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69 Cards in this Set
- Front
- Back
what are the first generation sulfonylureas? |
acetohexamide, chlorpropamide, tolazamide, tolbutamide I aced the chlorine totally B! |
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what are the second generation sulfonylureas? |
glipizide, glyburide, glimepiride triple G |
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what drugs are the meglitinides? |
nateglinide, repaglinide mega natty rap |
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what drugs are the biguanides? |
metformin |
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what drugs are in the thiazolidinedione class? |
pioglitaztine and rosiglitazone rosser is a pig |
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what bile acid sequestrant is used in diabetes? |
colesevelam |
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what dopamine agonist is used in diabetes? |
bromocriptine |
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what are the drugs in the SGLT-2 (sodium glucose cotransporter 2) inhibitor class? |
canagliflizoin, dapaglifozin, empaglifozin dad has a can of empathy |
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what are the drugs that are the DPP-4 inhitior (dipeptidyl peptidase 4 inhibitor) class? |
alogliptin, sitagliptin, saxagliptin, linagliptin sit sax all in line |
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what are the rapid acting insulins? what is the rapid inhaled insulin? |
lispro, aspart, glulisine LAG afrezza |
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what are the short acting insulins? |
humulin and novolin R |
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what are the intermediate acting insulins? |
humullin and novolin N |
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what is the ultra long acting insulin? |
degludec |
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what are the concentrated insulins? |
humulin r 0 300 and glargine u 300 |
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what is the only amylinomimetic for diabetes? |
pramlintide, this inhibits glucagon which decrease blood glucose |
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what are the GLP1(glucagon like peptide 1) agonists and mimetics? |
exenatide, liraglutide, albiglutide, dulaglutide Ex liar alex big dulces |
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what does amylin do? |
inhibits glucagon secretion |
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what is gestational diabetes? |
diabetes during the 24-28 week of gestation not known to have diabetes |
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when does the honeymoon phase happen? what type of diabetes? explain the physiology that causes type 1 dm? why does this cause hyperglycemia? |
type 1, following diagnosis when the pancreas is still able to produce enough insulin to manage glucose levels immune mediated beta cell destruction absolute deficiency in insulin and amylin |
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explain the physiology of type 2 diabetes. what causes hyperglycemia? |
impaired insulin secretion, insulin resistance because of upregulated basal insulin secretion, the pancreas in unable to maintain insulin production and basal insulin demand exceeds supply capacity of the pancrease, 60-90% of beta cell die insulin resistance with insuffcient supply of insulin to meet demand of body |
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what 2 factors are involved in the causation of type 2 diabetes? what does this cause what is this also known as? |
genes and environment insulin resistance and beta cell failure relative insulin deficiency |
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what organs/body parts are involved with diabetes? |
fat, kidney, muscle, liver, brain, pancreas, intestines |
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does alcohol cause hyper or hypoglycemia? |
hypo |
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what drugs cause hyperglycemia? |
diuretics, glucocorticoids, olanzapine, phenytoin, sympathomimetics(NE and E) |
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is there any recommended screening/diagnosing guidlines for type 1? type 2? |
None for type 1 test everyone over the age of 45, if normal repeat in 3 years |
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when would you consider screening for type 2 prior to the age of 45? |
if overweight or obese with one of the following physical inactivity, 1st degree relative, women who delieverd a 9 lb baby, polycyctic ovary syndrome, >140/90, HDL less 35 and TG gre 250, A1c greater than 5.7%, hx of CVD |
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normal fasting glucose? normal oral glucose tolerance test? normal A1c? |
less tha 100 less than 140 less than 5.7 |
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what is considered an impaired fasting glucose number? impaired oral glucose tolerance test? |
100-125 140-199 |
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what is fasting glucose in a diabetic? oral glucose tolerance test? a1c? |
greater or equal 126 greater or equal 200 greater or equal 6.5 |
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what is fasting glucose for those at increased risk for diabetes? oral glucose tolerance test? a1c? |
100-125 140-199 5.7-6.4 |
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symptoms of hyperglycemia? symptoms of hypoglycemia? |
blurry vision, difficulty concentrating, frequent urination, headache, fatigue, glucose in piss nevrousness, sweating, confusion, lightheaded, hunger, insomnia, blurry vision, weakness |
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what is needed for diabetes diagnosis? |
high fbg, ogtt, a1c and symptoms of hyperglycemia |
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what does a1c measure? |
glucose over 2-3 months, includes both postpradial blood glucose and fasting blood glucose |
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what did the a1c derived average glucose study show? how much does an a1c of 5 correlate with in average glucose? 6 |
a1c correlates with average glucose 97 120 add 30 for the rest |
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define insuline resistance syndrome, who gets this? |
impaired response to the physiological effects of insulin type 2 |
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what are the goals for diabetes? |
maintain glucose, prevent hyper/hypo, delay macro/micro complications, eliminate other risk factors, maintain qol |
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when should you use the ADA guidelines? ACCE/ACE guidelines? which one is more strict? |
elderly and frail young AACE/ACE |
