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ER Week 2 > Diabetes Medications > Flashcards

Diabetes Medications Flashcards

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1
Q

Metformin is the most common used drug in what class?

A

biguanides

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2
Q

WHat is metformin derived from?

A

french lilac

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3
Q

What does metformin do?

A
  1. inhibits the enzymes used for gluconeogenesis
  2. inhibits hepatic uptake of gluconeogenic substrates
  3. suppresses the mitochondrial repsiratory chain, increases insulin receptor tyrosine kinase activity and stimualtes GLUT4 transporters —– all increasing insulin sensitivity
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4
Q

What are the side effects of metformin?

A

about 50% complain of diarrhea with the initial dose

lactic acidosis is the most serious side effect

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5
Q

Why does the lactic acidosis happen?

A

the circulating lactate isn’t used as a substrate for gluconeogenesis, but those enzymes are inhibited

this means the lactate just builds up in the blood causing an acidosis

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6
Q

What are sufonylureas in general?

A

insulin secretagogues (meaning they promote insulin secretion)

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7
Q

What is the most commonly used sulfonylurea?

A

Glimepiride

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8
Q

How does Glimepiride work?

A

by binding to the SUR1 subunit of the ATP=sensitive potassium channel

it makes the channel close (essentially acting like glucose does)

This activates the Ca channels increasing intracellular Ca and thus triggering insulin release

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9
Q

What are the primary side effects of glimepiride?

A

hypoglyecmia

weight gain

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10
Q

Glimepiride is the most common, but what are some otherse?

A

First gen: tolbutamide, chlorporpamide

second gen: Glimepiride, glyburide, Glipizide

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11
Q

What made the second generations better than the first generations?

A

the first generations has half lives that were too long

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12
Q

How do they alter the pharmacokinetics of synthetic insulin preparations?

A

they use different amino acid substitutions in the alpha and beta chains

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13
Q

What insulin preparations are rapid acting?

A

Lispro
Aspart
Glulisine

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14
Q

What is the time of onset for the rapid acting? Peak effect? Duration?

A

15 minute to onset
max at .5-1.5 hours
Duration about 3-4 hours

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15
Q

What is the short acting insulin?

A

regular insulin!

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16
Q

What is the time of onset for insulin? Maximum effect? Duration?

A

30 minutes to onset
max at 2-3 hours
4-8 hr duration

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17
Q

What is the intermediate acting insulin?

A

NPH insulin

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18
Q

How long to onset? Maximum? Duration?

A

2-4 hours to onset
4-12 hours maximum effect
10-20 hour duration

19
Q

What are the two long acting insulins?

A

Glargine

Detemir

20
Q

How long does it take for the long acting to start having effect? WHen’s their max effect? Duration?

A

1-2 hours to onset
there’s no peak!!!
duration of 18-24 hours

21
Q

What are the main side effects of insulin?

A 
hypoglycemia (duh)
weight gain
allergic reaction to the preparation
atrophy or hypertrophy of subcutaneous fat at injection site
insulin resistance
22
Q

Which incretin do we make analogs of to promote insulin secretion and inhbit glucagon secretion?

A

GLP-1 analogs

23
Q

What is the main example of a GLP-1 analog?

A

Exenatide

24
Q

How is exenatide administered?

A

administered subq before a meal

25
Q

What are the side effects of exenatide?

A

nausea, vomiting and pancreatitis

26
Q

What’s another way we can use the action of GLP-1 in our favor?

A

We can use a DDP-IV enzyme inhibitor to prevent it’s degradation and increase it’s activity

27
Q

Name the DDP-IV inhibitor we learned.

A

Sitagliptin (Januvia)

28
Q

How do Meglitinides work?

A

they’re insulin secretagogues –block the K channel

29
Q

What are the two examples of Meglitinides?

A

Repaglinide

Nateglinide

30
Q

What are the main side effects of the melitinides?

A

hypoglycemia, weight gain, tremor, nausea, vomiting, dizziness

31
Q

How are the meglitinides administered?

A

orally, take with meal, duration of action 5-8 hours

32
Q

So…the meglitinides work sort of like what other class of drug?

A

sulfonylureas like glipizide

33
Q

What class of drugs will slow intestinal digestion and absorption of carbohydrates?

A

alpha-glucosidase inhibitors

the glucosidases hydrolyze carbs to monosaccharides

34
Q

What are the two alpha-glucosidase inhibitors we know?

A

acarbose

miglitol

35
Q

What would an amylin analog do?

A

delay gastric emptying and inhibit glucagon secretion
inhibit gluconeogenesis
increase satiety

36
Q

What’s the amylin analog we know?

A

PrAMLIntide

37
Q

How is Pramlintide administered?

A

SC administration before meals with peak concentration in 30 minutes

38
Q

Why would you probably not gives pramlintide in combo with insulin?

A

it can induce severe hypoglycemia

39
Q

What do the Thiazolidinediones do?

A

they are PPAR receptor agonists that increase glucose uptake and utilization by increasing synthesis and transport of GLUT transporter in muscle, adipose and liver

40
Q

What are the two thiazolidinediones we know?

A

Rosiglitazone

Pioglitazone

41
Q

So what do you need if the thiazolidinediones are going to work?

A

some level of insulin

42
Q

Why did a lot of doctors stop prescribing the thiazolidinediones?

A

there was maybe an increased risk of heart failure and cardiovascular events, but probably not now

43
Q

What group of people should you not use pioglitazone in?

A

those with previous or current bladder cancer - it’s been found to increase the risk

ER Week 2 (10 decks)

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