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Transcript
PART 8: Drugs Affecting
the Endocrine System
I. Thyroid and Antithyroid
Drugs:
 Thyroid replacement drugs:
 Levothyroxine.
 Liotrix.




Antithyroid drugs:
Carbimazole.
Propylthiouracil.
Methimazole.
Overview:
Thyroid function:
It is responsible for the secretion of three hormones essential for the proper regulation of metabolism:
thyroxin (T4), triidothyronine (T3), and clacitonin. It is close to and communicates with the parathyroid glands,
which lie just above and behind it. These glands are responsible for maintaining adequate levels of calcium in
the ECF, primarily by mobilizing calcium from bone. T4 and T3 are produced in the thyroid gland through the
iodination and coupling of the amino acid tyrosine.
Thyroid hormone synthesis: The iodide needed for this process is acquired from the diet.
Hypothyroidism:
Hypothyroidism is a lack of sufficient levels of thyroid hormones to maintain a normal metabolism. This
condition occurs in a number of pathophysiological states:
• Absence of the thyroid gland
• Lack of sufficient iodine in the diet to produce the needed level of thyroid hormone
• Lack of sufficient functioning thyroid tissue due to tumor or autoimmune disorders
• Lack of TSH due to pituitary disease
• Lack of TRH related to a tumor or disorder of the hypothalamus
Children who are born without a thyroid gland or who have a nonfunctioning gland develop a condition called
cretinism. If untreated, these children will have poor growth and development and mental retardation because
of the lack of thyroid hormone stimulation.
Severe adult hypothyroidism is called myxedema. Myxedema usually develops gradually as the thyroid slowly
stops functioning. Patients with myxedema exhibit many signs and symptoms. Some forms of hypothyroidism
may result in the formation of a goiter, which is an enlargement of the thyroid gland results from
overstimulation by elevated levels of TSH. The TSH level is elevated because there is little or no thyroid
hormone in the circulation. Hypothyroidism is treated with replacement thyroid hormone therapy.






Common symptoms
Thickened skin
Hair loss
Constipation
Lethargy
Anorexia
Hyperthyroidism:
Hyperthyroidism occurs when excessive amounts of thyroid hormones are produced and released into the
circulation. Graves’ disease, a poorly understood condition that is thought to be an autoimmune problem, is
the most common cause of hyperthyroidism. Thyroid storm is a severe and potentially life threatening
exacerbation of the symptoms of hyperthyroidism that is usually induced by stress or infection.
Hyperthyroidism may be treated by surgical removal of the gland or portions of the gland, treatment with
radiation to destroy parts or all of the gland, the metabolism of these patients then must be regulated with
replacement thyroid hormone therapy, or drug treatment to block the production of thyroxine in the thyroid
gland.






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
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Reported symptoms:
Flushing.
Increased appetite.
Muscle weakness.
Fatigue.
Palpitations.
Irritability.
Nervousness.
Sleep disorders.
Heat intolerance.
Pharmacology overview:
 Thyroid replacement drugs:
 Natural thyroid preparation: Thyroid.
 Synthetic thyroid preparations: levothyroxine, liothyronine and liotrix.
Mechanism of action: The thyroid drugs work in the same manner as the endogenous thyroid hormones,
affecting many body systems.
Indications: Levothyroxine is the preferred drug because its hormonal content is standardized; therefore, its
effect is predictable
Contraindications: Contraindications to thyroid preparations include known drug allergy to a given drug
product, recent myocardial infarction, and hyperthyroidism.
Adverse effects: Cardiac dysrhythmia is the most significant adverse effect
Toxicity:





Related to T4 levels.
Nervousness.
Heart palpitations.
Intolerance to heat.
Weight loss.
Interactions:
 May enhance the activity of oral anticoagulants.
 May decrease serum digitalis levels.
 Diabetic patients may require increased dosages of their hypoglycemic drugs.
Levothyroxine:





Its half-life is long enough that it only needs to be administered once a day.
It is available in oral form and in parenteral form.
Pregnancy category A.
Given once daily at morning before food ½ to 1 hour.
Steady state is achieved in 6-8 weeks.
 Antithyroid Drugs:
The treatment of hyperthyroidism may aim at treating either the primary cause or the symptoms of the
disease. Antithyroid drugs, iodides, ionic inhibitors, surgery, and radioactive isotopes of iodine are used to
treat the underlying cause, and drugs such as beta-blockers are used to treat symptoms. Here we will focus on
the antithyroid drugs.
Drugs:




