Diseases of the Adrenal Gland Online Medical Reference - discusses adrenal and endocrine dysfunction, and methods of diagnosis. Co-authored by Adriana G. Home > Articles > Cushing's Disease. Cushing's disease is common in older dogs, but both diagnosis and treatment can be complicated. In subjects with the late-onset (nonclassic.
Medical Care, Surgical Care, Consultations. Nour MA, Pacaud D. Height augmentation in 1. Int J Pediatr Endocrinol. Mornet E, Dupont J, Vitek A. Characterization of two genes encoding human steroid 1.
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Endocrinology Handbook. Imperial College Healthcare NHS Trust. Charing Cross, Hammersmith and St. Nifedipine, sold under the brand names Adalat among others, is a medication used to manage angina, high blood pressure, Raynaud's phenomenon, and premature labor. Mechanisms of Disease. Antiinflammatory Action of Glucocorticoids . Turk Rhen, Ph.D., and John A. 11-Deoxycorticosterone (DOC), or simply deoxycorticosterone, also known as 21-hydroxyprogesterone, as well as desoxycortone, deoxycortone, and cortexone, is a.
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Diseases of the Adrenal Gland. Anatomy and Physiology of the Adrenal Glands. Each adrenal consists of two functionally distinct endocrine glands: the cortex, derived from mesenchymal cells, and the medulla, derived from neuroectodermal cells. The adrenal cortex consists of three concentric zones: The outer glomerulosa secretes the mineralocorticoid aldosterone, the intermediate fasciculata secretes cortisol, and the inner reticularis secretes androgens. The endocrine cells of the adrenal medulla are the chromaffin cells, which are part of the sympathetic nervous system and produce the catecholamine epinephrine.
Back to Top. Adrenal Insufficiency. Etiology. Glucocorticoid insufficiency can be primary, resulting from the direct insult to the adrenal cortex, or secondary, from adrenocorticotropic hormone (ACTH) or corticotropin- releasing hormone (CRH) hyposecretion as a result of pituitary or hypothalamic dysfunctions.
Primary adrenal insufficiency affects glucocorticoid and mineralocorticoid secretion and may be fatal if untreated. Autoimmune destruction of the adrenal glands (Addison’s disease) is the most common cause of primary adrenal insufficiency in United States (7. Some other causes of primary adrenal insufficiency include bilateral adrenal hemorrhage, drugs (e. HIV infection, disseminated histoplasmosis, paracoccidiomycosis). HIV infection may result in both primary and secondary adrenal insufficiencies (AI). Addison’s disease may coexist with other autoimmune conditions, such as type 1 diabetes, hypothyroidism, or hypoparathyroidism.
Secondary and tertiary adrenal insufficiencies occur commonly after the discontinuation of glucocorticoids. Less frequently, ACTH deficiency may be caused by pituitary macroadenomas, pituitary surgery or radiation, and parasellar diseases. Megestrol acetate, an appetite stimulator used in some patients with advanced cancer or cachexia related to AIDS may be associated with secondary AI. Tertiary adrenal insufficiency results from the inadequate secretion of CRH. Secondary and tertiary adrenal insufficiencies only affect cortisol secretion, because ACTH has only a minor role in regulation of aldosterone secretion. Manifestations. All patients with primary adrenal insufficiency complain of fatigue, anorexia, and weight loss. Other clinical and laboratory manifestations of primary adrenal insufficiency are presented in Table 1.
Skin hyperpigmentation, initially on the extensor surfaces, palmar creases, and buccal mucosa, results from increased levels of ACTH and other pro- opiomelanocortin–related peptides, including melanocyte- stimulating hormone. Secondary adrenal insufficiency manifests more insidiously with lack of skin hyperpigmentation, salt craving, metabolic acidosis, and hyperkalemia, because mineralocorticoid secretion is intact. Fatigue, hyponatremia, and hypoglycemia are some of the clinical manifestations in secondary adrenal insufficiency.
Table 1 Clinical Manifestations of Primary Adrenal Insufficiency. Parameter. Frequency (%)Symptoms. Weakness, fatigue. Anorexia. 10. 0Nausea.
Vomiting. 75. Constipation. Diarrhea. 15. Abdominal pain. Salt craving. 16. Postural dizziness. Muscle and joint pain. Signs. Weight loss. Hyperpigmentation.
Vitiligo. 15. Hypotension (systolic blood pressure < 1. Hg)9. 2Laboratory Abnormalities.
