diabetes part 2 Flashcards
DKA
diabetic ketoacidosis, mainly occurs in type 1 DM, glucose is present so ketones aren’t used and cause acidosis in blood, can be caused by omitted insulin doses, emotional stress, and psychological problems complicated by eating disorders.
HHS
hyperosmotic hyperglycemia state, hyperglycemia leads to hypersomotic state, which can lead to polyuria, is characterized by hyperglycemia, profound dehydration, and neurologic manifestations in the absence of significant ketosis. mainly seen in type 2 DM where the cause is insulin resistance
chronic complications of DM
premature atherosclerosis (cardiac disease and stroke), retinopathy, rhinopathy, neuropathy, cellular toxicity in GLUT2 expressing cells (brain, kindney, RBC, lens, cornea), GLUT2 transport of glucose cause lead to advanced glycation end products and some can bind to the recpetor to form RAGE which cause inflammation
explain AGE and RAGE in cells
AGE is when glucose accumulates via GLUT2 and causes advanced glycation end products which can bind to receptors to form RAGE which can lead to inflammation which can cause cellular damage, including swelling and rupture, due to water retention and the formation of reactive oxygen species.
explain AGE and RAGE in the vasculature
AGE can also cause problems in the vasculature and cause RAGE induced pro inflammatory pathways in the vasculature, Can also condensate on hemoglobin forming glycalated hemglobin HbA1c or A1c
what are symptoms of hyperglycemia
polyuria, polydipsea, polyphagia, slow wood healing, recurrent infections, fatigue, blurred vission, dry mouth, dry itchy skin
Screening
don’t do for type 1. for type 2 start at age 45 and screen every 3 years if no risk factors,
what test values can diagnose DM
A1c over 6.5(must be lab not point of care!!), fasting BG over 126, 2 hour post glucose load over 200, random glucose over 200 with symptoms of the 3 P’s, testing should be done twice unless the random over 200 with symptoms is used. If the second test does not match diagnosis then repeat the test that was over threshold
BK has a fasting BG of 130. So we bring him in on another day and test his A1c and get 6.3.What is the diagnosis
Need to re run the fasting BG and if it is above threshold then he has diabetes
screening for gestational DM
at first visit if 2+ risk factors, at 24 and 28 weeks no matter what, can use one step or two step
explain the one step DM testing
for gestational, give 75 g glucose load, measure in 1 hour and 2 hours, diagnosed if fasting is over 92, if 1 hour is over 180 and 2 hours is over 153
2 step DM testing
for gestational, give 50g glucose, test after 1 hour if over 140 then go to step two, if not then negative test, step two) after fasting give 100 g test in 3 hours if over 140 then positive
prediabetic classification
impaired fasting glucose of 100-125, impaired glucose tolerance 2 hours after load of 140-199, A1C of 5.7-6.4
what are some meds that can cause secondary DM
meds that treat HIV/AIDS, corticosteroids, organ transplant drugs, antipsychoctics
what is the A1C goal for different populations?
under 7 for most, under 6.5 if you want to be more aggressive, under 8 if short life expectancy, severe hypoglycemia, CVD events, advanced micro or macrovascular events, under 7.5 for kids
what is the preprandial goal
80-130
what is the postprandial goal
under 180
what is the BP goal
under 140/90
goals for gestational
if acquired DM during pregnancy, pre prandial of less than 95, post of less than 140, 2 hour 120
if DM present before pregnancy than goals are more aggressive, fasting 60-99, and post prandial of 100-129, A1C of under 6
what are the bolus insulins
aspart, glulisine, lispo, regular,
what are the maintenance insulins
detrimir, NPH, glargine
which maintenance insulin can be mixed with bolus insulins?
NPH
if BK is switching from NPH 40 units BID to glargine qd what must be done
decrease daily dose by 20%
BK is switching from NPH 40units qd to glargine qd, what must be done
nothing
what is the structure of aspart
proline is changed to aspartic acid at carboxyl terminal of B chain
what is the structure of lispro
proline and lysine switch places at the carboxyl terminal end of B chain
what is the structure of glulisine
lysine is changed to glutamic acid and aspargine is changed to lyisine at carboxyl terminal end of B chain
how does NPH work
is bound to protamine which is degraded by enzymes once injected. This is a cloud suspension that need to be resuspended before injection
why can’t glargine be mixed in the same syringe as other insulins
increasing the ph causes it to precipitate out
which maintenance insulin remains soluble after injection
detemir
how does detemir work structurally
it self bonds with its hydrocarbon chains it can also bind to albumin