Carbimazole.
Methimazole.
Propylthiouracil.
Propranolol (beta-blocker), used to treat sympathetic stimulation.
Mechanism of action:
They act by inhibiting the incorporation of iodine molecules into amino acid tyrosine, a process required to
make monoiodotyrosine and diiodotyrosine, the precursors of T3 and T4. By doing so, these drugs impede the
formation of thyroid hormone. Propylthiouracil has the added ability to inhibit the conversion of T4 to T3 in the
peripheral circulation. Neither drug inactive already existing thyroid hormone, however. In pregnancy these
drugs should be avoided whenever possible.
Adverse effects: Liver and bone marrow toxicity.
Nursing implications:
 During pregnancy, treatment for hypothyroidism should continue
 Fetal growth may be retarded if maternal hypothyroidism is untreated during pregnancy
 Adjust dosage every 4 weeks to keep TSH at the lower end of the normal range
 Teach patient to take thyroxin once daily in the morning to decrease the likelihood of insomnia if taken
later in the day, and to take the medications at the same time every day and not to switch brands
without physician approval
 Teach patients to report any unusual symptoms, chest pain, or heart palpitations
 Teach patients not to take over-the-counter medications without physician approval
 Teach patients that therapeutic effects may take several months to occur
 Teach patients the importance of alerting health care providers of thyroid medication use
o
o
o




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May enhance activity of anticoagulants
Diabetic patients may need increased dosages of hypoglycemic meds
May decrease serum digoxin levels
Antithyroid medications
Better tolerated when given with food
Give at the same time each day to maintain consistent blood levels
Never stop these medications abruptly
Avoid eating foods high in iodine (seafood, soy sauce, tofu, and iodized salt)
 Monitor for therapeutic response
 Monitor for adverse effects
II.Antidiabetic Drugs:
Insulin:



Overview:
Glucose regulation:
Glucose is the leading energy source for the human body.
Glucose is stored in the body for rapid release in times of stress.
As a result, blood glucose levels can be readily maintained so that the
neurons always receive a constant supply of glucose to function.

Rapid-acting inslulins: Lispro.
Short-acting insulins: Regular.
Intermerdiate-acting insulins:
insulin isophane suspension
NPH.
Long-acting inslulins: insulin
glargine, insulin determir.
Oral hypoglycemic drugs:
 Insulin secretagenous:
Pancreas:
The pancreas is both exocrine and an endocrine gland. The endocrine
functions of the pancreas are the focus of this chapter. Two main
hormones are produced by the pancreas: insulin and glucagon. Both
hormones play an important role in the regulation of glucose
homeostasis, specifically the use, mobilization, and storage of glucose
by the body.
There is a normal amount of glucose that circulates in the blood to
meet requirements for quick energy. However, not all of the glucose
consumed is needed. When the quantity of glucose in the blood is
sufficient, the excess is stored as glycogen in the liver and, to a lesser
extent, in skeletal muscle tissue, where it remains until the body needs
it. Glucose is also stored in adipose tissue as triglyceride body fat.
When more circulating glucose is needed, glycogen-primarily that
stored in the liver-is converted back to glucose through a process is
called glycogenolysis. The hormone responsible for initiating this
process is glucagon. Glucagon is released from alpha cells of the islets
of langerhans in the pancreas. The beta cells of these same islets
secrete insulin.
There is a continuous homeostatic balance in the body between the
actions of insulin and those of glucagon. This natural balance serves to
maintain physiologically optimal blood glucose level, which normally
range between 70 and 100 mg/dL.
Insulin serves several important metabolic functions in the body. It
facilitates the transport of glucose into these cells. Other substances
such as cortisol, epinephrine, and growth hormone work
synergistically with glucagon to counter the effects of insulin and
cause increases in the blood glucose level.

The sulphonylureas:

Glibenclamide(Glibil, melix)/ also
known as glyburide.

Glipizide (minidiab).

Glimepiride (amaryl, glymax)

Glinides:

Repaglinide.

Nateglinide.


