Cushing's Syndrome
Original Editors - Jessica Stevenson from Bellarmine University's Pathophysiology of Complex Patient Problems project.
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Definition/Description
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Cushing’s syndrome is a general term for increased secretion of cortisol by the adrenal cortex. When corticosteroids are administered externally, a condition of hypercortisolism called iatrogenic Cushing’s syndrome occurs. [1] When the hypercotisolism results from an oversecretion of ACTH from the pituitary, the condition is called Cushing’s disease. The clinical presentation is the same for all of these conditions. [2]
- ACTH: Adrenocorticotropic hormone
Prevalence
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Non-iatrogenic Cushing’s syndrome occurs mainly in women, with an average age of onset of 20 to 40 years, although it can be seen in people up to age 60 years. [2]
Characteristics/Clinical Presentation[edit | edit source]
Clinical manifestations include “moon” face (very round), buffalo hump (truncal obesity with prominent supraclavicular and dorsal cervical fat pads) [3], protuberant abdomen with accumulation of fatty tissue and stretch marks with purple striae, muscle wasting and weakness, thin extremities, decreased bone density (especially spine), kyphosis and back pain (secondary to bone loss), easy bruising and poor wound healing due to thin and atrophic skin [3], acne, psychiatric or emotional disturbances, impaired reproductive function (decreased libido and changes in menstrual cycle, and diabetes mellatis. In women, masculinizing effects such as hypertrichosis, breast atrophy, voice changes, and other signs of virilism are noted. Cessation of linear growth is characteristic in children. [1] [3]
Associated Co-morbidities[edit | edit source]
Cushing’s syndrome involves the HPA axis causing excess cortisol release from the adrenal glands. When the normal function of the glucocorticoids becomes exaggerated, a wide range of physiologic responses can be triggered. [2]
Co-morbidities involved with Cushing’s disease are persistent hyperglycemia, cardiac hypertrophy and hypertension, proximal muscle wasting (protein tissue wasting), osteopenia or osteoporosis, hypokalemia, mental changes and memory loss, depression, renal calculi, increased susceptibility to infection, adrenal hyperplasia and adrenal tumors [2] [3] [1]
Medications[edit | edit source]
Initially, the patient’s general condition should be supported by high protein intake and appropriate administration of vitamin K. If clinical manifestations are severe, it may be reasonable to block corticosteroid secretion with metyrapone 250 mg to 1 g pot id or ketoconazole 400 mg po once/day, increasing to a maximum of 400 tid. Ketoconazole is more readily available but slower in onset and sometimes hepatatoxic. [3]
Adrenal inhibitors, such as metyrapone 500 mg pot id (and up to a total of 6 g/day) or mitotane 0.5 g po once/day, increasing to a maximum of 3 to 4 g/day, usually control severe metabolic disturbances (eg. Hypokalemia). When mitotane is used, large doses of hydrocortisone or dexamethasone may be needed. Measures of cortisol production may be unreliable, and severe hypercholesterolemia may develop. Ketoconazole 400 to 1200 mg po once/day also blocks corticosteroid synthesis, although it may cause liver toxicity and can cause addisonian symptoms. Alternatively, the corticosteroid receptors can be blocked with mifepristone (RU 486). Mifepristone increases plasma cortisol but blocks effects of the corticosteroid. Sometimes ACTH-secreting tumors respond to long-acting somatostatin analogs, although administration for > 2 years requires close follow-up, because mild gastritis, gall stones, cholangitis, and malabsorption may develop. [3]
Diagnostic Tests/Lab Tests/Lab Values[edit | edit source]
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Causes[edit | edit source]
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Systemic Involvement[edit | edit source]
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Medical Management (current best evidence)[edit | edit source]
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Physical Therapy Management (current best evidence)[edit | edit source]
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Alternative/Holistic Management (current best evidence)[edit | edit source]
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Differential Diagnosis[edit | edit source]
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Case Reports[edit | edit source]
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Resources
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References[edit | edit source]
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- ↑ 1.0 1.1 1.2 Goodman CC, Snyder KS. Differential Diagnosis for Physical Therapists: Screening for Referral. Philadelphia : W.B. Saunders Company; 2006: 473-475
- ↑ 2.0 2.1 2.2 2.3 Goodman CC, Fuller KS. Pathology: Implications for the Physical Therapist 3rd ed. St. Louis: Saunders Elsevier; 2009: 481-483.
- ↑ 3.0 3.1 3.2 3.3 3.4 3.5 Beers MH, Porter RS, Jones TV, Kaplan JL, Berkwits M. The Merck Manual of Diagnosis and Therapy 18th ed. Whitehouse Station:Merck Research Laboratories; 2006: 1212-1214.
