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D1 Spring > Pharmacology - Insulin, Oral Hypoglycemic Agents, Glucagon (Exam 5) > Flashcards

Pharmacology - Insulin, Oral Hypoglycemic Agents, Glucagon (Exam 5) Flashcards

1
Q

The principal hormone that’s dysregulated in diabetes

A

Insulin

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2
Q

What is signaled by the presence of usable energy and tells the body to store energy?

A

Insulin release

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3
Q

What is the structure of proinsulin?

A

A chain
B chain
C chain

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4
Q

Through the proteolytic cleavage of proinsulin, which chain gets cleaved?

A

C chain

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5
Q

T/F the C chain has no known physiological function

A

True

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6
Q

What is the active part of insulin?

A

A and B chain

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7
Q

What are A and B chains of proinsulin linked by?

A

Disulfide bonds

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8
Q

How do you inactivate insulin?

A

Hydrolyze the disulfide bond between A and B chain

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9
Q

Why do we care about the structure of insulin?

A

All therapies for type I diabetes are mimetics of insulin and have a similar structure

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10
Q

How fast is insulin’s half life?

A

3-5 mins

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11
Q

Where is endogenous insulin metabolized vs subcutaneously introduced insulin metabolized?

A

Endogenous: 60% liver, 40% kidney
Subcutaneous: 60% kidney, 40% liver

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12
Q

How much insulin does the pancreas hold?

A

8 mg (~200 units)

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13
Q

Which cells in the pancreas secrete insulin?

A

B cells

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14
Q

Name some secretory products of B cells

A

Insulin
C chain (peptide)
Proinsulin
Islet amyloid polypeptide (IAPP)

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15
Q

Which cells in the pancreas make glucagon?

A

A cells

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16
Q

T/F: The pancreas is mostly made up of alpha cells.

A

False! It’s mostly beta cells

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17
Q

Insulin secretion steps (7) (ON EXAM)

A
  1. High levels of glucose
  2. Glucose enters cell via GLUT2 and gets metabolized
  3. ATP is produced
  4. ATP phosphorylates and closes K+ channels
  5. Beta cell gets depolarized
  6. Voltage gated Ca2+ channels open
  7. Increased Ca2+ leads to the release of insulin
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18
Q

Most important step of insulin secretion

(this is what drugs that increase insulin secretion target)

A

When ATP closes the K+ channels and causes depolarization of the Beta cell

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19
Q

Insulin released from beta cells is a complex of what?

A

6 insulin molecules with 1 Zn atom

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20
Q

T/F when insulin is in a complex with Zinc, it cannot find its target receptor and it is NOT biologically active

A

True

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21
Q

Only the ___________ form of insulin is able to bind to the receptor

A

monomeric

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22
Q

3 insulin responsive tissues (ON EXAM)

A
  1. Liver
  2. Muscle
  3. Adipose
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23
Q

Insulin receptors have ___________ _________ activity

A

intrinsic enzymatic

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24
Q

Steps of insulin receptor signal transduction (ON EXAM)

A
  1. Insulin binds to insulin receptor
  2. IRS proteins are stimulated
  3. Glucose transporters (GLUT-4) move from intracellular vesicles to plasma membrane
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25
Q

Where is GLUT-2 transporter always located?

A

Plasma membrane

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26
Q

Where is GLUT-4 transporter located?

A

Translocates to the plasma membrane when activated by insulin receptor

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27
Q

Elevated levels of glucose leads to the release of ________ which leads to _________ _________

A

insulin; energy storage

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28
Q

Decreased levels of glucose leads to decreased levels of _________, which leads to the body using ________ ______ to make more ________

A

insulin; stored energy; glucose

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29
Q

Blood glucose levels serve as a ____________ for insulin action

A

surrogate

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30
Q

What are the physiologically most important roles of insulin? (ON EXAM)

A
  1. Increased glycogen synthesis
  2. Glucose uptake (removal from the blood)
31
Q

The improper synthesis or use of insulin characterized by hyperglycemia

32
Q

Diabetes differences in ethnic groups are because of?

A

Socioeconomic status

(NOT genetics)

33
Q

Common oral health problems associated w/ diabetes (7)

A
  1. Tooth Decay
  2. Periodontal disease
  3. Salivary gland dysfunction
  4. Fungal Infection
  5. Lichen planus and lichenoid reactions
  6. Infection and delayed healing
  7. Taste impairment
34
Q

What are the major classifications of diabetes?

A

Type I, II, III, and IV

35
Q

Which type of diabetes?

Insulin dependent diabetes mellitus

36
Q

Which type of diabetes?

Non-insulin dependent diabetes mellitus

37
Q

Which type of diabetes?

Diabetes linked to pancreatic disease, hormonal changes, drug side effects, or genetic defects

38
Q

Which type of diabetes?