Insulin sensitizers:
Biguanide: Metformin.

Thiazolidinediones:

Rosiglitazone.

Pioglitazone (actos)
 Alpha-glucosidase inhibitors:

Acarbose, Miglitol.
 Amylin mimetics: Pramlintide.
 Incretin mimetics: (Exentide,
Liraglutide).

Dipeptidyl peptidase-IV
inhibitors: Sitagliptin,
Vidagliptin.
Diabetes Mellitus:
Diabetes mellitus is primarily a disorder of carbohydrate metabolism that involves a deficiency of insulin, a
resistance of tissue to insulin, or both. Whatever the cause of the diabetes, the result is hyperglycemia.
Hyperglycemia is a state involving excessive concentrations of glucose in the blood.
Uncontrolled hyperglycemia correlates strongly with serious long-term macrovascular and microvascullar
complications. Macrovascular complications are usually secondary to large vessel damage caused by deposition
of atherosclerotic plaque. This compromises both central and peripheral circulation. In contrast, microvascular
complications are secondary to damage to the capillary vessels, which impairs peripheral circulation.
Two major types of diabetes mellitus are currently recognized and designated the American Diabetes
Association ADA: type 1 and type 2.
Type 1 (insulin dependent DM):
 Autoimmune destructions of beta cells in the pancreas lead to Lack of insulin production.
 Affected patients need exogenous insulin
 Fewer than 10% of all diabetes cases are type 1
 Complications: Diabetic ketoacidosis (DKA)
Type 2 (noninsulin dependent DM):
 Most common type: 90% of all cases
 Caused by insulin deficiency and insulin resistance
 Many tissues are resistant to insulin
 Reduced number of insulin receptors
 Insulin receptors less responsive
 Several comorbid conditions
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Obesity
Coronary heart disease
Dyslipidemia
Hypertension
Microalbuminemia (protein in the urine)
Increased risk for thrombotic (blood clotting) events
Major Long-Term Complications of DM:
 Macrovascular (atherosclerotic plaque)
 Coronary arteries
 Cerebral arteries
 Peripheral vessels
 Microvascular (capillary damage)
 Retinopathy
 Neuropathy
 Nephropathy
Gestational Diabetes:




