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Endocrine System

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Endocrine System CHAPTER XII PDL 101 HUMAN ANATOMY & PHYSIOLOGY Ms. K. GOWRI. M.Pharm., Lecturer. ENDOCRINE SYSTEM Introduction : Endocrine glands consist of groups of secretory cells surrounded by an extensive network of capillaries which facilitates diffusion of hormones. The endocrine glands are : 1. 1 pituitary gland 2. 1 thyroid gland 3. 4 parathyroid glands 4. 2 adrenal glands 5. The pancreatic islets 6. 1 pineal gland or body 7. 1 thymus gland 8. 2 ovaries in the female 9. 2 testes in the male . PITUITARY GLAND AND HYPOTHALAMUS : • Regulate activity of most of endocrine glands. • Pituitary gland lies in the hypophyseal fossa of the sphenoid bone. • Anterior pituitary & posterior pituitary • Thin strip of tissue called intermediate lobe. • Blood supply - arterial blood internal carotid artery • Venous blood - venous sinuses between duralayer The influence of the hypothalamus on the pituitary gland : • anterior pituitary - network of blood vessels forms part of the pituitary portal system. • Posterior pituitary – nerve cells called pituicytes hypothalamohypophyseal tract) ´ Anterior pituitary : Growth hormone (GH It release is stimulated by growth hormone releasing hormone (GHRH) & supressed by growth hormone release inhibiting hormone (GHRIH). • Sleep , exercise, hypoglycaemia, stimulates release. Thyroid stimulating hormone (TSH) : •Hormone thyroxine (T4) & triiolothyronine (t3). •Release decreases in evening & highest -> night. •Regulated by negative feed back mechanism. Adrenocorticotrophic hormone (corticotropin ACTH) •From hypothalamus -> synthesis of ACTH •Increases of conc of cholesterol & steroids within the adrenal cortex & the output. •Associated with sleep pattern -> shift work changes. •Secretion by negative feed back mechanism. Prolactin : •Stimulates lactation & has a direct effects on breasts immediately after parturition (child birth) •Lowered by prolactin inhibiting hormone. •Prolactin together & oestrogens, corticosteroids, insulin & thyroxine is involved. Gonadotrophins : •Sex hormones secreted by anterior pituitary in response to luteinising hormone releasing hormone (LHRH) also known as gonadotrophin releasing hormone (GnRH) •In females – LH & FSH ->oestrogen, progesteron •In males -> LH,ICSH - >testosterone. Posterior pitutary : • oxytoxin & antidiuretic hormone are synthesized in the hypothalamus. • they act on non-endocrine tissue and their release by exocytosis is stimulated by nerve impulses. Oxytocin •Stimulates two target tissues •Increased oxytocin during parturition •Positive feedback mechanism •Suckling inhibits the release of prolacting inhibiting hormone Antodiuretic hormone (ADH) or vaso pressin : •Reduce urine output •Reabsorption of water from glomerular filtrate is increased Glucagon : •Conversion of glycogen to glucose • glucogenesis Somastatin : • by hypothalamus • increase in insulin & glucagon. Pineal gland or body : •Metatonin • optic pathways light • coordination of circadian n diurnal rythms of tissues. • inhibition of growth. • synthesis of release of gonadotropins prevented . Thymus gland : • thymosin- by thymus gland • histamine , serotonin, prostaglandins • inflammatory response • potentiating pain, fever • regulating blood pressure • blood clotting • uterine contractions during labour • erythropoietin • gastrointestinal hormone Disorders of anterior pitutary : • commonly caused by tumours or autoimmune diseases . • hypersecretion of hormones. • hyposecretion of hormones. Hyper : • hyposecretion of hormone releasing factors by the hypothalamus. • damage to the optic nerves causing visual disturbances. • gigantism – excess GH • acromegaly – large extremities • hyperprolactinanemia Hyposecretion : • tumours of hypothalamus or pitutary . • trauma , usually caused by fractured base. •ischaemic neuroses • pitutary dwarfism ,genetic abnormality. • frohilch’s syndrome Disorders of posterior pitutary : • diabetes insipidus – hyposecretion of ADH THYROID GLAND THYROID DISORDER :- 9 . 9 – 30 9 . 9 . 9 (4) (3), . : , :- 9 . ( ) 9 . 9 . 9 . THYROID HORMONES 1. . 2. . 3. 4. 5. 6. 1. :- . . . 2. :- , 3. 4 3 :- . . . 3 4 . 4. 3 4 : 3 4 , . 3 4 . :- 1. . 2. . 3. . 4. , . . 5. . 6. . 7. . 8. , . 9. . 10. . :- 1. : 4-8 / ; 2 / ; 10-12 / ; 2. 4 : , 5-12 / 3 80-180 / 3. : 4 . 4. : DISEASE OF THE THYROID GLAND : : 9 . : 9 . 9 . 9 . 9 9 9 , . : 9 . 9 . 9 . : . . ’ . . ’ : ( ) , . . . . . : 1. : . 