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Pharmacology II > Exam 2: Diabetes Medications > Flashcards

Exam 2: Diabetes Medications Flashcards

1
Q

What makes the various insulin preparations

have differnt pharmacokinetic profiles?

A

They are modified with different amino acids.

This is reflected in their names:

Long Acting: Gly + Arg = glargine

Short acting: Lys + Pro = lispro,

Asp = aspart, Glu + Lys = glulisine

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2
Q

What is a rapid acting insulin?

A

Standard

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3
Q

Name in intermediate acting insulin

A

NPH = “isophane”

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4
Q

What are the two long-acting insulins

we need to know, and which one has no peak ?

A

Detemir

Glargine: no peak

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5
Q

What is the “Dawn Effect”

and how does that affect insulin dosing?

A

Corisol causes endogenous glucose production in the morning

so you need an overnight dose of insulin

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6
Q

What is the key side effect of insulin

and how do you treat it?

What will exacerbate this side effect?

A

Hyperglycemia (<70) due to excessive dose or mistimed dose

Tx: glucose or glucagon

Exacerbated by EtOH, beta blockers, salicylates

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7
Q

Your patient was just diagnosed with DM type 1.

She is a bright high school student who eats three good meals a day.

What medication would you provide?

A

Long acting insulin like Glargine or Detemir at bedtime

Short acting like Lispro or Aspart before each meal.

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8
Q

Your see your patient again in two weeks and look at her blood sugar diary.

Her blood sugar is low when she wakes up but tends to be high after meals. How do you adjust her dose?

A

Decrease her long acting bedtime dose.

Increase her mealtime doses.

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9
Q

What are the two key problems in DM Type 2?

Which one tends to happen first?

A

1st: decreased insulin sensitivity
2nd: decreased insulin secretion

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10
Q

You just diagnosed a new patient with DM type 2.

What is your first treatment of choice?

A

Lifestyle modification: increased exercise and weight loss

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11
Q

What is the MOA for Metformin?

A

Insulin sensitiation

Activation of AMP-dependent protine kinase AMPK

Leading to:

Decreased liver gluconeogenesis and lipogenesis

Increased liver fatty acid oxidation

Increased GLU uptake in muscles/fat cells

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12
Q

What is the first line medication for diabetes type 2?

A

Metformin

(Also for pre-diabetes)

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13
Q

What are the pros and cons of Metformin?

A

Pros: euglycemic, slight weight loss, decreased microvascular complications, ok during pregnancy,

somewhat additive effect with drugs with a different MOA.

Cons: N/V/D and metalic taste (which may lead to wt loss)

C/I re renal dysfunction and

severe liver dz (can lead to lactic acidosis)

NOTE: D/C before using contrast dyes

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14
Q

What is the MOA and effect of thiazolidenediones (TZDs)

Name one.

A

increase insulin sensitivity in target tissues

MOA: altering the expression of insulin responsive genes

via PPAR alpha receptor

Result: decreased FFA and increased GLU utilization in adipose tissue, decreased GLU output from liver

Pioglitazone

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15
Q

What are the pros and cons of TZDs

(Thiazolidenediones like Pioglitazone)

A

Pros: anti-inflammatory, improved lipids, no hypoglycemia, no lactic acidosis

Cons: fluid retention/edema, weight gain, decreased bone density and increased fractures

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16
Q

What is the MOA of insulin secretagogues?

A

They mimic glucose by getting beta cells to release insulin.

MOA: block K+ channel to increase depolarization and Ca+ influx leading to insulin release.

17
Q

What do secretatgogues need in order to work?

A

Beta cells!

Secretagogues do not work in patients with severe DM type 2 who have little or no remaining functional beta cells.

18
Q

How do secretagogues effect insulin sensitivity?

A

They don’t.

19
Q

What are the pros and cons of Sulfonureas?

Name one.

A

Pros: increase insulin secretion

Cons: severe hypoglycemia, weight gain, drug-drug interactions can either increase or decrease effectiveness

C/I: hepatic and renal disease

Glipizide

20
Q

What are the pros and cons of Non-sulfonurea Secretagogues?

(AKA Meglitinides)

Name one

A

Pros: increase insulin release from Beta cells

Cons: hypoglycemia (less than sulfonureas), drug-drug interactions can increase risk of hypoglycemia

NOTE: rapid absorption: good after a meal

Repaglinide

21
Q

What do GLP-1 Receptor Agonists do

and what is their MOA?

