chapter 57: drugs for DM Flashcards
the overall metabolic disturbances seen with diabetes is caused by what two things?
the lack of insulin and cellular insulin resistance
what is the hallmark sign of DM?
hyperglycemia
what two things characterize sustained hyperglycemia
impaired glucose uptake by the cells and increased glucose production
what is insulin released from
beta cells in the pancreas
what does the reaction of insulin stimulate?
the transport of glucose into the cells to be used for energy
where does glucagon come from?
alpha cells of the pancreas
what is glucagon an antagonist to
insulin
what does glucagon maintain
adequate glucose levels between meals
what does type 1 DM result from
an autoimmune disorder that destroys pancreatic beta cells
what type of onset does type one DM have
sudden
how do the glucose levels vary in type one DM
they have wide fluctuations
what are the classic clinical manifestations of type one DM
polyuria, polydipsia, polyphagia, weight loss.
what type of insulin do type 1 diabetics receive?
exogenous insulin
what is type II DM characterized by?
impaired insulin secretion and insulin resistance (desensitization)
what type of onset doest type II DM have
gradual onset
which type of diabetes has a more stable glucose levels
type 2
what type of factors are involved in the cause of type 2 DM
genetic and environmental factors
the amount of insulin required for type II DM declines due to what
increased workload of beta cells
most patients with type II diabetes are frequently what
obese
how long should you be NPO for a FPG test
8 hours
what is the normal FPG level
< 100 mg/dl
what is a prediabetic FPG level
100-125 mg/dl
what is a diabetic FPG level
> or equal to 126 mg/dl
what does a hemoglobin A1C provide information on?
long-term glycemic control
what is the goal for hemoglobin A1C
less than or 7%
what hemoglobin A1C is considered diagnostic
> or 6.5%
what is the principle stimulus of the secretion of insulin
elevated blood glucose levels
most of the body’s cells require insulin for what
to facilitate glucose entry into the cells
what is the exception of cells that need glucose entry?
cerebral cells
metabolic actions of insulin are what
anabolic
what 3 things promote the synthesis of complex molecules
CHO, amino acids, and lipids
what do CHO increase
glycogen storage
what are amino acids synthesized into
proteins
lipids are fatty acids that are incorporated into what
triglycerides
lack of insulin causes what type of effects
catabolic effects
what contributes to the s/sx of DM
favors breaking down complex molecules into their simpler forms
what is glycogen converted into
glucose
proteins are degraded into what
amino acids
fats are reduced to what two things
glycerol and free fatty acids
lack of insulin promotes hyperglycemia via what 3 mechanisms?
increased glycogenolysis, increased gluconeogensis, reduced glucose utilization
exogenous insulin mimics effects as what
endogenous insulin
what is the only effective treatment for type I DM
insulin
when is insulin required for a person with type II DM
when the person is unable to control disease with lifestyle changes and oral agents of needed during times of stress
what is insulin used to prevent or treat?
hyperglycemia induced by TPN or other medications
what three medications could induce hyperglycemia
loops, thiazides, corticosteroids
what electrolyte imbalance can insulin treat
hyperkalemia
why would you not want to give insulin orally
it is a protein and will be destroyed by gastric enzymes
what type of insulin can be given IV and mixed with other insulins
short duration insulins
what are examples of rapid acting, short duration insulins
lisper, aspart, glulisine
what are examples of slower acting short duration insulins
regular?
what is an example of an intermediate duration insulin
NPH
what kind of appearance does NPH have
cloudy
what is an example of a long duration insulin
Glargine U-100 and Deter
what type of insulin has no defined peak effect
long duration
what type of insulin is Glargine U-300 and Degludec
ultra long duration
what temperature should insulin be administered at
room temperature
what should you stress the importance of to people with DM
following a prescribed diet, exercise regimen and reducing stress levels
what is crucial to correlate for type I DM
timing of meals and administration of insulin
what is a loss of SQ fat and appears as slightly dimpling or pitting of SQ fat
atrophy?
