Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
27 Cards in this Set
- Front
- Back
|
what are the main benefits of using insulin |
unlimited dosing, accomdate lifestyle and preference, flexible dosing |
|
|
what are the limitations of insulin |
fear of needles, weight gain, less convenient, fear of hypo, horror story |
|
|
what is is in humulin 70/30? |
short acting insulin (regular) humulin R, and intermediate insulin humulin N |
|
|
what insulin dosing schedule is recommended? describe it |
method 8, 4 injections which includes 3 injections before meals with rapid acting (LAG) and ultra long injection before bed (glargine, detemir, degludec) |
|
|
what would you say to someone if they think treatment with insulin is unnatural? if it hurt someone before? |
it is what your body naturally produces, your just replacing it probably because they didnt get treated for it soon enough, we did not diagnose diabetes well years ago |
|
|
what are the characteristics of basal insulin? bolus? |
constantly secreted, no peaks, suppresses glucose between meals and during sleep, 50% of daily needs response to meals, limits hyperglycemia after meals, sharp peak,10-20% per meal |
|
|
what is the dawn phenonmenon? what is the somogyi effect? |
happens at 4-5 AM in which there is a surge of hormones to increase blood sugar for good stress, happens to everyone go hypoglycemic during sleep, and your liver increases glucose cause body thinks you will die from hypoglycemia, happens 2-3AM |
|
|
what do you do to treat the dawn phenomenon? why do you use that? |
use NPH=humulin or novolin N= intermediate acting insulin peak happens around 8 hours, right when you would have hyperglycemia |
|
|
what do you do to treat the dawn phenomenon? why do you use that? |
lower the amount of basal insulin
idk why |
|
|
at what point do you use a concentrated dose of insulin? |
if you need more than 200 units |
|
|
clinical pearl for treating type 1? type 2? |
multiple daily injections are prefered start with a long acting in the evening, then add pre prandial if basal only regimen is insufficient use biphasic insulin for cost savings |
|
|
what is the initial dose of insulin for type 1? what about on the honeymoon period? |
0.5-0.6 units/kg ABW 0.1-0.4 Units/kg ABW |
|
|
what is the initial dose for type 2? with insulin resistance? |
0.2-0.6 units/kg ABW 0.7-2.5 units/kg ABW |
|
|
if insulin needs to be adjusted, what should you fix first? what are the numbers on the adjustment? |
the fasting/basal/long acting insulin 1-2 units for ever 30-50 mg/dL above goal |
|
|
what does the 1500 rule estimate? 1800 rule? |
point drop in mg/dL for every unit of regular/short acting/novolin r/humulin r/nph point drop in mg/dL for every unit of rapid acting insulin/lispro/aspar/glusinine |
|
|
what are the approved injection sites for insulin? why are they used? |
abdomen, back of upper arm, upper ass or hip, outer thighs have a layer of fat beneath to absorb the insulin and not many nerves and is more comfortable, easier to get into the SQ tissue |
|
|
how do you manange hypoglycemia? |
eat or drink 15 grams of carbs.. juice, glucose tabs, hard candy |
|
|
what insulin do you roll? what does it mean to rotate an injection site |
cloudy insulin, dont shake pick when of the recommend areas and change where you inject the needle by a finger tip width, change the entire region once a week |
|
|
why is method 8 the best injection regimen? what does it include? |
it mimics natural release of insulin from the pancreas the basal dose has a long effect and supresses glucose between meals and overnight while the bolus insulin has a short effect and is used to suppress the glucose spike from meals |
|
|
describe the normal activity of beta cells |
glucose goes into beta cell using glut2, glycolysis produces ATP, increase in atp causing k channels to close, K ions build up in the cell and depolorize the cell, voltage gate ca channels open, Ca rushes in the cell and the beta cell releases insulin |
|
|
what is the mechanism of sulfonylureas? |
bind to SUR1 receptor that closes K channels and depolorizes the cell, ca channels open, causing the release of insulin insulin also binds receptors better when drug is present acts like glucose |
|
|
what does somatostain do? do sulfonylureas casue release of glucagon? |
provides feedback to alpha cells to inhibit the release of glucagon which decrease glucose no, decreases release of glucagon |
|
|
what is the mechanism of biguanides? |
increase insulin sensitvity, activate amp dependent protein kinase to block the breakdown of FA and inhibit hepatic gluconeogenesis and glycogenolysis, slows absoprtion of glucose from gut |
|
|
what is the mechanism of action of the thiazolidinediones? |
does not affect insulin secretion, enhances action of insulin at tartgets binds for nuclear hormone receptor peroxisome proliferator activated receptor gamma (PPARy) which binds rtinoid x receptor, which activates transcription of genes involved in glucose and lipid metabolism |
|
|
what does activation of PPARy normally do? |
control of glucose transport into cells, lipid metabolism, tissue sensitvity to insulin, tnfa and leptin |
|
|
what do the tzds do on muscle cells? liver? adipose? |
produce glut 4 decrease hepatic glucose production promotes uptake of glucose |
|
|
for now |
we are done |
