Cushing Hypertension

Antagonists of glucocoiticoid and mineral ocorticoid activity have found iacieased use clinically ia the treatment of hypertension, Cushing s disease, and heightened iatraocular pressure. 

Differential diagnoses include diabetes mellitus and metabolic syndrome because patients with these conditions share several similar characteristics with Cushing s syndrome patients (e.g., obesity, hypertension, hyperlipidemia, hyperglycemia, and insulin resistance). In women, the presentations of hirsutism, menstrual abnormalities, and insulin resistance are similar to those of polycystic ovary syndrome. Cushing s syndrome can be differentiated from these conditions by identifying the classic signs and symptoms of truncal obesity, "moon faces" with facial plethora, a "buffalo hump" and supraclavicular fat pads, red-purple skin striae, and proximal muscle weakness. 

Patients with secondary hypertension may complain of symptoms suggestive of the underlying disorder. Patients with pheochromocytoma may have a history of paroxysmal headaches, sweating, tachycardia, palpitations, and orthostatic hypotension. In primary aldosteronism, hypokalemic symptoms of muscle cramps and weakness may be present. Patients with hypertension secondary to Cushing s syndrome may complain of weight gain, polyuria, edema, menstrual irregularities, recurrent acne, or muscular weakness. 

Speciai risk Use with caution in the following situations Nonspecific ulcerative colitis if there is a probability of impending perforation, abscess, or other pyogenic infection diverticulitis fresh intestinal anastomoses hypertension CHF thromboembolitic tendencies thrombophlebitis osteoporosis exanthema Cushing syndrome antibiotic-resistant infections convulsive disorders metastatic carcinoma myasthenia gravis vaccinia varicella diabetes mellitus hypothyroidism, cirrhosis (enhanced effect of corticosteroids). 

Adverse reactions of corticosteroids are frequent with the long-term immunosuppressive regimens which are often needed and include an increased risk of infections, Cushing-like symptoms, hypertension, hyperglycemia, osteoporosis, growth retardation in children and mental reactions such as dysphoria, psychosis and depression. 

Adrenoicorticai insufficiency, increased intracraniai pressure, pseudotumor cerebri, impaired wound heaiing, Cushing s syndrome, HPA suppression, skin uicers, toier-ance, withdrawai, visuai impairment, ocuiar hypertension, cataracts... 

A specific cause of hypertension can be established in only 10-15% of patients. Patients in whom no specific cause of hypertension can be found are said to have essential or primary hypertension. Patients with a specific etiology are said to have secondary hypertension. It is important to consider specific causes in each case, however, because some of them are amenable to definitive surgical treatment renal artery constriction, coarctation of the aorta, pheochromocytoma, Cushing s disease, and primary aldosteronism. 

Quest Diagnostics use an LC-MS/MS panel for diagnosing cortisol-related disorders by urine analysis. This panel was designed to diagnose Cushings syndrome and the hypertensive conditions AME and GRA. The panel quantifies cortisone, cortisol, 6/j-hydroxycorlisol and 18-hydroxycortisol (18-OHF). The Quest analysis uses 2H4 cortisol as an internal standard and HTLC for on-line extraction. This panel has replaced the RIA and HPLC methods previously used by this commercial laboratory. Another recent publication describes MS/MS of cortisone and cortisol in serum using APPI and similar conditions and MRM transformations to those listed above [43]. 

I use Nipride, which I have never had fail to control the BP in patients with Cushing s, primary aldosteronism, renal artery stenosis, pheochromocytoma, and scleroderma with malignant hypertension. 

Corticosteroids should be used cautiously in the presence of congestive heart failure, myocardial infarction, hypertension, diabetes mellitus, epilepsy, glaucoma, hepatic disorders, osteoporosis, peptic ulceration, and renal impairment. Children are more susceptible to these adverse effects. To avoid cardiovascular collapse, steroids must be given slowly by intravenous injection. Large doses produce Cushing s syndrome (with moon face and sometimes hirsutism). 

Several relatively common disorders result in aldosterone secretion abnormalities and aberrations of electrolyte status. In Addison s disease, the adrenal cortex is often destroyed through autoimmune processes. One of the effects is a lack of aldosterone secretion and decreased Na+ retention by the patient. In a typical Addison s disease patient, serum [Na+] and [CL] are 128 and 96 meq/L, respectively (see Table 16.2 for normal values). Potassium levels are elevated, 6 meq/L or higher, because the Na+ reabsorption system of the kidney, which is under aldosterone control, moves K+ into the urine just as it moves Na+ back into plasma. Thus, if more Na+ is excreted, more K+ is reabsorbed. Bicarbonate remains relatively normal. The opposite situation prevails in Cushing s disease, however, in which an overproduction of adrenocorticosteroids, especially cortisol, is present. Glucocorticoids have mild mineralocorticoid activities, but ACTH also increases aldosterone secretion. This may be caused by an oversecretion of ACTH by a tumor or by adrenal hyperplasia or tumors. Serum sodium in Cushing s disease is slightly elevated, [K+] is below normal (hypokalemia), and metabolic alkalosis is present. The patient is usually hypertensive. A more severe electrolyte abnormality is seen in Conn s syndrome or primary aldosteronism, usually caused by an adrenal tumor. Increased blood aldosterone levels result in the urinary loss of K+ and H+, retention of Na+ (hypernatremia), alkalosis, and profound hypertension. 

Adrenal insufficiency Cushing s syndrome Peptic ulceration Osteoporosis Hypertension... 

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