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
give an example of biguanide
metformin
which oral medication for diabetes uses the matrix diffusion technology
metformin
which oral medication for diabetes uses osmotic gradient
sulfonylurias
which insulins do not really have a peak
detemir an glargine
list the insulins that do have peaks from the highest peak to the lowest
lispro, aspart, glulisine>regular>NPH
what is the most significant side effect of insulin
hypoglycemia ,longer duration of action=higher possibility of causing it
which oral medications deposits in the wall of the intestine which helps spread out its effects
metformin
which diabetic drug is an antihyperglycemic drug
metformin
what are the proposed mechanisms of metfromin
decreases hepatic glucose production, increases insulin sensitivity, slows absorption of glucose, it can also lower lipids
when is metformin contraindicated
Scr over 1.4 or 1.5, unstable heart failure, chronic metabolic acidiosis (DKA), when iodinated dies are used
which drug can cause lactic acidosis
metformin, rarely , symptoms are malaise, myalgia, respiratory distress, sleepiness and nonspecific abdominal pain, hypothermia, hypotension, bradycardia
what are the most common side effects of metformin
GI upset because a large daily dose is needed
what side effect can metformin users see after years of taking it
B12 deficiencies
which oral drug is highly bound in the blood
sulfonyurias
what is the mechanism of sulfonyurias
binds to SUR1 on the ATP sensitive K channels and inhibits K eflux
which sulfonyuria has the highest change for hypoglycemai
glyberide
what is the inpatient and outpatient hypoglycemia reversal
inpatient is D50W, outpatient it glucagon
how is insulin metabolized
glutathion insulin transhydrogenase (insulinase)
do we need to adjust insulin doses for end stage renal or liver disease
yes, decrease
how are sulfonyurias eliminated
CP2C9, glyberide and glybazide are more renal
what drug drug interactions can metformin have
can compete with other cations for excretion like cimetidine
why do iodinated dies cause an issue
can cause temporary renal dysfunction
what drug drug interactions can occur with sulfonyurias
cyp and binding in the blood
what diabetic drug decreases A1C the most
insulin
when should prediabetic patients use metformin
if they had gestational DM, BMI of over 35, and younger than 60 years
how to treat hypoglycemia
3-4 glucose tablets, 8-10 hard candies, 4-6oz of regular soda or juice, 8 oz of non fat milk , or dextors iv or glucagon
monitoring A1C
twice a year unless unstable or new therapy than every 3 months
eAG
28.7xA1C-46.7
what is the average daily requirement of insulin for type 1
.5-.6/kg/d
what is the daily requirement some are started on insulin for type 1
.1-.4/kg/d
how is the insulin does divided up for type one
2/3 daily does in the first dose 2:1 maintence to bolus (divide dose by 3 and multiple by 2 to get maintenence), evening dose is 1/3 daily dose and 1:1
whats the guidline for adjusting mealtime in type 1
1-3 units changes BG by 50mg/dL
1500/1800 rule
add up all the maitenance and regular doses to get daily dose and divide 1500 by that to find out how much 1 unit changes things, if using lispro, aspart, or glulisine then use 1800
which injection regimen most closely mimics the bodies normal insulin
4 injections
when should maitenence insulin be considered for type 2
A1c over 8.5 while on metformin, A1c over 8 when on dual meds, A1c over 10, symptoms of hyperglycemia (3 P’s)
what is the average amount of daily insulin for type 2
.7-2.5/kg/d
what are the does adjustments for fixing fasting in type 2
if over 180 then add 6 units, if 140-180 then add 4 units, if 110-139 then add 2 units, if 80-109 then don’t change, if 70-79 then decrease by 2, if under 20 then decrease by 4 or if taking over 60 units then decrease by 10%
what dosing should type 2 start on for insulin
if A1c is under 8 then .1-.2/kg/d, if A1c is over 8 then .2-.4/kg/d
when should mealtime insulin be added to type 2
when A1c is still not at goal, when glycemic control doesnt happen after .5-1/kg/d, or when experiencing hyperglycemia and hypo
what mealtime dose do you start with for type 2
4-10 units
what is the first line for gestational
10 units hs or 2:1 in the morning if experienceing postpradial hyperglycemia
what is the first, second, and third choice for type 1
1) glargine and mealtime
2) detemir and NPH
3) NPH and regular
what is the first, second, and third choice for insulin in type 2
1) NPH BID
2) glargine or detemir BID
3) pre mixed
what are the first choices for elder and frail for DM 2
1) glargine
2) NPH or detemire BID
3) NPH and regular
first line for gestational
NPH
what is the somogy effect
hypoglycemia in the night leads to morning hyperglycemia
whats the dawn effect
morning hyperglycemia is due to other factors like hormones
