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Pharmacology > Diabetes Drugs > Flashcards

Diabetes Drugs Flashcards

1
Q

What is the goal of insulin therapy for pts with T1DM?

A

Achieve normal glycemic control

Use basal insulin to replace insulin made under fasting conditions, and posprandial insulin for more rapid action

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2
Q

Insulin MOA (3 primary organs and its effects)

A

Liver
Inhibit secretion of glucagon from alpha cells, thus decreasing gluconeogenesis and glycogenolysis

Muscle
Upregulate GLUT4 and increase glucose uptake. Increase protein synthesis and inhibit proteolysis

Adipose
Increase glucose uptake and decrease lipolysis

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3
Q

Name the different forms of rapid acting insulin

A

Insulin aspart
Insulin lispro
Insulin glulisine

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4
Q

What is the intermediate acting insulin?

A

NPH Insulin

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5
Q

Name the long acting insulins

A

Insulin glargine

Insulin detmir

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6
Q

Insulin

Administration

A

SubQ via syringe, pen, or pump

Note: You should change site of administration over time, as insulin promotes lipid storage in adipose cells

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7
Q

Compare Conventional Insulin Therapy with Intensive Insulin Therapy

A

Conventional: Two injections per day containing both NPH insulin and regular insulin
Risk of hyperglycemia at night

Intensive: Once/twice daily basal insulin to lower fasting glucose, with pre-meal bolus of rapid insulin to control postprandial glucose
Needs more patient commitment; higher cost

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8
Q

Major symptoms of Hypoglycemia

A

Mild: Tremor, palpitations, sweating, hunger

Moderate: Headache, mood change, decreased attention, patients may need assistance

Severe: Unresponsive, Unconscious, convulsions, death

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9
Q

What is the best treatment for T2DM?

A

Diet and exercise

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10
Q

What is the DOC for patients unable to control T2DM with diet and exercise along?

A

Metformin

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11
Q

Metformin

MOA

A

Blocks complex 1 in mitochondrial oxidative phosphorylation, leading to an antagonization of adenylate cyclase in the liver (preventing gluconeogenesis). Also causes increased AMP, leading to higher AMPK, causing increased insulin sensitivity, glucose uptake.

Lower plasma glucose and insulin resistance

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12
Q

Metformin

Adverse Effects

A

Mostly well tolerated (some GI effects, potential B12 def)

Major AE: Lactic Acidosis that may be fatal
-Paritcular risk in high risk pt (elderly, renal/hepatic insufficiency)

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13
Q

Metformin

Contraindications

A

Pregnent/lactating women

Renal or hepatic insufficiency

Elderly (risk renal insufficiency)

Anyone at risk for lactic acidosis

Anyone taking iodinated contrast agent for radiography (risk of agent-induced acute renal failure)

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14
Q

What are the two Thiazolidinediones?

A

Pioglitazone

Rosiglitazone

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15
Q

Pioglitazone and Rosiglitazone

MOA

A

Agonist for PPARy
Increases gene transcription of GLUT4 in muscle, increased adiponectin

Increases Insulin SENSITIVITY

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16
Q

Pioglitazone and Rosiglitazone

Indications

A

Used in monotherapy or in combo with metformin, sulfonylureas, or insulin for T2DM

Decreases FASTING blood glucose

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17
Q

Pioglitazone and Rosiglitazone

Adverse Effects

A

Weight gain

Fluid retention and peripheral edema
-Increased risk HEART FAILURE

Increased risk bone fracture

Hepatotoxic

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18
Q

Pioglitazone and Rosiglitazone

Contraindications

A

Liver disease
Heart failure
Pregnancy

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19
Q

What two classes of drugs are known as insulin secretagogues? What is each of their durations?

A

Sulfonylureas (longer acting, primarily affect fasting glucose)

Meglitinides (shorter duration, primarily affect postprandial glucose)

20
Q

What sulfonylurea drugs are commonly used today?