Hyperglycemia that develops during pregnancy
Insulin must be given to prevent birth defects
Usually subsides after delivery
30% of patients may develop Type 2 DM within 10 to 15 years
Treatment of diabetes mellitus:
 Type 1
o
 Type 2
o
o
o
Insulin therapy
Lifestyle changes
Oral drug therapy
Insulin when the above no longer provide glycemic control
Pharmacology overview:
Antidiabetic Drugs:
 Inslulins:
 Oral hypoglycemic drugs
INSULINS:
Mechanism of action:
Administered insulin functions as a substitute for the endogenous hormone. It serves to replace the insulin that
is either not made at all or is made defectively in the body of a diabetic patient. The drug effects of exogenously
administered insulin are the same as those of normal endogenous insulin. That is, exogenously administered
insulin restores the diabetic patient’s ability to metabolize carbohydrates, fats, and proteins; to store glucose in
the liver; and to convert glycogen to fat stores.
Indications:
All insulin preparations can be used to treat both type 1 and type2 diabetes, but each patient requires careful
customization of the dosing regimen for optimal glycemic control. Additional therapeutic approaches such as
lifestyle modifications are also indicated and oral drug therapy as well, for type 2 diabetes.
Contraindications:
Contraindications to the use of all insulin products include known drug allergy to the specific product. Insulin
also should never be administered to an already hypoglycemic patient.
Adverse effects:
Hypoglycemia resulting from excessive insulin dosing can result in shock and possibly death. This is most
immediate and serious adverse effect of insulin. Other adverse effects of insulin therapy include weight gain,
lipodystrophy at the site of repeated injections, and in rare cases allergic reactions.
Interactions:
 Corticosteroids, thiazide and loop diuretics, sympathomimitic drugs, and thyroid hormones all can
anatagonize the hypoglycemic effects of insulin (which results in elevated blood glucose).
 Alcohol, anabolic steroids, sulfa drugs, and salicylates all can increase insulin’s hypoglycemic effects,
which lead to lower blood glucose levels.
 Beta-blockers may mask the signs and symptoms of hypoglycemia (tachycardia, tremor).
 Insulin increases the risk of hypoglycemia when administered with other hypoglycemic drugs.
Types of insulin:
There are currently four major classes of insulin, as determined by their pharmacokinetic properties: rapid
acting, short acting, intermediate acting, and long acting.
The duration of action ranges from several hours to over 24 hours depending on insulin class. The insulin
dosage regimen for all diabetic patients is highly individualized and may consist of one or more classes of
insulin administered at either fixed dosages or variable dosages in response to self-measurements of blood
glucose level.
 Rapid-Acting insulins: Insulin lispro.
There are currently three insulin products that are classified as rapid acting: insulin lispro, insulin aspart, and
insulin glulisine. These have the most rapid onset of action (roughly 15 minutes) as well as a shorter duration
of action than other insulin categories.
 Short-Acting insulin: Regular insulin.
Regular insulin is currently the only insulin that is classified as short-acting insulin. Regular insulin is the usual
insulin product to be dosed via intravenous bolus, intravenous infusion. These routes are often used in cases of
DKA or coma associated with uncontrolled type1 diabetes.
 Intermediate-Acting insulin: insulin isophane suspension NPH.
NPH is currently the only available intermediate-acting insulin product. NPH is an acronym for neutral
protamine Hagedorn insulin, the original name of this type of insulin. The suspension appears cloudy. NPH is
often combined with regular insulin to reduce the number of insulin injections per day.
 Long-Acting insulins: insulin glargine and insulin detemir.
Two long-acting insulin products are now available glargine and detemir. Insulin glargine is normally a clear,
colorless solution.Insulin glargine is usually dosed once daily, but the drug may be dosed every 12 hours
according to the patient response..
 Fixed-Combination insulins:
Currently available fixed-combination insulin products insulin:
NPH 70% and regular insulin 30%, NPH 50% and regular insulin 50%, Insulin aspart protamine suspension 75%
and insulin aspart 25%, Insulin lispro protamine suspension 75% and insulin lispro 25%. All of these premixed;
do not mix with other insulins.
Traditional oral drugs for diabetes:
1- Biguanide:
Mechanism of action:
Metformin is currently the only drug classified as biguanide. It is considered a first-line drug and is the most
commonly used oral drug for the treatment of type 2 diabetes. Metformin is decreasing glucose production by
the liver. It may also decrease intestinal absorption of glucose and improve insulin receptor sensitivity. This
results in increased peripheral glucose uptake and use.
Indications:
 Now recommended as the initial oral antidiabetic drug for treatment of newly diagnosed type2
diabetes.
 Because it may also cause moderate weight loss, it is particularly useful for the many diabetic patients
who are overweight or obese.
 May be used as monotherapy or in combination with other oral antidiabetec.
Contraindications:
 In patients with renal disease (serum Cr level higher than 1.5 mg/dL)
 Other contraindications include alcoholism, metabolic acidosis, hepatic disease, heart failure
Adverse effects:
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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
2- Sulfonylureas:
First-generation: Tolbutamide
Second generation: glipizide, glimepiride, and glyburide.
Mechanism of action:



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Stimulate insulin secretion from the beta cells of the pancreas, thus increasing insulin levels
Improve sensitivity to insulin in tissues
Result in lower blood glucose levels
Second generation drugs are primary used now.
Indications: Because they have different mechanisms of action, it can be used in combination with
metformin.
Adverse effects: Hypoglycemia, weight gain, skin rash, epigastric fullness and heart burn.
3- Glinides (repaglinide and Nateglinide):
Mechanism of action:
 Action similar to sulfonylureas, increase insulin secretion from the pancreas
Indications:
 Glinides can be used along with metformin and thiazolidinediones, but should never be combined with
sulfonylureas, because they share a similar mechanism of action.
Adverse effects:
 Hypoglycemia, which can occur particularly if food is not taken after a dose. Weight gain is also
commonly reported.
4- Thiazolidinediones (glitazones):
 Rosiglitazone.
 pioglitazone.
Mechanism of action:
 Increase insulin sensitivity in liver, adipose tissue, and skeletal muscle.
Side effects:
 Moderate weight gain, edema, mild anemia
 Hepatic toxicity—monitor ALT levels
5- Alpha-Glucosidase inhibitors:
 Acarbose.
 Miglitol.
Mechanism of action:
As the name implies, these drugs work by reversibly inhibiting the enzyme alpha-glucosidase that is found in
small intestine. This enzyme is responsible for the hydrolysis of oligosaccharides and disaccharides to glucose.
When this enzyme is blocked, glucose absorption is delayed. These drugs must be taken with food.
Indications: Used usually in combination with another oral hypoglycemic drug.
Adverse effects:
 Flatulence, diarrhea, abdominal pain
 Do not cause hypoglycemia, hyperinsulinemia, or weight gain
New antidiabetic drugs:
1- Amylin mimetics (pramlintide):

