DM Flashcards
What are the different types of diabetes
- Type 1: Juvenile onset ( IDDM) - childhood/puberty
- Type 1.5: LADA (Latent Autoimmune Diabetes of Adults) - Adults
- Type II: Maturity onset (NIDDM) - >35 years of age
- MODY (Maturity onset diabetes of the young) - 20-60 years of age
- Gestational - pregnant women
What is the prevalence of diabetes
9.3%
Which type of diabetes include autoantibodies that target B cells of the pancreas responsible for insulin production
- Type 1
2. LADA
in which type of diabetes is one considered undernourished
type 1
in which type of diabetes is one considered obese
type II
in which type of diabetes do you see insulin resistance
type 1, LADA (some)
in which type of diabetes do you see a genetic predisposition
- type I (polygenic and environmental)
- type II (polygenic and environmental)
- MODY (autosomal dominant–> monogenic)
What is the defect of deficiency of each type of diabetes?
- type I: Beta cells are destroyed
- LADA: slow progression to insulin dependence
- type II: inability of beta cells to produce adequate insulin
- MODY: defective insulin production or secretion
What are the classic symptoms of diabetes? (three P’s)
- polydipsia (always thirsty)
- polyuria (always urinating)
- polyphagia (always eating)
(signs include high blood sugar)
Therapy of diabetes include keeping A1-C below _____blood pressure below ____ and LDL cholesterol below ____
7.0; 140/80; 100
____% of diabetics are type 1
5
what does glycosylated hemoglobin bind to
red blood cells; the higher the levels of A1C, the higher the presumed glucose levels
what are normal glucose levels
70-110 mg/dl
what is the formula to determine eAG (estimated average glucose)
28.7 x A1C - 46.7
what does it mean when a patient tells you their A1C is 7?
That their average blood sugar is around 150
what are the diabetic drug classes
- oral hypoglycemics
2. injectable hypoglycemics (insulin and GLP- 1 agonists)
what are the oral hypoglycemic therapeutics
- biguanides
- sulfonylureas
- thiazolidinediones/glitazones
- DPP- 4 inhibitors
- SGLT 2 inhibitors
what is at the top of initial drug therapy for treating type II diabetic patients
metformin; efficacy in reducing hemoglobin A1 is high, and low risk for hypoglycemia
when do we prescribe insulin for diabetic patients? what is one of the key factors that is recognized in taking insulin?
when all else fails (tried mono therapy, two drug combinations and three drug combinations). key factor is weight gain.
what are the 3 classes of hypoglycemic agents that do not produce weight gain
- biguanides (metformin)
- DPP - 4 inhibitors
- GLP - 1 agonists
what is the trade name of metformin
glucophage
what is the indication for metformin
- diabetes mellitus type II
2. polycystic ovary syndroma (taken for infertility)
what is the MOA of metformin
Activates AMP activated protein kinase (AMPK) which in turn suppresses hepatic gluconeiogenesis and intestinal glucose absorption; increases insulin sensitivity.
what are AE of metformin
- headache
- metallic taste
- rash
what are serious AE of metformin
- lactic acidosis
2. megaloblastic anemia
which drugs/supplements increase blood sugar while taking metformin
fish oils and decongestants
while on metformin which drug/supplement causes a decrease in metformin
flaxseed
while on metformin, which drugs cause nephrotoxicity and induce lactic acidosis
- aminoglycosides
- amphotericin
- gancyclovir
- acyclovir
which drug masks hypoglycemia
beta blockers
T/F beta 2 causes gluconeogenesis and increased insulin relase
True
T/F alpha 2 causes decreased insulin release
true
which sulfonylureas have a greater potency…first generation or second generation?
second generation
what are the second generation sulfonylureas
- glipizide
2. glibenclamide
what is the indication for glipizide
DM type II
what is the MOA of glipizide
- stimulates pancreatic islet beta cell insulin release.
