Transcript Antidiabetic Medications & The Nursing Process

Antidiabetic
Medications
&
The Nursing Process
Karen Ruffin RN, MSN Ed.
Is it Diabetes or is it
Hyperglycemia???????????????
IS THERE A DIFFERENCE
AND
IF SO WHAT IS IT??
What is ???????

Hyperglycemia

Insulin

The primary source of energy for our
bodies
What is the difference
between

Basel Insulin

Prandial Insulin
Optimal Levels of Blood
Sugars

Preprandial-110 mg/dl

Postprandial-180 mg/dl
What happens to our bodies
when we are hyperglycemic?
hypertension
Vascular smooth
muscle cell growth
Release of chemokines
Release of cytokines
Expression of cellular
adhesion molecules
Hyper coagulation
Platelet Activation
Decreased Fibrinolysis
So what disease states are
you at risk for???
MI
 DVT
 PE
 Stroke
 AAA
 Retinopathy

What happens to our bodies
when we are hyperglycemic?
Increased Glucose
Decreased Insulin
Increased Glucose
Decreased Insulin
DID YOU KNOW ANY BLOOD
SUGAR >200
STUNS YOUR ???????? FOR
2WEEK
Criteria for Diagnosis of DM
DM Screening
Symptoms of diabetes + casual plasma glucose level less than
or equal to 200 mg/dL
OR
 Fasting plasma glucose higher than or equal to
126 mg/dL
OR
 2-hour postload glucose level higher than or equal to 200
mg/dL during an oral glucose tolerance test
 Impaired glucose tolerance (IGT)
◦ FPG <110 mg/dL: normal fasting glucose
◦ FPG ≥110 mg/dL but <126 mg/dL: impaired fasting glucose
(IFG)
◦ FPG ≥126 mg/dL: provisional diagnosis of diabetes mellitus

What is a HbA1c?

It is a test that allows healthcare
providers to see how diabetics have
managed their blood glucose level over
the last 2-3 months….

Why do you think this is important????
At what blood glucose level do we start
treating with sliding scale?
???????
So, what do you think we
are doing to our
patients???
What is the Difference??

Type 1 diabetes

Type 2 diabetes
Type 1 Diabetes

Lack of insulin production OR

Production of defective insulin

Affected patients need exogenous insulin

Complications
 Diabetic ketoacidosis (DKA)
 Hyperosmolar nonketotic syndrome

Oral antidiabetic drugs not effective
Diabetes Mellitus

Symptoms
Polyuria
 Polydipsia
 Polyphagia
 Glycosuria
 Unexplained weight loss
 Fatigue
 Hyperglycemia

Type 2 Diabetes

Most common type

Caused by insulin deficiency and insulin
resistance

Many tissues are resistant to insulin
 Reduced number insulin receptors
 Insulin receptors less responsive
 These people respond to oral
hypoglycemics
Type 2 Diabetes

•
Several comorbid conditions
metabolic syndrome OR insulin-resistance
syndrome OR syndrome X
◦
◦
◦
◦
◦
◦
◦
Obesity
Coronary artery disease
Dyslipidemia
Hypertension
Microalbuminemia (protein in the urine)
Enhanced conditions for embolic events (blood
clots)
Insulin Resistance
Coronary Artery Disease
Treatment DIfferences

Type 1
◦ Exogenous insulin
◦ Dietary control

Type 2
◦ Lifestyle changes
 Dietary control
 Weight reduction
 Exercise
◦ May require oral hypoglycemic therapy or
exogenous insulin
 Insulin when oral hypoglycemic medications can
no longer provide glycemic control
Gestational Diabetes
◦
Hyperglycemia that develops during pregnancy
◦
Insulin must be given to prevent birth defects
◦
4% of all pregnancies
◦
Must be reclassified if it persists 6 weeks postdelivery
◦
Usually subsides after delivery
◦
30% of patients may develop Type 2 DM within 10
to 15 years
Major Long-Term Complications
of DM (Both Types)
◦
Macrovascular (atherosclerotic plaque)




