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Pharm > Diabetes Drugs > Flashcards

Diabetes Drugs Flashcards

1
Q

What are the treatment goals for:
Fasting plasma glucose
2hr Peak postprandial glucose
HbA1C

A

Fasting plasma glucose: 90-130

2hr Peak postprandial glucose:

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2
Q

What is the only current treatment for type I diabetes?

A

Insulin

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3
Q

Insulin stimulates glucose uptake in liver, muscle, and adipose tissue via upregulation of ___ transporter

A

GLUT4 glucose transporter

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4
Q

Rapid acting Insulin

A

Insulin aspart
Insulin lispro
Insulin glulisine

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5
Q

Rapid acting insulin: (Insulin aspart, Insulin lispro, Insulin glulisine)
Onset
Peak
Duration

A

Onset: 5-15 mins
Peak : 45-75 mins
Duration: 2-4 hours

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6
Q

Rapid acting insulin: (Insulin aspart, Insulin lispro, Insulin glulisine) Usage

A

For meals or acute hyperglycemia

Can be inject immediately before meals

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7
Q

Regular insulin
Onset
Peak
Duration

A

Onset: 30-60 mins
Peak: 2-4 hours
Duration: 6-8 hours

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8
Q

Regular insulin Usage

A

For meals or acute hyperglycemia, needs to be injected 30-45 mins prior to meal

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9
Q

Intermediate acting insulin

A

NPH insulin (Isophane)

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10
Q

Intermediate acting insulin Formulation

A

Conjugated with protamine peptide- delays absorption until proteolytically cleaved by tissue proteases

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11
Q

Intermediate acting insulin
Onset
Peak
Duration

A

Onset: 1.5-2 hours
Peak: 6-10 hours
Duration: 16-24 hours

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12
Q

Intermediate acting insulin Usage

A

Provides basal insulin and overnight coverage

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13
Q

Long acting insulin

A

Insulin glargine

Insulin detmir

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14
Q

Long acting insulin formulation:
Insulin glargine
Insulin detmir

A

Insulin glargine: amino acid substituted insulin
Insulin detmir : insulin with fatty acid side chain that associates w/ tissue bound albumin

SLOWS ABSORPTION

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15
Q 
Long acting insulin formulation:
Insulin glargine
Insulin detmir 
Onset
Peak 
Duration
A 
Onset: 2 hours
Peak: no peak
Duration: 
Insulin glargine: 20-24 hours
Insulin detmir: 6-24 hours
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16
Q

Long acting insulin formulation:
Insulin glargine
Insulin detmir
Usage

A

Provides basal insulin and overnight coverage

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17
Q

Insulin administration

A

Give SQ

Syringe, pen, pump

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18
Q

Sites of insulin administration

A

upper arms, thighs, buttocks, abdomen

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19
Q

Sites of insulin admin should be rotated to avoid

A

lipodystrophy

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20
Q

Conventional insulin therapy

A

2 daily injections of pre-mixed intermediated insulin (NPH) + regular insulin

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21
Q

Risk of conventional insulin therapy

A

Hypoglycemia in afternoon or overnight (insulin> carb consumption)
Risk of hyperglycemia in the morning=Dawn phenomenon (cortisol raises glucose levels)

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22
Q

Intensive insulin therapy

A

One/twice daily basal insulin (NPH or glargine)- lowers fasting glucose
Pre meal rapid acting insulin- postprandial glucose

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23
Q

Dose of pre-meal bolus determined by

A

Blood glucose level
Size and composition of meal (amount of carbs)
Degree of anticipated physical activity

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24
Q

Drawbacks of intensive therapy

A

patient commitment and effort
higher cost
increased risk of adverse effects

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25
Q

Major adverse effect of insulin therapy

A

Hypoglycemia

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26
Q

Hypoglycemia

A

blood glucose

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27
Q

Treatment of mild-moderate hypoglycemia

A

Oral dose of simple carbohydrate

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28
Q

Treatment of severe hypoglycemia

A

IV glucose or glucagon

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29
Q

Non-drug therapies for type II DM

A

Diet and exercise
decrease refined sugar
decrease fat

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30
Q

Bariatric surgery in treatment of type II DM

A

Roux-en-Y gastric bypass surgery can restore normoglycemia in obese

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31
Q

Insulin sensitizers

A

Biguanides (Metformin)

