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ENDOCRINE SYSTEM, by prof D C MikULEacKY
- 1. THE ENDOCRINE SYSTEM D.C. MIKULECKY PROFESSOR OF PHYSIOLOGY AND FACULTY MENTORING PROGRAM
- 2. COMPARISON OF ENDOCRINE ANDNERVOUS 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
- 3. CATEGORIES OF HORMONES •PEPTIDES • AMINES • STEROIDS
- 4. PEPTIDES • HYDROPHILIC • DISSOLVEDIN PLASMA • RECEPTOR ON CELL SURFACE • cAMP OR CALCIUM AS SECOND MESSENGERS • ACTIVATE SPECIFIC GENES TO INITIATE PROTEIN SYNTHESIS
- 5. PEPTIDE HORMONES • HYPOTHALAMIC •PITUITARY • PANREATIC • PARATHYROID • GI • KIDNEY • LIVER • HEART
- 6. AMINES • THYROID HORMONE •CATECHOLAMINES • ALL DERIVED FROM AMINO ACID TYROSINE • UNIQUE SYNTHETIC AND SECRETORY PATHWAYS
- 7. STEROIDS • LIPOPHILIC • RECEPTORIN CYTOPLASM • ACTIVATE SPECIFIC GENES TO INITIATE PROTEIN SYNTHESIS • ADRENAL CORTICAL • GONADAL • PLACENTAL
- 8. PLASMA CONCENTRATION OF HORMONES •DEPENDS ON RATE OF SECRETION • NEGATIVE FEEDBACK • NEUROENDOCRINE REFLEXES • DIURNAL RHYTHMS
- 9. TYPES OF ENDOCRINE DISORDERS •HORMONE EXCESS • HORMONE DEFICIENCY • DECREASED RESPOSIVENESS OF RECEPTORS
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- 12. HYPOTHALAMIC-HYPOPHYSEAL PORTAL SYSTEM • VESSELSPASS THROUGH STALK OF PITUITARY FROM HYPOTHALAMUS TO ANTERIOR PITUITARY • CARRY HYPOTHALAMIC REGULATORY HORMONES
- 13. HYPOTHALAMIC REGULATORY HORMONES • TROPICHORMONES • CONTROL THE SECRETION OF OTHER HORMONES BY ACTING ON ENDOCRINE TISSUE
- 14. HYPOTHALAMIC RELEASING AND INHIBITINGHORMONES • 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
- 15. HIERARCHICAL CONTROL INPUT HORMONE 1(RELEASING/INHIBITING) HORMONE 2 (TROPIC) HORMONE 3 TARGET CELLS SYSTEMIC CIRCULATION SYSTEMIC CIRCULATION H/H PORTAL SYSTEM HYPOTHALAMUS ANTERIOR PITUITARY ENDOCRINE GLAND
- 16. NEGATIVE FEEDBACK INPUT HORMONE 1(RELEASING/INHIBITING) HORMONE 2 (TROPIC) HORMONE 3 TARGET CELLS SYSTEMIC CIRCULATION SYSTEMIC CIRCULATION H/H PORTAL SYSTEM HYPOTHALAMUS ANTERIOR PITUITARY ENDOCRINE GLAND
- 17. ANTERIOR PITUITARY HORMONES:TSH •THYROID GLAND • THYROID HORMONES (T3 & T4 )
- 18. ANTERIOR PITUITARY HORMONES:ACTH • ADRENALCORTEX • CORTISOL
- 19. ANTERIOR PITUITARY HORMONES:PROLACTIN • MAMMARYGLANDS • BREAST GROWTH AND MILK SECRETION
- 20. ANTERIOR PITUITARY HORMONES: GROWTHHORMONE • LIVER • SOMATOMEDINS • BONE • SOFT TISSUE • GROWTH • MANY TISSUES • INTERMEDIARY METABOLISM • INCREASE OR DECREASE
- 21. 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
- 22. CONTROL OF GROWTH •GENETIC • DIET • DISEASE • HORMONES
