1. CHAPTER 13
ENDOCRINE
SYSTEM

2. COMPARISON???

3. MORE SHORT TERM EFFECTS
ENDOCRINE
NERVOUS
MESSENGER
CHEMICAL/
HORMONE
IMPULSE
PATHWAY
BLOOD
NERVES
TIME
SLOWER/ USUALLY
FASTER
CONTROLS
MORE LONG TERM EFFECTS
MORE SHORT TERM EFFECTS
HOMEOSTASIS
RAPID, PRECISE CONTROL

4. GLAND TYPES EXOCRINE SECRETES INTO A DUCT ENDOCRINE
DUCTLESS, SECRETES INTO BLOOD STREAM
PARACRINE
AFFECTS NEIGHBORING CELLS
AUTOCRINE
AFFECTS SECRETING CELL

5. PARACRINE GLAND

6. AUTOCRINE GLAND

7. EXOCRINE AND ENDOCRINE

8. HORMONES SECRETED BY SMALL GROUPS OF SPECIALIZED CELLS ORGANS

9. HOW HORMONES TRAVEL

10. HORMONE STRUCTURE

11. HORMONE TYPES STEROID/ THYROID ADRENAL CORTEX SEX HORMONES AMINES
NEURONS
ADRENAL MEDULLA
PEPTIDE
POSTERIOR PITUITARY
HYPOTHALAMUS
PROTEIN
PARATHYROID
ANTERIOR PITUITARY
GLYCOPROTEIN

12. STEROID HORMONES

13. HORMONE STRUCTURE

14. PARACRINE SECRETIONS PROSTAGLANDINS
LIVER, KIDNEYS, LUNGS, HEART, THYMUS, PANCREAS, BRAIN REPRODUCTIVE ORGANS
LEUKOTRIENES
WHITE BLOOD CELLS

15. HORMONE ACTION ALTER METABOLIC PROCESSES
UP-REGULATION: INCREASE OF TARGET CELL RECEPTORS
DOWN-REGULATION ??

16. STEROID AND THYROID HORMONES
INSOLUBLE IN WATER
CARRIED ON PLASMA PROTEINS
LIPID SOLUBLE: DIFFUSES INTO TARGET CELL
COMBINE WITH PROTEIN RECEPTOR (USUALLY IN NUCLEUS)
HORMONE-RECEPTOR COMPLEX BINDS TO SPECIFIC DNA GENES
ACTIVATES OR REPRESSES THE GENES
ACTIVATED GENES FORM RNA
RNA DIRECTS PROTEIN SYNTHESIS
PROTEINS CARRY OUT FUNCTION FOR THE HORMONE

17. STEROID HORMONE ACTION

18. STEROID HORMONE ACTION PART 2

19. NONSTEROID HORMONE ACTION
WATER SOLUBLE
LIPID INSOLUBLE
HORMONE (FIRST MESSENGER) BINDS TO PROTEIN RECEPTOR ON TARGET CELL MEMBRANE AT BINDING SITE
RECEPTOR’S ACTIVITY SITE INTERACTS WITH MEMBRANE PROTEINS (SECOND MESSENGERS)
COMMONLY G PROTEIN STIMULATED TO ACTIVATE ADENYLATE CYCLASE WHICH REMOVES 2 PHOSPHATES FROM ATP FORMING cAMP

20. NONSTEROID HORMONE ACTION (CONTINUED)
cAMP ACTIVATES PROTEIN KINASES WHICH PHOSPHORYLATE SUBSTRATE MOLECULES
WHICH CHANGES THEIR SHAPE, ACTIVATING THEM WHICH THEN CAUSES THE CHANGE OF THE HORMONE

21. NONSTEROID HORMONE ACTION (III)
OTHER SECOND MESSENGERS:
DAG
cGMP
OR INCREASES CALCIUM IN CELLS BY DIFFUSION OR IP3 (INOTOSITOL TRIPHOSPHATE) ACTIVATING CALMODULIN WHICH THEN AFFECTS ENZYMES
UNLIKE STEROID HORMONES (DEPENDENT ON NUMBER OF RECEPTORS) WITH SECOND MESSENGERS THE MESSAGE CAN BE GREATLY AMPLIFIED ?