what is caused by administering insulin that is too cold
atrophy
what is the accumulation of SQ fat at the injection site due to repeated used of the same insulin site
hypertrophy
what develops at peak insulin times during the night
somogyi effect
what is an early morning increase in BG levels
dawn phenomenon
what is dawn phenomenon usually associated with
release of GH
what will help differentiate between dawn and somogyi
monitoring 0200/0300 blood glucose levels
what is a decrease in BG levels between 0200-0300 to hypoglycemic levels
somogyi effect
what does the somogyi effect result in the release of
counter regulatory hormones (epi, cortisol)
what does the release of counter regulatory hormones cause
elevated BG levels in the morning
what is the blood glucose level for someone with hypoglycemia
< 70 mg/dL
what does a rapid fall in BG levels cause
SNS activation (tachycardia and sweating)
what does a gradual fall in BG levels cause
CNS organ (headache, confusion, drowsiness)
rapid treatment of hypoglycemia is crucial why?
to prevent irreversible brain damage or death
how can glucagon be administered
IV, SQ, or IM
what does glucagon promote?
the breakdown of glycogen to glucose
what does glucagon reduce?
the conversion of glucose to glycogen
how much complex carb should you administer to a pt when regaining consciousness
15gm
if patient is still hypoglycemic 15 minutes after administering 15gm of CHO what should you administer
another 15gm of complex CHO
what is used to treat type II diabetes
oral anti diabetic agents
what class is metformin
biguanides
what agent could metformin be used as
weight-neutral agent. could be used for weight loss
what is the MOA of metformin
sensitizes insulin receptors, decreases hepatic glucose production, and decreases intestinal glucose absorption
who is metformin the drug of choice for
newly diagnosed patients
biguianides rarely causes what
hypoglycemia
what is the serious ADR biguanides
lactic acidosis
what could metformin cause when given with contrast dye
renal failure
when should you discontinue metformin before a test?
48 hours before
what does metformin decrease the absorption of
vitamin B12 and folic acid
what is the prototype for sulfonylureas
glipizide
what is the MOA of glipizide
stimulates release of insulin from pancreas
what is the ADR for for glipizede
hypoglycemia
what type of reaction is produced when alcohol is consumed with glipizide
disulfiram like reaction (N/V, flushing)
what does glipizde stimulate
the release of ADH
what can the stimulate of ADH release
SIADH
what class is repaglinide
meglitinides
what is the MOA for repaglinide
stimulates the release of insulin from the pancreas
when should you take repaglinide in regards to meals?
< or 30 meals before a meal with EACH meal
what class is pioglitazone
Thiazolidinediones
what is the MOA of pioglitazone
decreases insulin resistance by stimulating receptors on skeletal muscle and adipose tissues–> reduced production of glucose by the liver
what are the ADRs for pioglitazone
renal retention of fluid, increased risk of pathological fractures, increases LDL, increases HDL, decreases triglycerides
what drug inhibits enzymes in the small intestine that is responsible for breaking down complex carbs
acarbose
what form does CHO have to be in to be absorbed
monosaccharide
what should you teach the patinet about with acarbose
oral glucose tablets should be used if hypoglycemia symptoms are experienced
what is the MOA of sitagliptin
enhances the actions of incretin hormones by preventing their enzymatic breakdown by DPP-4
what are incretin hormones released in response to
glucose elevations that occur after a meal to maintain normal glucose levels
what do incretin hormones suppress
post prandial release of glucagon
what is the MOA for SGLT-2 inhibitors
blocks the SGLT-2 transport system
what are ADRs of SLGT-2 inhibitors
UTI (glucose in urine) and increased diuresis (hypovolemia and dehydration)
what is the prototype for amylin mimetic
pramlintide
what is amylin co released with
insulin
who is pramlintide used in
patients not able to achieve glucose control with insulin alone- acts synergistically with insulin
how is pramlinitide administered
SQ
when is pramlinitide administered
immediately before a major meal
how many carbs must a meal contain to be able to receive pramlinitide
30g
