diabetes - non insulin Flashcards
what are the 6 types of non-insulin meds used to treat type 2 DM? (broad MOA, not class)
- sensitize body to insulin / control liver glucose production
- stimulate pancreas to make more insulin
- slow absorption of starches
- act on incretins
- manipulate glucose excretion by kidneys
- synthetic amylin
what are the 2 classes of drugs that sensitize the body to insulin and or control glucose production by the liver?
- biguanides - Metformin
2. glitazones (TZD) - pioglitazone
what is the prototype for biguanides?
metformin (Glucophage)
“BIGuanides [big guys] = MetFORMIN [four men]” important meds, know these
what is the MOA of metformin? (2)
- increases sensitivity to insulin / decreases insulin resistance
- decrease glucose production by liver
what is our DOC + 1st line therapy for tx of type 2 DM?
metformin
what are SE of metformin? (1 broad) + what is most common one?
GI effects
MOST COMMON = flatulence
“the farts of 4 men (formin)”
what is the rare AE of metformin? what patients do we often see this in?
lactic acidosis MEDICAL EMERGENCY
often in renal patients or liver disease
b/c of risk of lactic acidosis with metformin, what lifestyle education should we give these patients?
avoid ETOH excess!!!
what is the prototype for TZD/”glitazones”?
pioglitazone
what is the MOA of pioglitazone?
- decrease insulin resistance
2. decrease glucose production by liver
SE of pioglitazone (4)
there’s another card for more serious/AE
- URI
- sinusitis
- HA
- myalgias
= inflammation + pain
AE of pioglitazone (4)
- fluid retention (increased fluid reabsorption in kidneys)
- bladder cancer
- fractures (suppressed bone formation)
- unintended pregnancy (stimulates ovulation)
b/c of one of the AE of pioglitazone, this drug should be used cautiously in what population of patient?
HF patients or those at risk for fluid retention
when should metformin be given?
with meals
metformin puts people at risk for deficiencies of what? (2)
- B12
2. folic acid
describe the risk of hypoglycemia and metformin use…..
low risk of hypoglycemia when used as MONOtherapy
metformin therapy has a contraindication with what? why? what are the protocols?
this contraindication is not supported by current evidence, but may take time to reflect in clinical practice
IV contrast dye
can cause ARF –> leading to lactic acidosis
protocol: stop 1-2 days before IV contrast and 2 days after
what are the 2 classes of drugs that stimulate the pancreas to make more insulin?
- sulfonylureas
- meglitinides / “glinides”
“Secrete More, Please”
(Sulfonylureas Meglitinides Pancreas)
what is the prototype for sulfonylureas?
glipizide
what is the MOA of glipizide? (2)
- stimulates insulin release from the pancreas
2. increase sensitivity of insulin receptors
patients should have functioning _______ to use glipizide (based on MOA)
PANCREAS
must still be making insulin b/c this causes a release of insulin from islet cells
most common SE of glipizide
hypoglycemia
dose dependent
SE of glipizide (3)
- hypoglycemia
- weight gain
- antabuse effect w/ETOH “no SIPS with GLIPS”
what is prototype of meglitinides / “glinides”?
rePAglinide
stimulates PAncreas
what is MOA of repaglinide?
stimulate pancreas to release insulin
short duration + rapid onset - very similar to body
what is duration of repaglinide?
2-4 hrs
when should we give repaglinide?
with meal or 30 mins before
what is SE of repaglinide? (2)
- hypoglycemia**
2. weight gain
the sulfonylureas and meglitinides have 2 SE in common. what are they? (think of mechanism of action)
- hypoglycemia
2. weight gain
what drug class are drugs that slow the absorption of starches?
alpha-glucosidase inhibitors
what is the prototype for alpha-glucosidase inhibitors?
acarbose
“A Carb, OH!!!!”
what is MOA of acarbose?
blocks enzyme in gut that breaks down starches
SE of acarbose (2 - one is long term)
- GI (abd cramping, diarrhea, flatulence, borborygmus) often intolerable
- long term –> liver dysfxn (elevation in other enzyme that damages liver)
when should acarbose be taken?
w/ 1st bite of food
does acarbose cause hypoglycemia?
