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Pharmacology > Diabetes Drugs > Flashcards

Diabetes Drugs Flashcards

1
Q

What is the ultimate result of T1 and T2 DM?

A

Hyperglycemia

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2
Q

Polyuria, polydipsia, glucosuria, unexplained weight loss despite polyphagia, fatigue & blurred vision and in some cases ketoacidosis

A

T1DM

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3
Q

Obesity, fatigue, polyuria and polydipsia can be present, although patients are often asymptomatic. IFG and IGT can be detected and precede the onset of diabetes.

A

T2DM

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4
Q

What are the treatment goals for diabetes?

A

Try to achieve and maintain glycemic control as close to the normal range as possible to prevent the chronic complications of sustained hyperglycemia

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5
Q

What is the main SE of intensive insulin therapy for diabetes?

A

Increased risk of hypoglycemia

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6
Q

What is the only treatment for T1DM?

A

Insulin

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7
Q

What transporter does insulin upregulate in liver, muscle and adipose?

A

GLUT4

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8
Q

What are the 4 classes of insulin?

A
  • Rapid acting
  • Regular
  • Intermediate acting
  • Long acting
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9
Q

What insulin type are detmir and glargine?

A

Long acting

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10
Q

What can happen if the same sites are continuously used for insulin?

A

Lipodystrophy - inappropriate lipid storage

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11
Q

Insulin SE

A

Hypoglycemia

  • Tremor
  • Palpitations
  • Intense Hunger
  • Headaches
  • Altered Mental Status
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12
Q

What is non-medical treatment for T2DM?

A

Change in diet and exercise - this can increase insulin sensitivity and decrease BP

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13
Q

What type of surgery can benefit T2DM patients?

A

Bariatric Surgery

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14
Q

What is the DOC for treating all T2DM patients?

A

Metformin

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15
Q

Is metformin associated with weight gain?

A

NO - actually can cause weight loss

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16
Q

What is the main advantage of metformin?

A

No hypoglycemia

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17
Q

Metformin Effects

A
  • Lowers fasting plasma glucose
  • Decreased hepatic gluconeogenesis
  • Increased insulin sensitivity
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18
Q

Metformin MOA

A

Inhibits the first unit of the electron transport chain which leads to decreased ATP and increased AMP which inhibits adenylate cyclase blocking glucagon’s pathway.

***Overall decreases gluconeogenesis and increases insulin sensitivity

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19
Q

Metformin SE

A
  • Inhibits absorption of Vitamin B12

- Lactic acidosis - rare but can be FATAL (high risk patients)

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20
Q

What is the mechanism of lactic acidosis in use of metformin?

A

Inhibition of gluconeogenesis decreases lactate being used up as a substrate which increases its concentration. When combined with another condition like decreased renal clearance of lactate, it can lead to toxic build-up.

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21
Q

Metformin Contraindications

A
  • Pregnancy and lactation
  • Impaired liver or renal function
  • Elderly
  • Use of contrast agent
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22
Q

What are the thiazolidinediones and what is their effect?

A
  • Pioglitazone
  • Rosiglitazone
    “Insulin sensitizers” that increase the sensitivity of adipose tissue, skeletal muscle and liver to the effects of endogenous insulin.
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23
Q

Pioglitazone/Rosiglitazone MOA

A

Thiazolidinediones are agonists for the peroxisome proliferator-activated
receptor-transcription factor (PPAR). Activation of the PPAR transcription factor by thiazolidinediones influences the expression of multiple genes involved in promoting 1) increased insulin sensitivity and 2) decreased plasma glucose levels

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24
Q

Pioglitazone/Rosiglitazone Indications

A
  • Mono or combo therapy for T2DM

* ** Takes time to see efficacy

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25
Q

Pioglitazone/Rosiglitazone SE

A
  • Weight gain
  • Fluid retention
  • Increased bone fracture risk in women
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26
Q

Pioglitazone/Rosiglitazone Contraindications

A
  • Liver disease
  • Heart failure
  • Pregnancy
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27
Q

What are the insulin secretagogues?

A
  • Sulfonylureas

- Meglitinides

28
Q

What are the sulfonylureas?

A
  • Glimepiride
  • Glyburide
  • Glipizide
29
Q

What are the meglitinides?

