ANGELES UNIVERISTY FOUNDATION

Angeles City

COLLEGE OF NURSING

ADDISON’S DISEASE

BONIFACIO, RAYNE KRISTINE

JARING, HANZ STEPEHN

ORTIZA, SVELTLANA JAN

TORNO, KRIZEL

BSN1-I
ADDISON’S DISEASE

Adrenal insufficiency commonly refers to the deficient production of the adrenal

cortical hormones cortisol, aldosterone, and adrenal androgens. Adrenal insufficiency is
divided into primary and secondary. Primary insufficiency, which is due to destruction of
all cells of the adrenal cortex, In contrast, secondary adrenal cortical insufficiency, is
due to lack of adrenocorticotropic hormone (ACTH) stimulation. The most common
cause of primary autoimmune insufficiency is autoimmune destruction of the adrenal
cortex, often referred to as Addison’s disease. In most cases, the disease results from
an autoimmune disorder in which destructive autoantibodies directed against adrenal
cortical cells and invading cytotoxic lymphocytes destroy the cortex.

As a result of a glucocorticoid deficiency, the glucose level is subnormal and may

decline during fasting to such a low level that symptoms develop. The body's ability to
regulate the content of sodium, potassium, and water in body fluids is disturbed as a
result of the mineralocorticoid deficiency. Blood volume and blood pressure fall, as does
the concentration of sodium in the blood, and blood potassium rises. The blood volume
may become reduced that the circulation can no longer maintain efficiently.

People with Addison’s disease also frequently exhibit increased pigmentation of

the skin, which is caused by secretion of ACTH, along with MSH, which is produced
from the same precursor molecule that gives ACTH. The MSH stimulates the melanin-
producing cells in the skin and is responsible for the increased skin pigmentation
characteristics of Addison’s disease. ACTH output is regulated by a negative feedback
mechanism. In Addison disease, secretion of cortisol is greatly diminished, which
causes ACTH to rise in an unsuccessful attempt to increase cortisol output. Treatment
of Addison’s disease consists of administering the deficient corticosteroid.
POSSIBLE CAUSES

Addison's disease is a rare disease that can occur at any age and in both sexes.
Most cases of Addison's disease are due to the destruction of more than 90% of both
adrenal glands caused by an autoimmune process. This occurs when the body's
autoimmune system mistakenly attacks the adrenal glands. Destruction of the adrenal
gland leads to lack of production of the hormones cortisol and aldosterone.

Other causes include long lasting infections like HIV, fungal infections, and
tuberculosis which can also harm the adrenal glands. Tuberculosis was once
considered as the main cause of Addison's disease but is now responsible for fewer
than 20% of adult cases. Family history of autoimmune disease may also predispose a
person to Addison's disease. Bilateral adrenalectomy, which is the surgical removal of
one or both adrenal glands, hemorrhage in the adrenal glands, neoplasms, are all
factors that can destroy the function of the cells in the adrenal glands which can all
result to Addison's disease.

Main cause:

- An autoimmune process can cause the destruction of more than 90% of both
adrenal glands

Other causes:

- Tuberculosis (most common cause)

- Bilateral adrenalectomy
- Hemorrhage into the adrenal gland
- Neoplasms
- Infections
- Family history of autoimmune disease
SIGNS AND SYMPTOMS

Cortisol deficiency causes weakness, fatigue, anorexia, nausea and vomiting,

hypotension, hyponatremia, and hypoglycemia. Mineralocorticoid deficiency produces
renal sodium wasting and potassium retention and can lead to severe dehydration,
hypotension, hyponatremia, hyperkalemia, and acidosis. Main symptoms of primary
adrenocortical insufficiency are hyperpigmentation, weakness and fatigue, weight loss,
anorexia, and gastrointestinal disturbances. Hyperpigmentation is the classic physical
finding, hyperpigmentation of the skin and mucous membranes is one of the earliest
manifestations of Addison disease.

- Weakness or fatigue caused by alterations in adrenal hormone balance

- Weight loss, nausea, vomiting and anorexia caused by glucocorticoid
deficiency
- Areas of vitiligo
- Hyperpigmentation of the oral mucosa
- Skin pigmentation of the face, resembling sun-induced tan

TREATMENT

Patients with Addison disease require life-long glucocorticoid and

mineralocorticoid therapy. In patients with autoimmune Addison disease, survival
approaches that of the normal population, and most patients’ lead normal lives. In
general, death from adrenal insufficiency now occurs only in patients with rapid onset of
disease who may die before the diagnosis is established and appropriate therapy
started.
References :

Merkle, C. (2004). Handbook of Pathophysiology. (2nd ed.). Philadelphia, US: Lippincott

Williams & Wilkins.

Reisener, E.G. & Reisener, H.M. (2017). Crowley's an introduction to human disease:
pathology and pathophysiology correlations. (10th ed.).5 wall street, Burlington
MA: Jone & Bartlett Learning.

Gardner, D., & Shoback, D. (2017). Greenspans Basic and Clinical Endocrinology,
Tenth Edition. McGraw-Hill Education.

Gardner, D. G., & Shoback, D. M. (2018). Greenspans basic & clinical endocrinology.
New York: McGraw-Hill Education.

Kleine, B., & Rossmanith, W. (2015). Hormones and Hormone System: Textbook of
Endocrinology. Erscheinungsort nicht ermittelbar: Springer International
Publishing AG.

Krause, W., & Stutz, N. C. (2010). Cutaneous manifestations of endocrine diseases.

Berlin ; Heidelberg: Springer.

Neighbors, M., Tannehill-Jones, R., & Neighbors, M. (2015). Workbook to accompany

Human diseases, fourth edition. Clifton Park, NY: Cengage Learning.

Pertsemlidis, D., Inabnet, W. B., & Gagner, M. (2017). Endocrine surgery. Boca Raton,
FL: CRC Press, Taylor & Francis Group.

Weiss, R. E., & Refetoff, S. (2016). Genetic diagnosis of endocrine disorders.

Amsterdam: Elsevier Acad. Press.