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Diabetes Mellitus (insulin (types of insulin (intermediate (NPH (humulin N…
Diabetes Mellitus
insulin
secreted from the islets of langerhans in the pancreas
alpha cells = glucagon
beta cells = insulin, amylin
secretion
basal = release in absence of stimuli; constance
stimulated/bolus = response to glucose load
administration
must be injected SQ
abdomen, arms, thighs, buttocks
do not shake suspensions
unopened vials/pens must be refrigerated
opened (in use) may be left at room temp
dose in units
drugs
U- 200 lispro (humalog), degludec (tresiba)
U-300 glargine (toujeo)
U-500 R insulin only
dosage forms
patches, vials, pens, pumps, inhalers
types of insulin
rapid acting injection
humalog and novolog
onset 10-15 minutes peak 1 hour duration 3-5 hours
short acting
regular (humulin R, novolin R, Relion R)
onset 30-60 min, peak 2-4 hour duration 6-8 hours
intermediate
NPH (humulin N, Novolin N, reliOn N
onset 2-4 hours, peak 4-10 hours, duration 10-18 hours
must roll to mix prior to injection
rapid and short are used for correction doses for hyperglycemia
mixed
usually a rapid or short acting combined with a intermediate
adverse effects of insulin (+sulfonylureas and meglitinides)
CNS: behavioral changes, confusion, HA, shallow respiration, coma, convulsions, death
adrenergic: anxiety, shakiness, palpitations
sweating, hunger, paresthesias
hypoglicemia
type 1 diabetes
absolute deficiency of insulin
autoimmune destruction of Beta-cells
most common diagnosed in younger ages
results in hyperglycemia
insulin must be used for survival
may developoe insulin resistance later in life in addition to autoimmune
signs and symptoms
polyuria, polydipsia,polyphagia, weight loss,nausea, vomiting, diarrhea, dehydration, weakness,diabetic ketoacidosis
HbA1c
glycosylated hemoglobin
measures % of hemoglobin irreversibly glycosylated
indicator of glycemic control past 2-3 months
1% change represents 25-30mg/dl change in average blood glucose
normal = 4.5-5.7%
check minimum of twice yearly
pathophysiology of type 2 diabetes
insulin resistance
defects in insulin secrection
dysregulated hepatic glucose production
dysregulated renal glucose reabsorption
other hormonal disturbances
GLP-1, amylin
GLP-1 agonist
bydureon, victoza, trulicity,adlyxin ozempic
second or third lid line therapy
mimics endogenous GLP-1 hormone
nausea, diarrhea, constipation weight loss, pancreatitis
activity
glucose dependent augmentation of insulin secretion, slows GI motility, suppresses inappropriate glucagon secretion
thiazolidinediones
add-on third line therapy
improves insulin sensitivity
full effect may take 2 months
edema, heartfailure, weight gain, fractures, macular edema, bladder cancer
actos, avandia
Metformin
glucophage, glumetza, fortamet, riomet
first line therapy
decreases glucose production from liver and improves insulin sensitivity, may take a few weeks for full effect
adverse effects diarrhea, weight loss, B12 deficiency
sulfonylureas
glimepiride (amaryl) glipizide (glucotrol) glyburide (micronase)
add-on third or later
stimulates insulin release from pancreas, must still have function
adverse effects include hypoglycemia, weight gain
DPP-4 inhibitors
add on second or third
januvia, onglyza
inhibits enzyme DPP-4 responsible for break-down of endogenous GLP-1
headaches, URI, pancreatitis, joint pain
SGLT-2 inhibitor
invokana, farxiga,jardiance
second third line therapy
inhibits sodium -glucose transporter in the kidney to increase urinary excretion of glucose
adverse;: orthostasis electrolyte changes, UTI, yeast infection, polyuria, weight loss,fracture risk, amputation risk, fournier gangrene
counterregulatory hormones maintain glucose homeostasis increase blood glucose
epinephrine
increases blood glucose
leads to symptoms of hypoglycemia
effective response may be lost after 10-20 years
glucagon
released from alpha cells
stimulate glucose release fromthe liver
cortisol, growth hormone
meglitinides
repaglinide (prandin) nateglinide (starlix)
stimulate insulin realese from pancreas duration of action @ 1.5 hours, taken with meals
hypoglycemia
alpha-glucosidase inhibitors
precose, glyset
add on, typically late and rare
inhibits enzyme in the intestines responsible for reducing polysaccharides into monosaccharides, delay absorption of carbs/sugar
type 2 diabetes
signs and symptoms
polyuria, polydipsia,polyphagia, weight gain, fatigue, recurrent UTIs, problems healing infections, blurred vision, asymptomatic
not prone to diabetic ketoacidosis
criteria for diagnosis
2 abnormal results unless obvious
fasting glucose >126mg/dl
oral glucose tolerance test (2hrs post load) >200 mg/dl
rando glucose w/signs and symptoms >200mg/dl
A1c >6.5%
hyopglycemia
hypoglycemia B G <70 mg/dl
treatment
4oz juice, 4oz soda, 1Tbs sugar, 5-6 lifesavers, 3-4 glucose tablets
if unconscious - glucagon injections
metabolic syndrome, prediabetes, and type 2 diabetes
do we know the cause?
visceral fat
more "lipolytically" active
likely to release FFAs to circulation and liver
insulin resistance
pancreatic dysfunction
stimulates hepatic glucose and VLDL production
can also accumulate in liver - fatty liver
undefined genetic predisposition
age
physical inactivity
high CHO diet >60% of calories
hgh saturated fat diet
glycemic goals of therapy
ADA guidelines
A1c <7%
preprandial/fasting 80-130
peak postprandial <180
general adverse effects of insulin
edema, weight gain,lipodystrophy