Hyponatremia. 90. Hyperkalemia. 64. Hypercalcemia. 5Azotemia. Anemia. 40. Eosinophilia. Evaluation. Evaluating a patient with suspected adrenal insufficiency is a three- step process: establishing the diagnosis, differentiating between primary and secondary adrenal insufficiencies, and looking for the cause of adrenal insufficiency.
Establishing the Diagnosis. Because of circadian secretion of cortisol and overlap among patients with adrenal insufficiency and those with normal adrenal function, determining the random serum cortisol level is only of value during stress (see later, “Adrenal Insufficiency in the Critically Ill Patient”). An algorithm for the evaluation of adrenal function is shown in Figure 1. An early morning (8 am) plasma cortisol level lower than 3 . Cortisol levels in the range of 3 to 1. The standard- dose CST uses an intravenous or intramuscular injection of 2. A normal response is a plasma cortisol concentration higher than 1.
Most individuals with normal adrenal function achieve much higher cortisol levels at 6. For this reason, the 1.
The standard- dose CST is excellent for excluding primary adrenal insufficiency. However, patients with mild partial or recent- onset pituitary ACTH or hypothalamic CRH deficiency (e. The sensitivity of CST to pick up mild adrenal insufficiency improves when using the low- dose CST (1 . The lack of a commercially available 1- . In most clinical situations, the 3. CST has a diagnostic accuracy close to that of a low- dose CST. The insulin tolerance test (ITT) and metyrapone test are generally used for the evaluation of patients suspected to have secondary adrenal insufficiency.
ITT is considered the gold standard test for the evaluation of hypothalamic- pituitary- adrenal (HPA) axis. The ITT is contraindicated in older patients (> 6. The result of the metyrapone test has been validated compared with the ITT. Metyrapone blocks the final step in cortisol biosynthesis, resulting in a reduction in cortisol secretion, which in turn stimulates ACTH secretion. This leads to higher levels of 1. The CRH stimulation test requires intact pituitary and adrenal glands for a response.
The test has not been well validated for the evaluation of adrenal function and its current role in the evaluation of adrenal function is limited to research protocols. Differentiation Between Primary and Secondary Adrenal Insufficiencies. This is done through the measurement of the basal plasma ACTH level. An elevated ACTH level is consistent with primary adrenal insufficiency. A low or normal- range ACTH level, with a low cortisol level, confirms the diagnosis of secondary or tertiary adrenal insufficiency.
Determining the Cause of Adrenal Insufficiency. When the biochemical workup is consistent with primary adrenal insufficiency, computed tomography (CT) scanning of the adrenal glands may help with the differential diagnosis. Enlarged adrenal glands or calcifications suggest an infectious, hemorrhagic, or metastatic cause.
In rare circumstances, CT- guided percutaneous fine- needle aspiration of enlarged adrenal glands may help establish the diagnosis. Patients with tuberculous adrenal insufficiency usually have evidence of active systemic disease. When the biochemical work up suggests secondary or tertiary adrenal insufficiency, magnetic resonance imaging (MRI) of the pituitary gland is indicated if glucocorticoid therapy as the cause of the secondary adrenal insufficiency has been ruled out. Treatment. Patients with Addison’s disease require lifelong replacement with glucocorticoids and mineralocorticoids. The minimal dosage to treat symptoms should be used, starting with hydrocortisone, 1.
Some patients may need another dose of 2. Patients require fludrocortisone, 0.
The dose is adjusted based on clinical status, including the presence or absence of orthostatic hypotension, hypertension, and electrolyte imbalance. Patients may need to double the dose of fludrocortisone or increase salt intake during the summer, when the weather is hot. Patients with secondary or tertiary adrenal insufficiency do not need mineralocorticoid replacement. During minor illness (e. The inability to ingest hydrocortisone tablets warrants parenteral administration. Most patients can be educated to self administer hydrocortisone, 1.
IM, and reduce the risk of an emergency room visit. Hydrocortisone, 7. Parenteral hydrocortisone, 1. Patients taking more than 1.
All patients should wear some form of identification indicating their adrenal insufficiency status. Adrenal Crisis. Acute adrenal insufficiency (adrenal crisis) is a life- threatening emergency, which usually manifests with nausea, vomiting, abdominal pain, and shock. Patients may be previously undiagnosed or have chronic primary adrenal insufficiency, with no or inadequate glucocorticoid replacement. Abdominal tenderness and fever are common findings, and adrenal crisis may manifest as an acute abdomen. In these cases, surgical exploration without glucocorticoid coverage can be lethal. The major hormonal factor precipitating adrenal crisis is mineralocorticoid deficiency. Therefore, adrenal crisis rarely occurs with secondary adrenal insufficiency.
