16/17: Diabetes - Dodge Flashcards
how many ppl have diabetes?
1/11
increased in native americans, hispanics, and lower education
increased in the south
what does calcium rushing into the islet cell in response to glucose cause?
ca2+ activates insulin gene expression via CREB –> exocytosis of stored insulin
insulin is created in…
beta islet cells of pancreas
insulin binding to cell receptors –>
glut 4 translocation to the cell membrane –> cell takes in glucose
common theme between dif. DM types
dysregulation of the insulin/glucose interplay leading to hyperglycemia
typeII DM
insulin resistance
95% of adult DM
type I diabetes is caused by…
complete or near complete insulin deficiency usually seen with >70% destruction of beta cells
no insulie
IDDM
insulin dependent diabetes mellitus
insulin is being used to treat
genetic component of DM type I
HLA DR3/DR4 gene
twin studies 50%
diabetic ketoacidosis –>
type I DM
30% children or adolescents diagnosed with type I DM after being treated for DKA
which type of DM has a higher genetic component?
type II
MODY
maturity onset diabetes of youth
- early onset of hyperglycemia, beta cell genetic defects
- appears morel like type 2 DM in a younger person
- AD, most common monogenetic syndrome associated with DM
LADA latent autoimmune diabetes of adults
WILL require treatment with insulin much like type I DM
- slow destruction of beta islet cells
- misdiagnosed as type 2
- tequire insulin due to insulin deficiency from autoimmune islet destruction
- will have low c peptide
drugs/medications that may cause diabetes
- thiazides
- pentamidine
- protease inhibitors
symptoms of DM
- always tired
- frequent urination
- wounds willnot heal
- blurry vision
- always thirsty
- vaginal infections
- numbness or tingling of feet
- sexual problems
- always hungry
- sudden weight loss
diabetes screening guidlines
every 3 yrs starting at age 45
if pt overweight with at least one additional risk factor screen earlier
prediabetes and diabetes fasting plasma glucose
100-125
>126
glucose tolerance test prediabetes; diabetes
140-199
>200
hemoglobin A1c prediabetes
- 7-6.4%
6. 5% —> diagnostic of diabetes**
what hemoglobin A1c level is diagnostic of diabetes?
> 6.5%
type I DM treatment :
require insulin!
- in basal/bolus (long and short)
- continuous infusion (short with short)
- split/mixed
does type 2 require insulin?
not at first, many will eventually require insulin as the disease progresses
> 10-12% A1c with ketosis and/or weight loss = insulin required; >10-12 alone is strongly recommended
standard oral therapy for type II DM
metformin
when do type II DM need more than one med?
greater than 9.0% A1c –> recommend treatment with two oral agents or insulin mono-therapy
intervention with A1c less than or equal to 7.5%
lifestyle and dietary changes
weight loss is _______ important than certain combinations of nutrients
more
MOA metformin
decreases hepatic gluconeogenesis and glycogenolysis with increase in peripheral insulin sensitivity and glucose uptake
severe side effect metformin
lactic acidosis
contraindications for metformin
- renal/hepatic impairment CR>1.5 in men or 1.5 in women
- no preggers
what may predispose ppl to lactic acidosis?
CHF with hypoperfusion or chronic hypoxemia
start dosing for metformin
500 mg once or twice daily with meals
if tolerate meds, double dose to 1000 mg twice daily
other oral therapies
sulfonylureas (stimulate insulin secretion by pancreas beta cells) (weight gain, hypoglycemia, increased CV events) (glyburide, glipizide, glimepiride)
and
Thiazolidinediones (pioglitazone)(increased risk for fluid retention and CHF)(bladder cancer risk)
which med can actually decrease the microvascular complications of diabetes?
sulfonylureas
similar to sulfonylureas, stimulate beta cells
glitinides
shorter half-life, dosed with meals
prevent absorption of simple sugars by decreasing carbohydrate breakdown
alpha-glucosidase inhibitors (acarbose)
increased incretin leads to increased insulin secretion
DPP4 inhibitors (sitagliptin)
increase insulin and decrease glucagon, increase satiety
GLP-1 receptor antagonist
no hypoglycemia, causes weight loss
block glucose resporption in kidney
sodium-glucose co-transporter 2 inhibitors
canagliflozin
*most effective medication to lower A1c
insulin therapy
insulin starting dose
0.1-0.2 units/kg initially - 10 units minimum
monitor morning fasting glucose and titrate insulin until goal of 70-130 is met
initial goal of insulin therapy =
obtain fasting glucose levels less than 130 mg/dL
glycemic treatment goals
less than 7% A1C
fasting glucose 70-130
peak glucose less tahn 180
3 annual screens for DM complications
- spot urine ablumin to creatinine ratio (want less than 30)
- foot exam with monofilament testing
- dilated eye exam by opthalmologist for diabetic retinopathy
main mechanism for chronic complication of diabetes
increased intracellular glucose leads to formation of advanced glycosylation end products AGEs
–> accelerate atherscleoris, promote glomerular dysfunction, reduce NO synthesis, endothelila dysfunction
can only have macular edema when…
non proliferative retinopathy present
