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Prevention of diseases of the endocrine system. Diabetes mellitus. Endemic goiter. Thyrotoxicosis. Sakharova Inna Ye., MD, PhD Hypothalamus • consists of very small clusters of cells that are located just above the pituitary gland • It controls the function of the pituitary gland, by producing hormones that induce the pituitary gland, which in turn affects hormone secretion of the other glands • Hormones secreted by hypothalamus include growth hormone-releasing hormone (GHRH), somatostatin and dopamine. Epiphysis (Pineal body) • Produce melatonin • Hypofunction: insomnia, increased anxiety, immune suppression, decreased basal body temperature and an elevated level of estrogen/progesterone ratio. • Hyperfunction: hypotension, inadequate function of the adrenal and thyroid glands, decreased estrogen/progesterone ratio, Seasonal Affective Disorder (SAD). Hypophysis (Pituitary gland) • “Master gland” of the organism • Produce endorphins ENDOCRINE GLAND HORMONES PITUITARY TSH •ANTERIOR ACTH LOBE FUNCTIONS •Thyroid to release hormones •Adrenal cortex to release hormones FSH,LH •Growth, maturation & GH/ SOMATOTROPIN •Growth of body tissues PROLACTIN/ LTH •Development of function of sex organs & bones mammary glands & lactation ENDOCRINE GLAND HORMONE ADH PITUITARY •POSTERIOR LOBE • INTERMEDIATE LOBE FUNCTION •Regulates water metabolism OXYTOCIN •Stimulate uterine MSH •Affects skin pigmentation contractions •release of milk Hypofunction (Hypopituitarism): • • • • • • • • • • • Head injuries Brain tumor Brain surgery Radiation treatment Autoimmune inflammation (hypophysitis) Stroke Infections of the brain, such as meningitis Tuberculosis Infiltrative diseases, such as sarcoidosi, histiocytosis Xand hemochromatosis Severe loss of blood during childbirth, which may cause damage to the front part of the pituitary gland (Sheehan syndrome, or postpartum hypopituitarism) Genetic mutations resulting in impaired pituitary hormone production Symptoms of hypopituitarism: • Growth hormone deficiency: - Congenital – dwarfism, nanism short stature (height more than 2 standard deviations below the mean for age and gender), muscle hypotonia, delayed motor development, “childs’ face”, high voice, hypogonadism, normal mental development - Aquired – growth retardation, memory problems, hypogonadism, decresed of muscles strength • FSH and LH deficiency: Deficiency of luteinizing hormone (LH) and folliclestimulating hormone (FSH), together referred to as the gonadotropins, leads to different symptoms in men and women. Women experience oligo- or amenorrhea (infrequent/light or absent menstrual periods respectively) and infertility. Men lose facial, scrotal and trunk hair, as well as suffering decreased muscle mass and anemia. Both sexes may experience a decrease in libido and loss of sexual function, and have an increased risk of osteoporosis (bone fragility). Lack of LH/FSH in children is associated with delayed puberty. - TSH deficiency: - Congenital hypothyroidism, cretinism increased birth weight, edemas, prolonged jaundice, low voice, enlarged tongue - ADH (vasopressin) deficiency: - Diabetes insipidus excessive thirst, polyuria, hypostenuria, normal level of glucose in blood, high sodium level Hyperfunction (Hypopituitarism): • Excessive production of growth hormone: Childhood: gigantism Adults: acromegaly Diagnostics: • Level of hormones in blood • X-ray of sella turcica • X-ray of hands (bone age) • MRI • CT scan ENDOCRINE GLAND HORMONE FUNCTION THYROID T3 & T4’ •Regulate metabolic rate •P,C,F metabolism •Regulate physical & mental growth & development THYROCALCITONIN PTH PARATHYROID •Decrease serum Ca by increasing bone deposition •Increase serum calcium by promoting bone decalcification • Hypofunction: • Endemic goiter, Aquired hypothyroidism, autoimmune thyroiditis • Hyperfunction: • Graves’ disease Classification of Goiter by Grades Classification Description Grade 0 No palpable or visible goiter. Grade 1 Mass in the neck that is consistent with an enlarged thyroid that is palpable but not visible when the neck is in the normal position. Moves upward in the neck as the patient swallows. Nodular alterations can occur even when the thyroid is not enlarged. Grade 2 Swelling in the neck that is visible when the neck is in a normal position and is consistent with an enlarged thyroid when the neck is palpated. From WHO/UNICEF Grave’s ophthalmopathy • Grefe symptom (uncovering sclera during patient is looking down) • Koher symptom (uncovering sclera during patient is looking up) • Rosenbah symptom (lids tremor) Diffuse toxic goiter (Graves disease) Lab. findings : – levels of T3 and T4 – Serum TSH, measured by the sensitive methods, is undetectable or subnormal • Simple goiter (the convertible terms are colloid goiter, adolescent goiter, juvenile goiter, nontoxic goiter) is an acquired enlargement of the thyroid gland with normal function that is not caused by an inflammatory process or a