Anatomy of adrenal glands
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Diseases of adrenal glands and hypophysis. thiology, pathogenesis, Diagnostics. Clinical pattern. Complications. Principles of treatment. The role of a doctor-dentist in early diagnostics and prophylaxis.
Anatomy of adrenal glandsLocation: the top of the kidney and weighting approximately 5 g each. Vascularization: a. suprarenalis superior (from a. phrenica inferior), a. suprarenalis media (from aorta abdominalis), a suprarenalis inferior (from a. renalis). Innervation: n. splanchnicus major (through plexus celiacus and plexus renalis), fibrae n. vagus and n. phrenicus.kidneyLeft renal arterya. suprarenalis inferior Left adrenal veinLeft adrenal glandLeft ovaria veinOvaria arteriesRight ovariaveinRena veinRightadrenal veinVena cava inferiora. supranenalis superiorAorta a. suprarenalis mediaa. phrenica inferior
Anatomy of adrenal glandsThe adrenals are divided into:1) outer area or cortex, which includes three zones: Glomerular (glomerulosa)Fascicular (fasciculata)Reticular (reticularis)
2) inner area or medulla
The pituitary gland is the master gland, which lies in a bony structure, the sella turcica, located at the base of the skull. The gland is a small organ about I cm long; it weighs 500 mg and is divided into two parts, anterior (adenohypophysis) and posterior (neurohypophysis).The anterior pituitary secretescorticotropin (ACTH)ProlactinSomatotropin (growth hormone (GH)gonadotropins [follicle-stimulating (FSH) and luteinizing (LH) hormones]thyrotropin (TSH)melanocyte-stimulating hormones (MSH).In the nerve endings of the posterior pituitary are stored Vasopressin (antidiuretic hormone, ADH)Oxytocin
The hypothalamus plays an important role in hormone regulation by secreting a series of small peptides which stimulate or inhibit the synthesis and release of hormones by the anterior pituitaryRealisingInhibitingCRGTRGLGRGFSRGGRH- GIH (somatostatin)PRG- PIF (dopamine)MRG- MIH
Action of mineralocorticoids:regulation of electrolyte balance in the organism:increasing the level of sodium (by sodium retention in distal nephron, colon, salivary gland) decreasing the level of potassium (by excretion).
Action of glucocorticoids:increasing of glycogen synthesis in liver and decreasing of glucose utilization by peripheral tissues, increasing gluconeogenesis;increasing of protein synthesis in liver and decreasing of its synthesis in muscles and increasing of protein destruction in muscles;increasing of lipolisis;anti-inflammatory function and immunomodulation;cardiovascular regulation (increasing of blood pressure).
RegulationFEEDBACK: Hormone secretion delivery to target cells hormone recognition by receptors in target cells biologic effect hormone degradation signal from target cells to stop further hormone secretion
Regulation of secretionglucocorticoids and androgens secretion is regulated by hypothalamic pituitary system
mineralocorticoids secretion is regulated by the renin angiotensin system, the level of Na+, K+ in blood, and to a lesser extent of ACTH
Action of catecholamines:modulate vascular tone;increase heart rate;antagonize insulin action.
CHRONIC ADRENOCORTICAL INSUFFICIENCY. It is an insidious and usually progressive disease resulting from adrenocortical hypofunction.
Classification.Primary adrenocortical insufficiency (Addisons disease).Secondary adrenocortical insufficiency .
Etiology of adrenal insufficiency:Primary:autoimmune processes (50 65 %);tuberculosis;neoplasm, metastatic carcinoma;inflammatory necrosis;amyloidosis; heamochromatosis;bilateral adrenal hemorrhage or infarction, intra adrenal hemorrhage (Waterhouse Friedrichsen syndrome following meningococcal septicemia); bilateral adrenalectomy; Secondary:hypothalamic or pituitary disease (primary injury of these organs leads to insufficiency of ACTH secretion that cause the two side atrophy of adrenal glands);glucocorticoid therapy.
Pathogenesis.Deficiency of adrenal hormones contributes to the hypotension and produces disturbances in carbohydrate, fat, and protein metabolism, and severe insulin sensitivity.
Symptoms and signs. Presentation may be acute and chronic. Frequently clinical signs of the primary chronic adrenocortical insufficiency are manifested in that time when adrenocortical tissue is destroyed on 70-90 %. The most common complaints are:weakness,malaise,weight loss,anorexia,depression.
Objective examination:Hyperpigmentation (in patients with primary adrenal insufficiency) is characterized by diffuse tanning of both exposed and nonexposed portions of the body, especially on pressure points (bony prominences), skin folds, scars, and extensor surfaces, black freckles over the forehead, face, neck, and shoulders; bluish black discoloration of the areolas and the mucous membranes of the lips, mouth, rectum and vagina are common. After compensation hyperpigmentation will decrease. Patients in 15 20 % of cases may have areas of vitiligo (depigmentation) as the sign of autoimmune process.
