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Pharm II Unit III > 2 Antidiabetic Drugs > Flashcards

2 Antidiabetic Drugs Flashcards

1
Q

Name the rapid-acting insulins

A

Insulin lispro (Humalog)
Insulin as part (Novolog)
Insulin glulisine (Apidra)
Insulin, inhaled (Afrezza)

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2
Q

Name the short-acting insulin

A

Regular Insulin (Novolin R, Humulin R0

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3
Q

Name the intermediate-acting insulin

A

NPH or Isophane Insulin (Humulin N, Novolin N)

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4
Q

Name the long-acting insulins

A 
Insulin glargine (Lantus)
Insulin detemir (Levemir)
Insulin degludec (Tresiba)
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5
Q

Ocular signs of chronic DM

A

Cataract and refractory changes in the lens

Retinopathy (—>blindness)

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6
Q

CV signs of chronic DM

A

Occlusive vascular disease of the lower extremity (gangrene)
Atherosclerosis
HTN
Coronary and cerebral atherosclerosis

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7
Q

Neurobiological signs of chronic DM

A

PERIPHERAL NEUROPATHY
Postural hypotension
Alternativing bouts of diarrhea and constipation
Inability to empty the bladder

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8
Q

Skin and mucous membrane signs of chronic DM

A

Chronic polygenic infection
Eruptive xanthomas
Shin spots
Candida infections, vulvo-vaginitis, pruritis

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9
Q

Diagnostic criteria for DM

A

Random blood glucose ≥200 mg/dL

Fasting blood glucose ≥126 mg/dL

Oral glucose challenge ≥200 mg/dL at 2 hr

HbA1C ≥ 6.5%

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10
Q

HbA1C is proportional to…

A

Long term blood glucose concentration

Used as an integrated index or marker of glycemic control

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11
Q

HbA1C of _____ indicates poorly controlled DM

A

> 10%

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12
Q

Release of insulin is activated by…

A 
Glucose and other sugars
Amino acids
Fatty acids
Ketone bodies
B2 adrenergic agonists
GLP-1 agonists
Vagal activation
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13
Q

Insulin release is inhibited by…

A

Alpha2 agonists

Conditions that activate the sympathetic nervous system

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14
Q

Insulin promotes entry of glucose into _______, _________, ________, and __________

A

Skeletal muscle, Heart muscle, Fat tissue, and leukocytes

Insulin NOT required for glucose transport into the brain, liver, or RBCs

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15
Q

What are the main treatment modalities for DM?

A

Insulin in Type 1 and Type 2

Antidiabetic agents in Type 2 ONLY
• Insulin secretagogues
• Insulin sensitizers
• Glucose uptake inhibitors
• Central modulators
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16
Q

What is the most important adverse effect of exogenous insulin?

A

HYPOGLYCEMIA

Causes tachycardia, confusion, vertigo, sweating

Repetitive hypoglycemic events —> cognitive dysfunction

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17
Q

Other adverse effects of insulin treatment

A 
Weight gain
Cough (inhaled only)
Local reactions (allergy)
Lipodystrophy and liphohypertrophy
Insulin resistance
Interactions with other drugs
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18
Q

What is the treatment for hypoglycemia

A

Give 50-100 ml of 50% glucose solution IV

0.5-1 mg glucagon (much less common)

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19
Q

Local allergic reactions are _______ more common than systemic allergic reactions to insulin

A

10x

Inflammation may persist for several days

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20
Q

Factors that increase insulin requirement

A

Fever, thyrotoxicosis, pregnancy, states of stress, surgery, trauma, infection, or any increased metabolic activity

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21
Q

Which type of insulin is first line in Type 2 DM?

A

Long-acting (basal)

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22
Q

What kind of insulin is used in insulin pumps?

A

Rapid-acting insulins

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23
Q

What type of insulin is preferred for less hypoglycemia?

A

Rapid acting over regular insulin

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24
Q

Hormone produced by alpha cells of the pancreas?

A

Glucagon

Regulates glucose, amino acids, and possibly free fatty acid homeostasis

Increases blood glucose levels by mobilizing hepatic glycogen when available

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25
Q

What are the therapeutic effects of glucagon?

A

Juveniles respond less favorably than adults with stable diabetes

Not very effective in patients with reduced glycogen stores

Potent inotropic and chronotropic effects on the heart (used in beta blocker overdose)

Produces profound relaxation of the intestine (used in radiology)

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26
Q

Non-diuretic thiazides, vasodilator, and hyperglycemic agent

A

Diazoxide (Proglycem)

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27
Q

MOA of Diazoxide (Proglycem)

A

Hyperglycemia by:

  • Directly inhibiting insulin secretion
  • Or decreasing peripheral glucose utilization
  • Or stimulating hepatic glucose production

Used in patients with INSULINOMA

Fairly long duration, oral administration

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28
Q

MOA for Metformin

A

Reduces glucose levels in a predominantly insulin-independent manner

Increases glucose removal from blood
Increases secretion of glucagon-like peptide (GLP-1)
Decreases glucose absorption from the GI
Decreases glucagon levels
Decreases gluconeogenesis
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29
Q

Initial drug of choice for Type 2 DM if A1C is <10%

A

Metformin

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30
Q

Glycemic effects of Metformin

A

HIGH - A1C decrease ~1-1.5%

Promotes a EUGLYCEMIC STATE

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31
Q

Cardiovascular effects of Metformin

A

15-20% reduction of plasma triglycerides

Decreased macrovascular events

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32
Q

Other benefits of metformin

A

Weight neutral
Decreases all-cause mortality events
Best pharmacological therapy for diabetes prevention (use in prediabetics)

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33
Q

What are the pharmacokinetics of Metformin?

