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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
What are the therapeutic effects of glucagon?
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)
26
Non-diuretic thiazides, vasodilator, and hyperglycemic agent
Diazoxide (Proglycem)
27
MOA of Diazoxide (Proglycem)
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
28
MOA for Metformin
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 ```
29
Initial drug of choice for Type 2 DM if A1C is <10%
Metformin
30
Glycemic effects of Metformin
HIGH - A1C decrease ~1-1.5% Promotes a EUGLYCEMIC STATE
31
Cardiovascular effects of Metformin
15-20% reduction of plasma triglycerides | Decreased macrovascular events
32
Other benefits of metformin
Weight neutral Decreases all-cause mortality events Best pharmacological therapy for diabetes prevention (use in prediabetics)
33
What are the pharmacokinetics of Metformin?
Oral admin Renal excretion Extended release available
34
Adverse effects of Metformin
Hypoglycemia is rare LACTIC ACIDOSIS**** (dose dependent) Diarrhea (53%)***
35
Contraindications for Metformin
Lactic acidosis conditions • Kidney disease (esp renal failure with GFR <30) • Hepatic disease • Alcoholism • Diseases predisposing to tissue hypoxia (CHF, COPD)
36
Name the GLP-1 agonists
``` Exenatide (Byetta, Bydureon) Liraglutide (Victoza) Dulaglutide (Trulicity) Albiglutide (Tanzeum) Lixisenatide (Adlyxin) ``` GULP DOWN THOSE TIDE PODS
37
MOA for GLP-1 agonists
GLP-1 agonists resistant to DPP-4 degradation —> increase the release of insulin
38
How are GLP-1 agonists administered?
S.C. Injections 2x/day —> 1x/week
39
Glycemic effects of GLP-1 agonists
High A1C decrease (1-1.5%)
40
Cardiovascular effects of GLP-1 agonists
LIRAGLUTIDE (Victoza) decreases macrovascular events Potential decrease in BP
41
Benefits of GLP-1 agonists
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
Adverse effects of GLP-1 agonists
Hypoglycemia (low risk) GI disturbance, N/V, diarrhea Hypersensitivity Associated with acute pancreatitis***
43
Contraindications for GLP-1 agonists
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
What drugs are the Dipeptidyl-peptidase-4 (DPP-4) inhibitors?
The “gliptins” Sitagliptin (Januvia) Saxagliptin (Onglyza) Linagliptin (Tradjenta) Alogliptin (Nesina)
45
MOA for DPP-4 inhibitors
Potentiates the effects of endogenous incretin hormones by inhibiting their breakdown by DPP-4
46
How are DPP-4 inhibitors administered?
Oral, once/day
47
Glycemic effects of DPP-4 inhibitors
Medium A1C decrease (0.5-1%) - not huge but nice addition to their treatments
48
CV effects of DPP-4 inhibitors
Neutral CVD effects Also weight neutral
49
Adverse effects of DPP-4 inhibitors
Low hypoglycemia risk Hypersensitivity reactions Associated with ACUTE PANCREATITIS*** Joint pain
50
Contraindications for DPP-4 inhibitors
Slow GI problems Renal impairment History of, or acute, PANCREATITIS
51
Which drugs are SGLT-2 inhibitors?
Canagliflozin (Invokana) Dapagliflozin (Farxiga) Empagliflozin (Jardiance) Ertugliflozin (Steglatro)
52
MOA for SGLT-2 inhibitors
Inhibits the sodium-glucose co-transporter 2 in the kidney
53
How are SGLT-2 inhibitors administered?
Oral
54
Glycemic effects of SGLT-2 inhibitors?
Medium A1C decrease (0.5-1%)
55
CV effects of SGLT-2 inhibitors
Empagliflozin decreases CV events (FDA approved, like Liraglutide) - probably due to WEIGHT LOSS Canagliflozin similar but not FDA approved Reduced BP
56
Adverse effects of SGLT-2 inhibitors
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
Contraindications of SGLT-2 inhibitors
Severe renal impairment or dialysis | Prone to UTIs or other genitourinary infections
58
What are the Thiazolidinediones?
Pioglitazone (Actos), Rosiglitazone (Avenida) “Insulin sensitizers” —> specifically targets insulin resistance
59
MOA for thiazolidinediones
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
Pharmacokinetics of thiazolidinediones
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
Glycemic effects of thiazolidinediones
High A1C decrease (1-1.5%)
62
CV effects of thiazolidinediones
Decreased TGs in long-term use Slight increase in HDL Also lower insulin resistance
63
Adverse effects of thiazolidinediones
``` 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
Contraindications for thiazolidinediones
HEPATIC DISEASE (troglitazone —> hepatotoxicity, taken off the market) Heart Failure
65
What drugs are the Alpha-glucosidase inhibitors?
Acarbose (Precose), Miglitol (Glyset) Used in both Type 1 (off label) and Type 2 DM
66
MOA for alpha-glucosidase inhibitors
Inhibit alpha-glucosidase in small intestine —> delayed carbohydrate digestion and absorption Addresses the diet issues but not the glucose issue***
67
How are alpha-glucosidase inhibitors taken?
Orally, pre-prandially
68
Glycemic effects of alpha-glucosidase inhibitors
LOW A1C decrease (0.5-1%) —> decreased postprandial glucose ONLY Also weight neutral
69
Adverse effects of alpha-glucosidase inhibitors
NEVER causes hypoglycemia Frequent GI effects - esp FLATULENCE Elevated hepatic enzymes, jaundice
70
Contraindications for Alpha-Glucosidase inhibitors
GI disease, GI obstruction, ileum, IBD, hiatal hernia Hepatic disease Renal impairment
71
MOA for sulfonylureas
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
Glycemic effects of sulfonylureas
High A1C decrease (1-1.5%)
73
CV effects of sulfonylureas
Short term: neutral Long term: decreased risk of MI and microvascular disease (better than placebo but not metformin)
74
Which noninsulin therapy has the highest risk of hypoglycemia?
Sulfonylureas
75
Adverse effects of sulfonylureas
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
Contraindications for sulfonylureas
Severe renal disease or hepatic dysfunction Allergies to SULFA DRUGS
77
Which are the first gen sulfonylureas?
Tolbutamide (short acting) Chlorpropamide (long acting - worst hypoglycemia***) Tolazamide
78
What are the second gen sulfonylureas?
Glyburide (worst hypoglycemia of the 2nd’s) Glipizide (least hypoglycemia of the 2nd’s) Glimepiride
79
Which drugs are Meglitinides?
Repaglinide (Prandin) Nateglinide (Starlix) They are not sulfas so can be used in sulfa allergic patients
80
MOA for meglitinides
Same as sulfonylureas (bind to and block ATP-sensitive K+ channels —> membrane depolarization and increased Ca2+ influx on beta cells) Mimic insulin***
81
Glycemic effects of Meglitinides
Low A1C decrease —> decrease postprandial glucose only
82
MOA for Colesevelam
Bile acid binding resin - unknown glycemic effect but good for combo with other antidiabetic agents to reduce basal plasma glucose
83
Most common toxic effect of Colesevelam
Constipation and bloating
84
MOA for Bromocriptine (Cycloset)
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
Glycemic effects of Bromocriptine
Low A1C decrease (but decreased postprandial glucose levels)
86
CV effects of Bromocriptine
Decreased free fatty acid and TG levels | Decreased CV end point problems
87
What is Pramlintide (Symlin)?
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
How is Pramlintide (Symlin) administered?
SC injection 3x/day (with meal bolus of insulin)

Pharm II Unit III (4 decks)

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