drug therapy for diabetes mellitus Flashcards
what is glucose
sugar in the blood, body primary energy source, brain almost exclusively. uses glucose for energy
what two major hormones stabilize glucose levels
glucagon and insulin
alpha cells secrete
glucagon, increase blood glucose levels
glucagon stimulates
the liver to convert some stored glycogen to glucose to use by the body
beta cells secrete
insulin, decrease blood glucose levels
glucagon is secreted with
low blood glucose; helps to maintain glucose between meals, works with insulin to maintain levels
glucose levels; between meals
decreased blood glucose -> into pancreas -> decreased insulin & increased glucagon secretion -> into liver -> release of stored glucose, breakdown of fat
glucose levels; after a meal
increased blood glucose -> into pancreas -> increased insulin secretion & decreased glucagon secretion -> into liver -> cellular uptake of glucose
insulin after a meal
pancreas recognizes rising glucose, secretes insulin to lower blood glucose; without insulin, glucose unable to enter cells
how does insulin act as transport to allow cells access to glucose
glucose can enter cells, cells store glucose as glycogen, converts lipids to fat, increase protein synthesis and stop glycogenesis
insulin helps to ______ glucose (blood sugar) when
lower blood sugar when levels are too high
hormones that can increase glucose
epinephrine, thyroid hormone(metabolism), growth hormone, glucocorticoids(steroids, promote glucose production in liver)
drugs that can increase glucose
phenytoin, beta blockers, NSAIDs, diuretics
drugs that can decrease glucose
alcohol, lithium, ACE inhibitors
what is diabetes mellitus
chronic metabolic disorder in which there is deficient insulin secretion or decrease sensitivity of insulin receptors resulting in hyperglycemia
classifications of DM
type I and type II
what is type I diabetes mellitus
common chronic disorder of childhood/ autoimmune disorder that destroys pancreatic beta cells difficult to control, sudden onset between ages 4-20, high incidence of complications and difficult to control, requires exogenous insulin administration
type I diabetes is dependent diabetes meaning
you have to administer insulin
what is type II DM
characterized by hyperglycemia and insulin resistance/ (beta cells are present and insulin present but unable to work), onset after age 40 years/ increasing prevalence among children and teens, gradual onset with less severe symptoms, 90% of people with diabetes have type 2
risk factors for development of type II DM
obesity, sedentary lifestyle, presence of metabolic syndrome, ethnicities (African American & hispanics)
metabolic syndrome r/t diabetes
abdominal obesity low HDL, hypertriglyceridemia, hypertension and/or impaired fasting glucose
s/sx of hyperglycemia (diabetes): fasting blood glucose levels greater than 126 mg/dL
polyuria, polyphagia (extremely hungry), polydipsia(extremely thirsty), glycosuria (kidneys clearing extra glucose), weight loss (bc of metabolic changes), fatigue
chronic complications of untreated DM
macrovascular and microvascular
what is macrovascular (big vessels)
HTN, MI, stroke, peripheral vascular disease (PVD)
what is microvascular (little vessels)
nephropathy (damage to kidneys), retinopathy (in eyes/ go blind), neuropathy (damage to nerve in PNS -> complete loss of sensation in extremities)
diabetes high risk to extremities
Peripheral vascular disease results from narrowing of blood vessels increasing the risk for reduced or lack of blood flow in legs. Feet wounds are likely to heal slowly contributing to gangrene(death of body tissue due to lack of blood flow) and other complications
acute complications of diabetes
diabetic ketoacidosis (DKA), hyperosmolar hyperglycemic nonketotic coma (HHNC)
what is diabetic ketoacidosis
life threatening, severe insulin deficiency, usually type I/ fat broken down for energy, results in ketones -> ketones reproduce faster than needed which cause a drop in pH (acidosis), usually type 1