◦
Coronary arteries
Cerebral arteries
Renal arteries
Peripheral vessels
Microvascular (capillary damage)



Retinopathy
Neuropathy
Nephropathy
Complications Associated with
Diabetes Mellitus
Cardiovascular disease, including
hypertension
 Peripheral vascular disease


Delayed healing
Visual defects, including blindness
 Renal disease
 Infection
 Neuropathies
 Impotence

Oral Hypoglycemics

Sulfonylureas (oldest)

Meglitinides

Biguanide

Thiazolidinediones
Indications for Oral
Hypoglycemics
They are used to lower blood sugar
levels in patients that diet and exercise
have failed.
 The patient must have some pancreatic
function left.
 They can be used as a monotherapy or
in conjunction with other oral
hypoglycemics.

Contraindications
Know drug allergy
 Active hypoglycemia
 Usually not used during pregnancy
subq insulin's are used then.
 Liver disease
 Kidney disease


Depending on the metabolic pathways of
the medication
Sulfonylureas

First generation:
 chlorpropamide
(Diabinese),
 tolazamide (Tolinase)
 tolbutamide (Orinase)

Second generation:
 glimepiride
(Amaryl)
 glipizide (Glucotrol)
 glyburide (DiaBeta, Micronase)
Sulfonylureas

Stimulate insulin secretion from the beta cells
of the pancreas, thus increasing insulin levels

Beta cell function must be present

Improve sensitivity to insulin in tissues

Result: lower blood glucose levels

First-generation drugs not used as frequently
now
Adverse Effects

Sulfonylureas






Hypoglycemia
hematologic effects
nausea
epigastric fullness
heartburn
many others
Interactions

Sulfonylureas

Hypoglycemic effect increases when taken with alcohol,
anabolic steroids, many other drugs

Adrenergics (beta blockers) may mask many of the
symptoms of hypoglycemia

Hyperglycemia: corticosteroids, phenothiazines, diuretics,
oral contraceptives, thyroid replacement hormones,
phenytoin, diazoxide and lithium.

Allergic cross-sensitivity may occur with loop diuretics
and sulfonamide antibiotics

May interact with alcohol/OTC medication containing
alcohol) - causing a disulfiram (Antabuse) -type reaction
(facial flushing, pounding headache, feeling of
breathlessness, and nausea)
Meglitinides

Meglitinides
repaglinide (Prandin)
 nateglinide (Starlix)


Meglitinides
Action similar to sulfonylureas
 Increase insulin secretion from the
pancreas

Adverse Effects

Meglitinides
Headache
 hypoglycemic effects
 Dizziness
 weight gain
 joint pain
 upper respiratory infection or flu-like
symptoms

Biguanides

Biguanides
 metformin (Glucophage)

Biguanides
 Decrease production of glucose


Increase uptake of glucose by tissues
Does not increase insulin secretion from
the pancreas (does not cause
hypoglycemia)
Adverse Effects

Metformin

Primarily affects GI tract: abdominal bloating,
nausea, cramping, diarrhea, feeling of
fullness

May also cause metallic taste, reduced vitamin B12
levels

Lactic acidosis is rare but lethal if it occurs

Does not cause hypoglycemia
Thiazolidinediones

Thiazolidinediones
 pioglitazone (Actos),
 rosiglitazone (Avandia)
 Also known as “glitazones”

Thiazolidinediones
 Decrease insulin resistance
 “Insulin sensitizing drugs”
 Increase glucose uptake and use in
skeletal muscle
 Inhibit glucose and triglyceride production in
the liver
Adverse Effects

Thiazolidinediones
Moderate weight gain
 Edema
 Mild anemia
 Hepatic toxicity—monitor liver function
tests

Alpha-glucosidase Inhibitors

Alpha-glucosidase inhibitors
 acarbose (Precose)
 miglitol (Glyset)

