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

THE ADRENAL GLAND

D. C. MIKULECKYPROFESSOR OF PHYSIOLOGYANDFACULTY MENTORING PROGRAM

THE ADRENAL GLANDS

CORTEX: STEROID HORMONES SECRETED

MEDULLA: CATECHOLAMINES (EPINEPHRIN AND NOR-EPINEPHRIN) SECRETED. IT IS A MODIFIED SYMPATHETIC GANGLION

CORTEX: STEROID HORMONES SECRETED

MINERALOCORTICOIDS

GLUCOCORTICOIDS

SEX HOMONES

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)

GLUCOCORTICOIDS AND THE IMMUNE RESPONSE

BLOCK CYTOKINE PRODUCTIONMAY ALSO KILL T-CELLS

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

SEX HOMONES

ANDROGENS (TESTOSTERONE)

ESTROGENS

LESS THAN GONADS

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

MEDULLA: CATECHOLAMINES

A MODIFIED SYMPATHETIC POST GANGLIONIC NEURON

EPINEPHRINE

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

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