22. NON-STEROID HORMONE ACTION 1

23. NON-STEROID HORMONE ACTION 2

24. NON-STEROID HORMONE ACTION 3

25. NON-STEROID HORMONE ACTION 4

26. AMPLIFICATION ??
STEROID
NON-STEROID
NOT MUCH
A LOT

27. NEGATIVE FEEDBACK ??

28. NEGATIVE FEEDBACK

29. ENDOCIRNE SYSTEM

30. HYPOTHALAMUS LINKS NERVOUS SYSTEM TO ENDOCRINE SYSTEM BY THE PITUITARY

31. HYPOTHALAMUS

32. HYPOTHALAMUS/ PITUITARY

33. ANTERIOR/POSTERIOR PITUITARY

34. HYPOTHALAMUS/PITUITARY CONTROL

35. PITUITARY HORMONES

36. ANTERIOR PITUITARY 5 TYPES OF EPITHELIAL CELLS AROUND BLOOD VESSELS
CONTROL BY HORMONES (RELEASING FACTORS) RELEASED BY THE HYPOTHALAMUS

37. ANTERIOR PITUITARY HORMONES
SOMATROPES: GH/ SOMATOTROPIN
GHRH (stimulates); SS (inhibits)
MAMMATROPES: PRL
PIH (DOPAMINE) (inhibits); MAYBE MORE THAN ONE PRF (stimulates)
THYROTROPES: TSH/THYROTROPIN
TRH (stimulates) OR LESS TRH
CORTICOTROPES: ACTH
CRH (stimulates); STRESS RELEASES MORE CRH
GONADOTROPES: FSH & LH/ICSH
MORE COMPLEX; GnRH (stimulates)
****ALL CONTROL FACTORS ARE RELEASED BY HYPOTHALAMUS

38. POSTERIOR PITUITARY
NERVE FIBERS AND PITUICYTES (NEUROGLIA); NEUROSECRETORY CELLS SECRETE:
ADH/ VASSOPRESSIN
RELEASE CONTROLLED BY:
OSMORECEPTORS IN HYPOTHALAMUS
STRETCH RECEPTORS OF BLOOD VESSELS
OXYTOCIN
STRETCHING OF UTERUS IN LATE PREGNANCY
SUCKLING

39. PITUICYTES

40. THYROID
ISTHMUS

41. FOLLICLES FOLLICULAR CELLS THYROGLOBULIN www-medlib.med.utah.edu
EXTRAFOLLICULAR CELLS

42. THYROID HORMONES T4/ THYROXINE T3/ TRIIODOTHYRONINE
TSH/ ANTERIOR PITUITARY
INCREASES ENERGY RELEASE FROM CARBOHYDRATES
INCREASES PROTEIN SYNTHESIS
INCREASES NERVOUS SYSTEM ACTIVITY
T3/ TRIIODOTHYRONINE
5X STRONGER THAN T4

43. CALCITONIN BY EXTRAFOLLICULAR CELLS
DIRECTLY: BLOOD CALCIUM LEVELS; DIGESTIVE HORMONES

44. CONTROL OF THYROID HORMONES
TRH FROM HYPOTHALAMUS STIMULATES TSH FROM ANTERIOR PITUITARY
TSH STIMULATES EPITHELIAL CELLS OF THYROID TO SECRETE HORMONES
INCREASE OF THYROID HORMONES HAS NEGATIVE FEEDBACK TO DECREASE PRODUCTION OF TRH AND TSH

45. PARATHYROID

46. PARATHYROID HORMONES
TIGHTLY PACKED SECRETORY CELLS WITH CAPILLARIES: CHIEF CELLS
PTH
BLOOD CALCIUM FEEDBACK
CALCITONIN AND PTH CONTROL BLOOD CALCIUM
PTH STIMULATES OSTEOCLASTS ?? (INCREASES NUMBER)
PTH ALSO CAUSES SMALL INTESTINES TO BECOME MORE EFFICIENT AT ABSORBING CLACIUM BY ACTIVATING VITAMIN D
PTH INCREASES WHEN BLOOD CALCIUM LEVEL DECREASES (NOT BY RELEASING FACTORS)
CAUSES KIDNEYS TO REABSORB MORE CALCIUM FROM URINE

47. ADRENAL GLAND

48. LOCATED BEHIND THE PERITONEUM, 12TH THORACIC VERTEBRAE, BENEATH ADIPOSE TISSUE
TWO PARTS:
CORTEX
MEDULLA

49. ADRENAL MEDULLA MEDULLA: MODIFIED POSTGANGLIONIC NEURONS
TIED TO SYMPATHETIC ns
EPINEPHRINE/ADRENALIN
NOREPINEPHRINE
AMINE
CONVERTED FROM NOREPINEPHRINE
STORED IN CHROMAFFIN GRANULES (VESSICLES)

50. EFFECTS OF ADRENAL MEDULLA HORMONES
SAME AS SYMPATHETIC NS NUEROTRANSMITTERS: ‘FIGHT OR FLIGHT’
LAST 10X LONGER
80% EPINEPHRINE 20% NOREPINEPHRINE
AFFECT ALPHA AND BETA RECEPTORS; NOREPINEHRINE AFFECTS ALPHA MORE
CONTROLLED BY SYMPATHETIC NEURONS FROM HYPOTHALAMUS