- 23. ANTERIOR PITUITARY HORMONES: GROWTHHORMONE • LIVER • SOMATOMEDINS • BONE • SOFT TISSUE • GROWTH • MANY TISSUES • INTERMEDIARY METABOLISM • INCREASE OR DECREASE
- 24. METABOLIC ACTIONS OFGROWTH HORMONE • MOBILIZES TRIGLYCERIDE FAT STORED IN ADIPOSE TISSUE • CONSERVES GLUCOSE FOR BRAIN
- 25. GROWTH PROMOTING ACTIONS OFGROWTH HORMONE • SOFT TISSUES: STIMULATES CELL DIVISION, INCREASES SIZE OF CELLS • STIMULATES ALMOST ALLASPECTS OF PROTEIN SYNTHESIS • INHIBITS PROTEIN DEGRADATION • PROMOTES UPTAKE OF AMINO ACIDS
- 26. GROWTH PROMOTING ACTIONS OFGROWTH HORMONE • BONE: PROMOTES GROWTH OF LONG BONES • THICKNESS • LENGTH • AT END OF ADOLESCENCE, SEX HORMONES STOP THIS ACTION
- 27. GROWTH HORMONE ACTS THROUGHSOMATOMEDINS • PEPTIDE MEDIATORS • PRODUCED IN LIVER AND OTHER TISSUES • ALSO PARACRINE EFFECTS
- 28. GHRH AND GHIH •ANTAGONIST IN CONTROL OF GROWTH HORMONE SECRETION • NEGATIVE FEEDBACK • DIURNAL RHYTHM: GH SECRETED AT NIGHT • EXERCISE, STRESS, HYPOGLYCEMIA
- 29. ABNORMAL GH SECRETION •DEFICIENCY: DWARFISM, REDUCED MUSCLE STRENGTH, DECREASED BONE DENSITY • EXCESS:GIGANTISM, ACROMEGLY
- 30. THE THYROID GLAND •OVER TRACHEA • THYROGLOBULIN • TETRAIODOTHYRONINE • TRIIODOTHYRONINE • IODINE REQUIRED FROM DIETARY INTAKE
- 31. 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
- 32. REGULATION OF THYROID SECRETION HYPOTHALAMUS TRH ANTERIORPITUITARY TSH THYROID GLAND TARGET ORGANS THYROID HORMONE STRESS COLD IN CHILDREN - +
- 33. 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
- 34. THE ADRENAL GLANDS •CORTEX: STEROID HORMONES SECRETED • MEDULLA: CATECHOLAMINES
- 35. CORTEX: STEROID HORMONES SECRETED •MINERALOCORTICOIDS • GLUCOCORTICOIDS • SEX HOMONES
- 36. MINERALOCORTICOIDS • ALDOSTERONE • ELECTROLYTEBALANCE • BLOOD PRESSURE • RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM
- 37. GLUCOCORTICOIDS • CORTISOL • GLOCONEOGENESIS •PERMISSIVE ACTIONS • STRESS ADAPTATION • ANTI-INFLAMITORYAND IMMUNOSUPPRESSANT
- 38. REGULATION OF CORTISOL SECRETION HYPOTHALAMUS CRH ANTERIORPITUITARY ACTH ADRENAL CORTEX TARGET ORGANS CORTISOL STRESS DIURNAL RHYTHM + + - - INCREASED BLOOD GLUCOSE BLOOD AA BLOOD FATTY ACIDS
- 39. SEX HOMONES • ANDROGENS(TESTOSTERONE) • ESTROGENS • LESS THAN GONADS
- 40. 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
- 41. ADRENAL INSUFFICIENY • CORTEX:ADDISON’S DISEASE • POOR RESPONSE TO STRESS • LACK OF PERMISSIVE ACTION • POTASSIUM RETENTION • HYPOTENSION
- 42. MEDULLA: CATECHOLAMINES • AMODIFIED SYMPATHETIC POST GANGLIONIC NEURON • EPINEPHRINE
- 43. ACTIONS OF EPINEPHRINE •MIMICS SYMPATHETIC NS • MOBILIZES STORED FAT AND CARBOHYDRATE • HEART AND BLOOD VESSELS