A
  • Repaglinide

- Nateglinide

30
Q

Sulfonylurea MOA

A

Bind Sur1 and block the channel leading to increased intracellular K+ leading to depolarization and activation of Ca2+ channels to release pre-formed insulin

31
Q

Sulfonylurea Indication

A

Reduce fasting plasma glucose - long duration of action

32
Q

What is the action of sulfonylureas dependent upon?

A

Functional beta cells

33
Q

Sulfonylurea SE

A
  • Hypoglycemia

- Weight gain

34
Q

Sulfonylurea Contraindications

A
  • Elderly (renal impairment)
  • Renal or liver disease
  • T1DM
  • Pregnancy
  • Sulfa allergy
35
Q

Sulfonylurea DDIs

A

Highly protein bound so can interact with:

  • Aspirin
  • Warfarin
36
Q

Meglitinide MOA

A

Bind different region of Sur1 leading to secretion of pre-formed insulin but has a RAPID and SHORTER duration that sulfonylureas

37
Q

What is melitinide dependent on?

A

Glucose - less risk of hypoglycemia

38
Q

Nateglinide affects primarily only _________

A

Postprandial glucose

39
Q

Repaglinide affects both ____________ and _____________.

A

Postprandial and fasting glucose

40
Q

Melitinide SE

A
  • Hypoglycemia

- Weight gain

41
Q

Meglitinide Contraindication

A
  • Liver disease

- Pregnancy

42
Q

What is the incretin effect?

A

Plasma insulin levels to oral glucose are significantly greater than to IV glucose

43
Q

GLP-1

A

Made by L cells of small intestine and mediates the incretin effect

44
Q

What degrades GLP-1?

A

DPP-IV

45
Q

Exenatide/Liraglutide Indications

A
  • Alternative to insulin in T2DM
46
Q

Exenatide/Liraglutide Effects

A
  • Reduce fasting and postpradial glucose

- Promotes weight loss

47
Q

Exenatide/Liraglutide SE

A

Minor GI effects

48
Q

Exenatide/Liraglutide MOA

A

GLP-1 homologs

49
Q

Sitagliptin/Saxagliptin MOA

A

DPP-IV inhibitors - increase half life of GLP-1

50
Q

Sitagliptin/Saxagliptin Indications

A
  • Decrease fasting and prostprandial glucose

- Mono or combo therapy for T2DM

51
Q

Acarbose/Miglitol MOA

A

Inhibit alpha-glucosidase which hydrolyzes dietary carbohydrates and delays the absorption of glucose

52
Q

Acarbose/Miglitol Indications

A
  • Postprandial hyperglycemia control
  • Less potent than sulfonylureas and metformin

NOT 1st line

53
Q

Acarbose/Miglitol SE

A
  • GI effects from unabsorbed carbohydrates

Do NOT cause hypoglycemia

54
Q

Acarbose/Miglitol Contraindications

A

GI diseases

55
Q

Canagliflozin/Dapagliflozin MOA

A

Inhibit SGLT2 in proximal renal tubule which prevents the normal process of glucose reabsorption

56
Q

Canagliflozin/Dapagliflozin Indications

A
  • Mono and combo therapy for T2DM
57
Q

What are the effects of Canagliflozin/Dapagliflozin?

A
  • Weight loss

- Decreased BP

58
Q

Canagliflozin/Dapagliflozin SE

A
  • UTIs
  • Thirst/dehydration
  • Increase LDL cholesterol
59
Q

Canagliflozin/Dapagliflozin Contraindications

A

Renal Impairment

60
Q

Bromocriptine MOA

A

DOPA D2 agonist - exact MOA for diabetes is unknown but thought to normalize morning DOPA levels

61
Q

Colesevalam MOA

A

Increases bile acid synthesis by increasing excretion of bile by binding to bile and preventing reabsorption -which leads to lowering of LDL

62
Q

Colesevalam Indications

A

Add on therapy to 1st line treatments for T2DM

63
Q

What is the most effective medication to lower hyperglycemia?

A

Insulin

64
Q

Pramlintide MOA

A

Amylin homolog - amylin is endogenous hormone that is co-secreted with insulin and contributes to post-prandial glucose control

65
Q

Pramlintide Effects

A
  • Inhibits hepatic gluconeogeneis
  • Slow gastric emptying
  • Inhibits glucagon
  • Increases satiety
66
Q

Pramlintide Indications

A

Adjunct therapy in T1 or T2 patients using insulin but are not at adequate control

67
Q

Pramlintide SE

A
  • Weight loss
  • GI effects
  • Risk for severe hypoglycemia

Pharmacology (74 decks)

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