E: Insulin Pharmacology

Front 1

What are the two forms of human insulin used in diabetes tx? Which is short-acting (6-8hrs)? Intermediate (12-20hrs)?

Back 1

regular and Neutral Protamine Hagedorn (NPH) Insulin
- short and intermediate, respectively.

Front 2

What are Aspart, Glulisine, and Lispro?
- how do they differ from human insulin in solution?

Back 2

Insulin analogues
- they're monomers, whereas the normal i is found as dimers and hexamers. These analogues have limited self-aggregation, in other words.

Front 3

Do the monomeric insulins have a different time of onset than normal human insulin?

Back 3

yes, they're faster, tend to peak @ 1hr.

Front 4

What is Glargine?
- what gives it it's unique properties?

Back 4

an insulin analog that is slow-acting because it precipitates in subQ tissue due to the pH. (Glargine likes an acidic solution ~4.0 in order to be soluble). It then is dissolved slowly --> protracted action.

Front 5

What is detemir? What makes it different from the other insulins?

Back 5

long-acting insulin analog; acts longer than NPH but shorter than glargine.

Front 6

Does the site of insulin injection matter re: absorption variability? Does exercise affect this? Hydration status?

Back 6

yes: abdomen > arm > thigh.

yes, they do.

Front 7

What is the rationale behind twice daily split-mixed insulin regimens?

Limitations?

Back 7

rapid-acting i limits the postprandial hyperG after breakfast and supper while the intermediate acting admin before breakfast and before dinner limits hyperG in the afternoon and the next morning.

the NPH dosing before dinner that attempts to control the next morning's hyperG can lead to hypoG.

Front 8

What is the rationale behind multiple daily insulin injections (MDI) of NPH and regular i @ mealtimes?

Limitations?

Back 8

more physiological than 2xdaily-mixed/split. Pt can adjust prandial regular insulin relative to food intake and other factors (heat, exercise, etc.)

regular insulin should be dosed ~30min before the meal in order for it's peak to be most effective --> inconvenient.
...there is also the potential for mismatch if unsure of food intake.
Finally, regular insulin's duration of action is 4-6hrs, and as such it is still active many hours after the meal and can result in hypoglycemia with changes in lvl of actv.

Front 9

Given the disadvantages of the NPH & normal i combo in MDI dosing, what might be a better idea?

Back 9

NPH or Glargine + Lispro, Aspart, or Glulisine w/ a MDI dosing framework.

Front 10

What is a Basal/Bolus insulin regimen?

Back 10

basal lvl = ~50% of daily needs --> kept near contant lvl

bolus insulin @ mealtimes limiting hyperG postprandially = ~10-20% of daily req @ each meal.

Front 11

How are pts with t1dm usually started on insulin tx?

What is the average insulin requirement in a t1dm pt?
- give example breakdown for a 60kg person.

Back 11

combo of basal bedtime glargine or NPH w/ prandial fast acting analogue boluses.

0.6 U/Kg/Day; 50% basal / 50% prandial
- 36U a day, 18 baseline and 6/6/6 prandially.

Front 12

How is insulin tx initiated in pts w/ t2dm?

Back 12

often done when dz is not adequately controlled on oral meds; BUT it CAN be done anytime.
--> NPH or glargine is added at bedtime, and all other oral agents are continued.
- pt is instructed to titrate this dosage based on their AM G readings.
- if this doesn't get it under control, add prandial boluses.

Front 13

In split/mixed insulin tx regimens, what determines the:
- fasting glucose (AM G)
- pre-lunch G?
- pre-supper G?
- bedtime G?

Back 13

- previous night NPH
- morning regular
- morning NPH
- pre-supper regular

Front 14

In MDI insulin tx regimens, what determines the:
- fasting G?
- pre-lunch, presupper, and bedtime?

Back 14

- nighttime long-acting (or intermediate acting)
- prandial short-acting dosages.

Front 15

What is the "somogyi effect?"

"dawn phenomenon"?

Explain how they relate to the eval of fasting hyperG i/ pts o/ insulin tx.

Back 15

low, excessive counterregulation of bedtime glucose (as measured @3am) causes rise in G by morning.

normal modest rise in F in early morning due to peaks of GH and cortisol.

check bedtime glucose. if it's too high, then you know what's up. If it's *not* high, then recheck @3am. If low (excessive) --> somogyi. If high/normal --> dawn phenomenon.

Front 16

Lipodystrophy seen with insulin can be two conditions = ?

Back 16

lipoatrophy
- immune mediated condition; loss of fat @ insulin injection sites. MUCH less freq w/ newer human insulins than w/ the old animal ones.

lipohypertrophy
- NON-immunological side effect resulting from repeated admin of insulin @ same injection site.

Front 17

What is insulin pump tx (CSII)?
- indications?

Back 17

a basal/bolus method with a variable basal rate.
- very motivated pt w/ interest and ability to assume substantial responsibility for own care.
+ also: variable schedule, hypoglycemia, dawn phenomenon, urgency to quickly optimize control (preggers)

Front 18

What are "smart pumps?"

"Sensor augmented pumps?"

Back 18

Calculates and recommends doses based on: (all and/or)
- current G lvls
- amount plan on eating
- personal preset info
- amount of insulin still active from previous dose.

These are even newer - have a G sensor which transmits the readings to the surface of the insulin pump.

Front 19

What is the preferred insulin regimen for the most flexibility?

Back 19

basal/bolus with glargine/NPH and monomeric short actings.

Front 20

What are the main medical risks of insulin therapy?

Back 20

hypoG and WG.