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Pharm II > Anti-diabetic Agents > Flashcards

Anti-diabetic Agents Flashcards

1
Q

What type of insulin preparation is represented by the blue line?

A

Rapid acting (Lispro, Aspart, Glulisine, Inhaled)

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2
Q

What type of insulin preparation is represented by the black line?

A

Short acting (Regular)

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3
Q

What type of insulin preparation is represented by the red line?

A

Intermediate (NPH)

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4
Q

What type of insulin preparation is represented by the pink and dark blue lines?

A

Long acting (Insulin detemir, Insulin glargine)

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5
Q

What is the classic triad of symptoms associated with DM?

A

Polyuria, polyphagia, polydipsia

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6
Q

Inability of the body to use glucose as an energy source leads to hyperlipidemia which causes what 2 associated conditions commonly seen with DM?

A

Atherosclerosis (of large and medium sized arteries) and HTN (with progressive renal involvement)

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7
Q

Aside from the classic triad, and atherosclerosis and HTN, what are other common sxs seen with DM? (4)

A

Peripheral neuropathy, acanthosis nigricans, myoglobinuria (increased muscle breakdown), microangopathy (unknown cause)

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8
Q

T1DM is characterized by virtually absent circulating insulin resulting in the need for exogenous insulin to be injected. What is the cause for this?

A

Pancreatic beta cells fail to respond to insulinogenic stimuli (glucose)

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9
Q

What is typically the trigger of sustained beta cell stimulation leading to hyperinsulinism and receptor insensitivity in T2DM?

A

Chronic over feeding

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10
Q

What may interrupt the disease cycle of T2DM?

A

Reduction of over feeding

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11
Q

Why is T2DM considered a progressive disease?

A

Start losing pancreas’ ability to produce insuline (T2DM → T1DM)

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12
Q

How does treatment progress as T2DM progresses?

A

Monotherapy → combo therapy → insulin

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13
Q

What are the 4 diagnosis methods for DM?

A
  1. DM sxs and random blood glucose (≥ 200mg/dL)
  2. Fasting blood glucose (≥ 126 mg/dL)
  3. Oral glucose challenge (blood glucose ≥ 200 @ 2 hrs)
  4. HbA1C ≥ 6.5%
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14
Q

Although an HbA1C level of ≥ 6.5% is diagnositc for DM, what is considered poorly controlled DM?

A

> 10%

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15
Q

You typically want a DM pt to have an HbA1C of < 6 BUT under what condition?

A

If you can safely get them to that level without hypoglycemic events

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16
Q

How is glycosylation affected as glucose levels increase?

A

Increases (A1C = glycosylated protein)

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17
Q

Preproinsulin → insulin yields what?

A

Insulin + C-peptide

(C-peptide provides long term marker for measuring insulin)

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18
Q

Release of insulin is activated by what?

A

Glucose, beta2 adrenergic agonist

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19
Q

Insulin promotes entry of glucose into what tissues? (2)

A

Skeletal muscle and fat tissue

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20
Q

Insulin is NOT required for glucose transport into what tissues? (2)

A

Brain and liver

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21
Q

Insulin release is stimulated by beta2 adrenergic agonists but inhibited by what?

A

Alpha2 agonists

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22
Q

How is insulin released from beta cells? (6 steps)

A
  1. Glucose transported via GLUT2
  2. Metabolism
  3. Increased ATP
  4. K+ channel closes and cell depolarizes
  5. Ca2+ channels open and Ca2+ enters cell
  6. Insulin released from cell via exocytosis
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23
Q

The following actions of insulin are considered what?

Decreased gluconeogensis and increased glycogen synthesis in the liver, and glucose uptake in muscle and adipose tissue

A

Anabolic actions (because insulin inhibtits catabolic actions)

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24
Q

Where do GLUT1 and GLUT3 act?

A

Brain

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25
Q

Where does GLUT2 act?

A

Beta cells of pancreas

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26
Q

Where does GLUT4 act?

