Antidiabetic Medications Flashcards
Which type of diabetes are oral antihyperglycemics commonly used?
for type 2 diabetes
7 types of antihyperglycemic?
biguanides
sulfonylureas
glinides
thiazolidinediones (glitazones)
a- glucose inhibitors
dipeptidyl- peptidase 4 inhibitors (DPP 4 inhibitors)
sodium-glucose cotransporter 2 inhibitor
Type 2 diabetes pathophysiology (2)
2 common treatment
insulin resistance
reduction in B cells
Treatment: lifestyle modification and oral hypoglycemics
lifestyle changes first before drug therapy (smoking cessation, diet, exercise)
Combination therapy is recommended if A1C exceeds?
What is Combination Therapy?
9 %
Two drugs from different classes
What is the A1C target?
less than 7 %
Effective treatment of TYPE 2 involves several elements: (4)
Lifestyle changes
Careful monitoring of blood glucose levels even if in oral medications
Therapy with one or more drugs
Treatment of associated comorbid conditions such as high cholesterol and high blood pressure
New-onset TYPE 2 diabetes treatment
Lifestyle interventions 1st
Oral biguanide lifestyle changes not effective
If lifestyle modifications and the maximum tolerated metformin dose do not achieve the recommended A1c goals after 3 to 6 months, additional treatment should be given with ______________ and ___________ or ______________.
dipeptidyl peptidase4 (DPP-4) inhibitors
glucagonlike peptide 1 (GLP-1) receptor agonists
Insulin
Insulin and oral hyper glycemic results in (2)
what 2 types of insulin?
better glycemic control
weight loss
intermediate or long acting
Diabetes Canada 2018 recommends
A1C of new-onset type 2 diabetes
treatments 2
new-onset type 2 diabetes with an A1C of less than 7 % be treated with lifestyle modifications for 2 to 3 months
ADD biguanides (metformin) if lifestyle changes not effective
Biguanides
-drug name
-what kind of therapy
-BMI use
metformin
first line drug therapy, BMI over 25
Biguanides mechanism of actions 5
Decrease GLUCOSE PRODUCTION in the liver
Decrease INTESTINAL ABSORPTION of GLUCOSE
Decrease liver production of triglycerides & cholesterol
IMPROVE INSULIN RECEPTOR SENSITIVITY- so more insulin can go into the cell
Improves glucose uptake by skeletal muscle, adipose and liver
Biguanides Does not increase insulin secretion from the pancreas and therefore does not cause ________
Biguanides do not cause _____ and _______ because it does not stimulate _______________
Does not increase insulin secretion from the pancreas and therefore does not cause hypoglycemia
Biguanides do not cause weight gain and hypoglycemia because it does NOT stimulate insulin production
Biguanides may be used in combination with ______, _______, and ________ when lifestyle measures are not successful
May be used in combination with
sulfonylureas
thiazolidinediones
incretin mimetics
when monotherapy & lifestyle measures are not successful
Biguanides adverse effects
Abdominal bloating, nausea, cramping, a feeling of fullness, and diarrhea (GI)
Metallic taste, hypoglycemia,
reduction in vitamin B12 levels after long-term use
Lactic acidosis is an extremely rare complication.
Biguanides indications
Initial oral drug, cause weight loss
Biguanides contraindications
include medications
kidney disease (creatinine <30 ml/min)
- metformin is excreted by kidneys and can accumulate if not eliminated, which can cause LACTIC ACIDOSIS
FUROSEMIDE
NIFEDIPINE (antihypertensives)
CIMETIDINE
DIGOXIN
(they can increase concentration)
Biguanides Interaction
IODINE BASED DYE
IODINATED RADIOLOGICAL CONTRAST which can cause KIDNEY INJURY and lactic acidosis
Discontinue _______ the day of the test and _____ after undergoing radiological study that requires radioactive iodine-based dye
This may lead to _____ and ______
Discontinue BIGUANIDES the day of the test and 48 HOURS after undergoing RADIOLOGICAL study that requires radioactive IODINE based DYE
This may leads to acute KIDNEY injury and LACTIC acidosis
What are 6 symptoms of lactic acidosis?
hyperventilation, cold and clammy skin, muscle pain, abd pain, irregular HR, dizziness
1 drug of Sulfonylureas
GLIclazide (important)
GLYburide
GLImepiride
What does Sulfonylureas need to work?
functioning B cells in the pancreas for sulfonylureas to be effective
Sulfonylureas is not used for?
why?