- actions involve binding to an ATP dependent K+ channel; blocked efflux leads to depolarization, Ca++ release and insulin vesicle effusion.
what are common AE of glipizide
- headache
- photosensitivity
- hypoglycemia
what are serious AE of glipizide
death
what are drug interactions of glipizide
- decongestants (antagonistic)
- steroids (antagonistic)
- flax seed oil (additive)
- fluoroquinolones (unpredictable)
- NSAIDS (prolonged effects)
T/F thiazolidinediones (TZD) are termed for their structural/molecular reference
True
what are the two TZDs
- Pioglitazone (actos)
2. Rosiglitazone (avandia)
what is the indication for pioglitazone
Diabetes mellitius type II
what is the MOA of Pioglitazone
A thiazolidinedione insulin sensitizer selectively stimulates nuclear receptor PPAR (peroxisome proliferator activated receptor) which increases insulin sensitivity in liver, skeletal muscle and adipose tissue.
when we talk about PPAR which subtype are we talking about?
gamma–> leads to transcription of certain substances that sensitize the body to insulin. Takes lipids out of circulation so that the body makes more use of the glucose.
what are common AE of pioglitazone
- fluid retention
- weight gain
- headache
- sinusitis
- pharyngitis
- dyspnea
what are serious AE of pioglitazone
- diabetic macular edema
2. bladder cancer
what are drug interactions of pioglitazone
- decongestants, corticosteroids, and sympathomimetics (antagonistic) –> dump sugar into bloodstream
- flaxseed (additive)
- beta blockers (mask hypoglycemia)
- azoles, trimethoprim (impaired metabolism)
which drug is a common DPP-4 inhibitor which does not cause weight gain
Sitagliptin
what is the MOA of sitagliptin
inhibits dipeptidyl peptidase 4, slowing incretin (GI hormones normally released during a meal) breakdown, increasing insulin synthesis/release, decreasing glucagon levels.
what are common AE of sitagliptin
headache
what are serious AE of sitagliptin
- renal failure
2. SJS
What is a common SGLT-2 inhibitor
Canagliflozin
what is the MOA of canagliflozin
inhibits sodium glucose cotransporter 2, reducing glucose reabsorption and increasing urinary glucose secretion.
what are common AE of canagliflizon
increased urination, thirst, and dehyrdation
what are serious AE of canagliflozin
- orthostatic hypotension
2. fractures, bone density loss–> we are losing calcium which is a key electrolyte responsible for bone mass.
Fluoroquinolones cause additive _____ while taken with canagliflozin
hypoglycemia
Dulaglutide is a _____ agonist which gets injected once a week for DM type II
GLP-1 agonist
what is the MOA of dulaglutide
activates glucagon like peptide-1 (GLP-1) receptor on beta cells, increasing insulin secretion, decreasing glucagon secretion, and delaying gastric emptying (incretin mimetic).
what are common AE of dulaglutide
tachycardia
what are serious AE of dulaglutide
- hypersensitivity
2. thyroid carcinoma
what are insulin based therapies that are long acting basal analogues
- insulin glargine (lantus) #6 highest selling drug in America!
- insulin detemir (levemir)
what are advantage of insulin
- universally effective
- unlimited efficacy
- decreased microvascular risk
What are disadvantage of insulin
- hypoglycemia
- weight gain
- mitogenicity: cell replication.
- injected
- training requirements
- “stigma”
what are the rapid acting insulin?
- lispro
- aspart
- glulisine
what are the intermediate acting insulin
NPH
what are the long acting insulin
- glargine
2. detemir
what is the MOA of insulin glargine
slow release, micro- crystalized rDNA insulin analog for stable day long blood sugar regulation to be used in post prandial combination with fast acting insulin.
what are common AE of insulin glargine
- hypoglycemia
- local lipo-dystrophy
- pruritus
- weight gain
- edema
when are you supposed to caution with use of insulin glargine
infection –> glucose is dumped into bloodstream, and blood becomes viscous. That viscosity impairs the mobility of immune cells that have been mobilized to fight the infection. So when a diabetic gets an infection and if they have poor blood sugar regulation, they will be more prone to complications from that infection due to high glucose in the bloodstream.