A

Muscle and adipose

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27
Q

The affinity for glucose is greatest/ least in which GLUT transporters?

A

GLUT2 < GLUT4 < GLUT1/ GLUT3

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28
Q

How is uptake of glucose unique with respect to the GLUT4 transporter?

A

Insulin-mediated (aka insulin dependent)

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29
Q

Overproduction or underutilization of glucose can cause what imbalance?

A

Lactic acidosis

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30
Q

Which drugs are approved for treatment of T2DM in pts who also have ASCVD? (3)

A

Liraglutide, Canaglifozin, Empagliflozin

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31
Q

What is typically considered 1st line treatment for DM?

A

Lifestyle modification (important in treatment and CV health)

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32
Q

What contributes to > 2/3 of all morbidity/ mortality/ costs of patients with DM?

A

CV disease

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33
Q

What has shown to be more important in treatment of patients with CV disease + DM?

A

Control of BP/ cholesterol levels > tightly controlled blood glucose levels

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34
Q

What 3 things must be treated simultaneously in patients with DM and CV disease?

A

A1C, BP, cholesterol

(bottom line = start intensive therapy immediately for best effect on CV health, but individuaize treatment and avoid hypoglycemia)

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35
Q

If a pt has a history of poor glycemic control, what might this indicate about intensive glycemic control?

A

No CV benefit

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36
Q

What is the MOA of insulin?

A

Stimulates GLUT4 (insulin mediated) uptake of glucose into muscle and adipose tissues

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37
Q

The goal of what DM treatment is to mimic what the body does (both meal-stimulated insulin and basal insulin)

A

Injections

(create insulin profile and eat to fill it)

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38
Q

Regular + intermediate insulin mix injection is given when?

A

1 hour before breakfast and dinner

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39
Q

Rapid-acting + long-acting insulin injections are given when?

A

Rpaid acting injected 1 hour before meals, long acting injected before bedtime

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40
Q

What DM treatment involves basal levels of rapid acting insulin maintained throughout the day but increased right before meal based on meal components (pt stimulated bolus)

A

Insulin pumps

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41
Q

What are the most common sxs of hypoglycemia? (4)

A

Tachycardia, confusion, vertigo, sweating

(dangerous b/c SEs will disappear w repeated events)

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42
Q

Besides hypoglycemia, what is a common side effect of insulin treatment for DM?

A

Weight gain (increased lipolysis)

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43
Q

What is the treatment for hypoglycemia? (2)

A

Give 50-100mL of 50% glucose solution IV, 0.5- 1mg glucagon injection

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44
Q

Which 2 types of insulin are given IV?

A

Rapid-acting and short-acting

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45
Q

Which 2 types of insulin are NOT given IV?

A

Intermediate-acting and long-acting (basal)

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46
Q

Why is rapid-acting insulin preferred over regular insulin (short-acting)?

A

Less hypoglycemia

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47
Q

What type of insulin is Insulin lispro (Humalog)?

A

Rapid-acting

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48
Q

What type of insulin is Insulin aspart (NovoLog)?

A

Rapid-acting

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49
Q

What type of insulin is Insulin glulisine (Apidra)?

A

Rapid-acting

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50
Q

What type of insulin is Insulin, inhaled (Afrezza) and what is a SE of it?

A

Rapid-acting, SE: cough

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51
Q

What are the short-acting insulins?

A

Regular insulin (Novolin R, Humulin R)

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52
Q

What are the intermediate acting insulins?

A

NPH insulin (Humulin N, Novolin N)

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53
Q

What type of insulin is Insulin glargine (Lantus)?

A

Long-acting (basal)

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54
Q

What type of insulin is Insulin detemir (Levemir)?

A

Long-acting (basal)

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55
Q

What type of insulin is Insulin degludec (Tresiba)?

A

Long-acting (basal)

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56
Q

What is 1st line treatment for T2DM when A1C is > 10%?