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
Mimics the natural hormone amylin
Slows gastric emptying
Suppresses glucagon secretion, reducing hepatic glucose output
Centrally modulates appetite and satiety
Used when other drugs have not achieved adequate glucose control
Subcutaneous injection
2- Incretin mimetics (Exentide, Liraglutide).
Incretins are hormones released by the GIT in response to food. The most important hormones that have been
identified so far are glucagon-like peptide 1 GLP-1 and gastric inhibitory peptide GIP. These hormones are
rapidly deactivated by the enzyme dipeptidyl peptidase- IV (DPP-IV).
Mechanism of action:
The incretin memitics are analogs of GLP-1 that exert their activity by acting as GLP-1 receptor agonists. These
agents are only available as S.C injection. These agents:







Improve glucose-dependent insulin secretion.
Slow gastric emptying time.
Decrease food intake.
Decrease postprandial glucagon secretion.
Promote beta-cell proliferation.
Weight gain and postprandial hyperglycemia are reduced.
HbA1c levels decline.
Adverse effects: Nausea, vomiting, diarrhea, and constipation.
3- Dipeptidyl peptidase-IV (DPP-IV) inhibitors (Sitagliptin (januvia) and vildagliptin (Galvus)):
Mechanism of action:
These drugs inhibit the enzyme DDP-IV, which is responsible for the inactivation of incretin hormones such as
glucagon-like peptide-1 GLP-1. Prolonging the activity of incretin hormones, results in increase insulin releasing
in response to meals and a reduction in inappropriate secretion of glucagon. They can be used as a
monotherapy or in combination with other drugs. Taken once daily with or without food.
Adverse effects:
 Is well tolerated.
 Headache is the most common side effects.
Hypoglycemia:
Hypoglycemia is an abnormally low blood glucose level. When the cause is organic and the effects are mild,
treatment usually consists of dietary medications, primarily a higher intake of protein and lower intake of
carbohydrates, to prevent a rebound postprandial hypoglycemic effect. Hypoglycemia is also a common
adverse effect of many antidiabetic drugs when their pharmacologic effects are greater than expected. Because
the brain needs a constant amount of glucose to function, early symptoms of hypoglycemia include the CNS
manifestations of confusion, irritability, tremor, and sweating. Later symptoms include hypothermia and
seizures. Without adequate restoration of normal blood and CNS glucose levels, coma and death can occur.
Glucose-Elevating Drugs:
 Oral forms of concentrated glucose: Buccal tablets, semisolid gel
 50% dextrose in water (D50W)
 Glucagon
Nursing implication:
 Before giving drugs that alter glucose levels:
 Assess the patient’s ability to consume food
 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
 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
 Is pregnant or lactating
 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 route
Correct type of insulin
Timing of the dose
Correct dosage
 Insulin order and prepared dosages are second-checked with another nurse
 Insulin






Check blood glucose level before giving insulin
Roll vials between hands instead of shaking them to mix suspensions
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
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 glucose levels, and injection site rotations
 Oral antidiabetic drugs




