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67 Cards in this Set

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Generally, what duration of action is regular insulin?
Short acting -> peaks at 2-4 hours
Generally, what duration of action is lispro insulin?
Very short acting -> peaks at 1-2 hours
(doesn't associate into hexaner around zing like standard insulin)
Generally, what duration of action is NPH insulin?
Intermediate acting -> peaks at ~8 hours, lasts for 16
Generally, what duration of action is Glargine insulin?
VERY LONG acting -> lasts ~24 hours

(Precipitates -> slowly resolubilizes)
Generally, what duration of action is detemir insulin?
Long -> lasts ~14 hours

(Has a lipid moiety)
Generally, what duration of action is Lente insulin?
Long-acting
Generally, what duration of action is Ultra Lente insulin?
Long-acting
How do the sulfonylureas work?
Block ATP-DEPENDENT K+ CHANNEL -> membrane depolarization -> CA2+ influx -> insulin release
How does tolbutamide work?
Block ATP-DEPENDENT K+ CHANNEL -> membrane depolarization -> CA2+ influx -> insulin release
How does glyburide work?
Block ATP-DEPENDENT K+ CHANNEL -> membrane depolarization -> CA2+ influx -> insulin release
Clinically AND biochemically, how are the metglinides different from the sulfonylureas?
Biochemically: They act at a distinct receptor site on the ATP-dependent K+ channel.

Clinically: They act more rapidly with a shorter duration -> better for post-prandial glucose control
Clinically AND biochemically, how does repaglinide different from the sulfonylureas?
Biochemically: They act at a distinct receptor site on the ATP-dependent K+ channel.

Clinically: They act more rapidly with a shorter duration -> better for post-prandial glucose control
Clinically AND biochemically, how is nateglinide different from the sulfonylureas?
Biochemically: They act at a distinct receptor site on the ATP-dependent K+ channel.

Clinically: They act more rapidly with a shorter duration -> better for post-prandial glucose control
What is the prototypical 1st generation sulfonylurea?
Tolbutamide
What is the prototypical 2nd generation sulfonylurea?
Glyburide
What are the main differences between a first generation sulfonylurea and a second generation sulfonylurea?
2nd generation have:

1) Greater potency

2) Longer half-life
What is tolbutamide?
a 1st generation sulfonylurea
What is glyburide?
a 2nd generation sulfonylurea
How is repaglinide dosed?
with meals, TID
What is the major difference in the metabolism of repaglinide and nateglinide?
Both are hepatically metabolized, but REPAGLINIDE is excreted in the bile.

Nateglinide is excreted in the urine. In fact 16% of it is secreted unchanged in the urine.

Also note that Nateglinide is metabolized by p450 -> solubilized -> readied for renal secretion.
How much of nateglinide is excreted in the urine without any alteration at all?
16% of it is secreted unchanged in the urine.
Which of the meglitinides is metabolized by p450?
Nateglinide
Which class of drugs is an insulin sensitizer?
Thiazolidiones (TZD's)

Glitazones
How do the TZD's work?
Insulin sensitizer.

Binds PPAR-y -> sensitizes to insulin
How do the glitazones work?
Insulin sensitizer.

Binds PPAR-y -> sensitizes to insulin
How rosiglitazone work?
Insulin sensitizer.

Binds PPAR-y -> sensitizes to insulin
How does pioglitazone work?
Insulin sensitizer.

Binds PPAR-y -> sensitizes to insulin
What are the side effects of the glitazones? (3)
1) Weight gain

2) Fluid retention -> contraindicated in CHF patients

3) Slight hepatotoxicity
What are the side effects of rosiglitazone? (3)
Rosiglitazone is an insulin sensitizer. It has the following side effects:

1) Weight gain

2) Fluid retention -> contraindicated in CHF patients

3) Slight hepatotoxicity
What are the side effects of the pioglitazone? (4)
Pioglitazone is an insulin sensitizer. It has the following side effects.

1) Weight gain

2) Fluid retention -> contraindicated in CHF patients

3) Slight hepatotoxicity
Which drug inhibits hepatic glucose production?
metformin
What are the mechanisms of metformin as an oral hypoglycemic? (4)
1) Decreases hepatic glucose production.