A

Oral admin

Renal excretion

Extended release available

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34
Q

Adverse effects of Metformin

A

Hypoglycemia is rare

LACTIC ACIDOSIS** (dose dependent)

Diarrhea (53%)***

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35
Q

Contraindications for Metformin

A

Lactic acidosis conditions
• Kidney disease (esp renal failure with GFR <30)
• Hepatic disease
• Alcoholism
• Diseases predisposing to tissue hypoxia (CHF, COPD)

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36
Q

Name the GLP-1 agonists

A 
Exenatide (Byetta, Bydureon)
Liraglutide (Victoza)
Dulaglutide (Trulicity)
Albiglutide (Tanzeum)
Lixisenatide (Adlyxin)

GULP DOWN THOSE TIDE PODS

37
Q

MOA for GLP-1 agonists

A

GLP-1 agonists resistant to DPP-4 degradation —> increase the release of insulin

38
Q

How are GLP-1 agonists administered?

A

S.C. Injections 2x/day —> 1x/week

39
Q

Glycemic effects of GLP-1 agonists

A

High A1C decrease (1-1.5%)

40
Q

Cardiovascular effects of GLP-1 agonists

A

LIRAGLUTIDE (Victoza) decreases macrovascular events

Potential decrease in BP

41
Q

Benefits of GLP-1 agonists

A

Slows gastric emptying —> patient eats less

WEIGHT LOSS, or at worst weight neutral (Liraglutide is the only one approved for weight loss)

Potential increased beta cell number and function

42
Q

Adverse effects of GLP-1 agonists

A

Hypoglycemia (low risk)
GI disturbance, N/V, diarrhea
Hypersensitivity
Associated with acute pancreatitis***

43
Q

Contraindications for GLP-1 agonists

A

Slow GI problems/GI disease
Other oral meds that cannot be exposed to stomach acid to long
Renal impairment

History of, or acute, PANCREATITIS

Thyroid cancer

44
Q

What drugs are the Dipeptidyl-peptidase-4 (DPP-4) inhibitors?

A

The “gliptins”

Sitagliptin (Januvia)
Saxagliptin (Onglyza)
Linagliptin (Tradjenta)
Alogliptin (Nesina)

45
Q

MOA for DPP-4 inhibitors

A

Potentiates the effects of endogenous incretin hormones by inhibiting their breakdown by DPP-4

46
Q

How are DPP-4 inhibitors administered?

A

Oral, once/day

47
Q

Glycemic effects of DPP-4 inhibitors

A

Medium A1C decrease (0.5-1%) - not huge but nice addition to their treatments

48
Q

CV effects of DPP-4 inhibitors

A

Neutral CVD effects

Also weight neutral

49
Q

Adverse effects of DPP-4 inhibitors

A

Low hypoglycemia risk
Hypersensitivity reactions
Associated with ACUTE PANCREATITIS***
Joint pain

50
Q

Contraindications for DPP-4 inhibitors

A

Slow GI problems
Renal impairment
History of, or acute, PANCREATITIS

51
Q

Which drugs are SGLT-2 inhibitors?

A

Canagliflozin (Invokana)
Dapagliflozin (Farxiga)
Empagliflozin (Jardiance)
Ertugliflozin (Steglatro)

52
Q

MOA for SGLT-2 inhibitors

A

Inhibits the sodium-glucose co-transporter 2 in the kidney

53
Q

How are SGLT-2 inhibitors administered?

A

Oral

54
Q

Glycemic effects of SGLT-2 inhibitors?

A

Medium A1C decrease (0.5-1%)

55
Q

CV effects of SGLT-2 inhibitors

A

Empagliflozin decreases CV events (FDA approved, like Liraglutide) - probably due to WEIGHT LOSS

Canagliflozin similar but not FDA approved

Reduced BP

56
Q

Adverse effects of SGLT-2 inhibitors

A

Hypoglycemia rare

Female genital mycotic infections, UTI and increased urinary frequency***

Increased urinary Na+ excretion and OSMOTIC DIURESIS

Increases in serum Cr, decreases in eGFR, and rarely renal impairment and AKI

Increased LDL-C

Increased incidence of bone fractures

57
Q

Contraindications of SGLT-2 inhibitors

A

Severe renal impairment or dialysis

Prone to UTIs or other genitourinary infections

58
Q

What are the Thiazolidinediones?