Type 1 because they do not have functioning B cells
Sulfonylureas mechanism of actions
bind to RECEPTORS on B cells in the pancreas to stimulate insulin
enhance the action of insulin in the liver, adipose and muscle
decrease glucagon secretion
Sulfonylureas is used as
a second-generation drug- used after the first line (second line for those A1C remains high after metformin)
oldest antihypergylcemic
Sulfonylureas adverse effects
hypoglycemia, weight gain, skin rash, nausea, epigastric fullness, and heartburn
WHAT to do if CBG is less than 4 mmol/L?
Hold insulin and oral antihyperglycemic drugs
Once insulin is started, _____ is stopped
Sulfonyureas
Sulfonyureas contraindications
ALCOHOL (induced vomiting and hypertension)
NPO
allergy to sulfonamide abx
Not used in pregnancy- only give insulin
severe liver and kidney disease
Sulfonyureas - Gliclazide
-onset
-duration
- interactions
rapid onset, short duration
Increased effect of hypoglycemia:
ALCOHOL*, anabolic steroids, β blockers, chloramphenicol (abx- meningitis), MAOI’s, oral anticoagulants, sulfonamides, garlic, ginseng
Decreased effect:
Adrenergics, corticosteroids, thiazides, thyroid drugs
Sulfonyureas - Gliclazide mechanism of action
stimulate pancreas to secrete insulin
transport excess glucose from blood to cells of muscle, liver, and adipose
has antiplatelet and antioxidant properties
Give Gliclazide- sulfonylureas immediate release
30 minutes before meals
1 medication of Glinides
Repaglinide
Glinides mechanism of actions
increase insulin secretion in the pancreas
Similar with sulfonylureas
Glinides duration of action?
when to give?
much shorter duration of action
give with meals
Glinides are useful for diabetics who have?
postprandial glucose levels and low insulin levels
Glinides cannot be combined with?
WHY?
sulfonylureas because of their similar mechanism of action
Glinides indications:
do not give (2)
diabetics with postprandial glucose levels
DO NOT give without meals
DO NOT GIVE with sulfonylureas
Thiazolidinediones: Glitazones
mechanism of actions
1 drug
Insulin sensitizing; enhance receptor sensitivity
* enhancing insulin receptor sensitivity > decrease insulin resistance
stimulate glucose uptake and storage
inhibit glucose and triglyceride production in liver
affects gene regulation
preservation of B cell function- slow disease progression
pioglitazone
Thiazolidinediones: Glitazones onset
slow onset up to months
1 drug of Thiazolidinediones
Reserved for pt who cannot tolerate or achieve gLucose control with metformin or sulfonylureas. WHY?
pioglitazone
due to cost, adverse effect, slow onset
Thiazolidinediones: Glitazones
Contraindications?
Heart disease- can worsen heart failure
Kidney/ liver disease
Thiazolidinediones adverse effects
peripheral edema
weight gain- water retention and increased adipose tissue
decrease bone density; increase risk for fracture
Thiazolidinediones: Glitazones interactions
erythromycin
ketoconazole
increases concentration
1 drug of Dipeptidyl peptidase 4 (DPP-4) Inhibitors
sitagliptin - Januvia
incretin hormones
increase insulin synthesis and decrease glucagon secretion
released throughout the day, after a meal
stimulate insulin secretion
reduce postprandial glucose production
slow gastric emptying
increase satiety
DPP-4 enzymes
metabolize incretin hormones which results in increased glucose
Dipeptidyl peptidase 4 (DPP-4) Inhibitors mechanism of action
Delay breakdown of incretin hormone by inhibiting enzyme DPP-4
increase insulin secretion
lower glucagon secretion
Dipeptidyl peptidase 4 (DPP-4) Inhibitors can be combined with?
