the adrenal gland d. c. mikulecky professor of physiology and faculty mentoring program
TRANSCRIPT
THE ADRENAL GLANDS
CORTEX: STEROID HORMONES SECRETED
MEDULLA: CATECHOLAMINES (EPINEPHRIN AND NOR-EPINEPHRIN) SECRETED. IT IS A MODIFIED SYMPATHETIC GANGLION
STEROID HORMONES
CHOLESTEROL IS A COMMON PRECURSOR
PREGNENOLONE IS A COMMON INTERMEDIATE
DERIVATIVES OF THE POLYCYCLIC PHENANTHRENE NUCLEUS
IMPORTANCE OF STEROID HORMONES:
REMOVAL OF CORTEX LEADS TO DEATH WITHIN 1 OR 2 WEEKS WITHOUT REPLACEMENT THERAPY
EVERY ORGAN SYSTEM IS AFFECTED
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
GLUCOCORTICOIDS
CORTISOLGLOCONEOGENESISPERMISSIVE ACTIONSSTRESS ADAPTATIONANTI-INFLAMITORY AND
IMMUNOSUPPRESSANTSEE TABLE I IN TEXT
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)
EFFECTS OF GLUCOCORTICOIDS ON ENERGY METABOLISM
MAINTAIN CARBOHYDRATE RESERVESHYPOGLYCEMIA IF ABSENTGLUCONEOGENESIS: DIRECT EFFECTS
AND INCREASES IN ENZYMESDECREASE UTILIZATION OF GLUCOSE
BY MUSCLE AND ADIPOSE TISSUE AND LOWER SENSITIVITY TO INSULIN. DIABETES MAY ACCOMPANY CUSHING’S DISEASE WHICH IS A HYPERSECRETION
ANTI-INFLAMITORY EFFECTS OF GLUCOCORTICOIDS
INFLUENCE ON PROSTAGLANDINS: SUPPRESS SYNTHESIS OF CYCLO-OXYGENASE
POSSIBLY INHIBIT HISTAMINE FORMATION
CYTOKINES (INTERLEUKIN-1)
REGULATION OF CORTISOL SECRETION
HYPOTHALAMUS
CRH
ANTERIOR PITUITARY
ACTH
ADRENAL CORTEX
TARGET ORGANSCORTISOL
STRESSDIURNALRHYTHM
+ +-
-INCREASEDBLOOD GLUCOSEBLOOD AABLOOD FATTY ACIDS
ACTION OF ACTH
STIMULATES STEROIDOGENESISINCREASES STEROID SECRETION
WITHIN 1 TO 2 MINUTESPEAK RATES IN ABOUT 15 MINUTEScAMP ---> PROTEIN KINASE AABSENCE LEADS TO ATROPHY OF
INNER ZONES OF ADRENAL CORTEX
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)
METABOLISM AND EXCRETION OF ADRENAL CORTICAL HORMONES
INACTIVATION MAINLY IN LIVERMAKES THEM UNRECONIZABLE
TO RECEPTORSEXCRETED IN URINE
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
ADRENAL INSUFFICIENY
CORTEX: ADDISON’S DISEASEPOOR RESPONSE TO STRESSLACK OF PERMISSIVE ACTIONPOTASSIUM RETENTIONHYPOTENSION
ACTIONS OF EPINEPHRINE
MIMICS SYMPATHETIC NS
MOBILIZES STORED FAT AND CARBOHYDRATE
HEART AND BLOOD VESSELS
GENERAL ADAPTATION SYNDROME
FLIGHT OR FIGHTEPINEPHRINECRH-ACTH-CORTISOLRENIN-ANGIOTENSIN-ALDOSTERONEVASOPRESSINCOORDINATED BY HYPOTHALAMUSCAN BE INDUCED PSYCHOSOCIALLY