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In the name of God.

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Presentation on theme: "In the name of God."— Presentation transcript:

1 In the name of God

2 هورمون ها اهداف آموزشی هورمونها تعریف هورمون
2- ساختمان ، بافت مترشح و بافت هدف را یاد بگبرد 3-نحوه انتقال هورمونها را بداند 4-متابولیسم -5ختلال ناشی از افزایش و کاهش ترشح هر کدام از هورمونها را بداند. 8-تستهای ازمایشگاهی هورمون ها هورمونهای پپتیدی هومونهای استروییدی هومونهای مشتق از اسید آمینه

3 Hypothalamuses-pituitary axis
Hypothalamose -pituitary stalk ADH, OX Pituitary hormones

4 Posterior Pituitary (neurohypophysis)
Cell bodies in SON (ADH) & PVN (Oxytocin) of hypothalamus Consists of neural endings with associated blood vessels Acts as storage area, secretory granules travel down axon Connects to hypothalamus via hypothalamic-hypophyseal tract Processes extend through infundibulum and end in Post. Pit

5 Primary positive signal
Fig. 4-10A Page 117

6 Pituitary hormones hypothalamus-Pituitary axis . Prolactin GH
Prolaction Structure function .

7 Regulation of prolactin

8 Laboratory tests Variation secretion TRH stimulate production
Normal level in women (up to 20ng/ml/12ng/ml Prolactin Excess In women:Milk production(galactorrhea), amenorrhes) In Men:Infertility, and impotence,Rarely breast enlargment(Gynecomastia) >200ng/ml: Pituitary tumores ng/ml: tumors 20-100: diurnal variation,medications,stress,…

9 Prolactin levels

10 Growth hormones Structure Function -Indirect -Direct

11 Regulation

12 Prolactin levels Marked diurnal Variation

13 Laboratory data GH Levels (single mea. Unless 1 h sleep)
RESPONSE TO Physiologic and pharmacologic changesS STIMULATORS:Exersise,Insulu Hypogly.GHRH(1mg/kg,clonidine(4mg/kg),l-dopa(0.5g)argenine(0.5g/kg) IGF-I and binding proteins IGF-1 best marker),<5 year very low Inhibition:liver disease,acute illoness,malnutreitient

14 Laboratory evaluation
GH over production Pituitary tumore (gigantism,acromegaly) Other effects:thickening, In.sweating,oilness of skin,hypertention,joint paint,hyperglecia GH deficiency

15 Sampling Transfering Blood increase Blood decrease

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19 Evolution of Adrenal function
Introduction Hypothalamic-pituitary-glucocorticosteroid Axis Biosynthesis Glococorticoids Mineral corticoids Sex Hormones Regulations

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22 Direct tests of the hypothalamic –pituitary –adrenal Axis
Cortisol,ACTH(stress) Cortisol(not specific), Synthetic stroids,CBG change. (↓Liver disease, malnutrition, ↑Est, pregnancy.) Urine Free cortisol Plasma cortisol exceeds protein binding capacity, ref.(20-90µg/day) Corticosteroid intermediates Evaluation for suspected congenital adrenal hyperplasia or carcinoma(17-hydroxysteriods, ). Adrenal Androgen production DHEA_S (plasma, urine), Testesteron (gonads),Weak androgens(from gonads and adrenal(measured)

23 Dynamic tests of the hypothalamic-pituitary-adrenal Axis
Dexamethasone suppression tests (DST) 1-Overnight DST(1 mg Dexa.). 2-Low doseDST(0.5 mg/6 h/2d) 3-high dose(2mg/6h/2d) Stimulatory stimulation 1- Cortrosyn stimulation(250 µg/0,30,60 min. after injection),7µg to µg, normal,1µg physiological dose? 2-Metyrapone Test(inhibites last step in cortisol synthesis) 3-Insulin hypoglycemia(Insulin, u/kg) 4- corticotropin –releasing hor. stimulation

24 Abnormalities of Glu. production
Suspected Cushing syndrome (excess Glu. Obesity, hypertention,virilization,hyperglycemia(hypokalemia and metabolic alkalosis may?) Diagnosis of Cushing syndrome UFC or Overnight DS Adrenal insufficiency Mineral cor. (dehydration, hyponatremia, hyperkalemia, non-anion gap metyabolic acidosis.) Glu. Deficeincy(weight loss, vometing, weakness) Primary insufficiency(addison disease). Pigmentation skin(POMC) Secondary adrenal insuficiency(pituitary). Neither min nor excess ACTH is present(Hyperglecimia) Diagnosing adrenal insufficiency Cortisol measument(18-20µg ruling out) Trea. Administration dexametasine, cotrosyn)

25 Congenital adrenal hyperplasia
21-hydroylase deficiency 11-hydroxylase deficiency

26 Laboratory tests of mineral and metabolism
Plasma calcium Total and active form (PH,complexing anion) Adjusted Ca(mg/dl)=totalCa(mg/dL)+0.8x(4-Albumin(g/dL) Free Calcium?

27 Phosphate Variation(Throuhgout the day and after meals↓) Single assay?
Renal failure? Monoclonal gammopathies Magnesium Plasma equilibrates with cell magnesium

28 PTH Mid-molecule or C-terminal assay measure long-lived,inactive metabolite Renal failure? PTH assay? Vitamin D assay 25-Hydroxyvitamin D assay proportion to deficiency or toxicity 1,25 Dihydroxyvitamin D(suspected ectopic) PTHr Urinary Mineral Excretion

29 Hypercalcemia Artifactual(protein bound)hypercalcemia
Primary hyperparathyroidism Hypercalcemia of Malignancy Uncommon causes of hypercalcemia

30 Hypocalcemia Artfactual Chronic Renal failure
Uncommon causes (hypoPTH,Hypomagnesemia)

31 Hyperphosphatemia Renal failure
Uncommon causes(HypoPTH,Vitamin D Toxicity,hyperthyroidism,Cell lysis sydromes)

32 hypophosphatemia Osteoporosis Vitamin D defiemcy Paget,s disease
Renal Osteodystrophy

33 Metabolic Bone disease


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