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IDT Spring Term > DM - Therapeutics - Dr. Frye > Flashcards

DM - Therapeutics - Dr. Frye Flashcards

1
Q

Trials:
IMPROVE-IT
DCCT

A

IMPROVE-IT - ezetimibe addition to statin therapy may help with recent coronary syndrome
DCCT - Tighter control increases the rate of hypoglycemia

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2
Q

If a patient has normal kidney function but is diabetic, should they be on an ACE or ARB?

A

No

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3
Q

What are FDA approved drugs to treat diabetic neuropathy? Off-label?

A

Duloxetine
Pregabalin
Tapentadol

Gabapentin
TCAs
Venlafaxine
Valproate

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4
Q

When is metabolic surgery recommended?

A

T2DM with BMI of >40 regardless of hyperglycemic control
T2DM with BMI 35-39 with inadequate control despite optimized lifestyle and meds
T2DM with BMI 30-34.9 with poor hyperglycemic control with optimized meds

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5
Q

Term:
Uncontrolled hyperglycemia, metabolic acidosis, increased total body ketone concentration, decreased bicarbonate (<15-18)

A

DKA

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6
Q

Term:

Severe hyperglycemia, hyperosmolarity, dehydration in absence of ketoacidosis

A

HHS (hyperosmolar hyperglycemic state)

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7
Q

What can cause DKA?

A

Missed insulin doses or acute infection

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8
Q

Which type of diabetes is more common in DKA?

A

Type I

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9
Q

Which type of diabetes is more common in HHS?

A

Type II. No absolute insulin deficiency, so little ketogenesis.

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10
Q

What are the treatments of DKA and HHS?

A

Fluids to correct dehydration
Insulin (IV first then SQ) to correct hyperglycemia
Potassium repletion and other interventions as necessary

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11
Q

Where is the line for critically significant hypoglycemia?

A

<54mg/dL

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12
Q

In hypoglycemia, what symptoms are the first seen? What type are they?

A

The autonomic/neurogenic symptoms are first seen in hypoglycemia. These are tremors, anxiety, sweating, irritability. These are related to the secretion of epinephrine.

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13
Q

In hypoglycemia, what symptoms are caused by deprivation of glucose to the brain? What are these called?

A

Confusion, lethargy, loss of consciousness and seizures are neuroglycopenic.

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14
Q

What is the treatment for hypoglycemic unawareness? How does this work?

A

Less tight A1C control. Increase epinephrine response to low blood sugar. Decrease sensitivity to glucose.

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15
Q

What is the adult dose of glucagon?

A

1.0mg

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16
Q

How many glucose tabs should be used to treat mild hypoglycemia?

A

3-4

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17
Q

Why should foods high in protein or fat be avoided when trying to treat hypoglycemia?

A

Because they will take longer to work.

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18
Q

What is CGM?

A 
Continuous glucose monitoring.
Useful in T1DM
Can see trends, help people nervous about highs and lows. 
Cost is an issue.
Need robust diabetes education.
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19
Q

How often should A1C be checked in those who are at goal? Not at goal?

A

In those at goal, check 2 times a year. In those not at goal, check 4 times a year at least.

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20
Q

What is fructosamine?

A

Measures glycated albumin, but not well standardized.

Indicated for pregnancy and hemoglobinopathies, and those with discordant A1C and CBC results.

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21
Q

What A1C does a 126 mg/dL average glucose reading indicate?

A

6%

22
Q

What is the general rule for conversion of A1C to glucose?

A

A1c-2 x 30
(so an A1C of 7.5: 7.5-2 = 5.5
5.5 x 30 = 150 + 15 = 165

23
Q

What is a reasonable A1C goal for a healthy adult?

A

<7%
This is associated with a reduction in microvascular complications
If implemented soon after diagnosis it is also associated with reduction of microvascular complications

24
Q 
What are the glycemic goals for the ADA?
A1C
Pre-prandial
Post-prandial
For the AACE?
A

A1C <7%
Pre-prandial 80-130
Post-prandial <180

A1C <6.5%
Pre-prandial <110
Post-prandial <140

25
Q

How was the ACCORD trial different than the others, such as UKPDS, ADVANCE, VADT, and DCCT/EDIC?

A

It found that there was increased mortality with more stringent A1C goals.

26
Q

Generally, when did trials find microvascular benefits with more stringent A1C goals?

A

With initial trial and long-term follow-up.

27
Q

Generally, when did trials find CVD benefits with more stringent A1C goals?

A

Some CVD benefits seen in follow-up

28
Q

Generally, when did trials find mortality benefits with more stringent A1C goals?

A

No change at all, too late.

29
Q

Why is lower A1C associated with a greater increase of mortality?

A

Higher A1C is associated with a greater risk of death, but the hypoglycemia associated with lower A1C contributed.

30
Q

What did the ACCORD trial find about the risks of hypoglycemia?

A

That hypoglycemia was associated with all sorts of negative outcomes.

31
Q

What are some potential mechanisms that hypoglycemia can increase CVD risk?

A

Cardiac arrhythmias
Increased thrombotic tendency
Cvd changes induced by catecholamines

32
Q

Metformin

a biguanide

A

MOA - Decreases liver gluconeogenesis and improves insulin sensitivity.
1st line
low cost
weight neutral
No hypoglycemia
Disadvantages: GI intolerance, B12 deficiency, increased risk of lactic acidosis
Continue use unless eGFR is <30. Don’t start metformin if eGFr is less than 45.

