DM Flashcards

1
Q

Risk factors for Diabetes

A
Obesity
Old age
African American
Native American
Hispanics
Family history (1st degree)
CVD
HTN
High Cholesterol
Physical inactivity
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2
Q

Long-term complications of Diabetes

A
Eye damage
Kidney damage
Amputations
Heart attack
Stroke
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3
Q

Criteria for diagnosing Diabetes

A

A1C >6.5%
or Fasting Glucose >120
or 2-hour Glucose >200
or Random Glucose >200

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4
Q

What is the definition of fasting (in regards to glucose testing)

A

No caloric intake for at least 8 hours

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5
Q

Blood (glucose/A1C/antibodies) should be used to screen for Type 1 Diabetes

A

A1C

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6
Q

Type 1 Diabetes Mellitus is common in (children/adults)

A

Children (autoimmune)

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7
Q

Diabetic Ketoacidosis is more commonly seen in Type (1/2) Diabetes

A

Type 1 (usually due to missed Insulin doses)

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8
Q

Diabetic Ketoacidosis in Type 1 Diabetics is usually due to…

A

missed insulin doses (or increased stress)

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9
Q

What autoimmune diseases are common in conjunction with Type 1 Diabetes

A

Grave’s disease
Celiac’s (gluten)
Pernicious Anemia (Intrinsic Factor)

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10
Q

3 main antibodies found with Type 1 Diabetes

A

Glutamic Acid Decarboxylase Antibody (GAD)
Islet Cell Antibody (ICA)
Insulin Autoantibody (IAA)

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11
Q

Factors that play into Type 2 Diabetes

A

Dec. glucose uptake
Dec. insulin and incretin (suppressed by fats)
Inc. glucagon
Inc. lipolysis

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12
Q

In Type 2 Diabetes, hyperglycemia leads to elevated _______________ _________ levels

A

fatty acid*

*suppressing insulin and it’s action

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13
Q

Type (1/2) Diabetes has a stronger genetic contribution

A

Type 2

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14
Q

Type (1/2) Diabetes is more common in adults

A

Type 2

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15
Q

C-peptide levels can be high-normal in Type 2 Diabetes (True or False)

A

True, but only in EARLY stages (will decline with time)

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16
Q

Best preventatives for Type 2 Diabetes

A

Diet
Exercise

*drugs are not used for prevention, only treatment

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17
Q

Suggested Lifestyle changes to PREVENT Diabetes

A

> 7% weight loss

>150 min/week of exercise

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18
Q

Blood sugar peaks around ___________ after eating

A

1 hour

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19
Q

Patients with diabetes are discouraged from drinking alcohol (True or False)

A

False, but must moderate within daily sugar intake

20
Q

How is physical activity beneficial for diabetics or pre-diabetics (besides the weight loss of course)

A

Inc. insulin sensitivity (helps prevent progression)

21
Q

What are the goals for Diabetics, in regards to glucose levels with treatment

A

Premeal glucose: 80-130
2-h post-meal: <180
HbA1c: <7%

22
Q

Which drug is considered the FIRST LINE agent for Diabetes and why?

A

Metformin

Has cardiovascular protection, lowers TG and LDL and doesn’t bottom out sugar levels

23
Q

MOA of Sulfonylureas and Meglitinides for Diabetes treament

A

Inc. Insulin release

24
Q

MOA of Metformin and Glitazones for Diabetes treatment

A

Inc. Insulin sensitivity (Metformin via AMPK) (Glitazones via PPARy)

25
Q

What liver enzyme does Metformin activate to increase Insulin sensitivity

A

AMP Kinase

26
Q

What enzyme do Glitazones activate in Adipose cells to inc. Insulin sensitivity

A

PPARy (inc. uptake of fatty acids to store)

27
Q

Disadvantages of Glitazones (as opposed to Meformin)

A

Weight gain
Fluid retention–> CHF
Inc. LDL

28
Q

MOA of Acarbose for Diabetes treatment

A

Delay sugar absorption (from gut) via a-Glocosidase inhibition

29
Q

Why is Acarbose not used too much for Diabetes

A

Poor patient adherence (makes them toot)

30
Q

Examples of most common drugs for Diabetes

A

Sulfonylureas (inc. insulin)

Metformin (inc. sensitivity)

31
Q

Examples of Insulin Secretagogues (2 total)

A

Sulfonylureas

Meglitinides

32
Q

Limitations and RISK for Sulfonylureas and Meglitinides (Insulin Secretagogues)

A

Requires functional Beta cells

Can cause HYPOglycemia

33
Q

Possible risk of Metformin (Inc. Insulin sensitivity)

A

Lactic acidosis (VERY RARE)

34
Q

Physiologic functions of the Incretins and Amylin

A

Promotes satiety
Stimulate Insulin release*
Inhibit Glucagon release
Slow gastric emptying

*Incretins only

35
Q

(IV/Oral) glucose has a much higher effect on Insulin secretion

A

Oral (due to Incretin effect in gut)

*Diabetics have stunted Incretin effect

36
Q

Examples of SGLT-2 Inhibitors (promote renal excretion) (3 total)

A

Canagliflozin
Dapagliflozin
Empagliflozin

37
Q

Benefit of Insulin Analogues vs. Human insulins

A

Analogues have limited self-aggregation, so stay as monomers in solution and act quicker

38
Q

Examples of Insulin Analogues (5 total)

A
Aspart
Glulisine
Lispro
Glargine*
Degludec*

*long acting

39
Q

Benefit of the Insulin Analogues Glargine and Degludec specifically

A

Actually a LONG acting formulations, slowly dissolving from hexamer to dimer to monomer

40
Q

Examples of LONG acting Insulin Analogues (2 total)

A

Glargine

Degludec (Tresiba)

41
Q

ALL patients with Type (1/2) Diabetes require insulin therapy

A

Type 1 (autoimmune attack, so no insulin production)

42
Q

When would you use Insulin for a Type 2 Diabetic?

A

When disease is not well controlled on oral meds

43
Q

What are some barriers to using Insulin

A

Fear of injections
Complex regimens
Lack of time/resources
Perceived significance of needing Insulin

44
Q

Immune-mediated loss of fat at the site of Insulin injections

A

Lipoatrophy

45
Q

Non-immune mediated gain of fat tissue at the site of repeated insulin injection

A

Lipohypertrophy