Objective examination:Hypotension or postural hypotension (88 90 %) with syncopal attacks can occur.Tachycardia.Weight loss (due to dyspeptic syndrome, true muscle tissue catabolism, dehydration).Anorexia, nausea, vomiting, abdominal pain, diarrhea are often. Gastritis, ulcer disease can occur.Decreased cold tolerance, with hypometabolism may be noted.Sexual disorders.Neurologic and psychiatric disorders: decreasing of the memory, mental activity, concentration of attention, depressions, hallucinations can occur due to chronic hypoglycemia which leads to changes of metabolism in brain tissue.Hypoglycemia.There are three stages of severity: mild, moderate and severe.
Laboratory findings.A low serum Na level and a high serum P level together with a characteristic clinical picture suggest the possibility of Addisons disease.Adrenal insufficiency can be specifically diagnosed by:low levels of plasma glucocorticoids and mineralocorticoids, or urinary 17 hydroxycorticosteroid (17 OHCS) or 17 ketogenic steroid (17 KGS);demonstrating failure to increase plasma cortisol levels, or urinary 17 OHCS or 17 KGS excretion, upon administration of ACTH (in patients with primary adrenal insufficiency, those with secondary adrenocortical insufficiency will have a significant increase in plasma cortisol or 24 - h urinary corticosteroid levels.)To distinguish between primary and secondary adrenal insufficiency, me have to find the level of plasma ACTH: primary shows increased, and secondary shows decreased level.
Instrumental findings.The ECG may decreased voltage and prolonged P R and Q T intervals.
Treatment.Etiologic: appropriate treatment of complicating infections (e.g., tuberculosis).Pathogenic:Diet (enough quantity of proteins, vitamins, salt and water).Glucocorticoids (normally, glucocorticoids are secreted maximally in the early morning hours, little being secreted at night).Average dosage is:cortisol: 20 25 mg daily;prednisolone 5 7.5 mg daily;hydrocortisone 30 40 mg orally daily. 2/3 of the dose can be given in the morning and 1/3 in the afternoon. Night doses should be avoided, as they may produce insomnia.
Mineraloocorticoids. DOCSA 5 mg orally daily should be used in patients with severe and moderate duration or fludrocortisone 0.1 0.2 mg orally once a day is recommended (this mineralocorticoid replaces aldosterone)Intercurrent illnesses (e.g., infections) should be regarded as potentially serious and the patient should double his dosage until he is well.If nausea or vomiting preclude oral therapy, medical attention should be sought immediately and parental therapy started.
Adrenal crisis - is a medical emergency caused by sudden marked insufficiency of adrenocortical hormones.
Precipitating factors.stress (infection (especially with septicemia), trauma, surgery, prolonged fasting, salt loss due to excessive sweating during hot weather);sudden withdrawal of adrenocortical hormone therapy in patients with chronic insufficiency.
Clinical features. An adrenal crisis is characterized byprofound asthenia, severe pains in the abdomen, lower back or legs; nausea, vomiting, diarrhea; peripheral vascular collapse; renal failure with azotemia. Body temperature may be subnormal, through severe hyperthermia due to infection is often seen.
Treatment.Therapy should be instituted immediately once a provisional diagnosis of adrenocortical failure has been made.Substitution therapyRehydrationTreatment of complications (hyperpyrexia, psychotic reactions).
Treatment.hydrocortisone 100 150 mg as a water soluble ester (usually the succinate or phosphate) is injected IV or acetate IMfollowed by infusion of 1 L of 5 % glucose in saline solution containing 100 mg hydrocortisone ester given over 2 h.Hydrocortisone acetate 50 75 mg IM each 4 6 hHydrocortisone therapy is given continuously to a total dosage in 24 h of 400 600 800 mg.After stabilization of BP (>100 mm Hg) we decrease the dosage of hydrocortisone acetate to 25 - 50 mg IM to 2 - 4 times a week
Treatment.Mineralocorticoids are not required when high dose hydrocortisone is givenIn a case of prominent hypotension DOKSA (5 mg), ftorhydrocortisone (cortinef 0,05 0,2 mg), fludrocortisone acetate (0.1 mg) have to be usedTotal infusion of saline and 5 % glucose - 2,5 3,5 l during first day
Prognosis. With a substitution therapy, the prognosis is excellent and a patient with Addisons disease should be able to lead a full life.
PHEOCHROMOCYTOMA.It is a tumor of chromaffin cells that secrete catecholamin