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CHAPTER 13 ENDOCRINE SYSTEM. COMPARISON???

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Presentation on theme: "CHAPTER 13 ENDOCRINE SYSTEM. COMPARISON???"— Presentation transcript:

1 CHAPTER 13 ENDOCRINE SYSTEM

2 COMPARISON???

3 ENDOCRINENERVOUS MESSENGERCHEMICAL/ HORMONE IMPULSE PATHWAYBLOODNERVES TIMESLOWER/ USUALLY FASTER CONTROLSMORE LONG TERM EFFECTS MORE SHORT TERM EFFECTS HOMEOSTASISRAPID, PRECISE CONTROL

4 GLAND TYPES EXOCRINESECRETES INTO A DUCT ENDOCRINEDUCTLESS, SECRETES INTO BLOOD STREAM PARACRINEAFFECTS NEIGHBORING CELLS AUTOCRINEAFFECTS 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 THYROID SEX HORMONES AMINESNEURONS ADRENAL MEDULLA PEPTIDE POSTERIOR PITUITARY HYPOTHALAMUS PROTEINPARATHYROID ANTERIOR PITUITARY GLYCOPROTEINANTERIOR PITUITARY

12 STEROID HORMONES

13 HORMONE STRUCTURE

14 PARACRINE SECRETIONS PROSTAGLANDINSLIVER, KIDNEYS, LUNGS, HEART, THYMUS, PANCREAS, BRAIN REPRODUCTIVE ORGANS LEUKOTRIENESWHITE 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 ?? STEROIDNON-STEROID NOT MUCHA 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 RELEASE CONTROLLED BY: STRETCHING OF UTERUS IN LATE PREGNANCY SUCKLING

39 PITUICYTES

40 THYROID ISTHMUS

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

42 THYROID HORMONES T4/ THYROXINE –TSH/ ANTERIOR PITUITARY –INCREASES ENERGY RELEASE FROM CARBOHYDRATES –INCREASES PROTEIN SYNTHESIS –INCREASES NERVOUS SYSTEM ACTIVITY T3/ TRIIODOTHYRONINE –TSH/ ANTERIOR PITUITARY –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, 12 TH 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 1.CONNECTIVE TISSUE 2.CORTEX 3.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: –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

61 ISLETS OF LANGERHANS

62 NEGATIVE FEEDBACK ???

63 http : //physiology-11.wikispaces.com/file/view/blood_glucose.jpg/ /blood_glucose.jpg

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 physnet/anatomynet/anatomy/endocrinesy stem.html

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 AT PUBERTY MATURATION OF REPRODUCTIVE SYSTEM DEVELOPMENT OF SECONDARY SEXUAL CHARACTERISTICS –PROGESTERONE MENSTRUAL CYCLE PLACENTA –ESTROGEN –PROGESTERONE

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 –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: –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 –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


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