33
Q

Sulfonylureas

A

MOA - increases insulin secretion by acting in the K channels of beta cells
Low cost
Effective
Generally well-tolerated
Disadvantages: Risk of hypoglycemia, weight gain
1st gen - Achexamide, Tolubutamide, Chloropropamide, Tolazamide
2nd gen - Glimipiride, glipizide, glyburide

34
Q

Which drug class is SIADH associated with?

A

Syndrome of Inappropriate Antidiuretic hormone… associated with 1st gen sulfonylureas

35
Q

Meglitinides

A

MOA - Increase insulin secretion by binding to the sulfonylurea receptor
Decrease postprandial glucose
Disadvantages: hypoglycemia, weight gain, frequent dosing, only modest efficacy, expensive, CYP 3A4 interactions
Repaglinide, nateglinide
If you miss a meal, skip the dose too

36
Q

TZDs

A

MOA - PPAR agonist, which increases sensitivity to insulin
Efficacious
Cheap
Disadvantages: 8-12 weeks for full effect, weight gain, edema (HF CI), bladder cancer, risk of fractures
no hypoglycemia, CVD benefits (PROactive trial), lipid benefits
“glitizones”

37
Q

Alpha-glucosidase inhibitors

A

MOA - Delays intestinal carb digestion by inhibiting enzymes in the small intestine
No hypoglycemia, reduces post-prandial hyperglycemia, decreases CVD events
Disadvantages: Flatulence, diarrhea, bloating/gas, modest efficacy
Acarbose, miglitol
LFTs needed for monitoring, initially every 3 months
Avoid use if SCr is >2mg/dL

38
Q

DPP4 inhibitors

A

MOA - increases insulin secretion (glucose dependent) and decrease glucagon secretion by inhibiting DPP4, increasing post-prandial incretin (GIP and GLP-1)
No hypoglycemia, well-tolerated, weight neutral
Disadvantages: Expensive, moderate efficacy, pancreatitis, joint pain, HF risk with saxagliptan
Sitagliptan, Saxagliptan, Linagliptan, Alogliptan

39
Q

What does GLP-1 do?

A 
Decreases appetite
Slows gastric emptying
Increases insulin secretion
Decreases glucagon secretion
Increases B-cell proliferation
Decreases B-cell apoptosis
Decreases glucose production
40
Q

Which DDP-4 inhibitor does not require renal or hepatic adjustment?

A

Linagliptan

41
Q

SGLT2 I’s

A

MOA - Blocks glucose reabsorption in the kidney, resulting in increased glucose excretion
Advantages: Weight loss, low hypoglycemia risk, modest BP lowering, CVD benefit (empagliflozin)
Disadvantages: All CI w/ renal dysfunction, UTIs, genital mycotic infections, euglycemic ketoacidosis, modest efficacy, high cost, bone fracture with canagliflozin
Canagliflozin, dapagliflozin, empagliflozin

42
Q

GLP-1 agonists

A

MOA - Increase insulin secretion, decrease glucagon secretion, slows gastric emptying, increases satiety
Efficacious, no hypoglycemia, weight reduction, improved beta-cell mass, Cvd benefit with liraglutide (LEADER trial)
Disadvantages: GI side effects, increased pancreatitis risk, high cost, no long term safety data
Black box warnings for all but exanitide for thyroid C cell tumors
Exanitide, liraglutide, albiglutide, dulaglutide

43
Q

Amylin analog

A

MOA - slows gastric emptying, decreases glucagon secretion, increases satiety
Adjunct to mealtime insulin only, moderately efficacious, decreases postprandial glucose, weight loss
Disadvantages: GI effects, no long term safety, frequent dosing, hypoglycemia potential with insulin use, high cost.
(Decrease insulin dose by 50% when taking)

44
Q

Insulin

A

MOA - facilitates cellular uptake of glucose, and reduces hepatic glucose production
Universally effective, unlimited efficacy, decreases microvascular complications
Disadvantages: weight gain, hypoglycemia, injectable, SMBG required, cost

45
Q

Human insulin vs insulin analogs:

A

Human: identical to endogenous insulin. Protamine and zinc can be added to create NPH, which has delayed peak and duration.

Insulin analogs are created by genetic engineering, which alters pharmacokinetics.

46
Q

When is U-500 insulin useful?

A

For when daily injections total 200 units or more

47
Q

What are the rapid-acting insulins?

A

Humalog
Novolog
Apidra
Take immediately before a meal

48
Q

What are the short-acting insulins?

A

Regular (R)
Novolin R
HUmulin R
Take 30 minutes before a meal

49
Q

What are the intermediate-acting insulins?

A

NPH
Novolin N
Humulin N
(The only cloudy insulins)

50
Q

What are the long-acting insulins?

A

detimir
glargine
degludec

51
Q

What is Afrezza?

A

Inhaled insulin.
Administer before meals.
Warnings of acute bronchospasm in patients with chronic lung disease

52
Q

What combos of split-mixed insulins can you use?

A

NPH and glassine, aspart, or lispro
NPH and regular

NO glargine, deter, or degludec

IDT Spring Term (7 decks)

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