Thiazolidinediones (Pioglitazone, Rosiglitazone)

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32
Q

Insulin Secretagogue

A

Sulfonylureas (Chlorpropamide, Tolbutamide, Glimepiride, Glyburide, Glipizide)

Meglitinides (Repaglinide, Nateglinide)

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33
Q

Incretin Mimics and Modulators

A

GLP-1 homologs (Exenatide, Liraglutide)

DPP-IV inhibitors (Sitigliptin, Saxagliptin)

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34
Q

Inhibitors of carbohydrate digestion

A

a-glucosidase inhibitors (acarbose, miglitol)

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35
Q

SGLT2 inhibitors

A

Canagliflozin

Dapagliflozin

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36
Q

Bile acid-binding resin

A

Colesevelam

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37
Q

Amylin Homolog

A

Pramlintide

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38
Q

What is the recommended initial drug of choice in the treatment of ALL types of DM 2 patients (unable to control with diet/exercise alone)?

A

Metformin

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39
Q

Metformin Actions

A

Anti-hyperglycemia drug
Lowers fasting plasma glucose
Decreases hepatic gluconeogenesis
Increases insulin sensitivity/glucose uptake

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40
Q

What does Metformin require for its effects?

A

presence of insulin

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41
Q

How much does Metformin lower HbA1c?

A

1-5.2%

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42
Q

Advantages of metformin

A

NO hypoglycemia
NO weight gain
Improves lipid prodile
Decreases MI, DM death, mortality

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43
Q

Metformin MOA

A

Inhibits complex I of mitochondrial oxidative phosphorylation
Block ATP, Increase in AMP
Antagonizes Glucagon by inhibiting AC activity (x hep gluc)
Indues AMP-dependent kinase (Inc insulin sens)

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44
Q

Metformin adverse effects

A

Well tolerated
GI effects
Bad taste
Inhibits absorption of Vit B12 (megaloblastic anemia, neuropathy)

LACTIC ACIDOSIS

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45
Q

Rare but serious adverse effect of metformin?

A 
Lactic acidosis
(Pts w/ renal/liver insuff, CHF, MI, hypoxia)
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46
Q

Symptoms of lactic acidosis

A

Deep and rapid breathing, vomiting, abdominal pain and severe weakening of muscles in the legs and arms
Increased lactic acid in the blood

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47
Q

Metformin contraindications

A 
Pregnant/lactating
Impaired renal/liver function
Elderly >80
Iodinated contrast agent (contrast induced renal failure)
Alcohol abuse
CHF
MI
Shock/septicemia
Acute illness
Hypoxia
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48
Q

Thiazolidinediones

“glitazones”

A

Pioglitazone

Rosiglitazone

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49
Q

Thiazolidinediones

“glitazones” description

A

Insulin sensitizers

Increase sensitivity of adipose, muscle, and liver to insulin

50
Q

Thiazolidinediones

“glitazones” MOA

A

Agonists of peroxisome proliferator activated recepor-Y TF (PPAR-y)
Increases insulin sensitivity
Decreased plasma glucose levels

51
Q

Thiazolidinediones

“glitazones” Indications

A

Monotherapy or combo w/ metformin, sulfonylureas or insulin for DM T2
Decreases fasting blood glucose, moderate effects on postprandial glucose

52
Q

How much do Thiazolidinediones

“glitazones” decrease HbA1C?

53
Q

How long does it take Thiazolidinediones

“glitazones” to have a max effect?

A

6-14 weeks

54
Q

Thiazolidinediones

“glitazones” adverse effects

A 
Weight gain (subQ)
Fluid retention > edema
Risk of heart failure
Bone fracture risk
Bladder cancer risk
Hepatotoxicity
55
Q

Thiazolidinediones

“glitazones” Contraindications

A

Liver disease
Heart failure (BLACK BOX)
Pregnancy

56
Q

Thiazolidinediones

“glitazones” BLACK BOX WARNING

A

Increased risk of heart failure (fluid retention)

57
Q

Sulfonylureas vs. Meglitinides onset and half life

A

Sulfonylureas: slow onset, long half life > fasting glucose
Meglitinides: Rapid onset, short half life > postprandial glucose

