  • DPP-4 is a serine protease that degrades GLP-1 and other incretins
  • so… we stop that shit
  • used as adjunctive therapy w/ diet and exercise
48
Q

Averse effects of the DPP-4 inhibitors

A
  • upper respiratory infections and nasopharyngitis
  • linked to acute pancreatitis
  • hypoglycemia
49
Q

Katp channel blockers

A
  • sulfonylureas 1st and 2nd gen

- Non-sulfonylureas (meglitinides)

50
Q

What’s the difference between 1st and second generation sulfonylureas?

A

-2nd gen has higher potency

51
Q

Clinical use of sulfonylureas

A

-type 2 diabetes as a monotherapy or in combo with insulin or other anti-diabetic drugs

52
Q

adverse effects of sulfonylureas

A
  • hypoglycemia
  • weight gain
  • secondary failure
  • Disulfiram-like effect of alcohol-induced flushing
  • Dermatological and general hypersensitivity reactions with other sulfonamides
53
Q

Drug interactions with sulfonylureas that enhance their hypoglycemic effect

A
  • displacing from binding with plasma proteins: sulfonamides, clofibrate, and salicylates
  • enhancing the effect on Katp channel: ethanol
  • inhibiting CYP enzymes: azole antifungals, gemfibrozil, cimetidine, etc..
54
Q

Drug interactions with sulfonylureas that decrease their glucose-lowering effect

A
  • inhibiting insulin secretion : beta-blockers, CCBs
  • antagonizing their effect on Kast channel: diaazoxide
  • Inducing hepatic CYP enzymes: phenytoin, griseofulvin, rifampin, etc…..
55
Q

MOA of Meglitinides

A

-Katp Channel inhibitiion

56
Q

clinical use of meglitinides

A
  • control of postprandial hyperglycemia in patients with type 2 diabetes
  • taken orally before the meal
  • can be used either alone or in combo with other antidiabetic drugs
57
Q

Side effects of meglitinides

A
  • hypoglycemia
  • secondary failure
  • weight gain
58
Q

Biguanides

A

Metformin!

59
Q

MOA of metformin

A
  • activation of AMP-dependent ptn kinase
  • exact mechanism unclear
  • Phophorylates stuff… leads to: inhibition of lipogenesis and gluconeogenesis, increase in glc uptake, glycolysis, and FA oxidation, lower glc levels in hyperglycemic (but not normoglycemic) states, increases insulin sensitivity
60
Q

Clinical use of metformin

A

-most commonly used oral agent to treat type 2 diabetes*… first line

61
Q

Why is metformin so great?

A
  • does better job of lowering glucose
  • does not cause hypoglycemia
  • no weight gain
  • taken orally
  • can be used either alone or in combo w/ other oral agents
62
Q

PK of metformin

A
  • not bound to plasma proteins
  • not metabolized
  • excreted unchanged by kidneys
63
Q

Adverse effects and contraindications of metformin

A
  • most common: GI complications like anorexia, vomiting, nausea, diarrhea, abdominal discomfort
  • decreased absorption of B12
  • lactic acidosis, especially under conditions of hypoxia, renal and hepatic insufficiency
  • contraindicated in conditions predisposing to tissue hypoxia, renal failure, chronic alcoholism, and cirrhosis
64
Q

Thiazolidinediones

A
  • Pioglitazone

- Rosiglitazone

65
Q

MOA of thiazolidinediones

A
  • Ligands of peroxisome proliferator-activated receptor-gamma (PPARy)
  • endogenous ligands: PG and FFAs and their derivatives
  • but TZDs have much igher affinity for PPARy
66
Q

What is PPARy?

A

a nuclear receptor expressed primarily in fat, muscle, liver tissue, and endothelium
-heterodimeric PPARy/RXR binds to specific DNA PPRE sequences to either increase or decrease gene transcription

67
Q

What are the effects of PPARy activation on gene expression?

A
  • increased GLUT4 in skeletal m.: enhanced glucose uptake, reduced hyperglycemia
  • same for adipocytes
  • increased IRS1,2, and PI3K: increased insulin sensitivity
  • Increased Adiponectin and other adipiokines: increased insulin sensitivity and decreased inflammation
  • decreases gluconeogenesis
  • decreases NFKB and AP-1 transactivation: decreased production of IL’s and other cytokines… antiinflammatory
68
Q

important PK thing for TZDs

A
  • it’s metabolized by the liver, so things that induce CYP will decrease its half life
  • safe to administer to patients with renal failure
69
Q

clinical use of TZDs?

A
  • type 2 diabetes
  • delays progression of prediabetes to type 3 diabetes
  • euglycemic drug…. no hypoglycemia when used alone
70
Q

Adverse effects of TZDs

A
  • weight gain, especially if with insulin
  • Edema: increased ENaC in kidneys
  • Exacerbation of heart failure
  • Link to the increased risk of bladder cancer
  • Osteoporosis
  • Increased TC and LDL-C (rosiglitazone
71
Q

SGLT2 inhibitors

A
  • Canagliflozin
  • Dapagliflozin
  • Empagliflozin
72
Q

MOA of SGLT2 inhibitors

A

-inhibit the SGLT2 transporter, which lets us excrete some glucose into the urine… reduces hyperglycemia

73
Q

Other effects of SGLT2 inhibitors

A
  • osmotic iduresis
  • induces weight loss
  • reduces blood pressure
  • reduce plasma levels of uric acid
  • do not cause hypoglycemia when used alone
74
Q

Clinical use of SGLT2 inhibitors

A
  • as an adjunct to diet and exercise in adults with type 2 diabetes
  • taken orally before the first meal once a day
  • in pts with hypovolemia, this condition should be corrected before the start of therapy
75
Q

Adverse effects of SGLT2 inhibitors

A
  • hypotension
  • hypovolemia: dizziness, syncope
  • Genital and urinary tract infections
  • hypoglycemia if combined with insulin or insulin secretagogues
  • increased LDL-C
  • renal function impairment: fall inglomerular filtration rate, increase plasma creatinine
  • hyperkalemia
  • development of ketoacidosis
76
Q

Alpha-glycosidase inhibitors

A
  • Acarbose

- Miglitol

77
Q

MOA of alph-glycosidase inhibitors

A
  • competitive inhibition of a-glycosidases, a family of enzyme located on the brush border of intestinal epithelium
  • only monosaccharaides are absorbed from GI into the blood
  • Enzyme inhibition defer digestion and thus absorption of ingested starch and disaccharides
  • lower postprandial hyperglyemia to creat an insulin-sparing effect
78
Q

Clinical use of alpha-glycosidase inhibitors

A
  • type 2 diabetes as monotherapy or in combo with other oral antidiabetic agents or insulin
  • taken orally at mealtime
  • do not cause hypoglycemia when used alone
  • do not cause weight gain
79
Q

Adverse effects of alpha-glycosidase inhibitors

A
  • most common: malabsorption, flatulence, diarrhea, and abdominal bloating
  • hypoglycemia has been described when combined with insulin or insulin secretagogues
80
Q

Drug interactions

A

-decrease absorption of digoxin and propranolol and ranitidine

Endocrine II midterm (13 decks)

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