Diabetes Mellitus Flashcards

1
Q

Thought to be an autoimmune disease in which pancreatic beta cells are destroyed.
Not caused by lifestyle. Nothing the patient did caused this to happen.
Insulin is the only treatment for this disorder.

A

Type 1 DM

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2
Q

Adipose and muscle tissue become less sensitive to the actions of insulin or the pancreas produces less insulin than the body needs. Either one causes increased glucose levels. Most are >30 y.o. Major risk factors include: obesity and family history. Both beta cell defects and insulin resistance found in these patients.

A

Type II DM

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3
Q

pregnancy causes women to become intolerant to glucose. Screening at 24 to 28 weeks. Causes not clear. Appear to be related to the anti-insulin effects created by progesterone, cortisol, and human placental lactogen. Usually after delivery, blood glucose will return to normal. First step is always lifestyle changes. These patients are 20-50% more likely to develop DM II as they age. If mom doesn’t control sugars during pregnancy it puts her at risk for a c-section due to a large baby.

A

Gestational Diabetes

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4
Q

What is the treatment goal for DM
American Diabetes assoc says ???
American association of endocrinologist says ???

A

HbA1C < 7.0%

Endo <6.5%

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5
Q

Normoglycemia is considered HbA1C of ??? with fasting glucose of ???

A

HbA1C : 4-5.6%
fasting glucose of <100
oral glucose tolerance test <140

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6
Q

Prediabetes criteria

A

A1C: 5.7-6.4%
fasting plasma glucose 140-199
oral glucose tolerance test 140-199

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7
Q

Diabetic criteria

A

A1C > 6.5
fasting plasma glucose >200
oral glucose >200
anyone who has an A1C result of >6.5 should be retested to confirm diagnosis
with a positive fasting plasm for OGTT you would repeat on another day to confirm diagnosis

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8
Q

Treatment goals for post prandial and BP

A

Preprandial plasma glucose should be 80-130 mg/dL-
Postprandial plasma glucose levels should be <180 mg/dL- his is two hours after a person eats.
Blood pressure should be <140/90 mm Hg- ACE (pril) and ARB (sartan) recommended therapy for B/P!

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9
Q

Which drug class decreases glucose production in the liver by decreasing glucogeneogenesis and glycogenolysis which is the breakdown of glucagon to glucose

A

Biguanides (metformin)

It moderately improves peripheral sensitivity to insulin by increasing the peripheral glucose uptake and utilization in the muscles of the body. Glucose comes out of the blood an into the muscle for utilization.

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10
Q

which DM drug has no action on the pancreas and no insulin release therefore you don’t have to worry about hypoglycemia from this drug alone

A

Biguanides (metformin)

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11
Q

Metformin absorption, distribution, metabolism, excretion

A

taking with food can slow absorption
50-60% bioavailable
does not bind to liver, primarily excreted in kidneys, **alcohol can cause decreased lactate metabolism causing lactic acidosis (or liver disease)

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12
Q

Biguanides (metformin) special populations

A

Preg cat. B
not recommended in children < 10
use with caution in pts over 80 (risk of dehydration)

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13
Q

Contraindications for metformin

A

renal or hepatic disease, alcoholics can have increase risk for lactic acidosis
existing acute or chronic metabolic acidosis
withhold drug day of and 48 hours after iodine contrast

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14
Q

come side effects of metformin

A

GI upset, D/N/V, bloating, flatulence, metallic tast in mouth, can cause some weight loss

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15
Q

which two drugs are considered the only options for DM II in pediatric patients

A

Metformin or insulin

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16
Q

max dose of metformin and education regarding dosing

A

max dose in 2250mg/day, you want to increase this dose every one to two weeks at 500 mg

17
Q

Which drug class has a MOA of an enzyme a-glucosidase is necessary for the absorption of starch and disaccharides. Produced by the brush border of the intestines. The drug acts by slowing the absorption of carbohydrates from the intestines, minimizing the postprandial rise in blood sugars.

A

Alpha-Glucosidase inhibitors

Acarbose (precose)
miglitol (glyset)

Most effective in patients with postprandial hyperglycemia, patients with high HgbA1c and poor dietary adherence. Useful in patients with high carb diets such as Asians and Hispanics

18
Q

Which drug has Starting dose of 25 mg three times a day at the start of each meal. Continue this for four to eight weeks. Then may increase to 50 mg three times a day if needed. After three months may increase to 100 mg TID. this can cause compliance issues. must take with first bite of meal

A

Alpha-Glucosidase inhibitors

Acarbose (precose)
miglitol (glyset)

19
Q

contraindications of alpha -glucosidase inhibitors

A

bowel disease, at risk for bowel obstruction
cirrhosis
renal dysfunction

20
Q

This drug increases flatus when eating high carbs

A

alpha-glucosidase inhibitors

21
Q

Which drug has local action in the gut, and more local metabolism instead of systemic,

A

alpha-glucosidase inhibitors

22
Q

How are labs drawn for patients taking alpha-glucosidase inhibitors?

A

need to monitor ALT/AST
do a two-hour, postprandial glucose not a fasting glucose- is not a good tool for evaluation because the medication is most effective two hours after a meal. Pt. needs to eat and then get the labs two hours later.

23
Q

Alpha-glucosidase inhibitors special population considerations

A
  • Pregnancy category B -only use if absolutely necessary. Pregnant mom is already having N/V/D. Does not need any added GI symptoms.
  • Not recommended in lactation.
  • Not recommended in children
24
Q

MOA of drug class that is rapid-acting insulin secretagogues that stimulate the release of insulin from the pancreas in response to a meal. Binding at characterized sites closes the ATP dependent potassium channels in the embraces of the beta cells. This causes depolarization of the beta-cells and an opening of calcium channels resulting in an increased influx of calcium causing insulin secretion.

rapid acting on post-prandial blood sugar

A

Meglitinides

-glinides

25
Q

Which drug is good for patients who get hypoglycemic with sulfonylureas

A

meglitinides

26
Q

pharmacokinetics for meglitinides

A

very highly protein bound

metabolized through the CYP system