Hemorrhage into adrenal gland
Tuberculosis, histoplasmosis, and cytomegalovirus
Family history of autoimmune disease
Hypopituitarism (causing decreased ACTH secretion)
Abrupt withdrawal of long-term corticosteroid therapy
Removal of an ACTH-secreting tumor
Pituitary injury by tumor or infiltrative or autoimmune process
Nausea, vomiting, anorexia, weight loss
Conspicuous bronze color of the skin, especially on hands, elbows, and knees; darkening of scars
Cardiovascular abnormalities, including orthostatic hypotension, decreased cardiac size and output, and weak, irregular pulse
Decreased tolerance for even minor stress
Craving for salty food
Similar to primary hypofunction; differences include:
hyperpigmentation absent because ACTH and melanocyte-stimulating hormone levels are low
possibly normal blood pressure and electrolyte balance because aldosterone secretion is near normal
usually normal androgen secretion.
Blood test for plasma cortisol levels confirms adrenal insufficiency.
Metyrapone test is used to detect secondary adrenal hypofunction.
Rapid corticotropin stimulation test by I.V. or I.M. administration of cosyntropin, a synthetic form of corticotropin, after baseline sampling for cortisol and corticotropin (samples drawn for cortisol 30 and 60 minutes after injection), differentiates between primary and secondary adrenal hypofunction. A low corticotropin level indicates a secondary disorder. An elevated level is indicative of a primary disorder.
Laboratory studies reveal decreased plasma cortisol level (less than 10 µg/dL in the morning; less in the evening) and decreased serum sodium and fasting blood glucose levels.
Serum chemistry reveals increased serum potassium, calcium, and blood urea nitrogen levels.
Complete blood count shows elevated hematocrit and increased lymphocyte and eosinophil counts.
X-rays show adrenal calcification if the cause is infectious.
Lifelong corticosteroid replacement, usually with cortisone or hydrocortisone, which have a mineralocorticoid effect
Pituitary hypersecretion of ACTH
Autonomous, ectopic ACTH secretion by a tumor outside the pituitary (usually malignant, frequently a pancreatic tumor or oat cell carcinoma of the lung)
Administration of synthetic glucocorticoids or steroids
Adrenal adenoma or a cancerous adrenal tumor
Fat pads above the clavicles, over the upper back (buffalo hump), on the face (moon face), and throughout the trunk (truncal obesity); slender arms and legs
Increased susceptibility to infection; decreased resistance to stress
Hypertension, left ventricular hypertrophy, bleeding and ecchymosis, and dyslipidemia
Increased androgen production — clitoral hypertrophy, mild virilism, hirsutism, and amenorrhea or oligomenorrhea in women; sexual dysfunction
Sodium and secondary fluid retention, increased potassium excretion, and ureteral calculi
Irritability and emotional lability
Little or no scar formation; poor wound healing
Purple striae, facial plethora, and acne
Pathologic fractures; skeletal growth retardation in children
Laboratory studies reveal hyperglycemia, hypernatremia, glucosuria, hypokalemia, and metabolic acidosis; elevated urinary free cortisol levels; elevated salivary free cortisol; and elevated serum cortisol.
Dexamethasone suppression test confirms the diagnosis and determines the cause, possibly an adrenal tumor or a nonendocrine, corticotropin-releasing tumor.
Ultrasound, computed tomography scan, and magnetic resonance imaging detect the presence of a pituitary or adrenal tumor.
Specific for cause of hypercortisolism — pituitary, adrenal, and ectopic
Surgery for tumors of adrenal or pituitary glands or other tissue, such as lung
Radiation therapy for tumor
Cortisol replacement therapy after surgery
Antineoplastic and antihormone agents
For inoperable tumor, drugs such as mitotane or aminoglutethimide to block steroid synthesis
Neurogenic: stroke, hypothalamic or pituitary tumor, cranial trauma, or surgery
Nephrogenic: X-linked recessive trait, end-stage renal failure
Psychogenic: primary polydipsia or sarcoidosis
Transient diabetes insipidus: certain drugs, such as lithium, phenytoin, or alcohol
progressive loss of nerve tissue and increased diuresis
polyuria and polydipsia, reflecting permanent loss of the ability to secrete adequate ADH.
Polydipsia and polyuria up to 20 L/d (cardinal symptoms)
Sleep disturbance and fatigue
Headache and visual disturbance
Abdominal fullness, anorexia, and weight loss
Changes in level of consciousness
Urinalysis shows almost colorless urine of low osmolality and low specific gravity.
Water deprivation test identifies vasopressin deficiency, resulting in renal inability to concentrate urine.
Vasopressin to control fluid balance and prevent dehydration until the cause of diabetes insipidus can be identified and eliminated
Hydrochlorothiazide with potassium supplement
Fluid intake to match output
type 1 — absolute insulin insufficiency
type 2 — insulin resistance with varying degrees of insulin secretory defects
gestational diabetes — manifested during pregnancy.
Environment (infection, toxins)
Stress, diet, and lack of exercise in genetically susceptible persons
Polyuria and polydipsia
Nausea; anorexia (common) or polyphagia (occasional)
Weight loss (usually 10% to 30%; persons with type 1 diabetes often have almost no body fat at diagnosis)
Headaches, fatigue, lethargy, reduced energy levels, and impaired school or work performance
Muscle cramps, irritability, and emotional lability
Vision changes such as blurring
Numbness and tingling
Abdominal discomfort and pain; diarrhea or constipation
Recurrent vaginal candidiasis
Two of the following criteria obtained more than 24 hours apart, using the same test twice or any combination, are indicators of the disease:
fasting plasma glucose level of 126 mg/dL or more
typical symptoms of uncontrolled diabetes and random blood glucose level of 200 mg/dL or more
blood glucose level of 200 mg/dL or more 2 hours after ingesting 75 g of oral dextrose.
Other criteria include:
diabetic retinopathy on ophthalmologic examination
other diagnostic and monitoring tests, including urinalysis for acetone and glycosylated hemoglobin (reflects glycemic control over the past 2 to 3 months).