Diabetes Medication Flashcards
what fasting plasma glucose and HbAIC levels consistute
- pre-diabetes?
- diabetes?
- fasting plasma glucose
- prediabetes: 100-125
- diabetes: 126 +
- HbA1C:
- prediabetes: 5.7-6.4%
- diabetes: 6.5% +
what “random” blood sugar levels are indicative of
- pre-diabetes?
- diabetes?
how are these levels obtained?
- pre-diabetic = 140 mg/dL
- diabetic = 200 mg/dL +
measured by oral glucose tolerance test (OGTT)
the treatment target for diabetes is a HbA1c of?
< 7%
discuss the mechanism by which glucose stimulate insulin secretion
- glucose enters beta cells on pancreas via GLUT-2 transporters
- it is phosphorylated to G-1-P by glucokinase, which traps it in the cell
- enters the glycolitic pathway to become ATP
- elevation in ATP/ATP ratio blcks ATP-sensitive K+ channel, trapping K+ in the cell
- the cells depolarizes, which opens voltage gated Ca++ channels
- increased cytosolic Ca++ triggers exocytosis of insulin granules
once released, how does insulin induce gucose uptake?
by inducing translalocation of GLUT-4, the glucose receptor on adipose & muscle cells, to he membrane
insulin replacement therapy - includes
- what classes of drugs?
- what are the drugs in each class?
- in which formulation is each drug?
- what are the drugs in each class?
- when is each class used?
- short duration - used to manage postprandial (post-meal) glucose
-
rapid acting short duration:
- lispro / aspart - injected
- afrezza - inhaled
-
slower acting short duration
- human insulin
-
rapid acting short duration:
- long duration - used for basal control of glucose
- glargine - injected
glargine
- what kind of drug?
- how is it given?
- long duration insulin replacement
-
injected sub-Q
- given once daily - manages glucose for 24 hrs
what are the major adverse effects of insulin replacement use?
how are each of these AEs managed?
- insulin overdose - can cause
-
hypoglycemia
- tx:
- dextrose
- glucagon
- tx:
-
hypokalemia
- tx
- K+ supplements
- tx
-
hypoglycemia
- insufficient insulin - can cause
-
ketoatcidosis (d/t prolonged hyperglycemia)
- this can lead to coma/death
- tx
- inc insulin dose (monitor K+)
- water / Na+ replacement
-
ketoatcidosis (d/t prolonged hyperglycemia)
pramlintide
- what kind of drug?
- MOA?
- clinical uses?
- AEs?
- drug-drug interaction?
- is an amylin mimetic
- clinical uses: management of post-prandial glucose levels in of Type I &Type II diabetes
- MOA:
- delays gastric emptying
- suppresses glucagon secretion
- AEs
- nausea
- hypoglycemia
what are the ways of treating pre-diabetes?
what is the goal of treaing pre-diabetes?
goal is to prevent/delay entry into Type II diabetes
- treatments
- lifestyle
- weight (calorie restriction)
- exercise: aerobic and resistant training both improve insulikn sensitivity
- pharmaceutical
- metformin - is the best available choice, tho technically not FDA approved
- lifestyle
ideal diet for tx of type II diabetes
–Carbohydrates 60-70%
–Protein 15-20%
–Polyunsaturated fat 10%
–Saturated fat less than 10%
–Cholesterol- less than 300 mg/day
metformin
- MOA
- indications
- AEs/CIs
- drug-drug interactions
- MOA: suppresses gluconeogeneis
- indication:
- type 2 diabetes
- can be used for pre-diabetes, but not technically FDA approved
- AEs:
- common: GI - nausea/flutulence/diarrhea, subside over time
- rare: lactic acidosis
- CI: in pts with GRF < 30 mL/min
- drug-drug interactions:
- nephrotoxic contrast agents
- acarbose
which patients must temporarily discontinue metformin?
those needing imaging that requires nephrotoxic contrast agents
sulfonuyreas
- include what drugs?
- MOA?
- AEs?
- drug-drug interactions?
- tolbutamide, glyburide
- MOA:
-
induce insulin release:
- bind ATP sensitive K+ channels in beta cells –> membrane depolarizes –> Ca++ influx induces insulin release
-
induce insulin release:
- AEs:
- hypoglycemia
- drug-drug interactions
- ethanol - facial flushing
- beta-blockers: b-blockers blunt drug effects
repaglinide
- what kind of drug?
- MOA?
- AEs/CIs?
- drug drug interactions?
- a meglitide
- MOA:
-
induces insulin release:
- bind ATP sensitive K+ channels in beta cells –> membrane depolarizes –> Ca++ influx induces insulin release
-
induces insulin release:
- AE
- hypoglycemia
- drug-drug interactions:
- gemfibrozil (a trigclyeride lowering drug): is a potent CYP2C8 inhibitor, which metabolizes repaglinide