Republic of the Philippines
CENTRAL MINDANAO UNIVERSITY
COLLEGE OF NURSING
University Town, Musuan, Maramag, Bukidnon
E-mail: nursing@cmu.edu.ph
NCM 74
(Care of Clients with Problems in Nutrition, and Gastrointestinal, Metabolism and
Endocrine, Perception and Coordination, (Acute and Chronic)
Submitted by:
Solis, Shiela Mae P.
Tuyco, Sherwin Kristoffer
Submitted to:
Ms. Neda Joy Espina, MAN, RN
Clinical Instructor
February, 2021
INTRODUCTION
Addison's disease is named after Thomas Addison, an English physician who
originally described the condition in the fundamental and local effects of disease of the
Suprarenal Capsules (1855). He called it "melasma suprarenale" at first, but it was later
given the medical name "Addison's disease" in honor of Addison's discovery. Initially,
the illness was thought to be a kind of anemia linked to the adrenal glands. Addison's
monograph detailing the illness was an unusual insight at the time because nothing was
known about the adrenal glands (then named "Supra-Renal Capsules"). Addison's
monograph became acknowledged as an important medical contribution and a classic
example of diligent medical observation as the adrenal function became more
understood.
Addison disease is an insidious, usually progressive hypofunctioning of the
adrenal cortex. It causes various symptoms, including hypotension and
hyperpigmentation, and can lead to adrenal crisis with cardiovascular collapse.
Diagnosis is clinical and by finding elevated plasma adrenocorticotropic hormone
(ACTH) with low plasma cortisol. Treatment depends on the cause but generally
includes hydrocortisone and other hormone therapy.
ETIOLOGY
There are two major classifications for Addison’s Disease, the primary adrenal
insufficiency and secondary adrenal insufficiency. Primary adrenal disease is caused by
severe damage to the cortex (the outer layer of the adrenal gland) that can no longer
produce enough hormones. This commonly results from an attack on the adrenal gland
by the body’s immune system. This is called an autoimmune disease. In an autoimmune
disease, the body’s immune system mistakes organs in the body. Antibodies are
produced against adrenal cortex cells, as well as +/- 21 hydroxylase enzymes within the
adrenal gland. These antibody production actually account for 70% of cases of
Addison's disease. Secondary adrenal insufficiency is caused by a lack of
adrenocorticotropic hormones (ACTH) made by the pituitary gland (located in the brain).
ACTH tells the adrenal gland when to produce its hormone. A lack of ACTH causes a
drop in the adrenal gland’s production of cortisol but the aldosterone is not affected. A
temporary form of secondary adrenal insufficiency occurs when people who have been
using glucocorticoids hormone (corticosteroids) such as prednisone for a long time to
treat a certain inflammatory condition such as rheumatoid arthritis, asthma,or ulcerative
colitis stops abruptly or interrupts taking the medication at once. This happens because
corticosteroids block the release of ACTH.
STATISTICS
Males and females are equally affected by Addison's disease. Addison's disease
affects about one in every 100,000 people in the United States. In the general
population, the prevalence is estimated to be between 40 and 60 persons per million.
It's difficult to estimate the true prevalence of Addison's disease in the general
population because some instances go undetected. Addison's disease can affect people
of any age, but it is most common in people between the ages of 30 to 50.
In a study published by the European Journal of Endocrinology in 2009, there were a
total of 811 Addison's disease patients identified, with 147 of them being deceased.
Females (1.18 (0.92-1.44) and males (1.10 (0.80-1.39) had similar SMRs of 1.15 (95
percent confidence intervals (CI) 0.96-1.35). SMR was significantly raised in patients
diagnosed before the age of 40, at 1.50 (95 percent CI 1.09-2.01), with males (2.03
(1.19-2.86) having the highest level (2.03 (1.19-2.86). Acute adrenal insufficiency was a
leading cause of death, with infection and sudden death occurring at higher rates than
in the general population. Females (75.7 years) and males (64.8 years) died at 3.2 and
11.2 years younger than the projected life expectancy, respectively.