58
Q

Sulfonylureas

A

First generation (rarely used)
Chlorpropamide
Tolbutamide

Second generation
Glimepiride
Glyburide
Glipizide

59
Q

Sulfonylureas Description

A

Oral drugs that lower blood glucose levels by stimulating beta cells to secrete insulin

60
Q

Sulfonylureas MOA

A

Directly bind to the regulatory subunit of the K channel (Sur1)
Mimic the effects of ATP, block channel
> K induced membrane depol
release of insulin

61
Q

Sulfonylureas Uses

A

Long duration of glucose lowering effect (16-24 h)
Stimulate insulin production in absence of glucose
REDUCE FASTING PLASMA GLUCOSE

62
Q

How much do Sulfonylureas reduce HbA1c?

63
Q

Activity of Sulfonylureas is dependent on

A

Functional beta cells

Most effective in pts w/ DM

64
Q

Sulfonylureas adverse effects

A 
Hypoglycemia (renal/hepatic impairment, eldly)
Weight gain (subQ)
65
Q

Sulfonylureas metabolism

A

Met in liver
Excreted in kidney

Glyburide and Glimepiride increase conc in R/H insuff

Glipizide is safer for patients with renal insufficiency

66
Q

Which Sulfonylurea is safer in pts with renal insufficiency and elderly?

67
Q

Sulfonylureas Contraindications

A 
Elderly (give Glipizide)
Impaired R/H function (give Glipizide or Repaglinide for R)
Type 1 diabetes
Pregnant (teratogenic)
Sulfa allergies
68
Q

Sulfonylureas Drug Interactions

A

Highly protein bound

Displacement > high risk of hypoglycemia

69
Q

Meglitinides (Insulin Secretagogues)

A

Repaglinide

Nateglinide

70
Q

Meglitinides Description

A

Short acting glucose-lowering oral drugs

Stimulate pancreatic beta cells to secrete insulin

71
Q

Meglitinides MOA

A

Trigger insulin secretion similarly to sulfonylureas but bind a different region of the SUR1 K/ATP channel

72
Q

Important difference between Meglitinides and Sulfonylureas

A

Rapid, shorter duration
Glucose dependent
**Decreased risk of hypoglycemia

73
Q

How much do Meglitinides reduce HbA1c?

74
Q

Meglitinides Indications

A

Post prandial glucose elevations

Often used in combo w/ drugs that affect fasting plasma glucose (metformin, thiazolidinediones)

75
Q

What is the difference between Nateglinide and Repaglinide?

A

Nateglinide affects POSTPRANDIAL glucose, and is rapidly reversed

Repaglinide affects postprandial and fasting glucose and effect is more prolonged

76
Q

Meglitinides metabolism

A

Repaglinide:
100% met in liver
90% fecal elimin
*good alternative to sulfonyl in renal insufficiency

Nateglinide:
80% met in liver
80% elim in urine
*Does not require dosage adjustment in renal insufficiency

77
Q

Meglitinides adverse effects

A

Hypoglycemia (less than sulfonyl)

Weight gain

78
Q

Meglitinides Contraindications

A

Liver disease

Pregnancy

79
Q

GLP-1 homologs

A

Exenatide

Liraglutide

80
Q

DPP-IV inhibitors

A

Sitagliptin

Saxagliptin

81
Q

GLP-1 homolog description

A

Analogs of GLP-1

GLP-1 is made in L cells of SI, mediates the incretin effect on plasma insulin

82
Q

GLP-1 MOA

A

Binds GLP-1 receptor on beta cells and potentiates glucose-induced insulin secretion
Suppresses hepatic glucose production (inhibits production of glucagon)
Promotes beta cells survival
Slows gastric emptying
Increases satiety

83
Q

GLP-1 homolog indications

A

Alterative to starting insulin in DM T2

Reduces both Fasting and postprandial glucose

84
Q

GLP-1 homolog duration of action

A

Exenatide: 6-8 hours
Liraglutide: 11-15 hours

85
Q

How much do GLP-1 homologs reduce HbA1c?

86
Q

GLP-1 homolog advantages

A

Little risk of hypoglycemia (glucose dependent)

Promotes weight loss

87
Q

GLP-1 homolog adverse effects

A

Frequent; nausea vomiting diarrhea

88
Q

DPP-IV inhibitors

A

Sitagliptin

Saxagliptin

89
Q

DPP-IV inhibitors

A

Decrease fasting and postprandial glucose

90
Q

How much do DPP-IV inhibitors reduce HbA1c?