A

Pioglitazone (Actos), Rosiglitazone (Avenida)

“Insulin sensitizers” —> specifically targets insulin resistance

59
Q

MOA for thiazolidinediones

A

Ligand of the nuclear PPAR-gamma receptor which can cause post-receptor insulin-mimetic action

—> increased glucose transporter synthesis in adipose
—> decreased hepatic glucose production

60
Q

Pharmacokinetics of thiazolidinediones

A

Oral
Plasma half-life long (takes awhile to take effect)
Metabolized to the liver
Onset and offset of action can take weeks to months

61
Q

Glycemic effects of thiazolidinediones

A

High A1C decrease (1-1.5%)

62
Q

CV effects of thiazolidinediones

A

Decreased TGs in long-term use
Slight increase in HDL

Also lower insulin resistance

63
Q

Adverse effects of thiazolidinediones

A 
Low risk hypoglycemia
Weight GAIN (possible edema)
EDEMA —> increased risk of HF in patients with CHF***
Increased risk of bone fracture
Back pain, fatigue, H/A
64
Q

Contraindications for thiazolidinediones

A

HEPATIC DISEASE (troglitazone —> hepatotoxicity, taken off the market)

Heart Failure

65
Q

What drugs are the Alpha-glucosidase inhibitors?

A

Acarbose (Precose), Miglitol (Glyset)

Used in both Type 1 (off label) and Type 2 DM

66
Q

MOA for alpha-glucosidase inhibitors

A

Inhibit alpha-glucosidase in small intestine —> delayed carbohydrate digestion and absorption

Addresses the diet issues but not the glucose issue***

67
Q

How are alpha-glucosidase inhibitors taken?

A

Orally, pre-prandially

68
Q

Glycemic effects of alpha-glucosidase inhibitors

A

LOW A1C decrease (0.5-1%) —> decreased postprandial glucose ONLY

Also weight neutral

69
Q

Adverse effects of alpha-glucosidase inhibitors

A

NEVER causes hypoglycemia

Frequent GI effects - esp FLATULENCE

Elevated hepatic enzymes, jaundice

70
Q

Contraindications for Alpha-Glucosidase inhibitors

A

GI disease, GI obstruction, ileum, IBD, hiatal hernia

Hepatic disease

Renal impairment

71
Q

MOA for sulfonylureas

A

Bind to and block ATP-sensitive K+ channel to cause membrane depolarization and increase Ca2+ influx on beta cells

Basically, squeeze the last bit of insulin out of the beta cells

72
Q

Glycemic effects of sulfonylureas

A

High A1C decrease (1-1.5%)

73
Q

CV effects of sulfonylureas

A

Short term: neutral

Long term: decreased risk of MI and microvascular disease (better than placebo but not metformin)

74
Q

Which noninsulin therapy has the highest risk of hypoglycemia?

A

Sulfonylureas

75
Q

Adverse effects of sulfonylureas

A

HYPOGLYCEMIA

  • highly dependent on their half-life
  • typically less of a problem with 2nd gen agents
  • why we don’t use these much anymore

Weight gain

GI side effects

76
Q

Contraindications for sulfonylureas

A

Severe renal disease or hepatic dysfunction

Allergies to SULFA DRUGS

77
Q

Which are the first gen sulfonylureas?

A

Tolbutamide (short acting)

Chlorpropamide (long acting - worst hypoglycemia***)

Tolazamide

78
Q

What are the second gen sulfonylureas?

A

Glyburide (worst hypoglycemia of the 2nd’s)

Glipizide (least hypoglycemia of the 2nd’s)

Glimepiride

79
Q

Which drugs are Meglitinides?

A

Repaglinide (Prandin)
Nateglinide (Starlix)

They are not sulfas so can be used in sulfa allergic patients

80
Q

MOA for meglitinides

A

Same as sulfonylureas (bind to and block ATP-sensitive K+ channels —> membrane depolarization and increased Ca2+ influx on beta cells)

Mimic insulin***

81
Q

Glycemic effects of Meglitinides

A

Low A1C decrease —> decrease postprandial glucose only

82
Q

MOA for Colesevelam

A

Bile acid binding resin - unknown glycemic effect but good for combo with other antidiabetic agents to reduce basal plasma glucose

83
Q

Most common toxic effect of Colesevelam

A

Constipation and bloating

84
Q

MOA for Bromocriptine (Cycloset)

A

Dopamine agonist - quick release

Augments low hypothalamic dopamine levels —> inhibits excessive sympathetic tone within the CNS —> decreased postmeal plasma glucose levels due to enhanced suppression of hepatic glucose production

85
Q

Glycemic effects of Bromocriptine

A

Low A1C decrease (but decreased postprandial glucose levels)

86
Q

CV effects of Bromocriptine

A

Decreased free fatty acid and TG levels

Decreased CV end point problems

87
Q

What is Pramlintide (Symlin)?

A

Amylin-like peptide - a hormone co-secreted with insulin

Only an adjunct to insulin therapy in type 1 and 2 DM

Works with insulin to regulate postprandial glucose by delaying gastric emptying, suppression of postprandial glucagon secretion, and centrally-mediated modulation of appetite (dec caloric intake)

88
Q

How is Pramlintide (Symlin) administered?

A

SC injection 3x/day (with meal bolus of insulin)

Pharm II Unit III (4 decks)

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