RISK FACTORS
Predisposing Factors
● Family history of Autoimmune disease
● Adrenal cortex autoantibody production
● Neoplasm
● Congenital adrenal hyperplasia
● Surgical removal of the adrenal gland
● Hypopituitarism
Precipitating Factors
● Tuberculosis infection
● Meningococcal infection w/ adrenal hemorrhage
● Use of medications such as etomidate, mitotane, & aminoglutethimide
● Metastatic carcinoma
● Infarction
● Abrupt removal of long-term corticosteroid therapy
PATHOPHYSIOLOGY
In primary adrenal insufficiency, there was significant bilateral damage to the
adrenal gland that led to impairment of entire gland cortex function. It results in many
things, first is the decreased serum levels of adrenal steroid hormones that exert
positive feedback on the pituitary gland and the increased production of ACTH in the
pituitary gland. The same gene that encodes ACTH also encodes melanocytes
stimulating hormone (MSH) that leads to coincidental increase in MSH production.
Then, MSH triggers the increased production of melanin by the melanocytes in the skin.
Second, is the decreased production of androgen from the zona reticularis that results
in decreased androgen levels in women. This decrease does not affect men much
because the testes are the major source of male androgen. Third, is the decreased
production of aldosterone from the zona glomerulosa that led to decreased sodium
channel and decreased sodium-potassium pump expression on principle cells of the
kidney. This results in decreased potassium pumped into kidney tubules leading to
increased potassium retention in serum, then decreased excretion of hydrogen ions
from kidneys, and increased sodium and water excretion because of decreased sodium
reabsorbed from the kidney tubules. Fourth is the decreased production of cortisol from
the zona fasciculata. This results in increased vasodilation because of lack of
cortisol-driven vasoconstriction of blood vessels. Also, because of decreased cortisol
production, there is an increased cortisol releasing hormone from the hypothalamus and
increased antidiuretic hormone released. There was also a decrease in cortisol
mediated gluconeogenesis and glycogenolysis. In secondary adrenal insufficiency, there
would be lack of adrenocorticotropic hormone (ACTH) that results to decrease cortisol
production
DIAGNOSTIC TOOLS
Blood and urine tests
- measures the levels of sodium, potassium and cortisol in the body. A low sodium,
high potassium or low cortisol level may indicate Addison's disease.
ACTH stimulation test
- ACTH signals the adrenal glands to produce cortisol. This test measures the
level of cortisol in your blood before and after an injection of synthetic ACTH.
- Addison's disease and most people who have had secondary adrenal
insufficiency for a long time have little or no increase in cortisol levels. The
adrenal glands may be too damaged to respond to ACTH.
Thyroid function test
- The thyroid gland produces hormones that control the body's growth and
metabolism. People with Addison's disease often have an underactive thyroid
(hypothyroidism), where the thyroid gland does not produce enough hormones.
- It is done by withdrawing blood from a vein in the arm. Thyroid blood tests are
used to tell if the thyroid gland is functioning properly by measuring the amount of
thyroid hormones in the blood.
Antibody test
- adrenal 21-hydroxylase antibody test also referred to as the adrenal antibodies
test, is used to investigate the insufficiency of the adrenal gland and to assess
the risk that a person may develop an autoimmune adrenal gland insufficiency
- A test result of 21-hydroxylase antibodies at 1 U/mL or higher indicates the
presence of adrenal autoantibodies, which is consistent with Addison disease.
CT Scan
- CT scans create images of organs and other inside structures using a
combination of x-rays and computer technologies. Adrenal gland alterations can
be detected with a CT scan of the abdomen. The glands in autoimmune
Addison's disease are tiny or normal in size and have no other apparent
abnormalities.
- In patients with Addison disease, an abdominal CT scan may be normal but
show bilateral enlargement of the adrenal glands due to TB, fungal infections,
adrenal hemorrhage, or infiltrating illnesses involving the adrenal glands.