symptoms of diabetic ketoacidosis
fruity odor to breath, ketones, kussmauls respirations(deep breathing), severe hyperglycemia (> 240), polyuria, polydipsia, N/V, coma
how to treat diabetic ketoacidosis
give a lot of IV fluids (flush out extra glucose and flush out some of the acid that’s making our blood so acidic), & give insulin (body can use those cells and reverse DKA)
what is hyperosmolar hyperglycemic nonketotic coma (HHNC)
life threatening, severe hyperglycemia, usually type 2; excessive glucose and electrolytes, severe dehydration
symptoms of hyperosmolar hyperglycemic nonketotic coma
extremely high glucose >600, polyuria, dehydration, drowsiness, confusion, coma
treatment for hyperosmolar hyperglycemic nonketotic coma
give lots of fluid, give insulin to bring down blood sugar
when to check blood sugar
before meals and at bedtime, if eating
abnormal fasting glucose number
> 126
diabetic AC (before meal, in morning) blood sugar goal
70-130
when to check blood sugar if NPO, or tube feeding or TPN
check every 6 hours
what is hemoglobin A1C
measure average blood glucose over a 3 month period, normal is < 7%
T or F. diabetes mellitus is a chronic, systemic disease characterized only by metabolic abnormalities
False; diabetes mellitus is a chronic, systemic disease characterized by a metabolic AND VASCULAR abnormalities. While a major clinical manifestation of DM is hyperglycemia, vacuum problems include atherosclerosis throughout the body, which results in HTN, MI, stroke and PVD
T or F. insulin is a hormone secreted by beta cells in the pancreas
true. insulin is a hormone secreted by beta cells in the pancreas that allows rapid entry of glucose into cells
signs of hyper-glycemia
Three P’s (polyuria, polyphagia, polydipsia), fatigue, weakness, dry skin (hot & dry= sugar high)
signs of hypo-gylcemia
sweating, tremors, tachycardia, hunger, confusion, drowsiness, seizures (cold & clammy= need some candy)
drug therapy for diabetes
control glucose levels and prevent complications
treatments for type 1 DM
insulin
treatment for type 2 DM; work in different parts of the body
sulfonylures, alpha glucosidase inhibitors, biguanide, thiazolidines, meglitinides, DDP 4 inhibitors, amylin analogs, incretin mimetics, SGLT2 inhibitors
what is insulin
human product; synthetic product is identical to endogenous insulin, synthesized in laboratories by altering the type or sequence of amnio acids
administration of insulin
CANNOT be given orally; most give subQ, regular can be IV; U-100 concentration in U.S. (100units/mL), orange tipped syringe or pen
rapid acting
lisper, aspart; rapid onset, shorter duration of action than regular (Onset: 15-30 min, P: 30min-2.5hr, D: 3-6hr)
short acting
regular; short onset, short duration of action (onset: 30-60 min, P: 1-5 hr, D: 6-10hr)
intermediate acting
NPH; slower absorption, prolonged action (onset: 1-2hr, P: 4-12hr, D: 16hr)
long acting
glargine, detemir; provide basal insulin over 24 hr period (Onset: 3-4 hr, P: continuous, D: 24hr)
ultra long acting
degludec; provide basal insulin over 42 hr period
mechanism of action for insulin
increased glucose uptake by cells, decreased glucose production by liver
uses of insulin
lower blood glucose, Renault may be given IM or IV in an emergency, can be used in children and older adults
contraindication of insulin
if they are hypoglycemia
timing insulin with meal
lispro (rapid): 15-30 mins before a meal, regular (short): 30-60 mins before a meal
adverse effects of insulin
hypoglycemia, local reactions, so you want to rotate sites
drug-drug interactions with insulin
any drug that affect glucose levels; beta blockers, MAOIs, NSAIDs, salicylates, alcohol, herbal preparations
nursing implications for insulin
be aware of mealtimes, rotate injection site (the abdomen is the best), monitor for hypoglycemia during sleep, insulin pumps (regular or rapid acting), considered a high risk medication (know policy)