Treatment of adrenal crisis should not be delayed. Diagnostic workup in a patient with no history of AI should include a plasma sample for cortisol and ACTH level determination, immediately followed by an IV bolus of hydrocortisone, 1. Hydrocortisone should be continued, 5. Adrenal Insufficiency in the Critically Ill Patient. The overall incidence of AI in critically ill patients is less than 1. The concept of total adrenal insufficiency has gradually been replaced by relative adrenal insufficiency, which may be fatal in critically ill patients.
Hypotension in patients with adrenal insufficiency may mimic hypovolemic or septic shock and should be considered in the differential diagnosis. Serial follow- up of adrenal function in critically patients with clinical features suggestive of AI is recommended. Intensive care unit (ICU) patients with hemodynamic instability, despite fluid resuscitation (especially in the presence of shock), should be tested for AI. A random serum cortisol level determination and the standard CST are the two commonly used tests for evaluating adrenal function in these patients. However, the cortisol level that reflects an adequate response is uncertain. In critically ill patients with near- normal albumin levels (> 2. L), a random plasma cortisol level lower than 1.
In patients with equivocal biochemical results, a trial of 2 or 3 days of stress dosage glucocorticoids is appropriate, as long as it will be discontinued in the absence of any significant hemodynamic improvement.
Nifedipine - Wikipedia. Nifedipine. Clinical data.
Trade names. Adalat, Procardia, others. AHFS/Drugs. com. Monograph. Medline. Plusa. 68. Pregnancycategory.
Routes ofadministrationby mouth, topical. ATC code. Pharmacokinetic data. Bioavailability. 45- 5. Protein binding. 92- 9. Metabolism. Gastrointestinal, Liver. Biological half- life.
Excretion. Kidneys: > 5. Biliary: 5- 1. 5%Identifiers. CAS Number. Pub. Chem. CIDIUPHAR/BPSDrug. Bank. Chem. Spider.
UNIIKEGGCh. EBICh. EMBLECHA Info. Card. Chemical and physical data. Formula. C1. 7H1. N2. O6. Molar mass.
D model (Jmol)Melting point. It may be used to treat severe high blood pressure in pregnancy. Its use in preterm labor may allow more time for steroids to improve the baby's lungs and time to transfer the mother to a well qualified medical facility before delivery. Nifedipine is taken by mouth and comes in fast and slow release formulations.
Serious side effects may include low blood pressure and heart failure. In hypertension, recent clinical guidelines generally favour diuretics and ACE inhibitors, although calcium channel antagonists, along with thiazide diuretics, are still favoured as primary treatment for patients over 5. African American patients.
It was once frequently prescribed as needed to people taking MAOIs for real or perceived hypertensive crises. Sublingual nifedipine causes blood- pressure lowering through peripheral vasodilation. It can cause an uncontrollable decrease in blood pressure, reflex tachycardia, and a steal phenomenon in certain vascular beds. There have been multiple reports in the medical literature of serious adverse effects with sublingual nifedipine, including cerebral ischemia/infarction, myocardial infarction, complete heart block, and death. As a result of this, the FDA reviewed all data regarding the safety and efficacy of sublingual nifedipine for hypertensive emergencies in 1.
A Cochrane review has concluded that it is comparable with magnesium sulfate and beta- agonists (such as ritodrine) with fewer side- effects. A 2. 00. 5 meta- analysis showed modest benefits (3. It is also used for the small subset of people with pulmonary hypertension. Nifedipine rapidly lowers blood pressure, and patients are commonly warned they may feel dizzy or faint after taking the first few doses.
Tachycardia (fast heart rate) may occur as a reaction. These problems are much less frequent in the sustained- release preparations of nifedipine. Extended release formulations of nifedipine should be taken on an empty stomach, and patients are warned not to consume anything containing grapefruit or grapefruit juice, as they raise blood nifedipine levels. There are several possible mechanisms, including the lowering of CYP3.
A4 activity. The adverse effects include lethargy, bradycardia, marked hypotension and loss of consciousness. The drug may be quantitated in blood or plasma to confirm a diagnosis of poisoning in hospitalized patients or to assist in a medicolegal death investigation. Analytical methods usually involve gas or liquid chromatography and specimen concentrations are usually in the 1. Although nifedipine and other dihydropyridines are commonly regarded as specific to the L- type calcium channel, they also possess nonspecific activity towards other voltage- dependent calcium channels. The American Society of Health- System Pharmacists. Retrieved Dec 1. 9, 2. Retrieved 2. 5 December 2.
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