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Med 1 Endo > Insulin Therapy > Flashcards

Insulin Therapy Flashcards

1
Q

If a patient comes in presenting with Diabetic Ketoacidosis, what should you do.

A

Monitor them frequently!

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2
Q

A patient with diabetes needs what type of treatment in regards to fluid and insulin.

A

Aggressive treatment if fluid deficit

Non-aggressive treatment of insulin (hypoglycemic episodes can occur with too much insulin)

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3
Q

Factors to consider when putting a patient on Insulin Therapy:

A
  1. Cost
  2. Lifestyle
  3. Compliance
  4. Patient Education
  5. Social Support
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4
Q

What types of Insulin therapy are there?

A
  1. Syringe
  2. Pen
  3. Continuous Pump
  4. Inhaled (coming soon)
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5
Q

Where do you normally administer insulin (for optimal results)?

A

Shoulder
Outer Thigh
Abdomen

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6
Q

What are three “rapid-acting” insulins on the market?

A
  1. Humalog
  2. Novolog
  3. Apidra
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7
Q

What is the benefit of combining insulin drugs (synergy)?

A

Helps non-compliant patients with their hyperglycemia

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8
Q

What is the disadvantage of combining insulin drugs (synergy)?

A

Increased risk for hypoglycemia

Weight gain possible

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9
Q

When should we use a concentrated insulin? (U500)

A

Patients with very high insulin resistance

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10
Q

Rapid Acting Insulin: Onset, Peak, Duration

A

Onset: 15 minutes
Peak: 30-90 minutes
Duration: 3-5 hours

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11
Q

Regular Insulin: Onset, Peak, Duration

A

Onset: 30 min - 1 hour
Peak: 2 hours
Duration: 6 hours

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12
Q

NPH (Humilin): Onset, Peak, Duration

A

Onset: 1-2 hours
Peak: 6-8 hours
Duration: 10-16 hours

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13
Q

Lantus/Levemir Insulin: Onset, Peak, Duration

A

Onset: 1 hour
Peak: None
Duration: 24 hours

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14
Q

What could cause hyperglycemia when you wake up?

A

Silent Hypoglycemia in the evening that rebounds in the morning

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15
Q

What is the Somogyi Effect?

A

The Somogyi effect can occur when a person takes long-acting insulin for diabetes. If the blood sugar level drops too low in the early morning hours, hormones (such as growth hormone, cortisol, and catecholamines) are released. These help reverse the low blood sugar level but may lead to blood sugar levels that are higher than normal in the morning. An example of the Somogyi effect is:

  • A person who takes insulin doesn’t eat a regular bedtime snack, and the person’s blood sugar level drops during the night.
  • A person’s body responds to the low blood sugar in the same way as in the dawn phenomenon, by causing a high blood sugar level in the early morning.
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16
Q

What is the Dawn Phenomenon?

A

Hormones (growth hormone, cortisol, and catecholamines) produced by the body cause the liver to release large amounts of sugar (glucose) into the bloodstream. These hormones are released in the early morning hours. These hormones also may partially block the effect of insulin, whether it’s insulin your body produces or insulin from the last injection.

This can happen in anyone, but when there is insulin resistance, this will cause a bad effect.

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17
Q

How to tell the difference between Somogy and Dawn?

A

The Somogyi effect can occur any time you or your child has extra insulin in the body. To sort out whether an early morning high blood sugar level is caused by the dawn phenomenon or Somogyi effect, check blood sugar levels around 2 a.m. to 3 a.m. for several nights.

If the blood sugar level is low at 2 a.m. to 3 a.m., suspect the Somogyi effect.
If the blood sugar level is normal or high at 2 a.m. to 3 a.m., it’s likely the dawn phenomenon.

18
Q

How do you dose insulin?

A
  1. Depends on patient’s weight

2. Estimate the total daily dosage (TDD) and how it’s being administered (shots vs. pump)

19
Q

Calculating Dosage

A

Rule of 500: (carb:insulin ratio) 500/TDD

Rule of 1800: (sensitivity/correction factor) 1800/TDD

20
Q

What does the Rule of 500 tell us?

A

Can use for calculating amount of meal-time insulin needed

21
Q

What does the Rule of 1800 tell us?

A

(When Jose is missing, 1800 is where it’s at)

Tells the amount of change in blood glucose from 1 unit of insulin

22
Q

What are the goals of treating DM

A
  1. Getting A1C below 7%

2. Less/Shorter Glycemic Excursions

23
Q

If this condition associated with DM is untreated it could be fatal.

A

Diabetic Ketoacidosis

24
Q

What causes DKA (Diabetic Ketoacidosis)?

A

Non-compliance
Infection
Trauma

25
Q

How can you become DKA

A

Having insulin deficiency results in excess free fatty acids from adipose tissue.
These FAs are substrates for ketone production in the liver

26
Q

How does DKA present?

A
  1. Acidosis
  2. Elevated Anion Gap
  3. Low glucose
  4. Serum and urine ketones are elevates
  5. Mental Health Status is Variable
27
Q

Clinical Features of DKA

A
  1. Polyuria, Polydipsia
  2. Hyperventilation (deep, rapid breaths (Kussmauls))
  3. Sweet Smelling Breath
  4. Hypokalemia
28
Q

What Labs would you order to check for DKA?

A 
CBC
CMP
Blood cultures
CXR
Drug Screen
Urine Culture
EKG
29
Q

How would you treat DKA?

A
  1. IVF hydration
  2. Electrolyte replacement
  3. Unsilun
  4. Potential bicar therapy in DKA if pH<6.9
  5. Eval underlying dz
30
Q

What is the goal of Treatment for DKA?

A
  1. Suppress Release of Free Fatty Acids and the Production of Ketones
  2. Suppress Liver Production of Glucose
31
Q

How do you calculate Serum Na?

A

Measured Serum Na+ + (Delta Serum Glucose/42)

32
Q

How do you calculate Osmolality?

A

2(Na + K) + Glucose

33
Q

How do you calculate Serum Anion Gap?

A

Serum Na - (Serum Cl-Bicarb)

34
Q

How do you know when the DKA has been successfully treated?

A

Normal Anion Gap
Ketone can persist
Mental Status Normal
Can Eat

35
Q

In a patient with DM II comes into clinic with altered mental status. Routine DM labs are completed and they show High Serum Glucose, with no ketones, elevated serum osmolality, and severe dehydration.
What does this pt have?

A

Hypeosmolar non-ketotic hyperglycemia

36
Q

Does Hypeosmolar non-ketotic hyperglycemia have a high or low mortality rate?

A

HIGH

37
Q

What can cause Hypeosmolar non-ketotic hyperglycemia?

A
  1. Steroids
  2. Infection
  3. Untreated/Recognized Type II DM
38
Q

What is happening in Hypeosmolar non-ketotic hyperglycemia? (Pathogenesis)

A

Insulin resistance in the body.

Have enough insulin to prevent ketone production (DKA), but not enough to prevent hyperglycemia.

39
Q

If a patient has suspected Hypeosmolar non-ketotic hyperglycemia, what labs should you run?

A 
CBC
CMP
Blood Cultures
CXR
Drug Screen
Urine Cultures
EKG
40
Q

What is the treatment for Hypeosmolar non-ketotic hyperglycemia, once confirmed?

A

IV Fluids (hydration)
Electrolyte Replacement
Unsilin
Evaluate Underlying Dz

41
Q

How quickly can this be resolved when found?

A

Relatively Quickly

Pt will become mentally alert and serum Osm should get below 315.

Med 1 Endo (9 decks)

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