CLINICAL MANIFESTATION
Primary Adrenal Insufficiency
● Conspicuous bronze color of the skin, especially in the creases of the hands and over
the metacarpophalangeal joints (hand and finger), elbows, and knees
● Darkening of scars, areas of vitiligo(absence of pigmentation), and increased
pigmentation of the mucous membranes, especially the buccal mucosa, due to
decreased secretion of cortisol, causing simultaneous secretion of excessive amounts
of corticotropin and melanocyte-stimulating hormone by the pituitary gland
● In women, decreased libido and lost of axillary and pubic hair
● Hyperkalemia
● Metabolic Acidosis
● Hyponatremia
● Craving for salty food due to decreased mineralocorticoid secretion (which normally
causes salt retention)
● Associated cardiovascular abnormalities, including orthostatic hypotension,
decreased cardiac size and output, and a weak, irregular pulse
● Postural dizziness
● Fasting hypoglycemia due to decreased gluconeogenesis
● Weakness and Body Malaise
● Muscle/joint pain
● Fatigue
● Weight loss
● Nausea, vomiting, and anorexia
● Decreased tolerance for even minor stress
Secondary Adrenal Insufficiency
● Similar to primary adrenal insufficiency, but without hyperpigmentation due to low
corticotropin and melanocyte stimulating hormone levels
● Possibly no hypotension and electrolyte abnormalities due to fairly normal aldosterone
secretion
● Usually normal androgen secretion
NURSING AND MEDICAL MANAGEMENT
Nursing Diagnosis 1: Risk for imbalanced nutrition: Less than body requirement
related to nausea and vomiting.
1.Medical
● Administer IV fluids, as ordered.
2.Pharmacological
Prescribed as ordered
● If the adrenal gland does not regain function, lifelong corticoid replacement,
usually w/ cortisone acetate or hydrocortisone (Cortef), both of which have a
mineralocorticoid effect.
3.Nursing
● Assess appetite and for the presence of nausea, vomiting, or diarrhea.
● Monitor trends in weight.
● Assess foods that the patient can tolerate.
● Monitor serum glucose levels.
● Assess for salt cravings.
● Ask the dietician to provide a high-protein, low-carbohydrate, high-sodium diet.
● Keep a late-morning snack available.
● Suggest need for frequent small meals.
● Instruct the patient to always carry a medical identification card stating that he
takes a steroid and giving the name of the drug and the dosage.
● Encourage rest periods after eating.
● Education about not missing a dose of medication.
● Explain to the patient the importance of taking antacids while on steroids.
Antacids will help to decrease gastric irritation caused by steroids.
Nursing Diagnosis 2: Risk for deficient fluid volume related to increased water and
sodium secretion and potassium retention.
1.Medical
● Start intravenous therapy as prescribed.
2.Pharmacological
Prescribed as ordered
● Oral fludrocortisone (Florinef), a synthetic mineralocorticoid, to prevent
dangerous dehydration, hypotension, hyponatremia, & hyperkalemia.
3.Nursing
● Assess vital signs, especially noting BP and HR for orthostatic changes.
● Assess skin turgor and mucous membranes for signs of dehydration.
● Assess for fatigue, sensory deficits, or muscle weakness, which may progress to
paralysis.
● Assess electrocardiogram rhythm, as available, for signs of hyperkalemia.
● Assess color, concentration and amount of urine.
● Monitor patient’s serum electrolytes and recommend electrolyte replacement
therapy (oral or IV) to the physician as needed.
● Commence a fluid balance chart, monitoring the input and output of the patient.
● Educate the patient/guardian on how to fill out a fluid balance chart at bedside.
● Must be taught never to miss a dose of medication.
● Instruct the patient to ingest salt additives in conditions of excess heat or
humidity.
● Encourage oral fluids as the patient tolerates.
Nursing Diagnosis 3:Risk for decreased cardiac output related to stress.
1.Medical
● Administer IV fluids, as ordered.
● If hypotension develops w/ signs of decreased CO, administer IV fluids rapidly.