programmed insulin order
given to regulate level between meals, set amount ordered, watch nutrition status, make sure patient is eating; if NPO do not give programmed insulin
example of programmed insulin order
5 units lispro subQ TID AC (with meals). Hold of BS <70
sliding scale insulin order (SSI)
dosing based on blood sugar level, notify MD if NPO
patient teaching about insulin
diet, weight control, exercise; know s/sx; teach family what to do; test BS as ordered; what to do if you’re sick; proper subQ injection technique; follow up appts
insulin SICK mimetic
S:sugar, I:insulin, C:carbs, K:ketones
T or F. insulin plays a major role primarily in the metabolism of carbohydrates
false; insulin plays a major role in metabolism of CARBOHYDRATE, FAT, and PROTEIN where the nutrients are broken down into simpler molecules (glucose, lipids, and amino acids)
for type 2: sulfonylureas; example med
glyburide
what does sulfonylureas do
stimulate pancreas to release insulin; bind to K+ channels on pancreatic beta cells, increase number of insulin receptors
what is sulfonylureas used for
injections for elevated serum glucose, must have some functioning pancreatic beta cell
adverse effects of sulfonylureas
hypoglycemia
contraindications for sulfonylureas
sulfa allergy, renal failure, liver failure
drug-drug interactions for sulfonylureas
beta blocker, alcohol
type 2: alpha glucosidase inhibitors example med
acarbose
what are alpha glucosidase inhibitors
delays digestion of complex carbohydrates; decrease the increase in blood sugar after meals, given in combo with sulfonylurea
uses for indications for alpha glucosidase inhibitors
decrease in postprandial glucose
adverse effects of alpha glucosidase inhibitors
hypoglycemia, GI upset
contraindications for alpha glucosidase inhibitors
hepatic disease, IBS
drug-drug interactions for alpha glucosidase inhibitors
can decrease digoxin levels
nursing implications for alpha glucosidase inhibitors
take at beginning of meal
type 2 biguanodes example med
metformin
what are biguanodes
decrease hepatic glucose production, increases use of glucose by muscle and fat cells, decreased intestinal absorption of glucose
uses for biguanodes
insulin resistance; commonly first choice for type 2 DM, used to treat PCOS
adverse effects for biguanodes
lactic acidosis, GI upset
contraindications for biguanodes
BLACK BOX warning to avoid over 80 year old, renal failure, ***hold metformin 48hrs before and after contrast media (CT dye, heart cath), testing to avoid renal failure
nursing implications for biguanodes
take with meals, increased effects if taken with furosemide, digoxin, vancomycin; monitor renal function
type 2 thiazolidinediones (TZDs) example med
rosiglitaxone
what are thiazolidinediones (TZDs)
stimulates insulin receptors on muscle, fat, and liver cells
uses for thiazolidinediones (TZDs)
insulin resistance; used in combo with insulin, sulfonylureas or biguanides
adverse effects of thiazolidinediones (TZDs)
hepatotoxicity, CHF, weight gain
contradictions of thiazolidinediones (TZDs)
liver disease, CV disease ***BLACK BOX warning of risk for CHF and MI
nursing implications for thiazolidinediones (TZDs)
take with meals, monitor liver functions, monitor pts for signs of HF, gemfibrozil may increase effects, may take 12 weeks to reach peak effects
type 2 meglitinides example med
repaglinide
what are meglitinides
stimulates pancreatic stimulation of insulin (need working beta cells)
uses for meglitinides
elevated serum glucose, used in combo with TZDs or biguanide
adverse effects of meglitinides
hypoglycemia less so than sulfonylureas, GI upset
contraindications for meglitinides
renal disease, liver disease, type 1 DM
nursing implications for meglitinides
take before meals (if meal skipped, skip dose; if meal added, add dose), gemfibrozil and itraconazole increase effects
type 2 dipeptidyl peptidase 4 inhibitors (DPP-4) example med
sitagliptin
what are dipeptidyl peptidase 4 inhibitors (DPP-4)
