the endocrine system
DESCRIPTION
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” - PowerPoint PPT PresentationTRANSCRIPT
D. C. MIKULECKY
PROFESSOR OF PHYSIOLOGYAND
FACULTY MENTORING PROGRAM
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
PEPTIDES
AMINES
STEROIDS
HYDROPHILIC DISSOLVED IN PLASMA RECEPTOR ON CELL SURFACE cAMP OR CALCIUM AS SECOND
MESSENGERS ACTIVATE SPECIFIC GENES TO INITIATE
PROTEIN SYNTHESIS
HYPOTHALAMIC PITUITARY PANREATIC PARATHYROID GI KIDNEY LIVER HEART
THYROID HORMONE CATECHOLAMINES ALL DERIVED FROM AMINO ACID
TYROSINE UNIQUE SYNTHETIC AND SECRETORY
PATHWAYS
LIPOPHILIC RECEPTOR IN CYTOPLASM ACTIVATE SPECIFIC GENES TO INITIATE
PROTEIN SYNTHESIS ADRENAL CORTICAL GONADAL PLACENTAL
DEPENDS ON RATE OF SECRETION NEGATIVE FEEDBACK NEUROENDOCRINE REFLEXES DIURNAL RHYTHMS
HORMONE EXCESS
HORMONE DEFICIENCY
DECREASED RESPOSIVENESS OF RECEPTORS
HYPOTHALAMUS
NEUROSECRETORYNEURONS
ANTERIOR PITUITARY
POSTERIORPITUITARY
SYSTEMICARTERY
SYSTEMICVEIN
VASOPRESSIN
OXYTOCIN
HYPOTHALAMUS
NEUROSECRETORYNEURONS
ANTERIOR PITUITARY:•TSH•ACTH•PROLACTIN•GROWTH HORMONE•LH•FSH
POSTERIORPITUITARY
VESSELS PASS THROUGH STALK OF PITUITARY FROM HYPOTHALAMUS TO ANTERIOR PITUITARY
CARRY HYPOTHALAMIC REGULATORY HORMONES
TROPIC HORMONES CONTROL THE SECRETION OF OTHER
HORMONES BY ACTING ON ENDOCRINE TISSUE
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
INPUT
HORMONE 1 (RELEASING/INHIBITING)
HORMONE 2 (TROPIC)
HORMONE 3
TARGETCELLS
SYSTEMIC CIRCULATION
SYSTEMIC CIRCULATION
H/H PORTAL SYSTEM
HYPOTHALAMUS
ANTERIOR PITUITARY
ENDOCRINE GLAND
INPUT
HORMONE 1 (RELEASING/INHIBITING)
HORMONE 2 (TROPIC)
HORMONE 3
TARGETCELLS
SYSTEMIC CIRCULATION
SYSTEMIC CIRCULATION
H/H PORTAL SYSTEM
HYPOTHALAMUS
ANTERIOR PITUITARY
ENDOCRINE GLAND
THYROID GLAND
THYROID HORMONES (T3 & T4 )
ADRENAL CORTEX
CORTISOL
MAMMARY GLANDS
BREAST GROWTH AND MILK SECRETION
LIVER SOMATOMEDINS BONE SOFT TISSUE GROWTH
MANY TISSUES INTERMEDIARY
METABOLISM INCREASE OR
DECREASE
LH:LETEINIZING HORMONE
SEX HORMONE SECRETION
F: ESTROGEN AND PROGESTERONE
M: TESTOSTERONE
FSH:FOLLICLE STIMULATING HORMONE
GAMETE PRODUCTION
OVA SPERM
GENETIC DIET DISEASE HORMONES
LIVER SOMATOMEDINS BONE SOFT TISSUE GROWTH
MANY TISSUES INTERMEDIARY
METABOLISM INCREASE OR
DECREASE
MOBILIZES TRIGLYCERIDE FAT STORED IN ADIPOSE TISSUE
CONSERVES GLUCOSE FOR BRAIN
SOFT TISSUES: STIMULATES CELL DIVISION, INCREASES SIZE OF CELLS
STIMULATES ALMOST ALL ASPECTS OF PROTEIN SYNTHESIS
INHIBITS PROTEIN DEGRADATION PROMOTES UPTAKE OF AMINO ACIDS
BONE: PROMOTES GROWTH OF LONG BONES
THICKNESS LENGTH AT END OF ADOLESCENCE, SEX
HORMONES STOP THIS ACTION
PEPTIDE MEDIATORS PRODUCED IN LIVER AND OTHER
TISSUES ALSO PARACRINE EFFECTS
ANTAGONIST IN CONTROL OF GROWTH HORMONE SECRETION
NEGATIVE FEEDBACK DIURNAL RHYTHM: GH SECRETED AT
NIGHT EXERCISE, STRESS, HYPOGLYCEMIA
DEFICIENCY: DWARFISM, REDUCED MUSCLE STRENGTH, DECREASED BONE DENSITY
EXCESS:GIGANTISM, ACROMEGLY
OVER TRACHEA THYROGLOBULIN TETRAIODOTHYRONINE TRIIODOTHYRONINE IODINE REQUIRED FROM DIETARY
INTAKE
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
