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THE ADRENAL GLAND

THE ADRENAL GLAND

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THE ADRENAL GLAND

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  1. THE ADRENAL GLAND D. C. MIKULECKY PROFESSOR OF PHYSIOLOGY AND FACULTY MENTORING PROGRAM

  2. THE ADRENAL GLANDS • CORTEX: STEROID HORMONES SECRETED • MEDULLA: CATECHOLAMINES (EPINEPHRIN AND NOR-EPINEPHRIN) SECRETED. IT IS A MODIFIED SYMPATHETIC GANGLION

  3. CORTEX: STEROID HORMONES SECRETED • MINERALOCORTICOIDS • GLUCOCORTICOIDS • SEX HOMONES

  4. STEROID HORMONES • CHOLESTEROL IS A COMMON PRECURSOR • PREGNENOLONE IS A COMMON INTERMEDIATE • DERIVATIVES OF THE POLYCYCLIC PHENANTHRENE NUCLEUS

  5. IMPORTANCE OF STEROID HORMONES: • REMOVAL OF CORTEX LEADS TO DEATH WITHIN 1 OR 2 WEEKS WITHOUT REPLACEMENT THERAPY • EVERY ORGAN SYSTEM IS AFFECTED

  6. MINERALOCORTICOIDS • ALDOSTERONE • ELECTROLYTE BALANCE • BLOOD PRESSURE • RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM • ALDOSTERONE SECRETION REGULATED BY RENIN SECRETION IN THE KIDNEY VIA ANGIOTENSIN II • NEGATIVE FEEDBACK CONTROL VIA MONITORING BLOOD VOLUME

  7. GLUCOCORTICOIDS • CORTISOL • GLOCONEOGENESIS • PERMISSIVE ACTIONS • STRESS ADAPTATION • ANTI-INFLAMITORY AND IMMUNOSUPPRESSANT • SEE TABLE I IN TEXT

  8. PERMISSIVE ACTION OF CLUCOCORTICOIDS • STRESS INCREASES OUTPUT OF ACTH FROM THE PITUITARY • THESE HORMONES SEEM TO GOVERN PROCESSES FUNDAMENTAL TO NORMAL FUNCTION IN MOST CELLS • TREATED AN ADRENALECTOMIZED ANIMAL PERMITTED THE RESUMPTION OF THESE FUNCTIONS (HANS SELYE, 1930’S)

  9. EFFECTS OF GLUCOCORTICOIDS ON ENERGY METABOLISM • MAINTAIN CARBOHYDRATE RESERVES • HYPOGLYCEMIA IF ABSENT • GLUCONEOGENESIS: DIRECT EFFECTS AND INCREASES IN ENZYMES • DECREASE UTILIZATION OF GLUCOSE BY MUSCLE AND ADIPOSE TISSUE AND LOWER SENSITIVITY TO INSULIN. DIABETES MAY ACCOMPANY CUSHING’S DISEASE WHICH IS A HYPERSECRETION

  10. ANTI-INFLAMITORY EFFECTS OF GLUCOCORTICOIDS • INFLUENCE ON PROSTAGLANDINS: SUPPRESS SYNTHESIS OF CYCLO-OXYGENASE • POSSIBLY INHIBIT HISTAMINE FORMATION • CYTOKINES (INTERLEUKIN-1)

  11. GLUCOCORTICOIDS AND THE IMMUNE RESPONSE • BLOCK CYTOKINE PRODUCTION • MAY ALSO KILL T-CELLS

  12. REGULATION OF CORTISOL SECRETION DIURNAL RHYTHM HYPOTHALAMUS STRESS + - + CRH ANTERIOR PITUITARY INCREASED BLOOD GLUCOSE BLOOD AA BLOOD FATTY ACIDS - ACTH ADRENAL CORTEX CORTISOL TARGET ORGANS

  13. ACTION OF ACTH • STIMULATES STEROIDOGENESIS • INCREASES STEROID SECRETION WITHIN 1 TO 2 MINUTES • PEAK RATES IN ABOUT 15 MINUTES • cAMP ---> PROTEIN KINASE A • ABSENCE LEADS TO ATROPHY OF INNER ZONES OF ADRENAL CORTEX

  14. SEX HOMONES • ANDROGENS (TESTOSTERONE) • ESTROGENS • LESS THAN GONADS

  15. ADRENAL STEROID HORMONES IN THE BLOOD • BOUND TO TRANSCORTIN OR CORTICOSTEROID BINDING GLOBULIN (CBG) • SECRETED BY LIVER BUT AT 1/1000 TH THE CONCENTRATION OF ALBUMIN • 95% CLUCOCORTICOIDS AND 65% ALDOSTERONE • LONG HALF LIFE (90 AND 30 MINUTES)

  16. METABOLISM AND EXCRETION OF ADRENAL CORTICAL HORMONES • INACTIVATION MAINLY IN LIVER • MAKES THEM UNRECONIZABLE TO RECEPTORS • EXCRETED IN URINE

  17. ADRENAL OVERSECRETION • MINERALCORTICOIDS: SODIUM RETENTION, POTASSIUM DEPLETION • CORTISOL:EXCESS GLUCONEOGENESIS-EXCESS GLUCOSE DEPOSITED AS FAT (CUSHING’S SYNDROME) • ANDROGEN: MASCULINIZATION, PSEUDOHERMAPHODITISM, PRECOCIOUS PSEUDOPUBERTY, NO EFFECT IN ADULT MALES

  18. ADRENAL INSUFFICIENY • CORTEX: ADDISON’S DISEASE • POOR RESPONSE TO STRESS • LACK OF PERMISSIVE ACTION • POTASSIUM RETENTION • HYPOTENSION

  19. MEDULLA: CATECHOLAMINES • A MODIFIED SYMPATHETIC POST GANGLIONIC NEURON • EPINEPHRINE

  20. ACTIONS OF EPINEPHRINE • MIMICS SYMPATHETIC NS • MOBILIZES STORED FAT AND CARBOHYDRATE • HEART AND BLOOD VESSELS

  21. GENERAL ADAPTATION SYNDROME • FLIGHT OR FIGHT • EPINEPHRINE • CRH-ACTH-CORTISOL • RENIN-ANGIOTENSIN-ALDOSTERONE • VASOPRESSIN • COORDINATED BY HYPOTHALAMUS • CAN BE INDUCED PSYCHOSOCIALLY

  22. EPINEPHRINE, CORTISOL, AND GROWTH HORMONE • ALL INCREASE BLOOD GLUCOSE AND FATTY ACIDS • CORTISOL INCREASES BLOOD AA AND DECREASES MUSCLE PROTEIN • GH DECREASES BLOOD AA AND INCREASES MUSCLE PROTEIN