metformin
Dipeptidyl peptidase 4 (DPP-4) Inhibitors indicators
adjunct to changes in diet and exercise habits to increase glycemic control
Dipeptidyl peptidase 4 (DPP-4) Inhibitors adverse effects
upper respiratory tract infection
headache
dizziness
hypopglycemia
Dipeptidyl peptidase 4 (DPP-4) Inhibitors contraindication
digoxin- increase levels
sulfonylureas
insulin
CYP3A4 inducers- carbamazepine, dexamethasone, phenobarbital, phenytoin, rifampin)
Sodium Glucose Cotransporter 2 Inhibitors: mechanism of actions
A decrease in blood glucose caused by an increase in RENAL GLUCOSE EXCRETION
Action: work independently of insulin to prevent glucose reabsorption from the glomerular filtrate, resulting in a reduced renal threshold for glucose and glycosuria
Other effects: may increase insulin sensitivity and glucose uptake in the muscle cells and decrease gluconeogenesis (use of glucose)
Results: improved glycemic control, weight loss, and a low risk of hypoglycemia
1 medication of Sodium Glucose Cotransporter 2 Inhibitors
canaglifozin (Invokana®), dapaglifozin (Forxiga®) > osmotic diuresis > intravascular volume depletion
a new class (2014) of oral drugs for the treatment of type 2 diabetes.
Sodium Glucose Cotransporter 2 Inhibitors: ADVERSE effects
vaginal yeast infections and UTIs due to increase glucose in those areas
Sodium Glucose Cotransporter 2 Inhibitors
What is the sodium-glucose cotransporter?
Inhibiting it results in?
inhibits sodium-glucose cotransporter (which is a protein that facilitates 90% of glucose reabsorption in kidneys)
reduce glucose
kidney glucose excretion is increased
Sodium Glucose Cotransporter 2 Inhibitors contraindication
interactions
Type 1 diabetes
DKA
kidney disease
digoxin, insulin (decrease efficacy)
What level is considered as Hypoglycemia?
Abnormally low blood glucose level (below 4 mmol/L)
HYPOGLYCEMIA: Mild cases can be treated with ____
Higher intake of ______ and lower intake of ______ to prevent rebound postprandial hypoglycemia
diet
high intake of protein and lower carbohydrates
Hypoglycemia Symptoms
Adrenergic: 5
CNS: 8
LATER SIGNS: 4
Adrenergic:
Anxiety, tremors, sensation of hunger, PALPITATIONS (fast), sweating
Central nervous system:
Difficulty concentrating, confusion, weakness, drowsiness, vision changes, difficulty speaking, dizziness and headache
Later signs:
HYPOTHERMIA (cold), seizures
Coma and death will occur if not treated
Glucagon
Concentrated glucose
IV glucose
Define Diazoxide
increase glucose; a natural hormone (can be given by injection)
Rapidly dissolving buccal tablets given and semisolid gels for oral use; better than regular sugar
Intravenous glucose solutions up to 50% D50W (IV from of glucagon)- hospital setting; severe hypoglycemia
Diazoxide: useful for long-term illness such as pancreatic cancer (oral)
Glucagon examples
4 glucose tabs
3 pack sugar
8 lifesavers
175ml softdrink
15 ml honey
2.1 mmol/L increase within 20 minutes
Glucose gels
must be swallowed; only 1 mmol/L increase at 20 minutes
Retest glucose __ minutes after glucose administration
Treat until CBG is above?
15 mins
4mmol/L
Continuous SC insulin infusion (CSII)
type 1 DM
CSII and Basal bolus regimen > intensive diabetes management
continuous delivery of basal insulin- rapid and consistent
achieve glucose and A1C levels that are lower than those with BBR therapy alone> decreases risk for hypoglycemia
Basal bolus regimen
insulin type combination?
long acting
rapid acting
DO not shake NPH insulin instead?
roll between hands
do not shake
rotate sites
Before giving drugs that alter glucose levels, obtain and document:
A thorough history
Vital signs
Blood glucose levels, HbA1c level
Potential complications and drug interactions
When to administer insulin?
Give if the tray arrives on the unit
Before giving drugs that alter glucose levels:
Assess the patient’s ability to consume food. (swallowing)
Assess for nausea or vomiting.
Hypoglycemia may be a problem if antidiabetic drugs are given and the patient does not eat.
If a patient is to take nothing by mouth (NPO) for a test or procedure, consult the primary care provider to clarify orders for antidiabetic drug therapy.