Gestational diabetes

39
Q

Difference in treatment betweeen Type I and Type II diabetes

A

Type I: do NOT have functioning B cells; patient provides their own insulin (replacement therapy)

Type II: less responsive to insulin; must secrete more insulin, reduce blood glucose from diet, or restore sensitivity to insulin

40
Q

Goals of Type I diabetes

A
  1. Stabilize glucose concentrations in blood
  2. Mediate all of insulins’s functions
41
Q

What are the advantages of glycemic control in Type I diabetes?

A
  1. Decrease swings in glucose levels
  2. Decrease glycated Hgb
  3. Decrease eye, kidney, nerve damage
42
Q

What are the disadvantages of glycemic control in Type I diabetes?

A
  1. Hypoglycemia risk
  2. Weight gain
43
Q

Differences between insulin preparations for treatment of Type I diabetes are __________

A

pharmacokinetic

(onset and duration of action is different for each one)

44
Q

What are the insulin delivery systems?

A
  1. Subcutaneous injection (needles/syringes, portable pen injectors)
  2. Continuous subcutaneous insulin infusion devices (insulin pump)
45
Q

What is the main problem in Type II diabetes?

A

Decreased insulin sensitivity

46
Q

Type II diabetes drugs have 3 therapeutic goals. What are they?

A
  1. Insulin release
  2. Increase insulin sensitivity
  3. Decrease blood glucose
47
Q

Name 2 insulin secretagogues. Which goal do they target?

A
  1. Sulfonylureas
  2. Meglitinides

Target: insulin release

48
Q

Name 2 insulin sensitizers. Which goal do they target?

A
  1. Biguanides
  2. Thiazolinediones

Target: increase insulin sensitivity

49
Q

Name one enzymatic inhibitor. Which goal does it target?

A

Alpha-glucosidase inhibitors

Target: decrease blood glucose

50
Q

Which drug increases glucose excretion?

A

Canagliflozin

51
Q

MOA of sulfonylureas

A
  1. Bind to K+ channel
  2. Block K+ channel
  3. Depolarize cell
  4. Increase intracellular Ca+
  5. Insulin release
52
Q

MOA of Meglitinides (Repaglinide)

A
  1. Regulate K+ flux through K+ channels
  2. Overlap w/ Sulfonylureas in binding site
  3. Rapid onset - peak effect within 1 hr
53
Q

What drug is a Biguanide?

A

Metformin (Glucophage)

54
Q

MOA of Metformin (Glucophage)

(most commonly prescribed!)

A
  1. Stimulates glycolysis in tissue
  2. Increase glucose removal
  3. Activates AMPK
  4. Decreases gluconeogenesis
  5. Slows glucose absorption from GI
  6. Decreases plasma glucagon levels
55
Q

Which drugs are thiazolinediones?

A

Pioglitazone
Rosiglitazone

56
Q

MOA of Pioglitazone and Rosiglitazone

A
  1. Acute post-receptor mimetic activity
  2. Bypass insulin receptor
  3. Stimulate signaling cascade at PPAR gamma receptor
  4. Work in liver, muscle, adipose
57
Q

Which drugs are alpha-glucosidase inhibitors

A

Acarbose (Precose)
Miglitol (Glyset)

58
Q

MOA of Acarbose (Precose) and Miglitol (Glyset)

A

Inhibit alpha-glucosidase, a brush border enzyme, decreasing carb absorption after meals

59
Q

Why does Acarbose and Miglitol cause GI distress?

A

They prevent breakdown of carbs, so your stomach will hurt

60
Q

What drugs are incretin-related drugs?

A

Exenatide
Sitagliptin

61
Q

MOA of incretin-related drugs (Exenatide and Sitagliptin)

A

Exenatide: binds GLP-1 receptors and NOT degraded by DPP-4

Sitagliptin: inhibits DPP-4

62
Q

What does Amylin maintain?

A

Glucose homeostasis

63
Q

What is Amylin?

A

37 amino acid protein secreted with insulin

64
Q

MOA of Amylin

A
  1. Decrease glucagon secretion
  2. Slow gastric emptying
  3. Decrease appetite
65
Q

Which drug is an Amylin analog given by injection at mealtime?

A

Pramlintide

66
Q

Which drug is a sodium-glucose cotransporter 2 (SGLT2) inhibitor?

A

Canagliflozin

67
Q

MOA of Canagliflozin

A
  1. Block Na+-glucose co-transporter in kidney
  2. Decrease glucose reabsorption
  3. Increase excretion of glucose
68
Q

This hormone increases cAMP production and facilitates catabolism of stored glycogen

69
Q

What pathways does glucagon increase?

A

Gluconeogenesis
Ketogenesis

70
Q

What does glucagon mimic in cardiac tissue?

A

B-adrenergic receptor cAMP effects

71
Q

What does glucagon do in smooth muscle?

A

Relax small intestine

72
Q

Counter hormone to insulin

73
Q

Causes glycogen breakdown to glucose and signals through glucagon receptor (GPCR linked to Gs)

74
Q

Clinical uses of glucagon (4)

A
  1. Treat hypoglycemia
  2. Diagnose endocrine disorders
  3. B-blocker poisoning
  4. Radiology of the bowel

D1 Spring (47 decks)

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