the endocrine system
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Transcript the endocrine system
THE ADRENAL GLAND
D. C. MIKULECKY
PROFESSOR OF PHYSIOLOGY
AND
FACULTY MENTORING PROGRAM
THE ADRENAL GLANDS
CORTEX: STEROID HORMONES
SECRETED
MEDULLA: CATECHOLAMINES
(EPINEPHRIN AND NOREPINEPHRIN) 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
CORTISOL
GLOCONEOGENESIS
PERMISSIVE ACTIONS
STRESS ADAPTATION
ANTI-INFLAMITORY AND
IMMUNOSUPPRESSANT
SEE 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 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
ANTI-INFLAMITORY EFFECTS
OF GLUCOCORTICOIDS
INFLUENCE ON PROSTAGLANDINS:
SUPPRESS SYNTHESIS OF CYCLOOXYGENASE
POSSIBLY INHIBIT HISTAMINE
FORMATION
CYTOKINES (INTERLEUKIN-1)
GLUCOCORTICOIDS AND THE
IMMUNE RESPONSE
BLOCK CYTOKINE PRODUCTION
MAY ALSO KILL T-CELLS
REGULATION OF CORTISOL
SECRETION
HYPOTHALAMUS
STRESS
+
CRH
+
-
DIURNAL
RHYTHM
ANTERIOR PITUITARY
INCREASED
BLOOD GLUCOSE
BLOOD AA
BLOOD FATTY ACIDS
ACTH
-
ADRENAL CORTEX
CORTISOL
TARGET ORGANS
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
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 LIVER
MAKES THEM UNRECONIZABLE TO
RECEPTORS
EXCRETED IN URINE
ADRENAL
OVERSECRETION
MINERALCORTICOIDS: SODIUM
RETENTION, POTASSIUM DEPLETION
CORTISOL:EXCESS GLUCONEOGENESISEXCESS GLUCOSE DEPOSITED AS FAT
(CUSHING’S SYNDROME)
ANDROGEN: MASCULINIZATION,
PSEUDOHERMAPHODITISM, PRECOCIOUS
PSEUDOPUBERTY, NO EFFECT IN ADULT
MALES
ADRENAL INSUFFICIENY
CORTEX: ADDISON’S DISEASE
POOR RESPONSE TO STRESS
LACK OF PERMISSIVE ACTION
POTASSIUM RETENTION
HYPOTENSION
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 FIGHT
EPINEPHRINE
CRH-ACTH-CORTISOL
RENIN-ANGIOTENSIN-ALDOSTERONE
VASOPRESSIN
COORDINATED BY HYPOTHALAMUS
CAN 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