Pathophysiology Cushing's and Management of Chusing's Syndrome

Pathophysiology and Management of Chusing's Syndrome

Pathophysiology Cushing's syndrome

Glucocorticoids (particularly cortisol) stimulate gluconeogenesis in the liver and inhibit glucose uptake in preferential cells. This hormone also stimulates lipolysis. With the breakdown of proteins in the periphery and the formation of plasma proteins (eg, angiotensinogen) in the liver, this hormone increases the formation of erythrocytes, platelets, and granulocytes (neutrophils), while this hormone also reduces the number of granulocytes eosinophils, With basophils, lymphocytes, monocytes.

This hormone also through the formation of lipocortin and phosphoprotein proteins, suppresses the release of histamine, interleukin, and lymphokines. By inhibiting fogfo lipase, glucocorticoids suppress the formation of prostaglandins and leukotrienes, these hormones inhibit the formation of antibodies and therefore act as immunosuppressives. 

Glucocorticoids suppress inflammation by inhibiting the proliferation of connective tissue, but at the same time inhibiting the synthesis and repair of collagen, these hormones stimulate the secretion of acid and pepsin in the stomach and slow down mucus formation. In addition, this hormone reduces plasma calcium and phosphate levels, in part by inhibiting the formation of calcitriol. 

This hormone also sensitizes blood vessels and the heart to catecholamines in part by inhibiting prostaglandin synthesis, stimulating norepinephrine release, and increasing nervous system excitability.

Mineralocorticoids, especially aldosterone, increase sodium and water retention in the kidneys. This hormone also facilitates an increase in blood pressure and stimulates the excretion of potassium, magnesium, and hydrogen in the kidneys, and simultaneously


stimulates intracellular potassium uptake, but at high plasma levels, cortisol also exhibits significant mineralocorticoid effects although it is largely inactivated in mineralocorticoid target cells. In addition to mineralocorticoids and glucocorticoids, dehydro-epiandrosterone (DHEA), which is a precursor to steroid sex hormones, is also formed in the adrenals. 

The metabolic effects of excess glucocorticoids encourage the onset of DM, namely steroid diabetes, namely increased insulin release. Free fatty acids formed by stimulation of lipolysis are used in the liver to produce very-low-density lipoprotein (VLDL) which will be released into the blood. In addition, the liver forms ketone bodies from fatty acids. 

The spread of fat tissue occurs due to differences in the sensitivity of peripheral adipose tissue to glucocorticoids and insulin, this causes centripetal fat storage on a round face or moon face and accumulation of fat in the neck (buffalo hump) while the legs remain thin. 

The breakdown of peripheral proteins causes a decrease in muscle mass, and osteoporosis (loss of bone matrix). Striae (breakdown of subcutaneous connective tissue and purpura, increased vascular fragility), because the repair is impaired, wound healing is delayed, its effect on bone is exacerbated by Ca HPO4 deficiency and in children causes stunted growth, its effect on the blood causes polycythemia. Thrombosis and increased coagulability. 

A weak immune system makes it easier for infections to occur. Circulation sensitization to catecholamines, among others, causes an increase in cardiac contractility and peripheral vasoconstriction, causing hypertension, which together with hyperlipidemia and blood coagulability will facilitate the formation of atherosclerosis, thrombosis, and vascular blockage, due to stimulation of hydrochloric acid and pepsin secretion as well as inhibition of mucus secretion in the stomach, gastric ulcers or ulcers will occur. duodenum (peptic). Its effect on the nervous system can trigger the endocrine psychogenic syndrome.

The increased influence of mineralocorticoids causes hyperplasia which in turn causes hypertension. This also causes hypokalemia, hypomagnesemia, and alkalosis which further causes an increase in neuromuscular excitability, the effects of which include disturbances in the formation of action potentials and conduction in the heart.

Androgen excess can cause masculinization and amenorrhea (virilism) in women and accelerated onset of sex characteristics in boys (incomplete precocious puberty).

Management of Chusing's Syndrome

1. Because more Cushing's syndrome is caused by pituitary tumors than adrenal cortex tumors, treatment is often directed at the pituitary gland. Surgical removal of the tumor via a transsphenoidal hypophysectomy is the treatment of choice because it is often successful. Adrenalectomy is the treatment for patients with primary adrenal hypertrophy.

2. After surgery, symptoms of adrenal insufficiency may begin 12 to 48 hours later as a result of a decrease in previously high blood levels of adrenal hormones. Temporary replacement therapy with hydrocortisone may be needed for several months until the adrenal glands begin to show a normal response to the body's needs. . If both adrenal glands are removed (bilateral adrenalectomy), replacement therapy with adrenal cortical hormones should be performed for life.

3. Adrenal enzyme-blocking preparations (ie, metyrapone, aminoglutethimide, mitotane, ketoconazole) may be used to reduce hyperadrenalism if the syndrome is caused by ectopic secretion of ACTH by a tumor that cannot be completely removed. Close monitoring is necessary because symptoms of adrenal insufficiency and side effects from these drugs can occur.

4. There are two groups of drugs that can be used, namely drugs that prevent the production of cortisol (Mitotane) and serotonin antagonists that can prevent the release of ACTH (Cyproheptadine).

5. If Cushing's syndrome results from the administration of external (exogenous) corticosteroids, the dose of the drug should be reduced or gradually discontinued until a minimal dose is adequate to treat the underlying disease process (eg, autoimmune disease and allergies and organ rejection are achieved) transplanted). Usually, therapy given every two days will reduce the symptoms of Cushing's syndrome and allow the restoration of the responsiveness of the adrenal glands to ACTH.

Supporting Examination

  • Dexamethasone suppression test.
  • Blood sampling.
  • 24-hour urine collection.
  • CRF stimulation.
  • Radioimmunoassay examination
  • CT, ultrasound or MRI scanner.

References

Smeltzer C. Suzanne, Brunner & Suddarth,   Buku Ajar Keperawatan Medikal Bedah, Jakarta, EGC ,2002.

Baradero  Mary,   Klien Gangguan Endokrin, jakarta, EGC, 2009.

NANDA, NIC, dan NOC

Sylvia A. Price; Patofisiolgi Konsep klinis Proses-Proses Penyakit ; 1994 EGC; Jakarta

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