tumor. Lab. findings: – N levels of T3, T4 – N level of thyroid-stimulating hormone (TSH) – negative thyroid antibodies Endemic goiter occurs iodine-deficient areas. predominantly in Test for diagnosing iodine deficiency: Extreme deficiency occurs when daily urine contains less then 25 g of iodine; moderate deficiency occurs when it is 25-50 g and an adequate intake is reflected by an excretion of 100-200 g/day. Lab. findings in early stages and small iodine deficiency: – N or slightly levels of T3, T4 – N or slightly level of thyroid-stimulating hormone (TSH), but these patients are clinically euthyroid. Recommended daily Intake of iodine Adults 150 micrograms/day Children 90-120 micrograms/day Pregnant Women 200 micrograms/day Diagnostics: • Labs • • • – Serum TSH (0.4 – 6.15 μU/mL) – Serum Free T4 (0.9 – 1.7 ng/dL) – Serum T3 (T3 70 – 220 ng/dL) – Serum T4 (4.5 – 11.5 μg/dL) – T3 Resin uptake test (25%-35%) – Thyroid antibodies – Serum thyroglobin Radioactive iodine uptake test Thyroid scan, radioscan, or scintiscan USD of thyroid gland ENDOCRINE GLAND HORMONES FUNCTION ADRENAL CORTEX ALDOSTERONE •Fluid & electrolyte balance; •Na reabsorption; •K excretion •Glycogenolysis; •Gluconeogenesis •Na & water reabsorption •Antiinflammatory •Stress hormone CORTISOL SEX HORMONES •Slightly significant ENDOCRINE GLAND HORMONE FUNCTION ADRENAL MEDULLA EPINEPHRINE NOREPINEPHRINE •Increase heart rate & BP •Bronchodilation, •Glycogenolysis •Stress hormone Adrenal glands hyperfunction: Cushing's syndrome (hypercorticism) Conn's syndrome (hyperaldosteronism) Congenital adrenal hyperplasia (CAH) Pheochromocytoma • Cushing's syndrome is a multisystem disorder resulting from chronic exposure to inappropriately elevated concentrations of free circulating glucocorticoids. Etiology of Cushing's syndrome Endogenous (ACTH dependent 85%) • Cushing's disease (pituitary) • Ectopic ACTH syndrome (small cell lung carcinoma) • Ectopic CRH syndrome (bronchial carcinoid tumours) ACTH independent 15% • Common: Adrenal adenoma, adrenal carcinoma • Less common: Micronodular hyperplasia, macronodular hyperplasia • Rare: McCune-Albright syndrome, gastric inhibitory polypeptide Exogenous • ACTH treatment • Glucocorticoid treatment Pseudo-Cushing's syndrome • Major depressive disorder • Alcoholism • Obesity Clinical features of Cushing's syndrome • 90% - Central (truncal) obesity. Fat • • • • • deposits may appear in the cheeks (moon facies), in the dorsocervical area (buffalo hump), and the supraclavicular area 85% - Hypertension 65% - Presence of multiple purple striae with a diameter >1 cm on the abdomen or proximal extremities 60% - Muscle wasting and weakness affect the proximal muscles of leg and shoulder girdle 40% - Easy bruising of the skin 40% - Osteoporosis • Hyperpigmentation (palmar creases and • • pressure points) in a patient with Cushing's syndrome strongly suggests an ACTH cause (Cushing's disease) Patients may have mild hirsutism and acne, but severe hirsutism and especially virilisation strongly suggest an adrenal carcinoma. Depression, lethargy, and insomnia often occur at the same time as other symptoms. In children the dominant clinical features are cessation of linear growth and weight gain; the clinical course is more aggressive than in adults. • Conn's syndrome is a disease of the adrenal glands involving excess production of a hormone, called aldosterone. Another name for the condition is primary hyperaldosteronism. Primary Hyperaldosteronism (Conn's syndrome) 1. 2. 3. 4. Solitary adrenal adenomas (80-90%) Bilateral adrenal hyperplasia (10-20%) Adrenal Carcinoma (rare) Unilateral Adrenal Hyperplasia (very rare) Clinical features of Conn's syndrome • Often asymptomatic • Frontal headache • Muscle weakness to flaccid paralysis • • decreased muscle strength (because of low potassium level) Polyuria and Polydipsia (carbohydrate intolerance) Hypertension Hypofunction of adrenal glands Addison's disease (primery adrenal insufficiency) The causes of Addison's disease include: • Actual destruction of the adrenal glands • • • through cancer, infection, or other diseases. Use of corticosteroids as a treatment causes a slow down in production of natural corticosteroids by the adrenal glands. Certain drugs used to treat fungal infections may block production of corticosteroids in the adrenal glands. Usually, the cause is unknown. Symptoms: • • • • • • • • • • • Weakness, Fatigue, Dizziness Arterial hypotension Dark skin Black freckles Bluish-black discoloration around the nipples, mouth, rectum, scrotum, or vagina Lack of appetite Weight loss Muscle aches Nausea, Vomiting, Diarrhoea Intolerance to cold Dehydration Diagnostics of adrenal glands disorders: • Hormons level in blood and urine • Products of hormons’ metabolism in blood • • • • • (hydroxyprogesteron) Products of hormons’ metabolism in urine (17-ketosteroids) Hormons supression tests Biochemical blood testing (pH, electrolytes) Molecular genetics MRI, CT scan, USD of adrenal glands QUESTIONS ?