A

Long-acting (basal)

(Insulin glargine (Lantus), Insulin detemir (Levemir), Insulin degludec (Tresiba))

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57
Q

What hormone antagonizes insulin?

A

Glucagon

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58
Q

What are the 3 routes of administration for glucagon?

A

SC, IM, IV (but gradual onset)

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59
Q

What is the MOA for glucagon?

A

Increase blood glucose levels by mobilizing hepatic glycogen (when glycogen stores available)

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60
Q

What are the indications for use of glucagon? (2)

A

Beta blocker overdose, radiology

(potent inotropic and chronotropic effects on heart via 2nd messenger, relaxation of intestine)

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61
Q

Glucagon drug class?

A

Hyperglycemic agents

62
Q

Diazoxide drug class?

A

Hyperglycemic agents

63
Q

How is Diazoxide administered?

A

Oral (long t1/2)

64
Q

What is the MOA for Diazoxide?

A

Directly inhibits insulin secretion

(decreases peripheral glucose utilization OR stimulates hepatic glucose production)

65
Q

Which hyperglycemic agent is a non-diuretic thiazide?

A

Diazoxide

66
Q

What is the indicated use of Diazoxide?

A

Insulinoma (insulin secreting tumor that leads to hypoglycemia)

67
Q

What are the only 2 anti-DM agents indicated for treatment of both T1 and T2?

A

Alpha-glucosidase inhibitors and Pramlintide

(Pramlintide used only as insulin adjunct)

68
Q

What is the administration method of most anti-DM agents?

A

Oral

69
Q

What are the the 4 compelling indications of anti-DM agents?

A
  1. Effect on ASCVD (#1 killer of DM pts)
  2. Effect on CKD
  3. Impact on weight (helps w weight loss = benefit)
  4. Hypoglycemia risk
70
Q

Metformin drug class?

A

Biguanide

71
Q

What is the MOA for Metformin? (2)

A

Decrease glucose levels in an insulin-independent manner, increase glucose removal from blood with AMPK

72
Q

What is the DOC for T2DM if A1C is < 10%?

A

Metformin

73
Q

What is the DOC for diabetes prevention (prophylaxis for pre-diabetic pts)?

A

Metformin

74
Q

Besides A1C and prophylaxis, what are the other uses of Metformin? (2)

A

PCOS (euglycemic state), decrease macrovascular events (but not direct CV drug)

75
Q

How is Metformin excreted?

A

Renally

76
Q

What are the SEs of Metformin? (4)

A

Hypoglycemia (rare), diarrhea (most common), lactic acidosis (most dangerous, dose dependent), reversible vit B12 deficiency (check levels anually)

77
Q

What are the contraindications to Metformin?

A

Kidney disease (GFR < 30), HbA1C > 10% (give basal insulin instead)

(kidney disease causes lactic acidosis which is a SE)

78
Q

How does Metformin impact weight and mortality events?

A

Weight neutral and decreases all cause mortality events

79
Q

Exenatide drug class?

A

GLP-1 agonist

80
Q

Liraglutide drug class?

A

GLP-1 agonist

81
Q

Semaglutide drug class?

A

GLP-1 agonist

82
Q

Which GLP-1 agonists are given as SC injections?

A

Exenatide and Liraglutide

83
Q

Which GLP-1 agonist is given orally?

A

Semaglutide

84
Q

What is the MOA of all GLP-1 agonists?

A

GLP-1 agonists that are resistant to DPP-4 degredation (inhibits glucagon release and increases insulin released from pancreas)

85
Q

What are the uses of GLP-1 agonists besides T2DM? (2)

A

Slows gastric emptying = weight loss, potential increase in beta cell # and function

86
Q

Which GLP-1 agonist decreases macrovascular events in T2DM and is independently approved for weight loss?