51. ADRENAL CORTEX MORE THAN 30 STERIODS DIE WITHOUT IT (1 WEEK)
ALDOSTERONE
ZONA GLOMERULOSA: MINERALOCORTICOID
KIDNEYS CONSERVE NA+ AND SECRETE K+
CONTROL: RENIN-ANGIOTENSIN SYSTEM

52. RENIN-ANGIOTENSIN SYSTEM
JUXTAGLOMERULAR CELLS STIMULATED BY DECREASE IN BLOOD PRESSURE OR PLASMA SODIUM CONCENTRATION: RELEASE RENIN
RENIN + ANGIOTENSINOGEN = ANGIOTENSIN 1
ACE CAUSE ANGIOTENSIN 1 TO BECOME ANGIOTENSIN 2 = RELEASE OF ALDOSTERONE
CONSERVES SODIUM/RETAINS WATER

53. CORTISOL/ HYDROCORTISONE
GLUCCOCORTICOID: AFFECTS GLUCOSE METABOLISM
ZONA FASCICULATA
INHIBITS PROTEIN SYNTHESIS: MORE BLOOD AA
USE OF FATTY ACIDS FOR ENERGY/ LESS GLUCOSE USED
LIVER CELLS: GLUCONEOGENESIS
CONTROL: HYPOTHALAMUS: CRH -> ANTRERIOR PITUITARY -> ACTH -> ADRENAL CORTEX -> CORTISOL

54. SEX HORMONES ZONA RETICULARIS
MALE ADRENAL ANDROGENS/ SOME CONVERTED TO ESTROGEN OF FEMALES
SUPPLEMENT SEX HORMONES FROM GONADS EARLIER IN LIFE

55. ADRENAL GLAND www.complab.nymc.edu CONNECTIVE TISSUE CORTEX
MEDULLA
4.ZONA FASCICULATA
5. ZONA RETICULARIS
6. MEDULLA

56. ADRENAL GLANDS

57. PANCREAS
en.wikipedia.org

58. PANCREAS EXOCRINE AND ENDOCRINE ?? ATTACHED TO DUODENUM
PANCREATIC ISLETS/ ISLETS OF LANGERHANS
ALPHA CELLS: GLUCAGON
BETA CELLS: INSULIN
DELTA CELLS: SOMATOSTATIN

59. HORMONES OF PANCREAS GLUCAGON: INSULIN: GLYCONEOGENESIS
FATS  FATTY ACIDS AND GLYCEROL
NEGATIVE FEEDBACK
INSULIN:
FORMS GLYCOGEN
INHIBITS GLUCONEOGENESIS
INCREASES FACILLITATED DIFFUSION OF CELLS WITH INSULIN RECEPTORS (CARDIAC, ADIPOSE AND RESTING SKELETAL TISSUE)
INCREASE PROTEIN SYNTHESIS
INCREASES STORAGE OF FAT

60. www. bing. com/images/search

61. ISLETS OF LANGERHANS

62. NEGATIVE FEEDBACK ???

63. NEGATIVE FEEDBACK???

64. SOMATOSTATIN (ALSO SECRETED BY HYPOTHALAMUS)
INHIBITS BOTH HORMONES

65. PINEAL GLAND

66. ABOVE THALAMUS
PINEAL CELLS + NEUROGLIA CELLS
SECRETES MELATONIN (MADE FROM SEROTONIN)
INCREASE LIGHT DECREASES MELATONIN PRODUCTION
DECREASE IN LIGHT INCREASES MELATONIN
INVOLVED IN CIRCADIAN RHYTHMS (SLEEP/WAKE, ETC. CYCLES)

67. THYMUS

68. THYMUS SHRINKS WITH AGE SECRETE THYMOSINS
PRODUCTION AND DIFFERENTIATION OF SOME WHITE BLOOD CELLS

69. REPRODUCTIVE ORGANS TESTES TESTOSTERONE AT PUBERTY
MATURATION OF REPRODUCTIVE SYSTEM
DEVELOPMENT OF SECONDARY SEXUAL CHARACTERISTICS
OVARIES
ESTROGEN
PROGESTERONE
MENSTRUAL CYCLE
PLACENTA

70. OTHERS HEART: ANP: ATRIAL NATRIURETIC POLYPEPTIDE FROM ATRIA
POWERFUL VASODILATOR
HOMEOSTASIS OF WATER, NA, K, FAT
RELEASED DUE TO HIGH BLOOD PRESSURE
REDUCES WATER, NA, AND ADIPOSE LOAD ON CIRCULATORY SYSTEM = ??
LESS PRESSURE

