THE ENDOCRINE SYSTEM D. C. MIKULECKY PROFESSOR OF PHYSIOLOGY AND FACULTY MENTORING PROGRAM.

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Presentation transcript:

THE ENDOCRINE SYSTEM D. C. MIKULECKY PROFESSOR OF PHYSIOLOGY AND FACULTY MENTORING PROGRAM

COMPARISON OF ENDOCRINE AND NERVOUS SYSTEMS NERVOUS SYSTEM “WIRED” CHEMICAL SIGNAL AT TARGET CELL RAPID BRIEF DURATION CLOSE ANATOMICAL PROXIMITY ENDOCRINE SYSTEM “WIRELESS” CHEMICAL SIGNAL AT TARGET CELL SLOW LONG DURATION SPECIFIC RECEPTORS

CATEGORIES OF HORMONES PEPTIDES AMINES STEROIDS

PEPTIDES HYDROPHILIC DISSOLVED IN PLASMA RECEPTOR ON CELL SURFACE cAMP OR CALCIUM AS SECOND MESSENGERS ACTIVATE SPECIFIC GENES TO INITIATE PROTEIN SYNTHESIS

PEPTIDE HORMONES HYPOTHALAMIC PITUITARY PANREATIC PARATHYROID GI KIDNEY LIVER HEART

AMINES THYROID HORMONE CATECHOLAMINES ALL DERIVED FROM AMINO ACID TYROSINE UNIQUE SYNTHETIC AND SECRETORY PATHWAYS

STEROIDS LIPOPHILIC RECEPTOR IN CYTOPLASM ACTIVATE SPECIFIC GENES TO INITIATE PROTEIN SYNTHESIS ADRENAL CORTICAL GONADAL PLACENTAL

PLASMA CONCENTRATION OF HORMONES DEPENDS ON RATE OF SECRETION NEGATIVE FEEDBACK NEUROENDOCRINE REFLEXES DIURNAL RHYTHMS

TYPES OF ENDOCRINE DISORDERS HORMONE EXCESS HORMONE DEFICIENCY DECREASED RESPOSIVENESS OF RECEPTORS

HYPOTHALAMUS AND POSTERIOR PITUITARY HYPOTHALAMUS NEUROSECRETORY NEURONS ANTERIOR PITUITARY POSTERIOR PITUITARY SYSTEMIC ARTERY SYSTEMIC VEIN VASOPRESSIN OXYTOCIN

HYPOTHALAMUS AND ANTERIOR PITUITARY HYPOTHALAMUS NEUROSECRETORY NEURONS ANTERIOR PITUITARY: TSH ACTH PROLACTIN GROWTH HORMONE LH FSH POSTERIOR PITUITARY

HYPOTHALAMIC-HYPOPHYSEAL PORTAL SYSTEM VESSELS PASS THROUGH STALK OF PITUITARY FROM HYPOTHALAMUS TO ANTERIOR PITUITARY CARRY HYPOTHALAMIC REGULATORY HORMONES

HYPOTHALAMIC REGULATORY HORMONES TROPIC HORMONES CONTROL THE SECRETION OF OTHER HORMONES BY ACTING ON ENDOCRINE TISSUE

HYPOTHALAMIC RELEASING AND INHIBITING HORMONES CONTROL THE SECRETION OF ANTERIOR PITUITARY TROPIC HORMONES TRH:THYROTROPIN-RELEASING HORMONE PRH:PROLACTIN RELEASING HORMONE PIH:PROLACTIN INHIBITING HORMONE GHRH:GROWTH HORMONE RELEASING HORMONE GHIH: GROWTH HORMONE INHIBITING HORMONE CRH:CORTICOTROPHIN RELEASING HORMONE

HIERARCHICAL CONTROL INPUT HORMONE 1 (RELEASING/INHIBITING) HORMONE 2 (TROPIC) HORMONE 3 TARGET CELLS SYSTEMIC CIRCULATION H/H PORTAL SYSTEM HYPOTHALAMUS ANTERIOR PITUITARY ENDOCRINE GLAND

NEGATIVE FEEDBACK INPUT HORMONE 1 (RELEASING/INHIBITING) HORMONE 2 (TROPIC) HORMONE 3 TARGET CELLS SYSTEMIC CIRCULATION H/H PORTAL SYSTEM HYPOTHALAMUS ANTERIOR PITUITARY ENDOCRINE GLAND