- 44. GENERAL ADAPTATION SYNDROME • FLIGHTOR FIGHT • EPINEPHRINE • CRH-ACTH-CORTISOL • RENIN-ANGIOTENSIN-ALDOSTERONE • VASOPRESSIN • COORDINATED BY HYPOTHALAMUS • CAN BE INDUCED PSYCHOSOCIALLY
- 45. CONTROL OF FUEL METABOLISM •GLYCOGENESIS • GLYCOGENOLYSIS • GLUCONEOGENESIS • PROTEIN SYNTHESIS • PROTEIN DEGRADATION • FAT SYNTHESIS • FAT BREAKDOWN
- 46. ANABOLISM VS CATABOLISM •BUILD UP VS BREAKDOWN OF LARGE MOLECULES • ANABOLISM REQUIRES ENERGY (ATP) • CATABOLISM:ENERGY PRODUCTION
- 47. PANCREATIC HORMONES • INSULIN •GLUCAGON
- 48. INSULIN: ACTION ONBLOOD SUGAR • BETA CELLS IN ISLETS OF LANGERHANS: INSULIN • FACILITIES GLUCOSE ENTRY INTO CELLS • STIMULATES GLYCOGENESIS • INHIBITS GLYCOGENOLYSIS • INHIBITS GLUCONEOGENESIS
- 49. INSULIN: ACTION ONFAT • INCREASES TRANSPORT INTO ADIPOSE CELLS • PROMTES TRIGLYCERIDE SYNTHESIS • INHIBITS LIPOLYSIS
- 50. INSULIN: ACTION ONPROTEIN • PROMOTES UPTAKE OF AA BY MUSCLE AND OTHER TISSUE • PROMOTES PROTEIN SYNTHESIS • INHIBITS PROTEIN DEGRADATION
- 51. CONTROL OF INSULINSECRETION • NEGATIVE FEEDBACK: BLOOD SUGAR • BLOOD AA • GI HORMONES • PARASYMPATHETIC ACTIVITY
- 52. TWO TYPES OFDIABETES MELLITUS • TYPE I: AUTOIMMUNE DESTRUCTION OF BETA CELLS, LACK OF INSULIN SECRETION • TYPE II: REDUCED SENSITIVITY OF INSULIN RECEPTORS
- 53. ACUTE EFFECTS OFDIABETES 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 • COMAAND DEATH
- 54. GLUCAGON • PANCREATIC ALPHACELLS • GENERALLY OPPOSES ACTIONS OF INSULIN • DECREASE GLYCOGEN SYNTHESIS • PROMOTE GLYCOGENOLYSIS • STIMULATE GLUCONEOGENESIS • PROMOTES FAT BREAKDOWN • ONLY IN LIVER: PROTEIN CATABOLISM
- 55. EPINEPHRINE, CORTISOL, AND GROWTHHORMONE • ALL INCREASE BLOOD GLUCOSE AND FATTY ACIDS • CORTISOL INCREASES BLOOD AA AND DECREASES MUSCLE PROTEIN • GH DECREASES BLOOD AAAND INCREASES MUSCLE PROTEIN
- 56. CONTROL OF CALCIUM METABOLISM •PARATHYROID HORMONE • CALCITONIN • VITAMIN D
- 57. PARATHYROID HORMONE • RAISESFREE PLASMA CALCIUM • FROM BONE • CONSERVATION IN KIDNEYS • INCREASES INTESTINAL ABSORPTION (VIA VITAMIN D ACTIVATION) • REGULATED BY FREE CALCIUM IN PLASMA (NEGATIVE FEEDBACK)
- 58. CALCITONIN • C CELLSOF THYROID GLAND • DECREASE IN CA MOBILIZATION FROM BONE • NOT AS IMPORTANT AS PTH AND VITAMIN D
- 59. VITAMIN D • ACTUALLYAHORMONE • RELEASED FROM SKIN BY SUNLIGHT • TWO STEPACTIVATION: LIVER AND KIDNEYS • INCREASES CALCIUM ABSORPTION IN INTESTINE
- 60. PTH HYPOSECRETION • LOWCALCIUM AND HIGH PHOSPHATE • MUSCLE SPASMS • MENTAL CHANGES
- 61. VITAMIN D DEFICIENCY •IMPARED ABSORPTION OF CALCIUM • PTH MAINTAINS PLASMA LEVELAT EXPENSE OF BONES • RICKETS IN CHILDREN • OSTEOMALACIA IN ADULTS