HYPOTHALAMUS
TRH
ANTERIOR PITUITARY
TSH
THYROID GLAND
TARGET ORGANSTHYROID HORMONE
STRESSCOLD INCHILDREN- +
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
CORTEX: STEROID HORMONES SECRETED
MEDULLA: CATECHOLAMINES
MINERALOCORTICOIDS
GLUCOCORTICOIDS
SEX HOMONES
ALDOSTERONE ELECTROLYTE BALANCE BLOOD PRESSURE RENIN-ANGIOTENSIN-ALDOSTERONE
SYSTEM
CORTISOL GLOCONEOGENESIS PERMISSIVE ACTIONS STRESS ADAPTATION ANTI-INFLAMITORY AND
IMMUNOSUPPRESSANT
HYPOTHALAMUS
CRH
ANTERIOR PITUITARY
ACTH
ADRENAL CORTEX
TARGET ORGANSCORTISOL
STRESSDIURNALRHYTHM
+ +-
-INCREASEDBLOOD GLUCOSEBLOOD AABLOOD FATTY ACIDS
ANDROGENS (TESTOSTERONE)
ESTROGENS
LESS THAN GONADS
MINERALCORTICOIDS: SODIUM RETENTION, POTASSIUM DEPLETION
CORTISOL:EXCESS GLUCONEOGENESIS-EXCESS GLUCOSE DEPOSITED AS FAT
ANDROGEN:MASCULINIZATION, PSEUDOHERMAPHODITISM, PRECOCIOUS PSEUDOPUBERTY, NO EFFECT IN ADULT MALES
CORTEX: ADDISON’S DISEASE POOR RESPONSE TO STRESS LACK OF PERMISSIVE ACTION POTASSIUM RETENTION HYPOTENSION
A MODIFIED SYMPATHETIC POST GANGLIONIC NEURON
EPINEPHRINE
MIMICS SYMPATHETIC NS MOBILIZES STORED FAT AND
CARBOHYDRATE HEART AND BLOOD VESSELS
FLIGHT OR FIGHT EPINEPHRINE CRH-ACTH-CORTISOL RENIN-ANGIOTENSIN-ALDOSTERONE VASOPRESSIN COORDINATED BY HYPOTHALAMUS CAN BE INDUCED PSYCHOSOCIALLY
GLYCOGENESIS GLYCOGENOLYSIS GLUCONEOGENESIS PROTEIN SYNTHESIS PROTEIN DEGRADATION FAT SYNTHESIS FAT BREAKDOWN
BUILD UP VS BREAKDOWN OF LARGE MOLECULES
ANABOLISM REQUIRES ENERGY (ATP) CATABOLISM:ENERGY PRODUCTION
INSULIN
GLUCAGON
BETA CELLS IN ISLETS OF LANGERHANS: INSULIN
FACILITIES GLUCOSE ENTRY INTO CELLS STIMULATES GLYCOGENESIS INHIBITS GLYCOGENOLYSIS INHIBITS GLUCONEOGENESIS
INCREASES TRANSPORT INTO ADIPOSE CELLS
PROMTES TRIGLYCERIDE SYNTHESIS INHIBITS LIPOLYSIS
PROMOTES UPTAKE OF AA BY MUSCLE AND OTHER TISSUE
PROMOTES PROTEIN SYNTHESIS INHIBITS PROTEIN DEGRADATION
NEGATIVE FEEDBACK: BLOOD SUGAR BLOOD AA GI HORMONES PARASYMPATHETIC ACTIVITY
TYPE I: AUTOIMMUNE DESTRUCTION OF BETA CELLS, LACK OF INSULIN SECRETION
TYPE II: REDUCED SENSITIVITY OF INSULIN RECEPTORS
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
PANCREATIC ALPHA CELLS GENERALLY OPPOSES ACTIONS OF
INSULIN DECREASE GLYCOGEN SYNTHESIS PROMOTE GLYCOGENOLYSIS STIMULATE GLUCONEOGENESIS PROMOTES FAT BREAKDOWN ONLY IN LIVER: PROTEIN CATABOLISM
ALL INCREASE BLOOD GLUCOSE AND FATTY ACIDS
CORTISOL INCREASES BLOOD AA AND DECREASES MUSCLE PROTEIN
GH DECREASES BLOOD AA AND INCREASES MUSCLE PROTEIN
PARATHYROID HORMONE CALCITONIN VITAMIN D
RAISES FREE PLASMA CALCIUM FROM BONE CONSERVATION IN KIDNEYS INCREASES INTESTINAL ABSORPTION
(VIA VITAMIN D ACTIVATION) REGULATED BY FREE CALCIUM IN
PLASMA (NEGATIVE FEEDBACK)
C CELLS OF THYROID GLAND DECREASE IN CA MOBILIZATION FROM
BONE NOT AS IMPORTANT AS PTH AND
VITAMIN D
ACTUALLY A HORMONE RELEASED FROM SKIN BY SUNLIGHT TWO STEP ACTIVATION: LIVER AND
KIDNEYS INCREASES CALCIUM ABSORPTION IN
INTESTINE
LOW CALCIUM AND HIGH PHOSPHATE MUSCLE SPASMS MENTAL CHANGES
IMPARED ABSORPTION OF CALCIUM PTH MAINTAINS PLASMA LEVEL AT
EXPENSE OF BONES RICKETS IN CHILDREN OSTEOMALACIA IN ADULTS