Diabetes Flashcards

1
Q

What are the diagnosing criteria for diabetes?

A

FBG > 100
GTT > 200
Random glucose: > 200
Hemoglobin A1C > 7.5%

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2
Q

Why do we use hemoglobin A1C in monitoring for diabetic patients?

A

It gives a reading of the blood sugar averages over the past 3 months

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3
Q

How do we treat T1DM?

A

Insulin therapy
Diet
Exercise

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4
Q

How do we treat T2DM?

A

Diet
Exercise
Drug therapy (PO or insulin therapy)

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5
Q

Rapid Acting Insulin

A

Used before meals
Onset: 5-15 minutes
Peak: 30-90 minutes
Duration: up to 5 hours

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6
Q

Short Acting Insulin

A

Can also be used before meals
Onset: 30-60 minutes
Peak: 2-3 hours
Duration: 5-8 hours

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7
Q

Intermediate Acting Insulin

A

Used between meals to help maintain blood sugar
Onset: 2-4 hours
Peak: 4-10 hours
Duration: 10-14 hours

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8
Q

Long Acting Insulin

A

Used to maintain blood sugar over a 24 hours period
Onset: 2-8 hours
No peak
Duration: up to 24 hours

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9
Q

What is the first line drug choice to T2DM?

A

Biguinides (metformin)

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10
Q

What is the mechanism of action of biguinides?

A

Inhibits glucose production and output from the liver

Can also sensitize insulin receptors and reduce glucose absorption in the gut

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11
Q

What are common side effects of biguinides?

A

GI symptoms (N/V/D, loss of appetite), Vitamin B12 deficiency

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12
Q

What is a severe adverse effect of biguinides?

A

lactic acidosis (most common with AKI/CKD)

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13
Q

When are biguinides contraindicated?

A

Renal impairment and heart failure due to the increased risk for lactic acidosis

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14
Q

How much do biguinides lower A1C?

A

1-2%

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15
Q

What is the mechanism of action of sulfonylureas?

A

Promote insulin release by stimulating the pancreatic beta cells

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16
Q

What are common side effects of sulfonylureas?

A

hypoglycemia and weight gain

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17
Q

What medication class should be avoided with sulfonylureas and why?

A

Beta blockers due to the fact that they can reduce the effectiveness by decreasing insulin release

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18
Q

What at the sulfonylurea drug names?

A

Glipizide, Glimepiride, and Glyburide

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19
Q

How much do sulfonylureas lower A1C?

A

1-2%

20
Q

What is the mechanism of action of the glinides?

A

Stimulate the pancreas to release insulin, primarily used prior to meals

21
Q

What is the mechanism of action of the SGLT-2 inhibitors?

A

They block the reabsorption of glucose in the kidneys (promote increased glucose excretion)

22
Q

What is a common side effect from SGLT-2 inhibitors

A

Elevated glucose levels in the urine which can cause UTI’s, yeast infections, and dehydration
hypotension is also a common side effect

23
Q

Should SGLT-2 inhibitors be given to a patient with renal impairment?

A

No as glucose can further damage the kidneys

24
Q

How much do SGLT-2 inhibitors lower A1C?

A

0.7-1.2%

25
Q

What are things to monitor for patients on SGLT-2’s?

A

Kidney functions, BP, urine glucose levels

26
Q

What is a piece of education for patients on SGLT-2’s?

A

Promote hydration as the increase in glucose excretion can increase dehydration levels

27
Q

What is a benefit to the SGLT-2’s?

A

cardiovascular protection, possible weight loss, no hypoglycemia

28
Q

What is the SGLT-2 inhibitor endings?

A

-gliflozin

29
Q

What is the mechanism of action of the TZDs?

A

decrease blood glucose by decreasing insulin resistance, increases insulin sensitivity

30
Q

What are common side effects of TZDs?

A

Weight gain, URI, headaches, sinusitis, myalgia, hyperlipidemia

31
Q

What is a strong adverse effect of TZDs?

A

fluid retention

32
Q

What a contraindication for TZD use?

A

CHF as it can increase fluid volume and promote fluid retention and edema, thus worsening heart failure

33
Q

How much to TZDs lower A1C?

A

0.5-1%

34
Q

What is the only TZD on the market at present time?

A

Pioglitazone

35
Q

What is the mechanism of action of the DPP-4 inhibitors?

A

Enhance incretin hormones that stimulate glucose-dependent release of insulin and suppress post-prandial release of glucagon by inhibiting the DPP-4 enzyme

36
Q

What are common side effects of DPP-4’s?

A

URI, headache, inflammation of nasal passage

37
Q

What is a severe adverse effect of the DPP-4’s?

A

pancreatitis

38
Q

What is the ending of the DPP-4 inhibitors?

A

-gliptins

39
Q

What is the advantage of DPP-4 inhibitors over GLP-1 receptor agonists?

A

DPP-4’s are an oral formulation whereas GLP-1’s are an injection

40
Q

What is the mechanism of action of the GLP-1 receptor agonists?

A

Activate the GLP-1 receptors which slow gastric emptying, stimulate glucose-dependent release of insulin, inhibit postprandial release of glucagon, and suppresses appetite

41
Q

What is a benefit of the GLP-1’s?

A

Weight loss

42
Q

What are some adverse effects of GLP-1’s?

A

N/V/D, injection site soreness, puritis pancreatitis, renal impairment, tertatogenic effects, hypoglycemia when combined with sulfonylureas

43
Q

When are GLP-1’s contrainidacted?

A

Patients with ESRD as they are excreted in the urine, unchanged

44
Q

What is the black box warning for the GLP-1’s?

A

Thyroid cancer, history of thyroid cancer, or family history of medullary thyroid cancer

45
Q

What do the GLP-1 receptor agonists end in?

A

-glutide (except exantide)