Pharm - Diabetes Flashcards by mhari scott

Hallmark signs/symptoms of DM

Hyperglycemia (sustained)

Polyuria

Polydipsia

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What FPG levels are considered impaired?

Btw 100 and 125

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What OGTT levels are considered impaired?

140-199

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What A1C level is associated with prediabetes?

5.7-6.4%

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When should healthy adults be screened for DM?

At age 45 and every three years (if results are normal).

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How to diagnose diabetes?

FPG 126** or above

2-h PG over 200** during OGTT

A1C over 6.5%**

Symptoms & random PG over 200.

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What is primary goal of diabetes management/treatment?

Control blood glucose to PREVENT long-term complications.

(Goal is not feeling better. Glucose can feel good in the bloodstream.)

Controlling BP and lipids is also important.

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What is the first-line oral therapy for DM2?

Biguanide (metformin)

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MOA of biguanide

Decreases liver’s production of glucose

Increases sensitivity of liver and muscle tissues to glucose uptake.

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Does metformin/biguanide target post-prandial or fasting?

Fasting (FPG)

(Usually have to control the FPG first. Better effect on CV risk. This is why we use metformin first).

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Most common S/E of biguanide?

Diarrhea. This is why we start low and go slow.

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What is the BBW for biguanide/metformin?

Lactic acidosis: don’t use if patient has renal impairment.

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What are the other adverse effects of metformin/biguanide?

Metallic taste in mouth
B12 absorption inhibition
(And diarrhea)

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MOA of sulfonylureas?

Binds to sulfonylurea receptors on beta cells, increasing insulin secretion.

Targets postprandial glucose (PPG)
(Not fasting).
This is why it’s not first-line.

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Why do sulfonylureas get discontinued?

Have squeezed the last drop of insulin out of the beta cells… no more left.

Called “secondary burnout”

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What is the big side effect for sulfonylureas?

Weight gain.

(Also hypoglycemia can occur).

(There’s a possibility of higher CV risk… still finding out.)

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How do thiazolidinediones work?

-increases glucose uptake in muscles and adipose
-decreases glucose output by liver
(Insulin sensitized)

Targets FPG

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What are the A/Es of Thiazolidinediones?

Weight gain
HF exacerbation

(BBW: HF warnings: weight gain over 3kg, acute edema, SOB or fatigue without any cause).

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What is Incretin/GLP-1 (Glucagon-like peptide)’s MOA? What do we want to take to imitate it?

Slows down stomach emptying

Promotes insulin release

Inhibits glucagon release (so the liver isn’t told to release glucose).

Suppresses appetite.

GLP-1 receptor agonists.

What is the route of GLP-1 receptor agonists?

Injections only

What does GLP-1 target? (PPG or FPG)?

Both!

Except for exenatide, which only targets PPG

Biggest advantages of GLP-1 receptor agonists?

Weight loss
Lowers BP
Might preserve beta cells
Low risk for hypoglycemia. 
Both FPG and PPG effects (for most).

A/Es of GLP-1 receptor agonists?

GI Discomfort is the big one.

Also, can interact with warfarin (monitor INR), oral contraceptives and ABX.

Pt education for GLP-1 receptor agonists?

Prime the pen once before the first dose

Don’t freeze.

What GLP-1 receptor agonists need mixing?

Bydureon and Tanzeum

What should the pt know about Byetta?

Eat no more than 1 hour beforehand

MOA of DPP-4 Inhibitors?

Inhibits DPP-4 (degrades incretin hormones). Increases insulin synthesis and release from beta cells Decreases glucagon secretion from alpha cells

Major S/E of DPP-4 inhibitors

Severe joint pain | But overall, well-tolerated

Why would a pt use DPP-4 inhibitors instead of GLP-1 inhibitors?

They’re oral. But the GLP-1’s have better S/E profile.

SGLT2 inhibitors MOA?

Excrete glucose in the urine (proximal convoluted tubule).

Other advantages of SGLT2 inhibitors?

Weight loss Low hypoglycemia risk BP reduction (maybe) FPG and PPG

S/Es of SGLT2 inhibitors?

Mycotic infections of the genitals (esp females) UTIs Polyuria/Dehydration Bone fractures

Contraindications of SGLT2 inhibitors?

Renal impairment (Severe) End-stage renal disease Dialysis

MOA: alpha-glucosidase inhibitors?

Slows down the stomach so that glucose isn’t absorbed as quickly in the intestine.

``` What is the primary S/E of Acarbose/Precose? What class is it in? ```

Gas, bloating, GI effects. It’s an alpha-glucosidase inhibitor.

What are our lab goals for DM pts?

A1C less than 7% FPG 80-130 PPG less than 180 mg/dl (Also control BP and cholesterol)

What are the insulin sensitizers?

Biguanides | Thiasolidinediones

What are the Insulin secretagogues?

Sulfonylureas

What are the Incretin-based therapies?

GLP-1 agonists | DPP-4 inhibitors

What are the glucose absorption inhibitors?

SGLT2 Inhibitors

Functions of insulin?

Decreases glucose output from the liver Increases glycogen synthesis Increased glucose uptake by the muscles

What’s the most effective drug available to treat diabetes? Why?

Insulin. No ceiling for A1C reduction. (The oral medications usually only reduce it by 1%). Natural hormone. Easy to individualize (adjustable) Good data for reducing microvascular complications

What are patients most afraid of with insulin use?

Fear of needles Fear of side effects (Weight gain, hypoglycemia) (Also embarrassment and change in lifestyle)

What does U100 mean?

100 units of insulin per ml.

What are the concentrated formulations of insulin? Why would they be used?

U500, U300, U200 Very Insulin-resistant patients.

What is the standard concentration of insulin?

U100