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2nd Semester Nursing > Pharm - Diabetes > Flashcards

Pharm - Diabetes Flashcards

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1
Q

Hallmark signs/symptoms of DM

A

Hyperglycemia (sustained)

Polyuria

Polydipsia

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2
Q

What FPG levels are considered impaired?

A

Btw 100 and 125

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3
Q

What OGTT levels are considered impaired?

A

140-199

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4
Q

What A1C level is associated with prediabetes?

A

5.7-6.4%

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5
Q

When should healthy adults be screened for DM?

A

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

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6
Q

How to diagnose diabetes?

A

FPG 126** or above

2-h PG over 200** during OGTT

A1C over 6.5%**

Symptoms & random PG over 200.

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7
Q

What is primary goal of diabetes management/treatment?

A

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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8
Q

What is the first-line oral therapy for DM2?

A

Biguanide (metformin)

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9
Q

MOA of biguanide

A

Decreases liver’s production of glucose

Increases sensitivity of liver and muscle tissues to glucose uptake.

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10
Q

Does metformin/biguanide target post-prandial or fasting?

A

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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11
Q

Most common S/E of biguanide?

A

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

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12
Q

What is the BBW for biguanide/metformin?

A

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

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13
Q

What are the other adverse effects of metformin/biguanide?

A

Metallic taste in mouth
B12 absorption inhibition
(And diarrhea)

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14
Q

MOA of sulfonylureas?

A

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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15
Q

Why do sulfonylureas get discontinued?

A

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

Called “secondary burnout”

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16
Q

What is the big side effect for sulfonylureas?

A

Weight gain.

(Also hypoglycemia can occur).

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

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17
Q

How do thiazolidinediones work?

A

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

Targets FPG

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18
Q

What are the A/Es of Thiazolidinediones?

A

Weight gain
HF exacerbation

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

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19
Q

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

A

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.

20
Q

What is the route of GLP-1 receptor agonists?

A

Injections only

21
Q

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

A

Both!

Except for exenatide, which only targets PPG

22
Q

Biggest advantages of GLP-1 receptor agonists?

A 
Weight loss
Lowers BP
Might preserve beta cells
Low risk for hypoglycemia. 
Both FPG and PPG effects (for most).
23
Q

A/Es of GLP-1 receptor agonists?

A

GI Discomfort is the big one.

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

24
Q

Pt education for GLP-1 receptor agonists?

A

Prime the pen once before the first dose

Don’t freeze.

25
Q

What GLP-1 receptor agonists need mixing?

A

Bydureon and Tanzeum

26
Q

What should the pt know about Byetta?

A

Eat no more than 1 hour beforehand

27
Q

MOA of DPP-4 Inhibitors?

A

Inhibits DPP-4 (degrades incretin hormones).

Increases insulin synthesis and release from beta cells

Decreases glucagon secretion from alpha cells

28
Q

Major S/E of DPP-4 inhibitors

A

Severe joint pain

But overall, well-tolerated

29
Q

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

A

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

30
Q

SGLT2 inhibitors MOA?

A

Excrete glucose in the urine (proximal convoluted tubule).

31
Q

Other advantages of SGLT2 inhibitors?

A

Weight loss
Low hypoglycemia risk
BP reduction (maybe)

FPG and PPG

32
Q

S/Es of SGLT2 inhibitors?

A

Mycotic infections of the genitals (esp females)

UTIs

Polyuria/Dehydration

Bone fractures

33
Q

Contraindications of SGLT2 inhibitors?

A

Renal impairment (Severe)

End-stage renal disease

Dialysis

34
Q

MOA: alpha-glucosidase inhibitors?

A

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

35
Q 
What is the primary S/E of Acarbose/Precose?
What class is it in?
A

Gas, bloating, GI effects.

It’s an alpha-glucosidase inhibitor.

36
Q

What are our lab goals for DM pts?

A

A1C less than 7%

FPG 80-130
PPG less than 180 mg/dl

(Also control BP and cholesterol)

37
Q

What are the insulin sensitizers?

A

Biguanides

Thiasolidinediones

38
Q

What are the Insulin secretagogues?

A

Sulfonylureas

39
Q

What are the Incretin-based therapies?

A

GLP-1 agonists

DPP-4 inhibitors

40
Q

What are the glucose absorption inhibitors?

A

SGLT2 Inhibitors

41
Q

Functions of insulin?

A

Decreases glucose output from the liver

Increases glycogen synthesis

Increased glucose uptake by the muscles

42
Q

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

A

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

43
Q

What are patients most afraid of with insulin use?

A

Fear of needles
Fear of side effects (Weight gain, hypoglycemia)

(Also embarrassment and change in lifestyle)

44
Q

What does U100 mean?

A

100 units of insulin per ml.

45
Q

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

A

U500, U300, U200

Very Insulin-resistant patients.

46
Q

What is the standard concentration of insulin?

A

U100

2nd Semester Nursing (18 decks)

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