Overall concerns for any patient with diabetes increase when the patient is at risk for
Is under stress
Is pregnant or lactating
Has an infection
Has an illness or trauma
Nursing consideration highlights
Blood glucose monitoring (CBG & A1C)
Proper injection techniques for insulin or continuous pump therapy (mimics pancreas response to insulin)
Emphasize non-pharm: weight & dietary management, exercise, foot care(damage to BVs/ nerves- PVD, results in loss of sensation, nor enough BF- decreased healing), eye care
Use of medic alert bracelet
Keep a hypoglycemic kit on hand
Oral hypoglycemics may cause photosensitivity
A drug that can increase BG?
Corticosteroids- suppress the immune system, anti-inflammatory
hyperglycemia breath smell
acetone smelling breath
Thorough patient education is essential regarding:
Disease process
Diet and exercise recommendations
Self-administration of insulin or oral drugs
Potential complications
When insulin is ordered, ensure:
Correct drug
Correct route
Correct type of insulin
Correct dosage
Insulin order and prepared dosages are second-checked with another registered nurse (or per agency policy).
When giving insulin
Check blood glucose level before giving insulin.
To mix suspensions, roll vials between hands instead of shaking them.
Ensure correct storage of insulin vials.
Only use insulin syringes, calibrated in units, to measure and give insulin.
Ensure correct timing of insulin dose with meals.
Provide thorough patient education regarding self-administration of insulin injections, including timing of doses, monitoring of blood glucose levels, and injection site rotations.
Which kind of insulin should you draw up first
CLEAR insulin (REGULAR/ RAPID) first then cloudy insulin (INTERMEDIATE)
When drawing up two types of insulin in one syringe, always withdraw the regular or rapid-acting (clear) insulin first.
Oral antidiabetic drugs nursing implications
Always check blood glucose levels before administering.
Usually given 30 minutes before meals
α-Glucosidase inhibitors are given with
the first bite of each main meal.
Metformin is taken with
Metformin will need to be discontinued if the patient is to undergo studies with________ because of possible renal effects; check with the prescriber.
meals to reduce gastrointestinal effects.
contrast dye
Nursing Implications
Assess for signs of hypoglycemia.
Administer oral form of glucose if the patient is conscious.
Give the patient glucose tablets, liquid, or gel; corn syrup; honey; fruit juice or nondiet soft drink; or have the patient eat a small snack, such as crackers or a half sandwich
Deliver ____ or ____ glucagon if the patient is unconscious.
Deliver D50W or IV glucagon if the patient is unconscious.
Monitor therapeutic response.
Decrease in blood glucose levels to the level prescribed by physician
Measure HbA1c to monitor long-term compliance with diet and drug therapy.
Watch for and monitor hypoglycemia and hyperglycemia.
Hyperglycemia a fasting glucose of?
non fasting glucose of?
7 mmol/L or higher
or non-fasting glucose of 11.1 mmol/L or higher
The current key diagnostic criterion for diabetes
glucose level
and A1C level
is hyperglycemia with a fasting plasma glucose of higher than
7 mmol/L or a hemoglobin
A1C level greater than or equal to
6.5%.
An A1C level of ___% is the threshold for the development
of microvascular disease and a predictor for the development of
macrovascular disease
6.5 %
Define diabetes and 2 types
Often regarded as a syndrome rather than a disease
disorder of carbohydrate metabolism
Type 1 and 2
Normal CBG
4 to 7 mmol/L as per brenda
4 to 6 in book
Pancreas> ductless endocrine
secrete hormones into the bloodstream> insulin and glucagon for homeostasis
Glucose
energy for cells
simplest from of carbs is dextrose
Glycogen
stored excess glucose in liver, muscles, and adipose
Glycogenolysis
glycogen in liver converted back to glucose
Hormone GLUCAGON
released from a-cells of the islet of Langerhans in the pancreas
stimulate glycogen back to glucose
INSULIN
created by?
metabolic functions?
what does it store in the liver?
explain fat metabolism
stimulates _____ synthesis
from B-cells
metabolic functions: stimulate carbohydrate metabolism (glucose into cells)
In the liver> insulin converts glucose to glycogen
Fat metabolism (lipogenesis > inhibit lipolysis and release of fatty acids from adipose cells)
Stimulate protein synthesis
What would happen if there is no INSULIN?
Kidney?
Energy source?