2) Some insulin sensitization: Increases insulin-mediated glucose uptake by fat and muscle cells.

3) Absorption inhibitor: Decreases GI glucose absorption.

4) Inhibits adipose tissue lipolysis
A T2DM patient presents to the ER complaining of shortness of breath. A careful history reveals that his primary care doctor put him on a new drug a few weeks ago. Physical examination of the patient reveals that he is taking rapid, deep breaths. As you finish your exam, he mentions that he has also been told that his diabetes has damaged his kidneys or something. Diagnosis? What was the drug?
Lactic acidosis -> caused by giving METFORMIN to a patient with renal insufficiency
Which two classes of drugs lower plasma triglycerides?
Metformin and the glitazones (TZD's).

Both inhibit adipose tissue lipolysis.
Which two drugs inhibit alpha-glucosidases?
Acarbose

Miglitol


(MIGLITOL, MIGLITOL, MIGLITOL)
What does miglitol do?
Inhibits alpha-glucosidase -> delays breakdown and absorption of complex CHO in intestines.
What does acarbose do?
Inhibits alpha-glucosidase -> delays breakdown and absorption of complex CHO in intestines.
What is an incretin? Classic example?
Incretins are endogenous molecules that increase insulin production.

Classic example: GLP-1
What is GLP-1?
Endogenously-produced peptide molecules that increase insulin production.
What effects does GLP-1 have on the body? (4)
1) Increased insulin release

2) decreased glucagon release

3) Decreased gastric emptying

4) Lowers appetite, increases satiety, and causes nauseousness
What effects does exendin-4 have on the body? (4)
Remember, it's modified GLP-1, so it:

1) Increased insulin release

2) decreased glucagon release

3) Decreased gastric emptying

4) Lowers appetite, increases satiety, and causes nauseousness
What effects does liraglutide have on the body? (4)
Remember, it's modified GLP-1, so it:

1) Increased insulin release

2) decreased glucagon release

3) Decreased gastric emptying

4) Lowers appetite, increases satiety, and causes nauseousness
What are the two GLP-1 analogues?
Exendin-4

Liraglutide
What is Exendin-4?
GLP-1 analogue
What is liraglutide?
GLP-1 analogue
Which GLP-1 analogue binds to albumin?
liraglutide
What two classes of oral hypoglycemics cause weight loss?
Metformin

GLP-1 analogues
What two classes of oral hypoglycemics cause weight gain?
Sulfonylureas

Glitazones (TZD's)
What endogenous enzyme normally breaks down GLP-1?
DPP-4
What drug inhibits DPP-4?
Vildagliptin inhibits DPP-4, thus increasing the concentration of GLP-1.
What does vildagliptin do?
Inhibits DPP-4, thus increasing the concentration of GLP-1.
What does DPP-4 do?
It breaks down GLP-1.

Inhibitors of DPP-4 indirectly increase the concentration of GLP-1.
What is somatrem?
Recombinant GH with extra methionine.
What is bromocriptine?
semi-selective D2 agonist used to treat hyperprolactinemia
What is desmopressin?
Long-acting version of anti-dieuretic hormone
What is sermorelin acetate?
GHRH
What is cabergoline?
more selective D2 agonist for the treatment of hyperprolactinemia -> less nausea from D1 agonism.
What is octreotide?
somatostatin analogue

More potent than somatostatin but not as effective outside of the CNS.
What do perchlorate and thiocyanate have in common?
They are competitive blockers of iodide transport into the thyroid.ii
What is levothyroxine?
T4
What is clomophene?
estrogen receptor antagonist used in the treatment of infertility
What is pergolide?
Long-lasting dopamine receptor agonist used in the treatment of Parkinson's.
What is vasopressin?
anti-dieuretic hormone
What is Liothyroxine?
T3
What is raloxifene?
estrogen receptor antagonist in breast and uterus, but an agonist in the bone -> used in the treatment of postmenopausal osteoporosis
What is lotrix?
T4:T3 mixture in a 4:1 ratio.
What do thioureylenes, propylthiouracil, and methimazoles all have in common?
They all block multiple steps in the creation of T3, including thyroperoxidase function and peripheral conversion of T4 to T3.