ANTERIOR PITUITARY HORMONES:TSH THYROID GLAND THYROID HORMONES (T 3 & T 4 )

ANTERIOR PITUITARY HORMONES:ACTH ADRENAL CORTEX CORTISOL

ANTERIOR PITUITARY HORMONES:PROLACTIN MAMMARY GLANDS BREAST GROWTH AND MILK SECRETION

ANTERIOR PITUITARY HORMONES: GROWTH HORMONE LIVER SOMATOMEDINS BONE SOFT TISSUE GROWTH MANY TISSUES INTERMEDIARY METABOLISM INCREASE OR DECREASE

ANTERIOR PITUITARY HORMONES: LH & FSH: ACT ON GONADS LH:LETEINIZING HORMONE SEX HORMONE SECRETION F: ESTROGEN AND PROGESTERONE M: TESTOSTERONE FSH:FOLLICLE STIMULATING HORMONE GAMETE PRODUCTION OVA SPERM

CONTROL OF GROWTH GENETIC DIET DISEASE HORMONES

ANTERIOR PITUITARY HORMONES: GROWTH HORMONE LIVER SOMATOMEDINS BONE SOFT TISSUE GROWTH MANY TISSUES INTERMEDIARY METABOLISM INCREASE OR DECREASE

METABOLIC ACTIONS OF GROWTH HORMONE MOBILIZES TRIGLYCERIDE FAT STORED IN ADIPOSE TISSUE CONSERVES GLUCOSE FOR BRAIN

GROWTH PROMOTING ACTIONS OF GROWTH HORMONE SOFT TISSUES: STIMULATES CELL DIVISION, INCREASES SIZE OF CELLS STIMULATES ALMOST ALL ASPECTS OF PROTEIN SYNTHESIS INHIBITS PROTEIN DEGRADATION PROMOTES UPTAKE OF AMINO ACIDS

GROWTH PROMOTING ACTIONS OF GROWTH HORMONE BONE: PROMOTES GROWTH OF LONG BONES THICKNESS LENGTH AT END OF ADOLESCENCE, SEX HORMONES STOP THIS ACTION

GROWTH HORMONE ACTS THROUGH SOMATOMEDINS PEPTIDE MEDIATORS PRODUCED IN LIVER AND OTHER TISSUES ALSO PARACRINE EFFECTS

GHRH AND GHIH ANTAGONIST IN CONTROL OF GROWTH HORMONE SECRETION NEGATIVE FEEDBACK DIURNAL RHYTHM: GH SECRETED AT NIGHT EXERCISE, STRESS, HYPOGLYCEMIA

ABNORMAL GH SECRETION DEFICIENCY: DWARFISM, REDUCED MUSCLE STRENGTH, DECREASED BONE DENSITY EXCESS:GIGANTISM, ACROMEGLY

THE THYROID GLAND OVER TRACHEA THYROGLOBULIN TETRAIODOTHYRONINE TRIIODOTHYRONINE IODINE REQUIRED FROM DIETARY INTAKE

THYROID HORMONE’S EFFECTS METABOLIC RATE: INCREASED BMR CALOROGENIC: INCREASED HEAT PRODUCTION SYMPATHOMIMETIC: FLIGHT OR FIGHT CARDIOVASCULAR:INCREASES RESPONSIVENESS OF HEART GROWTH: ESSENTIAL FOR NORMAL GROWTH NERVOUS SYSTEM:DEVELOPMENT AND ADULT ACTIVITY

REGULATION OF THYROID SECRETION HYPOTHALAMUS TRH ANTERIOR PITUITARY TSH THYROID GLAND TARGET ORGANS THYROID HORMONE STRESS COLD IN CHILDREN - +

ABNORMALITIES OF THYROID FUNCTION HYPO REDUCED BMR POOR TOLERANCE OF COLD GAIN OF WEIGHT FATIGUE SLOW, WEAK PULSE SLOW REFLEXES AND MENTATION MYXEDEMA GOITER CRETINISM HYPER GRAVE’S DISEASE:TSI EXOPHTALMOS GOITER

THE ADRENAL GLANDS CORTEX: STEROID HORMONES SECRETED MEDULLA: CATECHOLAMINES

CORTEX: STEROID HORMONES SECRETED MINERALOCORTICOIDS GLUCOCORTICOIDS SEX HOMONES

MINERALOCORTICOIDS ALDOSTERONE ELECTROLYTE BALANCE BLOOD PRESSURE RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM

GLUCOCORTICOIDS CORTISOL GLOCONEOGENESIS PERMISSIVE ACTIONS STRESS ADAPTATION ANTI-INFLAMITORY AND IMMUNOSUPPRESSANT

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

SEX HOMONES ANDROGENS (TESTOSTERONE) ESTROGENS LESS THAN GONADS

ADRENAL OVERSECRETION MINERALCORTICOIDS: SODIUM RETENTION, POTASSIUM DEPLETION CORTISOL:EXCESS GLUCONEOGENESIS- EXCESS GLUCOSE DEPOSITED AS FAT 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

CONTROL OF FUEL METABOLISM GLYCOGENESIS GLYCOGENOLYSIS GLUCONEOGENESIS PROTEIN SYNTHESIS PROTEIN DEGRADATION FAT SYNTHESIS FAT BREAKDOWN

ANABOLISM VS CATABOLISM BUILD UP VS BREAKDOWN OF LARGE MOLECULES ANABOLISM REQUIRES ENERGY (ATP) CATABOLISM:ENERGY PRODUCTION

PANCREATIC HORMONES INSULIN GLUCAGON

INSULIN: ACTION ON BLOOD SUGAR BETA CELLS IN ISLETS OF LANGERHANS: INSULIN FACILITIES GLUCOSE ENTRY INTO CELLS STIMULATES GLYCOGENESIS INHIBITS GLYCOGENOLYSIS INHIBITS GLUCONEOGENESIS

INSULIN: ACTION ON FAT INCREASES TRANSPORT INTO ADIPOSE CELLS PROMTES TRIGLYCERIDE SYNTHESIS INHIBITS LIPOLYSIS

INSULIN: ACTION ON PROTEIN PROMOTES UPTAKE OF AA BY MUSCLE AND OTHER TISSUE PROMOTES PROTEIN SYNTHESIS INHIBITS PROTEIN DEGRADATION

CONTROL OF INSULIN SECRETION NEGATIVE FEEDBACK: BLOOD SUGAR BLOOD AA GI HORMONES PARASYMPATHETIC ACTIVITY

TWO TYPES OF DIABETES MELLITUS TYPE I: AUTOIMMUNE DESTRUCTION OF BETA CELLS, LACK OF INSULIN SECRETION TYPE II: REDUCED SENSITIVITY OF INSULIN RECEPTORS

ACUTE EFFECTS OF DIABETES MELLITUS EXTRACELLULAR GLUCOSE EXCESS GLUCOSE IN URINE EXCESS FLUID LOSS CIRCULATORY FAILURE RENAL FAILURE NERVOUS SYSTEM MALFUNCTION DUE TO DEHYDRATION EXCESSIVE FOOD INTAKE PROGRESSIVE WEIGHT LOSS MOBILIZTION OF FAT KETOSIS ACIDOSIS COMA AND DEATH

GLUCAGON PANCREATIC ALPHA CELLS GENERALLY OPPOSES ACTIONS OF INSULIN DECREASE GLYCOGEN SYNTHESIS PROMOTE GLYCOGENOLYSIS STIMULATE GLUCONEOGENESIS PROMOTES FAT BREAKDOWN ONLY IN LIVER: PROTEIN CATABOLISM

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

CONTROL OF CALCIUM METABOLISM PARATHYROID HORMONE CALCITONIN VITAMIN D

PARATHYROID HORMONE RAISES FREE PLASMA CALCIUM FROM BONE CONSERVATION IN KIDNEYS INCREASES INTESTINAL ABSORPTION (VIA VITAMIN D ACTIVATION) REGULATED BY FREE CALCIUM IN PLASMA (NEGATIVE FEEDBACK)

CALCITONIN C CELLS OF THYROID GLAND DECREASE IN CA MOBILIZATION FROM BONE NOT AS IMPORTANT AS PTH AND VITAMIN D

VITAMIN D ACTUALLY A HORMONE RELEASED FROM SKIN BY SUNLIGHT TWO STEP ACTIVATION: LIVER AND KIDNEYS INCREASES CALCIUM ABSORPTION IN INTESTINE

PTH HYPOSECRETION LOW CALCIUM AND HIGH PHOSPHATE MUSCLE SPASMS MENTAL CHANGES

VITAMIN D DEFICIENCY IMPARED ABSORPTION OF CALCIUM PTH MAINTAINS PLASMA LEVEL AT EXPENSE OF BONES RICKETS IN CHILDREN OSTEOMALACIA IN ADULTS