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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
Insulin (any) - clinical indications
DM1, DM2, gestational DM, severe hyperkalemia
26
Treating severe hyperkalemia
Insulin + glucose + furosemide
27
Adverse effects of insulin (4)
- Hypoglycemia - Lipodistrophy (using same injection site) - IgE hypersensitivity (rare) - Hypokalemia
28
Natural things that activate Gs on beta cell
Epinephrine, GLP-1 receptor agonists (incretins), Glucagon
29
Thing that activates Gi on beta cell
Somatostatin
30
Pramlintide - use
Adjunct to insulin before meals to prevent postprandial hyperglycemia
31
Pramlintide - MoA (4)
Inhibit glucagon, enhance insulin sensitivity, slow gastric absorption, satiety
32
Pramlintide - side effects (2)
- Severe hypoglycemia (must reduce insulin dose) | - Constipation (if on anticholinergics)
33
GLP-1 agonists - general functions (3)
- Increase glucose-related insulin release - Inhibit glucagon release (i.e. gluconeogenesis) - Slows gastric emptying
34
Liraglutide - how different than Exenatide?
Lira = more GLP-1 homology, longer 1/2 life (lipid-modified = binds albumin)
35
GLP-1 agonists - clinical indication
Type 2 DM - not adequately controlled w/ Metformin/Sulfonylureas/TZDs
36
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
GLP-1 agonist LESS risk of hypoglycemia (w/ insulin) - stimulates insulin release during hyperglycemia ONLY
37
GLP-1 agonists - adverse effects
Pancreatitis, pancreatic cancer
38
DPP-4 - function
Serine protease that inactivates GLP-1
39
DPP-4 inhibitors - use
DM2 - alone or with other drugs
40
DPP-4 inhibitors - adverse effects
URIs, nasopharyngitis
41
Sulfonylureas - MoA
Block K-ATP channel, causing membrane depolarization and insulin release
42
Sulfonylureas - use
DM2 - alone or w/ others
43
Sulfonylureas - adverse effects (5)
- Hypoglycemia - 2º resistance - Weight gain (increased insulin release) - Facial flushing - Sulfa drug allergy/cross-reactivity
44
Sulfonylurea + Sulfonamides or Salicylates Sulfonylurea + alcohol Sulfonylurea + gemfibrozil/cimetidine/azole
- Displaced from albumin = high action - Enhanced action at K-channel - CYP inhibition = high actioin
45
Sulfonylurea + B-blocker/CCB Sulfonylurea + diazoxide Sulfonylurea + phenytoin/rifampin
- Low insulin release = opposing actions - Less action at K-channel = less action - CYP activation = less action
46
Meglitinides - MoA
Inhibit K-ATP channel (like sulfonylureas), causing insulin release
47
Meglitinides - use
DM2 - postprandial hyperglycemia control (alone or with others)
48
Meglitinides - adverse effects
Hypoglycemia, 2º resistance, weight gain
49
Metformin - MoA
Inhibits OxPhos complex 1, leading to activation of AMP-dependent protein kinase, causing phosphorylation of targets that increase insulin action
50
Metformin - use
DM2 (common) - 1st line
51
Why is Metformin so heavily used? (4)
- NO HYPOGLYCEMIA - NO WEIGHT GAIN - ORAL - Vascular complication decrease
52
Metformin - adverse effects
- GI upset (like the rest) | - Lactic acidosis (do NOT give if renal disease)
53
Thiazolidinediones - MoA
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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