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Endocrine Module > Diabetes Pharmacology > Flashcards

Diabetes Pharmacology Flashcards

(69 cards)

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1
Q

What chemical is in the mouth utilized for the digestion of carbs?

A

Alpha Amylase

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2
Q

What chemicals are in the small intestine that are utilized for the digestion of carbohydrates?

A

Alpha Amylase, Hydrolases, Glucosidases

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3
Q

What is the role of insulin in carbohydrate homeostasis?

A

Leads to storage of glucose, synthesized in pancreas, released in response to increasing blood glucose levels

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4
Q

What is the role of glucagon in carbohydrate homeostasis?

A

Stimulates release of glucose, synthesized in the pancreas, and prevents hypoglycemia

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5
Q

Glucogneogenesis

A

Formation of glucose not from glycogen

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6
Q

Glycogenolysis

A

Formation of glucose from glycogen

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7
Q

Glycolysis

A

Breakdown of glucose for energy

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8
Q

Glycogenesis

A

Formation of glycogen

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9
Q

Lipolysis

A

Breakdown of fat

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10
Q

Lipogenesis

A

Formation of fat

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11
Q

Beta Cells in the Pancreas do what?

A

Produce insulin and amylin
Insulin and C-Peptide are stored and CO-released together

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12
Q

Alpha Cells in the Pancreas do what?

A

Regulate glucagon secretion and hepatic glucose output

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13
Q

What is the Primary regulator of insulin release?

A

Glucose

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14
Q

What are the steps in insulin release?

A
  1. glucose into beta cells by FACILITATED diffusion (GLUT1)
  2. glucokinase phosphorylates glucose to Glucose 6 Phosphate
  3. glucose 6 phosphate INCREASES ATP levels via glycolytic pathway
  4. increased ATP:ADP ratio INHIBITS K+ Channels
  5. membrane depolarization of B cell, INFLUX of Ca2+
  6. calcium influx leads to EXOCYTOSIS of INSULIN granules
  7. insulin secretion via incretins
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15
Q

What does SUR (Sulfonylurea Receptor) do?

A

Block of SUR keeps K+ Channel Closed = Facilitation of Insulin Secretion with no regard to glucose levels

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16
Q

Does IV or Oral Glucose cause a higher Incretin Effect?

A

Oral (ingestion) of glucose causes more insulin release than an equivalent rise in blood glucose induced by IV, due to it going through the GI tract

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17
Q

What gut derived hormones are released proportionally to nutrient load?

A

GLP-1 and GIP

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18
Q

What type of diabetes has an impaired incretin effect?

A

Type 2, worse insulin response/release

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19
Q

How does the insulin receptor cause glucose transportation?

A
  1. insulin binds to the receptor
  2. receptor TYROSINE phosphorylates
  3. casacade activated
  4. PIP3 and Akt involved in translocation GLUT4 to cell membrane
  5. Glucose transported into the cell
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20
Q

Where are insulin receptors located?

A

Liver, muscle, and fat = ALL peripheral tissues

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21
Q

Where is GLUT4 located?

A

ON the cell MEMBRANE, important for storage of glucose

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22
Q

What does insulin activate for phosphorylation of glucose in the liver?

A

Hexokinase = trapping phosphorylated glucose in liver

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23
Q

What enzymes does insulin activate for glycogen synthesis?

A

Phosphofructokinase and Glycogen Synthase = promoting production of glycogen from excessive glucose

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24
Q

How are fatty acids exported from the liver?