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what is the FBG for ADA? a1c? BP? AACE/ACE? a1c? BP? |
80-130, less than 7, less than 140/90 less than 110, less than or equal to 6.5, less than 130/90 |
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what are features that can be modified in treating a diabetic? |
patient attitude, treatment efforts, resources, support |
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what drugs should you consider for a patient that is in increased risk for diabetes? how much excercise a week? |
metformin, pioglitazone, orlistat if severly obese 150 mins per week, no more than 2 consecutive days w/o excercise |
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why would you give an ACE to a diabetic? |
prevents progression to macroalbuminuria ffor type 1 |
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should a type 1 diabetic check BG? how often should they check a1c? GFR and urinary albumin? Eyes? what vaccines? |
3 or more times a day 3-6 months 5 or more years after diagnosis and annually influenza, pneumococcal, hepatitis B (HIP) |
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what is different about the excercise regimen for type 2? what is unique about CAD prevention in diabetics? |
includes resistance training BP less than 140/90, statin, ACE, use aspirn if 10 year risk is greater than 10% |
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what is unique about the monitoring for type 2? how much weight should diabetics lose? |
includes annual feet exam 5-10% |
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what is the therapy for type 1? gestational? |
insulin that mimics body phsilogical secretions insulin, oral sulfonyurea or metformin |
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describe the treatment algorithm for ADA |
diet excercise, metformin, if a1c in not achieved after 3 months do dual therapy, add anything, if a1c is not achieved in 3 months do triple therapy, then try injectables (metformin, insulin, mealtime insulin or glp) |
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describe the treatment algorith for AACE |
depends on entry a1c, if less than 7.5 monotherapy, if greater than 7.5 dula therapy, if greater than 9 and no symptoms do dual or triple therapy, if greater than 9 w symptoms add insulin and other agents |
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what does a fasting value indicate? post meal? |
microvascular problems macrovascular problems |
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what 4 people received a nobel prize for insulin? |
fredrick banting, jj macloed, charles best, jb collin |
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what hormone is synthesized by the beta cells? what happens to this? what happens to proinsulin? |
a preprohormone called preproinsulin leaves ER and part of N termins is cleaved to create proinsulin in golgi, PC and PC2 cleave the connecting peptide leaving the a and b chain attached by disulfide bonds |
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what type of recptor is the insulin receptor? describe the structure? is the recptor found only in a dimeric form? |
tyrosine kinase like receptor that autophosphorylates heterodimeric, external alpha subunit and beta transmembrane subunit (tyrosine kinase activity) no tetrameric form, has greater affinity |
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explain the sig transduction after insulin binds? |
binding, autophosphorylation of beta, aggregation of alpha and beta, beta phosphoraltes IRS1 (insulin receptor substrate 1), gene expression, insertion of GLUT transpoorters into cell membrane, increase uptake of blood glucose |
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describe the different forms of insulin molecules and how it affects absorption |
hexameric state is not absorbed, this eventually turns into the dimeric state which is slowly abosrbed, then this breaks down to the monmeric state which is rapidly absorbed |
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what are the effects of zinc and protamine? |
increase onset of action and half life |
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how is lispro different from natural insulin? is there any difference in binding? |
proline at 28 and lysine at 29 are reversed, this allows lispro to dissociate from hexmeric form to monomeric after injection bind insulin receptor the same, greater affinity for IGF1 receptor |
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how is insulin aspart different from natural insulin? |
Proline at position 28 of b chain is replaced with aspartic acid, which allows dissociate from hexmeric to monomeric form after injection |
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how is insulin glulisine different from natural insulin? |
b chain aspargine at 3 is replaced with lysine b chain lysine at 29 is replaced with glutamic acid |
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how are the short acting insulins different from natural insulin? intermediate acting insulins? |
has zinc and crystals has zince and protamine |
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how is insluin glargine different from natural insulin? |
2 arg residues added to c termine of B and 21 asparagine is replaced with glycine, makes peptide less soluble |
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how is insulin degludec different from natural insulin? what are the effects? |
B 30 threonine is deleted and is conjugated to hexadecanedioic acid on b 29 lysine, causes hexamers to form which favors slow release of insulin |
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what are the main differences between glut 4 and glut 2? |
glut 2 does not depend on insulin for diffusion and is found in the liver and kidney glut 4 is found in adipose and muscle and only works if insulin is present |
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Afrezza what is the time until onset? time until peak? duration? |
5-10 minutes 10-14 minutes 2-3 hours |
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rapid acting insulin lispro/aspart/glusine onset of action? peak? duration? |
5-15 min 1-2 hour 3-5 hour |
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Regular insulin (humulin R and Novolin R/short acting insulin) onset? peak? duration? |
30-60 min 2-4 hours 6-10 hours |
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intermediate insulin (NPH) onset? peak? duration? |
1-2 hours 4-8 hours 10-20 hours |
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long acting insulin glargine onset? peak? duration? |
2-4 hours none 24 hours |
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long acting insulin detemir onset? peak duration? |
2-4 horus none 12-24 hours |
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