Alpha-glucosidase inhibitors
 Reversibly inhibit the enzyme alpha-glucosidase in
the small intestine
 Result: delayed absorption of glucose
 Must be taken with meals to prevent excessive
postprandial blood glucose elevations (with the
“first bite” of a meal)
Adverse Effects

α-glucosidase inhibitors
Flatulence
 diarrhea
 abdominal pain


Do not cause hypoglycemia,
hyperinsulinemia, or weight gain
Insulins

Mechanism of Action

Substitute for & same effects as endogenous insulin


Restores the diabetic patient’s ability to:
 Metabolize carbohydrates, fats, and proteins
 Store glucose in the liver
 Convert glycogen to fat stores
Some derived from porcine sources

Most now human-derived, using recombinant DNA technologies

Goal: tight glucose control

To reduce the incidence of long-term complications
Indications

To treat both types of diabetes

Each patient requires careful
customization of the dosing regimen for
optimal glycemic control
Contraindications

Anyone who is hypoglycemic?????
Adverse Effects

Are all signs and symptoms of
hypoglycemia including shock and
death.
Human-Based Insulins

Rapid-Acting


Most rapid onset of action
Shorter duration
Insulin
Onset
(mins)
Peak (hrs)
Duration (hrs)
aspart (Novolog)
2-33
1-3
3-5
lispro (Humalog)
2-33
30mins – 2.5
3-6.5
glulisine (Apidra)
2-33
30mins – 1.5
1.-25
May be given SC or via continuous SC infusion
pump (but not IV)
Human-Based Insulins

Short-Acting

regular insulin (Humulin R, Novolin R)
Insulin
Onset (mins)
Peak (hrs)
Duration
(hrs)
Humulin R
30 mins to 4 hrs
2.5-5
5-10
Novolin R
30
2.5-5
8

Onset 30 – 60 minutes
 The
only insulin product that can be
given by IV bolus, IV infusion, or even IM
Sliding-Scale Insulin Dosing

SC rapid or short-acting doses adjusted
according to blood glucose test results

Typically used in hospitalized diabetic patients


Or in patients on TPN / enteral tube feedings or
receiving steroids
Subcutaneous insulin is ordered in an amount
that increases as the blood glucose increases
Human-Based Insulins

Intermediate-Acting

isophane insulin suspension (also called NPH) (Humulin N, Novolin
N)

isophane insulin suspension & insulin injection
(Humulin 50/50 , Humulin 70/30, Novolin 70-30)

Lispro protamine suspension (Humalog 75/25, Novolog Mix 70/30)

insulin zinc suspension (Lente, Novolin L)


Cloudy appearance
Slower in onset and more prolonged duration than
endogenous insulin
Human-Based Insulins
Intermediate-Acting
Insulin
Onset (hrs)
Peak (hrs)
Duration (hrs)
Humulin N
1-4
4-12
16-28
Novolin N
1-5
4-12
24
Humulin 50/50
0.5
4-8
24
Humulin 70/30
0.5
4-12
24
Novolin70/30
0.5
2-12
24
Isophane (NPH):
Isophane & Insulin:
Human-Based Insulins
Intermediate-Acting
Insulin
Onset
(hrs)
Peak (hrs)
Duration (hrs)
Humalog Mix 75/25
0.25-0.5
0.5-1.5
12-24
Novolog Mix 70/30
0.2-0.33
2.4
24
Lente Iletin II
1-1.5
8-12
24
Novolin L
1-4
7-15
20-28
lispro protamine & lispro:
Insulin Zinc Suspension:
Human-Based Insulins

Combination Insulin Products

NPH 70% and regular insulin 30%
(Humulin 70/30, Novolin 70/30)

NPH 50% and regular insulin 50%
(Humulin 50/50)

insulin lispro protamine suspension 75%
and insulin lispro 25% (Humalog Mix
75/25)
Human-Based Insulins
Long-Acting
Insulin
Onset
Peak
Duration
glargine (Lantus
1
No peak activity
24 (when
administered at hs)
detemir (Levemir)
1
6-8
6-28
DM Monitoring – Daily
AC & HS