Increased PG
Kidneys unable to reabsorb excess glucose and they would excrete large amounts of glucose and ketones into urine
Loss of energy source which leads to polyphagia, weight loss and malnutrition
presence of glucose in kidney > draws large amount of water into urine > osmotic diuresis > leads to polyuria, polydipsia, dehydration
polyuria
polydipsia
increased urination
increased thirst
Hypergycemia
excessive concentrations of glucose in the blood
Hyperglycemia diagnostic criteria
fasting
A1C
fasting- 7 mmol/L or higher
A1C- greater than/ equal to 6.5 %
diabetes pathophysiology
deficiency of insulin: lack of insulin > destruction of B cells in pancreas> inability to produce insulin
defect in insulin receptors: resistance to insulin
or both
2 types of hyperglycemia complications
macrovascular- secondary to large vessel damage, caused by deposition of atherosclerotic plaque, impairs central and peripheral
microvascular- secondary to capillary vessels, impairs peripheral circulation
autonomic/ somatic nerve damage- comprised circulation
glycoproteins define?
when insulin receptors become defective, they no longer respond to insulin, what happens to glucose?
insulin receptors
when insulin receptors become defective, they no longer respond to insulin> and glucose remains in the blood rather than kept in cells
Type 1 diabetes
2 effects on insulin
And why?
lack of insulin production
OR
production of defective insulin
due to the destruction of B cells (insulin-producing cells)- leads to lack of endogenous insulin by pancreas
Type 1 requires ____ for treatment
2 complications
needs exogenous insulin to decrease CBG
Complications:
Diabetic ketoacidosis- extreme hyperglycemia, ketones, acidosis, electrolyte imbalance [younger than 65, insulin required]
Hyperosmolar hyperglycemic state- extreme hyperglycemia [34 mmol/L, 65 yr or older, insulin not required in most cases, more than 5 days]
Fewer than 10% of all cases are type 1.
DKA
elevated glucose and no insulin to allow glucose to be used for energy production= body may break fatty acids for fuel and produce ketones
treatment- fluids, electrolytes, IV therapy
Type 2
2 effects on insulin
most common; genetic and environmental factors
Caused by insulin deficiency and insulin resistance
insulin resistance; insulin receptors are reduced and has decreased sensitivity to insulin (people can have normal insulin but has high BG)
insulin deficiency (reduced insulin secretion due to loss of normal response of B cells to increased glucose, when B cells do not recognize glucose, they do not secrete insulin > decreased response of insulin receptors
Many tissues are resistant to insulin.
Reduced number of insulin receptors
Insulin receptors less responsive
Insulin (hormone) actions in the body 3
facilitates the uptake of glucose so it can be used as an energy source
facilitates the transfer of glucose into cells
glucose to glycogen
Diabetes symptoms?
fasting glucose of _____
A1C of _____
Polyuria
Polydipsia
Polyphagia- excess hunger
Glycosuria
Weight loss
Fatigue
Blurred vision
Elevated fasting blood glucose (higher than 7 mmol/L) or a hemoglobin A1c (HbA1c) level greater than or equal to 6.5%
Several comorbid (associated with a disease) conditions
The comorbidities are reffered to as?
Obesity
Coronary heart disease
Dyslipidemia- high cholesterolol
Hypertension
Microalbuminemia (protein in the urine)
Increased risk for thrombotic (blood clotting) events
These comorbidities are collectively referred to as metabolic syndrome or cardiometabolic syndrome.
Gestational Diabetes
Define
Treatment
Hyperglycemia that develops during pregnancy
Insulin must be given to prevent birth defects (Insulin: Prevents hypoglycemia in babies, decreases stillbirth, and weight gain)
Usually subsides after delivery
30% of patients may develop type 2 diabetes within 10 to 15 years.
Major Long-Term Complications of Both Types of Diabetes
Macrovascular (atherosclerotic plaque)
Coronary arteries
Cerebral arteries
Peripheral vessels
Microvascular (capillary damage)
Retinopathy
Neuropathy
Nephropathy
Screening for Diabetes: prediabetes
A1C
FASTING PG
HbA1c of 6.0 to 6.4%
Fasting plasma glucose levels higher than or equal to 6.1 mmol/L but less than 6.9 mmol/L
Impaired glucose tolerance test (oral glucose challenge)
Screening is recommended every _ ____ for all patients 40 years of age and older
Screening is recommended every 3 years for all patients 40 years of age and older
Nonpharmacological Treatment Interventions
Type 1: Always requires insulin therapy
Type 2
Weight loss
Improved dietary habits
Smoking cessation
Reduced alcohol consumption
Regular physical exercise
Glycemic Goal of Treatment
A1C
FASTING PG
2 HOURS POSTPRANDIAL TARGET
HbA1c of less than 7%
Fasting blood glucose goal for diabetic patients: 4 to 7 mmol/L
2-hour postprandial target of 5 to 10 mmol/L
Treatment for Diabetes
TYPE 1
TYPE 2
Type 1
Insulin therapy
Type 2
Lifestyle changes
Oral drug therapy
Insulin when the above no longer provide glycemic control
Types of Antidiabetic Drugs
Insulins
Oral hypoglycemic drugs
A combination of oral antihypoglycemic and insulin controls glucose levels.