A

Lipoproteins

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25
How does insulin resistance affect the liver?
Gluconeogenesis causes glucose production despite hyperglycemia, glucagon is not inhibited
26
How does insulin resistance affect the muscle?
Decreased ability to take up glucose
27
How does insulin resistance affect the adipocytes?
Lipase enzyme is not inhibited leading to increased plasma FFA and decreased ability to take up glucose
28
What are the functions of Amylin?
Slows gastric emptying, decreases speed of glucose absorption, suppresses glucagon output, increases satiety, and is co-released with insulin
29
What type of insulin is used for bolus/prandial dosing?
Rapid
30
What type of insulin is used for basal dosing?
Long/Ultra Long
31
Why must you always pair insulin with food?
HYPOglycemia
32
What is the inhaled insulin on the market?
Afrezza
33
What is the artificial pancreas on the market?
Medtronic MiniMed
34
What are the adverse effects of insulin?
Hypoglycemia, Weight Gain, and Insulin Allergy
35
What is the MOA of Sulfonylureas?
Increase insulin release from beta cells in pancreas by closing K-ATP channels SUR, decreases serum glucagon
36
Are sulfonylureas independent or dependent on glucose?
Insulin Secretion is INDEPENDENT, risk of hypoglycemia
37
What drugs are classified as Sulfonylureas?
Glyburide, Glipizide, and Glimepiride
38
What is the MOA of Meglitinides/Glindies?
Block ATP sensitive potassium channels in beta cells to increase insulin release
39
Are Meglitinides/Glindies independent or dependent of glucose?
Insulin release, somewhat DEPENDENT on glucose levels, less risk of hypoglycemia
40
What drugs are classified as Meglitinides/Glinides?
Repaglinide and Nateglinide
41
What are the pearls of Repaglinide?
Hypoglycemia possible, weight gain, Glucuronidation required for metabolism
42
What are the pearls of Nateglinide?
Risk of hypoglycemia and weight gain
43
What is the MOA of Biguanides?
Increases insulin sensitivity in muscle and liver involving activation of AMP Kinase (AMPK), decreases hepatic glucose formation, and stimulation of glucose uptake by increasing GLUT4
44
Is Biguanide dependent on functioning beta-cells?
NO
45
What drugs are classified as Biguanide?
Metformin
46
What are the pearls of Metformin?
Rare hypoglycemia, EUGLYCEMIC Agent, do not use with impaired kidney function, GI upset/diarrhea
47
What is the MOA of Thiazolidinediones?
Agonists at PPAR-y, nuclear receptor, encouraging redistribution of fat from central to periphery, increases secretion of adiponectin
48
Are Thiazolidinediones independent or dependent on insulin?
DEPENDENT, REQUIRE insulin to be present for them to work
49
What drugs are Thiazolidinediones?
Pioglitazone and Rosiglitazone
50
What are the pearls of Pioglitazone and Rosiglitazone?
Raise HDL levels, weight gain, CHF (black box), increased bone fracture, decreased hematocrit
51
What is the MOA of A-Glucosidase Inhibitors?
Inhibition of a-glucosidase in intestines, delay digestion and absorption of starch, inhibit glucose uptake from GI
52
What drugs are A-Glucosidase Inhibitors?
Acarbose and Miglitol
53
What are the pearls of Acarbose and Miglitol?
No weight gain, no effect on plasma lipids, no hypoglycemia, flatulence, diarrhea, abdominal pain, and bloating
54
What is the MOA of GLP-1 Agonists?
GLP-1 receptor activation increases cAMP levels, increasing insulin synthesis and release in a glucose-dependent manner
55
What drugs are classified as GLP-1 Agonists?
Exenatide, Liraglutide, Albiglutide, and Dulaglutide
56
What are the pearls of Exenatide, Liraglutide, Albiglutide, and Dulaglutide?
N/V (dose dependent), weight loss, and pancreatitis
57
What drug is a GLP-1 and GIP Agonist?
Tirzepatide/Mounjaro
58
What are the pearls of Tirzepatide?
Decrease A1c and BW, nausea/diarrhea, vomiting, dyspepsia, acute pancreatitis, acute gallbladder dysfunction, black box for c-cell thyroid tumors
59
What is the MOA for DPP-4 Inhibitors?
Block degradation of GLP-1 and GIP by dipeptidyl peptidase 4, increasing levels of GLP-1 and GIP
60
What drugs are classified as DPP-4 Inhibitors?
Alogliptin, Sitagliptin, Saxagliptin, and Linagliptin
61
What are the pearls of Alogliptin, Sitagliptin, Saxagliptin, and Linagliptin?
No satiety or gastric emptying effects
62
What is the MOA of Amylin analogs?
Slows gastric emptying, decreases appetite, decreases glucagon release
63
What drug is classified as an Amylin analog?
Pramlintide
64
What are the pearls of Pramlintide?
Weight loss and N/V
65
What is the MOA of SGLT2 Inhibitors?
Inhibits SGLT2, causing less glucose reabsorption, increase glucose in urine
66
What drugs are classified as SLGT2 Inhibitors?
Canagliflozin, Dapagliflozin, and Empagliflozin
67
Are SGLT2 Inhibitors dependent or independent of insulin?
Independent
68
What are the pearls of Canagliflozin, Dapagliflozin, and Empagliflozin?
Low risk of hypoglycemia, some weight loss, and glucose in urine = increase UTIs
69
What does SGLT2 stand for?
Sodium glucose transporter 2

Endocrine Module (16 decks)

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