2.Pharmacological
Prescribed as ordered
● I.V. bolus of hydrocortisone, 100mg q6hrs for 24hrs; then, 50 to 100mg IM or
diluted w/ dextrose in saline solution & given IV until patient condition stabilizes.
● During stressful procedures or significant illness, additional supplementary
therapy w/ glucocorticoids is required to prevent addisonian crisis.
● Administer antipyretics as needed for fever.
3.Nursing
● Assess level of consciousness.
● Monitor vital signs with frequent monitoring of BP.
● Include assessment for orthostatic hypotension.
● Monitor for dysrhythmias.
● Monitor urine output.
● Monitor oxygen saturation.
● Minimize stress situations and promote a quiet environment.
● Provide rest periods.
● Assist the patient with activities, as needed
● Educate about not to miss doses of medication.
● Warn the patient that stress may necessitate additional cortisone to prevent
adrenal crisis. Review stress management techniques.
MAINTENANCE STEROID THERAPY
● Arrange for a diet that maintains sodium and potassium balances.
● If the patient is anorexic, suggest six small meals per day to increase calorie
intake. Ask the dietitian to provide a diet high in protein and carbohydrates. Keep
a late-morning snack available in case the patient becomes hypoglycemic.
● Explain that lifelong steroid therapy is necessary.
● Teach the patient the symptoms of steroid overdose (swelling, weight gain) and
underdose (lethargy, weakness).
● Tell the patient that the dosage may need to be increased during times of stress
(when he has a cold, for example).
● Warn that infection, injury, or profuse sweating in hot weather may precipitate
adrenal crisis.
● Instruct the patient to always carry a medical identification card stating that he
takes a steroid and giving the name of the drug and the dosage.
● Teach the patient and his family how to give a hydrocortisone injection.
● Tell the patient to keep an emergency kit available containing hydrocortisone in a
prepared syringe for use in times of stress.
● Explain to the patient the importance of taking antacids while on steroids.
Antacids will help to decrease gastric irritation caused by steroids.
● Warn the patient that stress may necessitate additional cortisone to prevent
adrenal crisis. Review stress management techniques. Encourage adequate rest
and nutrition.
PROGNOSIS
If treated
Addison's disease cannot be cured but can be significantly improved with hormone
replacement therapy and the avoidance of common triggers. If treated properly,
Addison's disease can be brought under control and you can be better assured of living
a long and healthy life. Patient should:
● Continue replacement steroid therapy
● Have regular check-ups
● Keep spare medicine as necessary or emergency kit
● Take medicine every day at the right time
If untreated
If Addison's disease is left untreated, the levels of hormones produced by the adrenal
gland gradually decrease in the body. This causes the symptoms to get progressively
worse and eventually lead to a life-threatening situation called an adrenal or Addisonian
crisis.
● Addison’s crisis
● Higher complication rate of secondary sepsis or intestinal perforation
● Symptoms get progressively worse
● Death
References:
● Addison’s disease - Diagnosis and treatment - Mayo Clinic. (2020, November 24). MayoClinic.Org.
https://mayocl.in/3szBQkF
● Addison’s disease symptoms and treatments. (2021, November 1). NHS Inform. https://bit.ly/3M0KhNv
● Grossman, A. B. (2022, February 22). Addison Disease. MSD Manual Professional Edition.
https://www.msdmanuals.com/professional/endocrine-and-metabolic-disorders/adrenal-disorders/addison-di
sease
● Munir, S., Rodriguez, B., Waseem, M., & Haddad, L. (2022, January 9). NCBI - Addison Disease (Nursing).
NCBI. https://www.ncbi.nlm.nih.gov/books/NBK568775/
● NHS website. (2022, February 4). Addison’s disease. Nhs.Uk. https://bit.ly/3ss1yHK
● Vera, M. B. (2019, April 9). 3 Addison’s Disease Nursing Care Plans. Nurseslabs.
https://nurseslabs.com/3-addisons-disease-nursing-care-plans/
