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Pharmacology > Antidiabetic Drugs > Flashcards

Antidiabetic Drugs Flashcards

1
Q

what causes insulin secretion

A
  • glucose
  • amino acids
  • GI hormones called incretins: glucagon like peptide-1 (GLP-1) and gastric inhibitory peptides (GIP)
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2
Q

mechanism of insulin secretion

A

hyperglycemia –> increase in ATP levels –> closes ATP dependent K+ channels –> depolarization and opening of voltage gated calcium channels –> influx of Ca2+ –> pulsatile insulin exocytosis

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3
Q

what degrades insulin

A

inuslinase found in liver gets rid of 60% and kidney the other 40% (roles reversed in insulin dependent diabetics getting SC injections)

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4
Q

mechanism once insulin bind to its receptor

A
  • insulin receptor has two covalently linked heterodimers that have an alpha (extracellular and recognition site) and a beta subunit (contains tyrosine kinase)
  • insulin binds to recognition site at the alpha subunit on outside of cell
  • this activates the tyrosine kinase on the beta subunit
  • tyrosine kinase and cytoplasmic proteins become phosphorylated
  • first proteins phosphorylated: insulin receptor substrate proteins (IRS)
  • IRS interacts with other signaling molecules to activate gene expression, metabolism, and growth
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5
Q

how does insulin increase uptake of glucose in muscle and adipose tissue

A

upregulating the GLUT-4 transporter –> hence promoting uptake of glucose by muscle and fat

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6
Q

how does insulin affect lipid metabolism

A
  • inhibits hormone sensitive lipase so decreasing circulating fatty acids
  • increases synthesis of fatty acids and TAGs and their storage in adipose tissue by providing glycerol-3-phosphate
  • increases lipoprotein lipase providing FA for esterification
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7
Q

what are the four types of insulin preparations

A
  • Rapid acting: fast onset and short duration
  • Short acting: rapid onset of action
  • intermediate acting
  • slow acting: slow onset of action
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8
Q

what are the rapid acting insulin preparation (talks about mechanism)

A

hexamers slow down the absorption of insulin and reduce its post prandial peak as seen in native insulin but those listed below do not form hexamers

Insulin Lispro
Insulin Aspart
Insulin Glulisine

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9
Q

describe how each of the rapid acting insulin preparations was created

A

Insulin Lispro: proline and lysine at pos 28 and 29 in B chain are reversed so proline on pos 29 and lysine on pos 28; low propensity to form hexamers

Insulin Aspart: substitution of the B28 proline by aspartate

Insulin Glulisine: replace asparagine with lysine at B3 and lysine by glutamate at B29

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10
Q

what are rapid acting insulin given

A

they mimic the prandial release of insulin and are less likely to cause hypoglycemia

usually given with a longer acting insulin to ensure proper glucose control

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11
Q

what is the short acting insulin and when should it be given

A

Regular insulin – given 30 minutes before a meal

safe in preggos

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12
Q

what is the intermediate acting insulin

A

Neutral Protamine Hagedorn Insulin (NPH) aka Isophane Insulin

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13
Q

why is intermediate acting insulin delayed (name it)

A

NPH insulin aka Isophane Insulin

delayed absorption of insulin because of conjugation of insulin with protamine

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14
Q

what are the long acting insulins

A

Insulin Glargine

Insuline Detemir

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15
Q

how is insulin glargine produced

A
  • two arginine residues added to the C terminus of the B chain
  • an asparagine in A21 is replaced with glycine on the A chain
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16
Q

what happens to insulin glargine in different pH solutions

A

soluble in acidic solution but precipitates in neutral pH

17
Q

what does insulin glargine’s acidic pH (4) prevent it from

A

can’t be mixed with short acting insulin preparations (insulin lispro, aspart, and glulisine) because they are formulated at neutral pH

18
Q

describe the peak of insulin glargine

A

it has a peakless absorption profile

19
Q

describe how was insulin detemir was created

A

terminal threonine is removed from the B30 position and myristate is attached to the new terminal B29 lysine

20
Q

what has a lower risk of hypoglycemia in comparison to NPH insulin

A

Insulin Glargine

Insulin Detemir

21
Q

benefits of rapid acting insulin over regular human insulin

A
  • rapid acting can be taken right before a meal

- improved post prandial glycemic control and less risk of hypoglycemia

22
Q

overall benefit of using rapid and long acting insulin over NPH and regular human insulin

A
  • improvements in HbA1C levels
  • better glycemic control
  • reduced hypoglycemia
23
Q

what type of insulin is used when IV therapy is warranted

A

regular human insulin

24
Q

AE of inhaled insulin

A

cough
throat pain or irritation
hypoglycemia

25
Q

contraindications of inhaled insulin

A

asthma
COPD
smokers

26
Q

goal of SC insulin therapy

A

replace the normal basal (overnight, fasting, and between meals) as well as bolus or prandial (meal time) insulin

27
Q

two methods used to simulate normal insulin release pattern

A
  • basal bolus insulin regimen: once to twice a day dose of basal insulin coupled with premeal doses of rapid or short acting insulin
  • insulin pump therapy: delivers various basal amounts of insulin over 24 hours as well as meal related boluses
28
Q

AE of basal bolus insulin regimen and insulin pump therapy

A
  • hypoglycemia
  • allergic reactions
  • lipodystrophy at injection site
29
Q

drugs that commonly causes hypoglycemia

A

BES

beta blocker
ethanol
salicylates

30
Q

how does ethanol cause hypoglycemia

A

inhibits gluconeogenesis

31
Q

how do beta blockers cause hypoglycemia

A
  • block the effects of catecholamines on gluconeogenesis (beta 2 causes increase in glycogenolysis and gluconeogenesis)
  • also blocks the symptoms of hypoglycemia by blocking tremors and tachycardia
32
Q

how does salicylates cause hypoglycemia

A
  • weak insulin like activity in periphery

- enhance pancreatic beta cells sensitivity to glucose and potentiating insulin secretion

33
Q

Drugs that cause hyperglycemia by countering the actions of insulin

A

HAGE

HIV protease inhibitors
Atypical antipsychotics
Glucocorticoids
Epinephrine

34
Q

drugs that cause hyperglycemia by inhibiting insulin secretion directly and indirectly

A

Directly:
Phenytoin
Clonidine
Calcium channel blockers

Indirectly:
diurectics by depleting K+

35
Q

non insulin antidiabetic agents

A

BIT BAGID

  • Biguanides
  • Insulin Secretagogues: Sulfonylurea and Meglitinides
  • Thiazolidinediones (TZDs)
  • Bile acid sequestrants
  • Amylin Analogs
  • alpha-Glucosidase inhibitors
  • Incretin analogs
  • DPP-IV inhibitors
36
Q

what are the “oral hypoglycemics”

A
  • Biguanides
  • Insulin Secretagogues: Sulfonylurea and Meglitinides
  • Thiazolidinediones (TZDs)

-alpha-Glucosidase inhibitors

37
Q

what are the insulin secretagogues

A

sulfonylurea and meglitinides

38
Q

what are the sufonylureas

A

Chlorpropamide
Glyburide
Glipizide
Glimepiride

Pharmacology (79 decks)

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