71. KIDNEYS:
ERYTHROPOIETIN ??

72. STRESS STRESSOR: ?? STRESS ??
CONDITION IN BODY
INCREASES ACTIVITY OF SYMPATHETIC NS AND ADRENAL CORTEX

73. TYPES OF STRESS PHYSICAL PHYSIOLOGICAL
DAMAGES TISSUE
EXTREME HEAT/COLD, LOW O2, INFECTION, DISEASES, HEAVY EXERCISE, LOUD SOUNDS
OFTEN PAINFUL
PHYSIOLOGICAL
REAL/IMAGINED DANGER, LOSS, NO SOCIAL LIFE, UNPLEASANT SOCIAL INTERACTIONS,
FEELINGS LIKE: ANGER, DEPRESSION, GREIF, ANXIETY, GUILT
PLEASANT STIMULI: JOY, HAPPINESS
CHANGES OVER AGE, DIFFERENT IN DIFFERENT PEOPLE

74. STRESS RESPONSE HYPOTHALAMUS INITIATES: FIGHT OR FLIGHT RESPONSE
GENERAL STRESS SYNDROME
TO DO WHAT ???
FIGHT OR FLIGHT RESPONSE
RAISE BLOOD SUGAR AND GLYCEROL AND FATTY ACIDS, HEART AND BREATHING RATE, BLOOD PRESSURE, DILATES AIR PASSAGES
SHUNTS BLOODFROM SKIN & DIGESTION TO SKELETAL MUSCLES
WHY??
ALSO ADRENAL MEDULLA RELEASES EPINEPHRINE WHY??

75. CONTINUED HYPOTHALAMUS RELEASES CRH
STIMULATES ANTERIOR PITUITARY TO RELEASE ACTH
STIMULATES ADRENAL CORTES TO RELEASE CORTISOL
CAUSES: DIVERTS GLUCOSE TO BRAIN AND AMINO ACIDS AND OTHER ENERGY SOIURCES TO CELLS

76. PANCREAS RELEASES GLUCAGON ANTERIOR PITUITARY RELEASES GH
MORE ENRGY SOURCES
ANTERIOR PITUITARY RELEASES GH
MORE ENERGY SOURCES, REPAIR OF INJURED TISSUE
POSTERIOR PITUITARY RELEASES ADH
KIDNEYS RETAIN H2O: DECREASE URIN PRODUCTION/ INCREASE BLOOD VOLUME
KIDNEY RELEASES RENIN
KIDNEYS RETAIN SODIUM (THROUGH ALDOSTERONE)
VASOCONSTRICTION TO MAINTAIN BLOOD PRESSURE
WHY???

77. LIFE SPAN CHANGES
GLANDS DECREASE IN SIZE AND BECOME MORE FIBROUS (LESS SECRETORY CELLS); MORE LIPOFUSCIN (LIPID PIGMENT GRANULES)
GH: NOT AS MUCH SECRETED AT NIGHT: DECLINING STRENGTH OF MUSCLES AND SKELETON: SUPPLEMENTS CAN INCREASE BP & BLOOD SUGAR AND ENLARGE SOME ORGANS
ADH LEVELS INCREASE: BUT BECAUSE IT IS NOT BROKEN DOWN AS FAST: REABSORB MORE WATER
THYROID SHRINKS: SMALLER FOLLICLES, MORE FIBROUS TISSUE: NODULES DEVELOP: T3 AND T4 DIMMINISH BUT CONTROL IS SAME ; CALCITONIN DECREASES: OSTEOPOROSIS

78. PTH: MALE: PEAK PRODUCTION AT 55; FEMALE
DECREASES TILL 40 THAN INCREASES AND COULD CAUSE
OSTEOPOROSIS; FAT ACCUMULATES
ADRENAL GLANDS: INCREASE IN FIBROUS TISSUE,
LIPOFUSCIN, AND ABNORMAL CELLS; FINE TUNING
OF NEGATIVE FEEDBACK KEEPS GLUCOCOTICOIDS
AND MINERALCORTICOIDS IN NORMAL RANGE;
HOMEOSTASIS OF OSMOTIC PRESSURE, BLOOD
PRESSURE, ACID/BASE BALANCE, AND SODIUM
AND POTASSIUM CONCENTRATIONS MAY DECREASE
GLUCOSE REGULATION: PANCREAS CAN MAINTAIN
PRODUCTION OF INSULIN AND GLUCAGON BUT
INCREASE FAT, LESS EXERCISE MAY INCREASE INSULIN;
INSULIN RESISTANCE: LESS GLUCOSE UPTAKE,
SO PANCREAS PRODUCES MORE INSULIN: TYPE 2
DIABETES