A

0.48-0.61%

91
Q

DPP-IV inhibitors MOA

A

Inhibitors of DPP-IV, promotes actions of GLP-1

92
Q

DPP-IV inhibitors adverse effects

A

metabolism of other hormones?

93
Q

Alpha-glucosidase inhibitors

A

Acarbose

Miglitol

94
Q

Alpha-glucosidase inhibitors Description

A

Reduce postprandial glucose

Inhibit digestion of polysaccharides in small intestine

95
Q

Alpha-glucosidase inhibitors MOA

A

Inhibit alpha-glucosidase (enzyme in brush border of SI - hydrolysis of dietary carbs)

96
Q

Alpha-glucosidase inhibitors Indications

A

Control of postprandial glucose (needs to be taken with meal)
Not considered first line anti-diabetic drug
Less potent than sulfmet
NO hypoglycemia

97
Q

How much do Alpha-glucosidase inhibitors lower HbA1c?

98
Q

Alpha-glucosidase inhibitors Adverse effects

A

GI (abd pain, flatulence)

99
Q

Alpha-glucosidase inhibitors Contraindications

A

Chronic intestinal disease
Inflammatory bowel disease
Colonic ulceration/ intestinal obstruction

100
Q

SGLT2 Inhibitors

A

Canagliflozin

Dapagliflozin

101
Q

SGLT2 Inhibitors Description

A

Drugs that reduce hyperglycemia by promoting glucose excretion in the urine

102
Q

SGLT2 Inhibitors MOA

A

Inhibit sodium-glucose linked transporter 2 protein (SGLT2)

prevents glucose reabsorption in proximal renal tubules

103
Q

SGLT2 Inhibitors Indications

A

Mono/ combo
Low risk of hypoglycemia when used mono
Decreases body weight
decreases BP

104
Q

How much do SGLT2 Inhibitors decrease HbA1c?

105
Q

SGLT2 Inhibitors Adverse Effects

A 
UTI
Thirst/Dehydration
Hypotension
Increased LDL cholesterol
Hyperkalemia
106
Q

SGLT2 Inhibitors Contraindications

A

Renal impairment

107
Q

Bromocriptine description

A

Sympatholytic dopamine D2 receptor agonist
Normalize decreased AM dopamine levels in DMT2

Take within 2 hours of waking

108
Q

How much does Bromocriptine lower HbA1c?

109
Q

Colesevelam Description

A

Bile acid binding resin
LDL-lowering drug
Used as adjunct
Indirectly increases GLP-1

110
Q

Colesevelam MOA

A 
Bind bile acids in SI
Form insoluble complexes
Excreted in feces
Prevents bile acid reabsorption
Bile acid bind to TGR5 in colon >stimulation GLP-1 secretion
111
Q

Colesevelam Indications

A

+ metformin, sulf, insulin
NOT 1st line
Helpful in pts w/ high LDL

112
Q

How much does Colesevelam lower HbA1c?

113
Q

Which medication should be considered as initial therapy for patients presenting with HbA1c >1%

114
Q

Who requires more insulin - DM Type 1 or 2?

A

Due to insulin resistance, type-2 diabetics require considerably more Insulin compared to the doses used in the treatment of type-1 diabetes

115
Q

Amylin homolog

A

Pramlintide

116
Q

Amylin homolog Description

A

Synthetic analog of amylin (co-secreted with insulin, helps with postprandial glucose control)
Amylin is absent in diabetics
Used w/ insulin in DM T1&2

117
Q

Pramlintide actions

A

Decreases hepatic gluconeogeneiss
Decreases postprandial glucagon
Slows gastric emptying
Increases satiety

118
Q

Amylin homolog (pramlintide) indications

A

Adjunct + insulin
Post prandial glucose control
Effects are ADDITIVE to sinulin (reduce insulin by 50%)
Weight loss

119
Q

How much does amylin homolog lower HbA1c?

120
Q

Amylin homolog adverse effects

A

Nasuea, vomiting, anorexia, headache

Increases risk of severe hypoglycemia (w/ insulin)

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