balance the release of insulin and limit the release of additional glucose from the liver, inhibition of glucagon secretion, delayed gastric emptying, and induction of satiety (need working beta cells)
uses for dipeptidyl peptidase 4 inhibitors (DPP-4)
elevated serum glucose, used in combo with TZDs or biguanide
adverse effects of dipeptidyl peptidase 4 inhibitors (DPP-4)
upper resp tract infections, heart failure
contraindications for dipeptidyl peptidase 4 inhibitors (DPP-4)
type 1 Dm, insulin use, renal failure
nursing implications for dipeptidyl peptidase 4 inhibitors (DPP-4)
one daily with or with out meal
type 2 amylin analogs example med
pramlintide
what are amylin analogs
suppresses postprandial glucagon secretion, increases sense of satiety
uses for amylin analogs
regulate the postprandial rise in blood glucose, used in addition to insulin, sulfonylureas or biguanides
adverse effects of amylin analogs
hypoglycemia ***BLACK BOX warning for severe hypoglycemia if mixed with insulin
nursing implications for amylin analogs
monitor blood sugars closely, avoid giving with anticholinergics, may promote weight loss, subQ injection before meals
type 2 incretin mimetics example med
exenatide
what are incretin mimetics
stimulates the pancreas to secrete the right amount of insulin based on the food that was just given
uses for incretin mimetics
postprandial glucose elevations, used in combo with oral medications
adverse effects of incretin mimetics
hypoglycemia, GI distress and nausea, pancreatitis
contraindications for incretin mimetics
liver disease, ***BLACK BOX warning for risk of thyroid cancer
nursing implications for incretin mimetics
subQ injection within 1 hour of breakfast and diner, must be refrigerated, some ER versions available (dulaglutide) only need 1/weekly injection, may promote weight loss
type 2 sodium glucose contransporter 2 inhibitors (SGLT2) example med
canaglifozin
what are sodium glucose contransporter 2 inhibitors (SGLT2)
blocks reabsorption of glucose In the kidney, promotes excretion of glucose in urine
uses of sodium glucose contransporter 2 inhibitors (SGLT2)
improved glucose control, used in combo with other anti-diabetics
adverse effects of sodium glucose contransporter 2 inhibitors (SGLT2)
dehydration, hypotension, electrolyte imbalance, bone loss, increased risk of leg/foot amputations
contraindications for sodium glucose contransporter 2 inhibitors (SGLT2)
renal failure
nursing implications for sodium glucose contransporter 2 inhibitors (SGLT2)
take with first meal of day, use caution in combo with meds that decrease BP, risk for dehydration or syncope
general patient education about diabetes
consistent diet and exercise = best control; maintain normal weight; unopened bottles of insulin stored in fridge; know s/sx and what to do; teach family; maintain BS to prevent complications; follow up appts; don’t start new meds/herbs with put telling MD; alert MD if BS is >250
patient education on hyperglycemia management: seek MD if
BS > 250, ketones in urine, fever above 101, vomiting & diarrhea, miss multi doses of a med
patient education on hypoglycemia management
rapidly absorbed sugar (10-20mins), if patient is alert (4oz of juice/soda, 1 tube glucose gel, 2-3 glucose tabs), if patient is unable to swallow (dextrose 50% half ampule, glucagon IM/SQ), avoid taking so much sugar that you cause hyperglycemia
managing diabetes on sick days
illness can cause stress response and increase bS, continue to take anti-diabetic meds, test for ketones in urine, check glucose at least 4x daily, if unable to continue liquids (15g carbs every 1-2 hrs, gatorade, drink 2-3 quarts of fluids, water)
a patient with type 2 DM is scheduled for a heart catheterization in 1 week. The nurse instructs the patient to stop taking which med 2 days before the procedure
metformin; biguanides like metformin can cause kidney failure if given 48 hrs before or after receiving contrast dye