Some new injectable hypoglycemic drugs may be used in addition to insulin or antidiabetic drugs.
A1C IS AN INDICATOR OF
indicator of glycemic control 2 to 3 months (lifespan of RBC)
A1C for very sick patients
7 to 8.5 %
Insulins function as a substitute for?
effects are the same as those normal?
synthesized in labs using
Function as a substitute for the endogenous hormone
Effects are the same as those of normal endogenous insulin
RDNA technology
Insulin restores the diabetic patient’s ability to:
Metabolize carbohydrates, fats, and proteins
Store glucose in the liver
Convert glycogen to fat stores
Four Major Classes of Insulins and their examples
Rapid Acting (insulin lispro)
Short Acting (regular insulin)
Intermediate Acting (insulin NPH)
Long Acting (insulin detemir and glargine)
Human insulin
derived using?
recombinant insulin produced by?
goal (2)
Derived using recombinant deoxyribonucleic acid (DNA) technologies
Recombinant insulin produced by bacteria and yeast
Goal: tight glucose control
To reduce the incidence of long-term complications
Individualized dose
exogenous insulin:
substitute for endogenous
replace insulin
restore ability to metabolize carbs, fats and protein
does not reverse damage to receptors
Rapid-acting treatment for types 1 and 2 diabetes
Onset
Peak
Duration
When to give?
2 names of medications
Can it be given via CSIP? what about via IV?
Most rapid onset of action (10 to 15 minutes)
Peak: 1 to 2 hours
Duration: 3 to 5 hours (shorter duration)
Patient must eat a meal after injection
Insulin lispro (Humalog®)
~~~~Action similar to that of endogenous insulin
Insulin aspart (NovoRapid®)/ Insulin glulisine (Apidra®)
May be given subcutaneously or via continuous subcutaneous infusion pump (but not intravenously)
Insulin lispro
facilitates uptake of excess glucose at hepatic insulin receptor sites for storage in liver as glycogen
facilitates glucose to glycogen in liver
RAPID ACTING- given when?
eat a meal after injection of rapid acting
Short-Acting Insulins
Onset
Peak
Duration
When to give?
2 names of medications
Can it be given via IV?
Regular insulin (Humulin R®, Novolin ge Toronto®)
Routes of administration: intravenous (IV) bolus, IV infusion, intramuscular, subcutaneous
Onset (subcutaneous route): 30 minutes
Peak (subcutaneous route): 2 to 3 hours
Duration (subcutaneous route): 6.5 hours
for DKA/ COMA
Intermediate-Acting Insulins
names
apperance
O
P
D
Insulin isophane suspension (also called NPH), Humulin N, NovoliN ge NPH
CLOUDY appearance
Often combined with regular insulin
Onset: 1 to 3 hours
Peak: 5 to 8 hours
Duration: up to 18 hours
What is often combined with Intermediate-Acting Insulins?
Regular insulin (short-acting)
Intermediate-Acting Insulins ONSET AND DURATION
slower onset and longer duration
Long-Acting Insulins
Onset
Peak
Duration
CAN BE DOSED….
2 names of medications
provides
Insulin glargine (Lantus®) & Detemir
Clear, colourless solution
Constant level of insulin in the body
Usually dosed once daily
Can be dosed every 12 hours
Referred to as basal insulin
Onset: 90 minutes
Peak: none
Duration: 24 hours
Bolus insulin
rapid-acting
short -acting
treats at time of meals
Basal insulin
intermediate- acting
long-acting
fasting periods and in between meals
Insulin detemir duration of action and effect on frequency
Insulin detemir
Duration of action is dose-dependent.
