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Endocrine 2 > Diabetes - Konorev > Flashcards

Diabetes - Konorev Flashcards

1
Q

Rapid-acting insulin

A

LAG - Lispro, Aspart, Glulisine

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2
Q

Short-acting insulin

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 - classes

A

Incretin mimetics

K-ATP channel blockers

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7
Q

Incretin mimetics - classes (secretagogue)

A

GLP-1 agonist

DPP-4 inhibitors

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8
Q

K-ATP channel blockers - classes (secretagogue)

A

Sulfonylureas

Meglitinides

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9
Q

GLP-1 agonists (secretagogue)

A

Exenatide, Liraglutide

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10
Q

DPP-4 inhibitors (secretagogue)

A

“-gliptin” x4

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11
Q

First generation sulfonylureas (secretagogue)

A

Chlorpropamide, Tolbutamide, Tolazamide

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12
Q

Second generation sulfonylureas (secretagogue)

A

Glipizide, Glyburide, Glimepiride

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13
Q

Meglitinides (secretagogue)

A

Nateglinide, Repaglinide

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14
Q

Biguanides

A

Metformin

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15
Q

Thiazolidinediones

A

Pioglitazone, Rosiglitazole

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16
Q

SGLT2 inhibitors

A

Canagliflozin, Dapagliflozin, Empagliflozin

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17
Q

Alpha-glycosidases

A

Acarbose, Miglitol

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18
Q

Rapid insulin - why rapid?

A

Mutations = no dimers/hexamers = faster absorption

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19
Q

Rapid insulin - use

A

Postprandial hyperglycemia - avoidance

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20
Q

Regular insulin - why not rapid?

A

Forms hexamers, too bulky for immediate transport to bloodstream

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21
Q

Regular insulin - use

A

Basal maintenance, night coverage

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22
Q

NPH - why longer than regular insulin?

A

Protamine = digested before insulin can be absorbed

23
Q

NPH - use

A

Basal maintenance, night coverage

24
Q

Detemir vs. Glargine - why long?

A

Detemir - Lys 29 has lipid, binds albumin in blood

Glargine - AA subs enhance stability at physiologic pH (∆pKa)

25
Q

Insulin (any) - clinical indications

A

DM1, DM2, gestational DM, severe hyperkalemia

26
Q

Treating severe hyperkalemia

A

Insulin + glucose + furosemide

27
Q

Adverse effects of insulin (4)

A
  • Hypoglycemia
  • Lipodistrophy (using same injection site)
  • IgE hypersensitivity (rare)
  • Hypokalemia
28
Q

Natural things that activate Gs on beta cell

A

Epinephrine, GLP-1 receptor agonists (incretins), Glucagon

29
Q

Thing that activates Gi on beta cell

A

Somatostatin

30
Q

Pramlintide - use

A

Adjunct to insulin before meals to prevent postprandial hyperglycemia

31
Q

Pramlintide - MoA (4)

A

Inhibit glucagon, enhance insulin sensitivity, slow gastric absorption, satiety

32
Q

Pramlintide - side effects (2)

A
  • Severe hypoglycemia (must reduce insulin dose)

- Constipation (if on anticholinergics)

33
Q

GLP-1 agonists - general functions (3)

A
  • Increase glucose-related insulin release
  • Inhibit glucagon release (i.e. gluconeogenesis)
  • Slows gastric emptying
34
Q

Liraglutide - how different than Exenatide?

A

Lira = more GLP-1 homology, longer 1/2 life (lipid-modified = binds albumin)

35
Q

GLP-1 agonists - clinical indication

A

Type 2 DM - not adequately controlled w/ Metformin/Sulfonylureas/TZDs

36
Q

A patient w/ DM2 is still having hyperglycemia while on Metformin. The doc suggests either Pramlintide or a GLP-1 agonist to supplement. Which might be better?

Why? Explain

A

GLP-1 agonist

LESS risk of hypoglycemia (w/ insulin) - stimulates insulin release during hyperglycemia ONLY

37
Q

GLP-1 agonists - adverse effects

A

Pancreatitis, pancreatic cancer

38
Q

DPP-4 - function

A

Serine protease that inactivates GLP-1

39
Q

DPP-4 inhibitors - use

A

DM2 - alone or with other drugs

40
Q

DPP-4 inhibitors - adverse effects

A

URIs, nasopharyngitis

41
Q

Sulfonylureas - MoA

A

Block K-ATP channel, causing membrane depolarization and insulin release

42
Q

Sulfonylureas - use

A

DM2 - alone or w/ others

43
Q

Sulfonylureas - adverse effects (5)

A
  • Hypoglycemia
  • 2º resistance
  • Weight gain (increased insulin release)
  • Facial flushing
  • Sulfa drug allergy/cross-reactivity
44
Q

Sulfonylurea + Sulfonamides or Salicylates
Sulfonylurea + alcohol
Sulfonylurea + gemfibrozil/cimetidine/azole

A
  • Displaced from albumin = high action
  • Enhanced action at K-channel
  • CYP inhibition = high actioin
45
Q

Sulfonylurea + B-blocker/CCB
Sulfonylurea + diazoxide
Sulfonylurea + phenytoin/rifampin

A
  • Low insulin release = opposing actions
  • Less action at K-channel = less action
  • CYP activation = less action
46
Q

Meglitinides - MoA

A

Inhibit K-ATP channel (like sulfonylureas), causing insulin release

47
Q

Meglitinides - use

A

DM2 - postprandial hyperglycemia control (alone or with others)

48
Q

Meglitinides - adverse effects

A

Hypoglycemia, 2º resistance, weight gain

49
Q

Metformin - MoA

A

Inhibits OxPhos complex 1, leading to activation of AMP-dependent protein kinase, causing phosphorylation of targets that increase insulin action

50
Q

Metformin - use

A

DM2 (common) - 1st line

51
Q

Why is Metformin so heavily used? (4)

A
  • NO HYPOGLYCEMIA
  • NO WEIGHT GAIN
  • ORAL
  • Vascular complication decrease
52
Q

Metformin - adverse effects

A
  • GI upset (like the rest)

- Lactic acidosis (do NOT give if renal disease)

53
Q

Thiazolidinediones - MoA

A

Increases insulin sensitivity -Activates PPAR-gamma (nuclear receptor) in fat, muscle, liver, endothelium

–> increased GLUT4, increased insulin signaling molecules, adiponectin, inhibited gluconeogenesis, inhibited inflammation

Endocrine 2 (12 decks)

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