2. : ( I 131 ) 3. : 4. : . . ’ ( ) 5. : , . ANATOMY AND PHYSIOLOGY OF ADRENAL GLANDS ♥10 grams in weight ♥4cm long and 3cm thick ADRENAL CORTEX ♥Produces three groups of hormones ♥Glucocorticoids ♥Mineralocorticoides ♥Androgens(sex hormones) ADRENAL GLANDS GLUCOCORTICOIDS PRODUCED BY ZONE OF FASICULATA 21 carbon steroids. Stimulated by ACTH by anterior pituitary and stress. High levels ofharmones occur between 4am to 8am and lowest between midnight and 3am. BIOCHEMICAL FUNCTION Effect of Carbohydrate Metabolism. Effert on Lipid Metabolism. Effect on Water and Electrolye Metabolism. Effect on Protien and Nucleic acid Metabolism. MECHANISM OF ACTION Binds to specific receptor on target cell and bring about the action. Act at transcription level and control the protine synhtesis. MINERALOCORTICOIDS Most active and potent mineralocorticoids is aldosterone. It promote sodium reabsorption at distal convulated tubules of kidney. Sodium retention is accompanied by excretion of potassium,hydrogen and ammonium ions. REGULATION OF ALDOSTERONE SYNTHESIS Renin angiotension. Potassium. Sodium. ACTH. MECHANISUM OF ACTION It binds to specific receptors on the target tissues and promotes transcription and translation. Stimulates the active transport and absorption of sodium ions. ADDISON’S DISEASE • Addison’s disease is a disorder that results in insufficient amounts of certain important like glucocorticoids and mineralocorticoids CLINICAL FEATURES Weight and decreasd appetite Glucocorticoids Insufficiency Malaise,Anorexia,Nausea,vomiting Gastrointestinal diarrhea Constipation HYPOGLYCEMIA Increased ACTH secrtion Pigmentation – Sun exposed area,HYPOTENTION Decreased body hair espically in female Mineralocorticoids insufficiency Postural hypotension Loss of Adrenal Androgen CAUSES COMMON AUTOIMMUNE Spordiac Polyglandular deficiency type 1 Polyglandular deficiency type 2 Tuberculosis Bilateral adrenalectomy RARE Metastatic tumour Lymphoma Amyloid Bleeding into the adrenal glands Other infections on adrenal glands spread of cancer to the adrenal glands INVESTIGATION ACTH stimulation test o Measurment of plasma ACTH Blood glucose o Plasma rennin activity and aldosterone o Plasma electrolytes Insulin induced hypoglycemia test o Imaging tests TREATMENTS Required treatment with glucocorticles and mineralocorticoides Hydrocortisone 20 mg in morning and 10mg in evening Glucocorticles of choice cordisone 12.5mg -37.5mg orally daily Fludro Cortisone -50mg -30mg orally/daily. Accute adrenocortical insufficincy. Addisional crisis Treatment with salt, water, glucose should be replaced with I.V.dextrose.(5%) plus isotonic saline solution. Hydrocortisone 100mg I.V.should be given immediately.same oral hydrocortisone and cortisone is started with high doses 50mg every six hours of hydrocortisone and maintaince dose according to the requirement. ADRENAL CORTICAL HYPERACTIVITY CUSHING’S SYNDROME Cushing’s syndrome, also known as hypercortisolism,occurs when a person’s tissuesare exposed to an excess of the hormone cortisol. APPROPRIATE AMOUNT OF CORTISOL Regulate blood pressure Energy production Ability to fight disease CLINICAL FEATURES Extremed weight gain Growth retardation Missed periods in teenage girls Excess hair growth Acne Reddish-blue streaks on the skin High blood pressure Tiredness and weakness Either very early or late puberty Muscle and bone weakness Moodiness, irritability,or depression Sleep disturbance High bloodpressure Menstual disorders in women and decreased fertility in man. CAUSES ´ Persons take certain hormones for a long time as a treatment for another disorders or disease,taking steroidal anti-inflammatory for arthrities. ´ The body produces too cortisol, when the pituitary and adrenal glands are not working properly. ´ Certain type of cancerous tumors in other part of the body ´ Growth on the adrenal glands,that may or may not be cancerous, can cause the adrenal glands to relase extra cortisol ´ A noncancerous tumor of the pituitary gland that produces incresed amount of the ACTH produces adrenal glands to produces too munch cortisol . ´ This form of cushing’s syndromes is known “Cushing’s disease” INVESTIGATION Seeing if there is too much cortisol in the body. ´ Discovering the cause of extra cortisol. ´ A urine test to measure cortisol is being produced. ´ Dexamethasone suppresion test. ´ CRH stimulation tests. ´ Scans –This may inculde CT and MRI scans of pituitary, adrenal gland,chest and abdomen. ´ Ultrasound imaging of the adrenal gland. ´ Chests X-rays. ´ Iodo cholestrol scan. ´ Petrosal sinus sampling. TREATMENT ´ Treament upon the specific reasons for cortisol excess and include ´ Oral medication. ´ Radiation ´ Surgery to remove a tumour ´ A combination of tumour that pepends upon the causes.
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