A

Liraglutide

87
Q

What are the SEs of GLP-1 agonists? (2)

A

Hypoglycemia (low risk), acute pancreatitis

88
Q

What are the precautions of GLP-1 agonists? (2)

A

GI disease, on meds that can’t be exposed to stomach acid too long (b/c GLP-1 agonists slow gastric emptying)

89
Q

What are the contraindications of GLP-1 agonists? (2)

A

Hx of/ current acute pancreatitis, personal/ family hx of thyroid CA (black box warning)

90
Q

Sitagliptin drug class?

A

DPP-4 inhibitor

91
Q

Linagliptin drug class?

A

DPP-4 inhibitor

92
Q

How are the DPP-4 inhibitors administered?

A

Orally

93
Q

What is the MOA of DPP-4 inhibitors?

A

DPP-4 inhibitors, potentiates effects of endogenous incretin hormones (inhibits breakdown by DPP-4)

94
Q

How is Sitagliptin eliminated?

A

Renally

95
Q

How is Linagliptin eliminated?

A

Liver/ GI elimination

96
Q

What are the SEs for the DPP-4 inhibitors? (2)

A

Hypoglycemia (low risk), acute pancreatitis

97
Q

What is the precaution for Sitagliptin?

A

Renal impairment

98
Q

What are the contraindications to DPP-4 inhibitors?

A

Hx of/ current acute pancreatitis

99
Q

Canagliflozin drug class?

A

SGLT-2 inhibitor

100
Q

Dapagliflozin drug class?

A

SGLT-2 inhibitor

101
Q

Empagliflozin drug class?

A

SGLT-2 inhibitor

102
Q

What is the MOA for SGLT-2 inhibitors?

A

SGLT-2 inhibitors, inhibits sodium-glucose co-transporter 2 in kidney = glucose not reabsorbed and then excreted in the urine

103
Q

What are the uses for SGLT-2 inhibitors aside from T2DM? (2)

A

Decreased BP, weight loss

104
Q

Which SGLT-2 inhibitors are used to decrease CV events?

A

Canagliflozin and Empagiflozin

105
Q

Which SGLT-2 inhibitors are used to decrease CKD progression?

A

Canagliflozin

106
Q

Which SGLT-2 inhibitors are used to decrease HF hospitalizations?

A

Canagliflozin and Dapagliflozin

107
Q

What are the most common SEs of the SGLT-2 inhibitors? (3)

A

Genital candida infection, UTI, increased urinary frequency

108
Q

What are the less common SEs of SGLT-2 inhibitors? (3)

A

Hypoglycemia (rare), osmotic diuresis, renal impairment/ AKI

109
Q

What are the contraindications to SGLT-2 inhibitors? (3)

A

Females with recurrent UTIs, ESRD, dialysis

110
Q

Pioglitazone drug class?

A

Thiazolidinedione

111
Q

Rosiglitazone drug class?

A

Thiazolidinedione

112
Q

The following is the MOA for which drug class?

Binds to nuclear PPAR𝛄 receptor → post-receptor insulin mimetic action (induces insulin response w/o insulin present) → ↑ insulin sensitivity, ↑ GLUT 4 and ↓ hepatic glucose production

A

Thiazolidinediones (insulin sensitizers)

113
Q

What is 2nd line treatment for diabetic prophylaxis?

A

Thiazolidinediones

(1st line = Metformin)

114
Q

What are the SEs for Thiazolidinediones? (4)

A

Hypoglycemia (low risk), weight gain, edema, increased bone fracture risk

115
Q

What are the contraindications to Thiazolidinediones? (2)

A

HF and hepatic disease

116
Q

Acarbose drug class?

A

𝝰-glucosidase inhibitor

117
Q

Miglitol drug class?

A

𝝰-glucosidase inhibitor

118
Q

What is the MOA for 𝝰-glucosidase inhibitors?

A

𝝰-glucosidase inhibitors, taken right before a meal = delayed carb digestion/ absorption

119
Q

𝝰-glucosidase inhibitors can be used to treat what?