Always check blood glucose levels before giving
Usually given 30 minutes before meals
Alpha-glucosidase inhibitors are given with the first bite of each main meal
Metformin is taken with meals to reduce GI effects
 Assess for signs of hypoglycemia
 If hypoglycemia occurs:
 If the patient is conscious, give oral form of glucose
 Give the patient 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 a half sandwich
 If the patient is unconscious, give D50W or glucagon, intravenously
 Monitor blood glucose levels
 Monitor for therapeutic response
 Decrease in blood glucose levels to the level prescribed by physician
 Measure hemoglobin A1c to monitor long-term compliance with diet and drug therapy
 Monitor for hypoglycemia and hyperglycemia
III. Adrenal drugs:
Overview:
The adrenal gland is an endocrine organ that sits on top of the kidney like a cap. It is composed of two distinct
parts called the adrenal cortex and the adrenal medulla that both structurally and functionally are very
different from one another.
The adrenal medulla secrets two important hormones, both of them are catecholamines. These are
epinephrine or adrenalin and norepinephrine or noradrenaline.
The hormones secreted by the adrenal cortex, which are the focus of this chapter, are broadly referred to as
corticosteroids. There are two types of corticosteroids- glucocorticoids and mineralcorticoids. In humans the
only physiologically important mineralcorticoid is aldosterone. Cortisol is the principle human glucocotricoids.
The oversecretion of adrenocortical hormones can lead to a group of signs and symptoms called Cushing’s
syndrome. The undersecretion of adrenocortical hormones causes a condition known as Addison’s disease.
Adrenal drugs:





Can be either synthetic or natural
Many different drugs and forms
Glucocorticoids : Topical, systemic, inhaled, nasal
Mineralocorticoid: Systemic
Adrenal steroid inhibitors: Systemic
 Glucocorticoids
o Beclomethasone (several formulations)
o Fluticasone propionate
o Cortisone
o Methylprednisolone
o Prednisone………….and many others
 Mineralocorticoid
o Fludrocortisone acetate
o Hydrocortisone (several formulations)
 Adrenal steroid inhibitor
o Aminoglutethimide
Glucocorticoids:
Indications: There are a wide variety of indications:




Adrenocortical deficiency
Dermatologic diseases
Exacerbations of chronic respiratory illnesses, such as asthma and COPD
Organ transplant (decrease immune response)
Glucocorticoids administration




By inhalation for control of steroid-responsive bronchospastic states
Nasally for rhinitis and to prevent the recurrence of polyps after surgical removal
Topically for inflammations of the eye, ear, and skin
As oral form (tab, susp) and as injection.
Contraindications:
 Drug allergies
 Serious infections, including septicemia, systemic fungal infections, and varicella
 Cautious use in patients with
o Gastritis, reflux disease, ulcer disease
o Diabetes
o Cardiac/renal/liver dysfunction
Adverse effects:

Prolonged use of high doses of glucocorticoids:









Bone thinning and osteoporosis.
Muscle weakness and wasting.
Effects on carbohydrate metabolism.
Suppression of stress responses.
Growth retardation in children.
Skin thinning, acne and stretch marks.
Gastric ulceration.
Diabetes.
Oedema.
Corticosteroid drugs can cross the placenta and produce fetal abnormalities. For this reason, they are classified
as pregnancy category C drugs. They may be secreted in breast milk and cause abnormalities in the nursing
infant. One important point about long-term use of steroids is that must not be stopped abruptly. These drugs
require a tapering of the daily dose, because the administration of these drugs causes the endogenous
production of the hormones to stop. This suppression can cause impaired stress response and place the patient
at risk of developing hypoadrenal crisis in times of increased stress.
Antiadrenals (adrenal steroid inhibitors)
 aminoglutethimide
 Used in the treatment of Cushing’s syndrome, metastatic breast cancer, and adrenal cancer
Nursing implications:
 Assess for edema and electrolyte imbalances. Be aware that these drugs may alter serum glucose and
electrolyte levels
 Assess for contraindications to adrenal drugs, especially the presence of peptic ulcer disease
 Systemic forms may be given by oral, IM, IV, or rectal routes (not SC).Oral forms should be given with
food or milk to minimize GI upset
 Clear nasal passages before giving a nasal corticosteroid
 After using an orally inhaled corticosteroid, instruct patients to rinse their mouths to prevent possible
oral fungal infections
 Teach patients on corticosteroids to avoid contact with people with infections and to report any fever,
increased weakness, lethargy, or sore throat
 Patients should be taught to take all adrenal medications at the same time every day, usually in the
morning, with meals or food. Patients should not take with alcohol, aspirin, or NSAIDs
 Sudden discontinuation of these drugs can precipitate an adrenal crisis caused by a sudden drop in
serum levels of cortisone, doses are usually tapered before the drug is discontinued.