A

Increase glucose dependent insulin secretion

Decrease gastric emptying and increased satiety, decreased hepatic fat, possible decreased beta cell apoptosis

MOA: GLP-1 mimetics: enter the beta cell via the same receptor

22
Q

Name a GLP-1 receptor agonist.

How is it formulated?

A

Exenatide and Exendatide LAR extended release

Formulation: injectable

23
Q

What are the pros and cons of GLP-1 Receptor Agonists?

A

Pros: increase insulin secretion (they require glucose!), weight loss, decreased hepatic fat, increased beta cell mass

Cons: N/V/D (44%) which can decrease with use or can lead to acute renal failure

Increase hypoglycemia if used with secretagogues.

C/I: gastroparesis

24
Q

What is the MOA and effect of DPP-4 Inhibitors?

(Dipeptidyl Peptidase 4 Inhibitors)

A

MOA: stop metabolism of GLP-1 by DPP-4

leading to prolonged GLP-1 action

Effect: increased incretin > insulin secretion

leading to increased glucose mediated insulin secretion

25
Q

What are the pros and cons of DPP-4 Inhibitors?

Name one.

A

Pros: increased insulin secretion, weight neutral

Cons: increased hypoglycemia with secretagogoes

potentially fatal hepatic failure

hypersensitivity reactions (urticaria, etc)

possible severe disabling joint pain (Tx: D/C)

Sitagliptin

the “gliptins”

26
Q

What is the MOA and effect of Alpha-glucosidase Inhibitors?

Name one.

A

MOA: inhibit alpha-glucosidase, which metabolizes small sugars.

Effect: decreased digestion of carbs leading to

decreased GLU absorption in GI (take at mealtime)

Acarbose (carbs not absorbed)

27
Q

What are the pros and cons of alpha-glucosidase inhibitors?

A

Pros: decreased blood sugar

Cons: abdominal pain, diarrea, gas

(decrease with use or dose titration)

increased hypoglycemia with sulfonureas or insulin

NOTE: Tx hypoglycemia with oral glucose, NOT dissacharides because cannot digest them!

C/I: chronic bowel disease due re abdominal pain

28
Q

What is the MOA and effect of Renal SGLT-2 Inhibitors?

Name one.

A

MOA: inhibit Sodium-dependent GLucose Transporter in proximal tubule of kidney

Effect: decreased glucose reabsorption leading to decreased blood sugar.

Canagliflozin (CAN affect GLucose FLO)

29
Q

What are the pros and cons of SGLT-2 Inhibitors?

A

Pros: possible weight loss and possible improved cardiovascular disease (re Na+ loss)?

Cons: increased glucose in urine can lead to UTIs and genital mycotic infections (3-15%)

Electrolyte changes (increased K+, Mg++, Phos)

C/I: DM type I (not tested yet)

30
Q

What is the MOA and the effect of Amylin Agonists?

A

MOA: mimics beta cell amylin,

which causes decreased glucagon release

Effect: decreased gastric emptying and increased satiety

31
Q

What are the pros and cons of Amylin Agonists?

What is its formulation?

A

Pros: decreased blood glucose, increased satiety

Cons: hypoglycemia, N, HA, anorexia

Formulation: injectible, taken like insulin before meals

for type 1 and type 2 DM

32
Q

Your patient is on metformin but needs another medication to better control his type 2 DM.

Your patient also has high LDL and arthritis.

What do you prescribe?

What would you warn the patient about?

A

Pioglitazone (thiazolidenedione)

Because: anti-inflammatory and improves lipid profile

Warn patient about edema (peripheral, pulmonary, macular) and risk of fracture

33
Q

Which two types of medications

have the greatest risk of hypoglycema?

A

Insulin

Sulfonylureas

34
Q

Which medications do NOT lead to weight gain?

A

Weight loss: Biguanides (Metformin)

GLP-1 receptor agonists (Exenatide)

Weight Neutral: DPP-4 Inhibitors (Sitagliptin)

35
Q

Your patient has been a type 2 diabetic for 20 years and now has virtually no beta cells left.

What can you prescribe?

A

Insulin

Metformin and Thiazolidenediones (insulin sensitizers)

Alpha-glucosidase Inhibitors (decreased digestions of carbs)

Renal SGLT-2 inhibitors (decreased renal GLU reabsorption)

36
Q
A

Pharmacology II (11 decks)

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