A

T1 AND T2DM

120
Q

What are the SEs to 𝝰-glucosidase inhibitors? (3)

A

GI effects/ flatulence, increased hepatic enzymes, jaundice

(flatulence b/c bacteria thrive on excess carbs)

121
Q

What is a precaution to treatment with 𝝰-glucosidase inhibitors?

A

Hepatic and renal disease

122
Q

What is the contraindication to 𝝰-glucosidase inhibitors?

A

GI condition/ obstruction

123
Q

Glyburide drug class?

A

Sulfonylureas

124
Q

Glipizide drug class?

A

Sulfonylureas

125
Q

Glimepride drug class?

A

Sulfonylureas

126
Q

The following is the MOA for which drug class?

Bind and block/ close K channel → membrane depolarization → ↑ Ca into cell → ↑ insulin release

A

Sulfonylureas

127
Q

The long half life of Sulfonylureas allows for what?

A

Insulin secreted all day

128
Q

What are the SEs for Sulfonylureas? (4)

A

Hypoglycemia (highest risk), weight gain, GI SEs, progressive disease process of DM

129
Q

Which drug class has the highest risk for hypoglycemia?

A

Sulfonylureas

130
Q

Of the Sulfonylureas (Glyburide, Glipizide, Glimepride) how does the risk for hypoglycemia compare?

A

Glyburide = worst hypoglycemia (24 hr effect)

Glipizide = least hypoglycemia (2-4 hr t½)

Glimepiride = no hypoglycemic effect (once a day dosing)

131
Q

What are the precautions of the Sulfonylureas? (2)

A

Severe renal disease and hepatic dysfunction

132
Q

What is a contraindication to the Sulfonylureas?

A

Sulfa allergy

133
Q

Repaglinide drug class?

A

Meglitinides

134
Q

Meglitinides have the same MOA as Sulfonylureas (bind and block/ close K channel → membrane depolarization → ↑ Ca into cell → ↑ insulin release) with the exception of what?

A

They are not sulfonamides so they are safe in pts with sulfa allergies

135
Q

What is important about the pharmacokinetics of Repaglinide?

A

Short t1/2 = rapid acting (better at mimicking insulin), postprandial

136
Q

What is a SE of Repaglinide?

A

Hypoglycemia (moderate risk, less than all Sulfonylureas)

137
Q

What is a precaution to treatment with Repaglinide?

A

Liver impairment

138
Q

What is a contraindication to treatment with Repaglinide?

A

Do not use with Sulfonylureas

139
Q

Colesevelam drug class/ MOA?

A

Bile acid binding resin

(but MOA unknown for glycemic effect)

140
Q

How is Colesevelam used?

A

Used in combo to decrease basal plasma glucose, also decreases LDL (CV effects)

141
Q

What are the SEs to Colesevelam? (2)

A

Constipation and bloating

142
Q

Bromocriptine drug class?

A

Dopamine agonist

143
Q

What is the MOA of Bromocriptine?

A

Dopamine agonist (quick release), enhanced suppression of hepatic glucose production

144
Q

What is the use of Bromocriptine?

A

Post-prandial glucose

145
Q

What is the precautions with Bromocriptine?

A

Caution w/ CYP3A4 inhibitors/ inducers/ substrates

146
Q

Pramlintide drug class?

A

Amylyn-like peptide

147
Q

What is the MOA for Pramlintide?

A

Amylyn-like peptide, synthetic analog of amylin, regulates post-prandial glucose by ↓ gastric emptying

(amylin = hormone co-secreted with insulin)

148
Q

How is Pramlintide used/ what are its uses?

A

IN COMBO w/ insulin for glycemic control in T1 and T2DM, weight loss

149
Q

How is Pramlintide administered?

A

SC injection, 3x per day (in additional to insulin injections)

150
Q

What is a SE of Pramlintide if used with insulin?

A

Hypoglycemia

151
Q

What is the contraindication to Pramlintide?

A

Gastroparesis (slow stomach emptying)

Pharm II (13 decks)

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