Ante Cibum: before meals

HS: Hour of Sleep: prior to taking any HS snack

Rapid or short acting insulin used to cover any blood sugar
(accucheck, chemstrip)
 Dose by protocol (protocols are usually hospital-based)
for any result greater than 150mg/dL
 Usually 1-2U for every 50mg/dL >150 with special
instructions to notify physician if >300 mg/dL
Injection Sites
External
Insulin Pumps
Internal
Hypoglycemia
Adverse Effect of Insulin

Early
◦ Confusion, irritability, tremor, sweating
Later
◦ Hypothermia, seizures
◦ Coma and death will occur if not treated

Abnormally low blood glucose level

Mild cases can be treated with diet—higher intake of
protein and lower intake of carbs—to prevent a rebound
postprandial hypoglycemia

(<50 mg/dL)
Good way to remember!!!
Diabetic Ketoacidosis


State of hyperglycemia with ketosis
Usually results from infection, environment, or emotional stressor
 As a result of Lack of Insulin, Breakdown:
 Fat – free fatty acids in liver – ketone bodies – ketones in
urine
 Protein – to form new glucose / increased BUN
 Glycogen to glucose (decrease use of glucose because of
decreased insulin)
 Osmotic diuresis
 Dehydration / Electrolyte Imbalance
 Hyperosmolality Hemoconcentration
 Acidosis
 Death
Diabetic Ketoacidosis






Sudden onset
Factors: infection, stressors, inadequate insulin
Kussmaul respiration / fruity odor to breath, nausea, abdominal
pain
Dehydration, electrolyte imbalance, polyuria, polydipsia, weight
loss, dry skin, sunken eyes, soft eyeballs, lethargy, coma
Glucose >300 mg/dL
pH <7.35 / Bicarbonate < 15 mEq/L
Cr >1.5 mg/dL
 Blood & Urine Ketones - Positive

Na – low / K+ </> /
Hyperglycemic-hyperosmolar
nonketotic syndrome (HHNS)
State of hyperglycemia without ketosis
 Little breakdown of fat (little or no ketone
bodies)
 Breakdown


Glycogen– formation of new glucose –
hyperglycemia
 Very
high levels of glucose >800mg dL
Osmotic diuresis – extracellular dehydration
 Renal insufficiency – hyperosmolality –
intracellular dehydration
 Hypokalemia – shock – tissue hypoxia - Coma

Hyperglycemic-hyperosmolar
nonketotic syndrome (HHNS)









Gradual onset
Factors: infection, other stressors, poor fluid intake
Altered CNS function – neurologic symptoms
Dehydration / electrolyte loss
Glucose > 800 mg/dL
pH >7.4 / Bicarbonate >20 mEq/L
Na & K+ normal or low
Bun & Cr – elevated
Blood & Urine Ketones - negative
Hyperglycemic-hyperosmolar
nonketotic syndrome (HHNS
Treatment
 Rehydrate with NS (if severe) or ½ NS


IV insulin According to Sliding Scale


Use CVP or PCWP / UO / blood pressure monitoring
Never Reduce hyperglycemia by 10% /hr
Replace Potassium (will not be as severe as
DKA)
Antidiabetic Drugs:
Nursing Implications

Before giving any drugs that alter glucose
levels, obtain and document:
A thorough history
 Vital signs
 Blood glucose level, HbA1c level
 Potential complications and drug interactions

Antidiabetic Drugs:
Nursing Implications

Before giving any drugs that alter glucose levels:

Assess the patient’s ability to consume food

Assess blood glucose level

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 NPO for a test or procedure, consult physician to
clarify orders for antidiabetic drug therapy
Antidiabetic Drugs:
Nursing Implications

Keep in mind that overall concerns
for any diabetic patient increase
when the patient:

Is under stress

Has an infection

Has an illness or trauma
Antidiabetic Drugs:
Patient Education

Thorough patient education is essential regarding:
◦ Disease process
◦ Other Risk Factors:
 Smoking
 HTN
 CAD
◦ Self-Care:
 Medication
 Psychological adjustment
 Nutrition
 Activity and Exercise
 Blood-glucose testing
 Self-administration of insulin or oral drugs
◦
Potential complications
 How to recognize and treat hypoglycemia and hyperglycemia
FIGURE 36-3 Diabetes health care plan.
Mosby items and derived items © 2007, 2004 by Mosby, Inc., an affiliate of Elsevier Inc.
Nursing Implications
Insulin

When insulin is ordered, ensure:
◦
◦
◦
◦

Correct route
Correct type of insulin
Timing of the dose
Correct dosage
Insulin order and prepared dosages are
second-checked with another nurse
◦
◦
◦
◦
◦
Check blood glucose level before giving insulin
Roll vials between hands them to mix suspensions – no shaking!
Ensure correct storage of insulin vials
ONLY insulin syringes, calibrated in units, to administer insulin
Ensure correct timing of insulin dose with meals
Nursing Implications
Insulin

Insulin

When drawing up two types of insulin in one
syringe:
 Always
withdraw the regular or rapid-acting
insulin first

Provide thorough patient education regarding
self-administration of insulin injections, including
timing of doses, monitoring blood glucoses, and
injection site rotations
Nursing Implications Oral
Antidiabetic drugs

Always check blood glucose levels before giving

Usually given 30 minutes before meals
 Administer the medication at exact time – with meal
or when food is in sight*

Alpha-glucosidase inhibitors are given with the first bite of
each main meal

Metformin is taken with meals to reduce GI effects
Nursing Implications
Insulin & hypoglycemic medications
Assess for signs of hypoglycemia
 If hypoglycemia occurs:

Give glucagon or
 Have the patient eat glucose tablets or
gel, corn syrup, honey, fruit juice, or
nondiet soft drink or
 Have the patient eat a small snack
such as crackers or half a sandwich


Monitor blood glucose levels
Nursing Implications

Monitor for therapeutic response

Decrease in blood glucose levels to the
level prescribed by physician

Measure hemoglobin A1c to monitor longterm compliance to diet and drug therapy

Watch for hypoglycemia and
hyperglycemia
Review

When administering insulin, the nurse must
keep in mind that the most immediate and
serious adverse effect of insulin therapy is
which of the following?
A: Hyperglycemia
 B: Hypoglycemia
 C: Bradycardia
 D: Orthostatic Hypotension

Review

A dose of long acting insulin has been ordered
for bedtime for a diabetic patient. The nurse
expects to give which type of insulin?
A: Regular
 B: Lente
 C: NPH
 D: Glargine (Lantus)

Review

A Patient is to be placed on an insulin drip to
control his high blood glucose levels. The
nurse knows that which of the following is the
only type of insulin that can be given IV?
A: Regular
 B: Lente
 C: NPH
 D: Ultralente

Review

While monitoring a patient who is receiving
insulin therapy, the nurse observes for signs of
hypoglycemia, such as which of the following?
A: Decreased pulse and respiratory rate and flush
skin.
 B: Increased pulse rate and a fruity, acetone breath
odor.
 C: Weakness, sweating, and confusion.
 D: Increased urine output and edema.

Review

When giving oral acarbose (Precose),
the nurse should administer it at what
time?
A: 15 minutes before meal
 B: 30 minutes before meal
 C: with the first bite of a meal
 D: 1 hour after eating

Review

A patient taking rosiglitazone (Avandia) tells
the nurse, “There’s my insulin pill!” The nurse
describes the mechanism of action of Avandia
by explaining that this drug is not insulin but it
works by:
A: Stimulating the beta cells of the pancreas to
produce insulin.
 B: Decreasing insulin production.
 C: Inhibiting hepatic glucose production.
 D: Decreasing intestinal absorption of glucose.