Lower doses require twice-daily dosing.
Higher doses may be given once daily.
Long acting insulin
provides a ____ level of insulin
referred to as
Provides a constant level of insulin
referred to as basal insulin
Fixed-Combination Insulins
Fixed combinations
Humulin 30/70
Novolin 30/70, 40/60, 50/50
NovoMix® 30
Humalog Mix25®
Humalog Mix50®
Each contains two different insulins, fixed combinations: What are the two?
One intermediate-acting type
Either one rapid-acting type (Humalog, NovoLog) or one short-acting type (Humulin)
intermediate + (rapid or short)
Insulin contraindicated for drug allergy
*patients with dietary restrictions to pork products
Insulin adverse effects
Hypoglycemia
Tachycardia, palpitations
Headache, lethargy, tremors
Blurred vision, dry mouth, hunger
Insulin interactions
What drugs cause? >Reduced effects which result in elevated blood glucose: 5
Increased effects resulting in lowered blood glucose: 7
Β blockers, corticosteroids, epinephrine, furosemide, thyroid hormones
Alcohol, anabolic steroids, sulfa drugs, ACE inhibitors, MAOIs, propanolol and salicylates
Special Considerations
Hospitalized patients may be put on a ‘sliding scale’ protocol to try and achieve better glycemic control (not preferred)
Some controversy to this but some conditions or NPO status or TPN alters the maintenance normalcy for patients as compared to home
__________ has been proven to be more effective
Basal bolus strategy
Sliding-Scale Insulin Dosing
* type of insulins
* used for which patients
* relationship to glucose levels
Subcutaneous rapid-acting (lispro or aspart) or short-acting (regular) insulins are adjusted according to blood glucose test results.
Typically used in hospitalized diabetic patients or those on total parenteral nutrition or enteral tube feedings
Subcutaneous insulin is ordered in an amount that increases as the blood glucose increases.
Recent research does not support sliding-scale use; nonetheless, sliding scale is still commonly used.
Disadvantage of Sliding-Scale Insulin Dosing
Delays insulin administration until hyperglycemia occurs, resulting in large swings in glucose control.
Basal-Bolus Insulin Dosing
* types of insulin
* describe what it does
Preferred method of treatment for hospitalized patients with diabetes
Mimics a healthy pancreas by delivering basal insulin constantly as a basal and then as needed as a bolus
Basal insulin is a long-acting insulin (insulin glargine).
Bolus insulin (insulin lispro or insulin aspart [rapid acting] )
Special Considerations
Be aware of special dosing guidelines for children
Insulin therapy is the only currently recommended drug therapy for pregnant women
Reduce risk of congenital anomalies, stillbirth~~~Helps with milk production (hyperglycemia impedes this)
Other Injectable Antidiabetic Drugs
Amylin agonist
pramlintide (Symlin®)
Incretin mimetics
exenatide (Byetta®)
liraglutide (Victoza®)
Amylin agonist
Mimics hormone amylin
Slows gastric emptying
Suppresses glucagon secretion, reducing hepatic glucose output
Used when other drugs have not achieved adequate glucose control
Subcutaneous injection
Incretin mimetic
action?
used only in?
Mimics the incretin hormones
Enhances insulin secretion from β cells of the pancreas
Used only for type 2 diabetes
Exenatide: injection pen device
Injectable Antidiabetic Drugs: Adverse Effects
Amylin agonist
Nausea, vomiting, anorexia, headache
Incretin mimetics
Nausea, vomiting, and diarrhea
Rare cases of hemorrhagic or necrotizing pancreatitis
Weight loss
a- glucosidase inhibitor
- mechanism of action
- a glucosidase enzyme function
- important FACT
inhibits a-glucosidase enzymes > which delays glucose absorption
a glucosidase enzyme> responsible for the hydrolysis of oligosaccharides and disaccharides into glucose
must be taken with food > first bite of a meal, so that post-prandial elevation can be prevented.
a glucosidase inhibitor 1 drug
acarbose (less commonly used)
a- glucosidase
interactions
contraindications
interactions- digoxin, ranitidine, propanolol
contraindication: IBS, malabsorption, intestinal obstruction
a glucosidase indication
indication- controlling elevated postprandial glucose levels
a-glucosidase AE
AE: GI effects- flatulence, diarrhea, abd pain