NO, not as monotherapy
if hypoglycemia develops from acarbose therapy, what does the patient need? what will NOT work?
patient needs oral glucose
sucrose won’t work b/c of how acarbose works
what are incretins?
hormones released by intestine following a meal when blood glucose is elevated –> tell pancreas to increase insulin secretion and liver to stop producing glucagon
what are the 2 drug classes that act on incretins?
- DPP-4 inhibitors “gliptins” (prevent the breakdown of incretins): sitagliptin
- GLP-1 receptor agonists (incretin mimetics): exenatide
what is the prototype for DPP 4 inhibitors / “gliptins”?
sitagliptin
what is MOA of sitagliptin?
enhance action of incretin hormones (for pts that can make insulin)
SE of sitagliptin (1)
cold symptoms
“SIT down, get some LIPTIN tea, you have a cold”
rare AE of sitagliptin (2)
- pancreatitis
2. hypersensitivity rxns
what is the prototype for incretin mimetics/ GLP-1 receptor agonists ?
exantide
“incretins EXIT from the GI”
what is MOA of exantide?
mimics actions of incretins (stimulate pancreas to release insulin)
what is dosing/admin of sitagliptin?
one pill daily w/or w/o food
what is dosing/admin of exantide?
subQ BID ; 30-60 mins BEFORE meal
you gotta go under the tide to swim (sub) and the tide goes out 2x/day + you should eat BEFORE so you have strength to swim
SE of exantide (1 - broad)
- GI
* working on pancreas / GI system = GI effects*
re: exantide and the GI side effects, what can we do to mitigate the nausea?
low fat diet ◡̈
rare AE of exenatide (2)
- pancreatitis
2. hypersensitivity rxns
exantide can cause hypoglycemia if combined with what drug class?
sulfonylureas
re: oral drugs and exantide, what should happen regarding administration?
give oral drugs 1 hr before injection b/c exantide slows gastric emptying (incretin)
what is the drug CLASS that mimics kidney excretion of glucose?
SGLT-2 inhibitors
“So much Glucoe is Leaving your Tubes”
canagliflozin
what is the prototype for SGLT-2 inhibitors?
canagliflozin
“So much Glucose Leaving your Tubes”
“your GLucose is FLOwin’ into the CAN”
what is MOA of canagliflozin?
increases glucose excretion through urine
SE of canagliflozin (4)
- UG fungal infections (b/c of increased glucose)
- UTI
- polyuria
- weight loss
canagliflozin puts patient at a risk of what (think what the MOA is…)
DEHYDRATION
“your GLucose is FLOwin’ into the CAN”
rare/serious AE of canagliflozin (3)
- DKA
- urosepsis
- pyelonephritis (kidney infection)
what is prototype for synthetic amylin / amylin mimetics?
pramlintide (Symlin)
“baby Amy Lin is in her little pram”
what is MOA of pramlintide? (3)
- delays gastric emptying
- suppresses glucagon secretion
- decrease post meal glucose elevations
what is admin (r/t food) / route for pramlintide? + interaction with oral meds?
subQ w/meals
give oral drugs 1 hr before pramlintide b/c of delayed gastric emptying
what type of DM is pramlintide used with?
both type 1 and type 2 DM
SE of pramlintide (2; 1 ONLY if used with another drug)
- nausea
2. hypoglycemia (only if used with insulin)
nursing protocols for hypoglycemia tx (5)
will be on order, but some general ideas
- start with least invasive 1st if can swallow and alert + oriented + are not NPO
- 120 mL oj, non diet soda, spoon of honey, candy, glucose tabs
- foods with protein to sustain
- IV 50% dextrose
- glucagon