A

Glipizide
Glimepride
Glyburide

21
Q

Sulfonylurea

MOA

A

Inhibit Sur1 subunit of the Kir6.2 channel on beta cells. Causes an increase in intracellular K+, stimulatign Ca2+ influx and causing release of insulin-containign granules

22
Q

Sulfonylureas

Indications and Uses

A

Long duration of glucose lowering effect, primarily affecting fasting plasma glucose

Activity is dependent on function of beta cells, which will likely lose function over time

23
Q

Sulfonylureas

Adverse Effects

A

Hypoglycemia– seen more in pts with renal or hepatic insufficiency

Weight gain

24
Q

Describe the metabolism of Glipizide, Glyburide, and Glimepride and how that affects their potential uses and toxicites

A

Glyburide and Glimepride are metabolized in liver to active metabolites, so they may cause increased drug conc and toxicity in renal or hepatic insufficiency

Glipizide is metabolized in liver to an inactive metabolite, so it is safer to use in patients with renal insufficiency

25
Q

Sulfonylureas

Contraindications

A

Elderly people with renal or liver insufficiency

T1DM

Pregnant/lactating women

Sulfa allergy

26
Q

Sulfonylureas

Drug Interactions

A

Sulfonylureas are highly protein bound drugs, so it is easy to knock them off with other drugs (salicylates, B blockers, warfarin, fibrates) and cause toxicity

27
Q

Meglitinides

MOA

A

Bind a different part of Sur1 subunit of the Kir6.2 channel on Beta cells, inhibiting it and causing increase in intracellular K+, then ca2+, then release of insulin granules

28
Q

What is the major difference between meglitinides and Sulfonylureas?

A

Meglitinides are much more rapid acting and used to affect postprandial blood glucose

They are glucose-dependent, whereas sulfonylureas are not

29
Q

Name the two Meglitinides

A

Repaglinide

Nateglinide

30
Q

Meglitinides

Adverse Effects

A

Hypoglycemia

Weight gain

31
Q

Meglitinides

Contraindications

A

Liver disease

Pregnancy

32
Q

What is the major difference between Nateglinide and Repaglinide?

A

Nateglinide does not require dose adjustment in renal insufficiency

33
Q

List the GLP-1 homologs

A

Exenatide

Liraglutide

34
Q

Describe the Incretin Effect

A

Oral glucose induces a much better plasma insulin response than IV glucose does because of release of incretins form intestines, which potentiate insulin release at beta cells

35
Q

Exenatide

MOA

A

Binds GLP-1 receptor on beta cells and potentiates glucose-induced insulin release

Suppresses glucagon production

Makes periphery more sensitive to insulin

36
Q

What is the advantage of giving exenatide over recombinant GLP-1?

A

GLP-1 has a very short half life (2 min) because it is rapidly broken down by DPP-IV

Exenatide acts longer than GLP1 itself, and exenatide reduces both fasting and postprandial glucose

37
Q

List the DPP-IV Inhibitors

A

Sitagliptin

Saxagliptin

38
Q

DPP-IV Inhibitors

MOA

A

Inhibit breakdown of GLP1 by DPP-IV, thus allowing more activity of GLP1

39
Q

Alpha-glucosidase inhibitors

MOA

A

Reduce postprandial blood glucose by inhibiting the digestion of polysaccharides in the small intestine (inhibit alpha-glucosidase enzyme)

40
Q

Alpha-glucosidase inhibitors

Adverse Effects

A

May cause GI side effects – do not use when pt has any GI disorder

Do NOT treat any hypoglycemia with complex carbs because the patient won’t be able to break them down

41
Q

SGLT2 Inhibitors

MOA

A

Work to inhibit SGLT2 Na+/Glucose linked transporter protein in the kidney

Promotes glucose excretion from kidney by preventing its reabsorption in the PCT

42
Q

SGLT2 Inhibitors

Adverse Effects

A

Increased risk UTIs
Thirst/dehydration
Hypotension
Hyperkalemia

43
Q

Bromocriptine

MOA

A

Direct D2 agonist

Given in quick release in early morning

Decreases gluconeogenesis, lipolysis, and lipogenesis

44
Q

Colesevelam

MOA

A

Bile acid binding resin that is also used to treat dyslipidemia

Prevent bile acid from being reabsorbed in the small intestine. Bile acids can then bind receptors in the colon to stimulate GLP1 secretion and thus potentiate insulin release

45
Q

Pramlintide

MOA

A

Amylin homolog that inhibits hepatic gluconeogenesis, slows gastric emptying, and lowers glycogenolysis

Reduces POSTPRANDIAL glucose excursion

46
Q

Pramlintide

Indications

A

Used as an adjunct to insulin therapy

Increases risk of severe hypoglycemia, so insulin dosage should be lowered before adding pramlintide

Pharmacology (67 decks)

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