CHAPTER 13 ENDOCRINE SYSTEM. COMPARISON??? .

CHAPTER 13

ENDOCRINE

SYSTEM

COMPARISON???

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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

GLAND TYPES

EXOCRINE SECRETES INTO A DUCT

ENDOCRINE DUCTLESS, SECRETES INTO BLOOD STREAM

PARACRINE AFFECTS NEIGHBORING CELLS

AUTOCRINE AFFECTS SECRETING CELL

PARACRINE GLAND

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AUTOCRINE GLAND

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EXOCRINE AND ENDOCRINE

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HORMONES SECRETED BY

• SMALL GROUPS OF SPECIALIZED CELLS

• ORGANS

www.parathyroid.com

www.heartinfo.org/

HOW HORMONES TRAVEL

www.emc.maricopa.edu

HORMONE STRUCTURE


HORMONE TYPES

STEROID/THYROID

ADRENAL CORTEXTHYROID

SEX HORMONESAMINES NEURONS

ADRENAL MEDULLAPEPTIDE POSTERIOR PITUITARY

HYPOTHALAMUS

PROTEIN PARATHYROIDANTERIOR PITUITARY

GLYCOPROTEIN ANTERIOR PITUITARY

STEROID HORMONES


HORMONE STRUCTURE


PARACRINE SECRETIONS

PROSTAGLANDINS LIVER, KIDNEYS, LUNGS, HEART,

THYMUS, PANCREAS, BRAIN

REPRODUCTIVE ORGANS

LEUKOTRIENES WHITE BLOOD CELLS

HORMONE ACTION

• ALTER METABOLIC PROCESSES• UP-REGULATION: INCREASE OF TARGET

CELL RECEPTORS• DOWN-REGULATION ??

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

STEROID HORMONE ACTION


STEROID HORMONE ACTION PART 2


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

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

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 ?

NON-STEROID HORMONE ACTION 1


AMPLIFICATION ??

STEROID NON-STEROID

NOT MUCH A LOT

NEGATIVE FEEDBACK ??


NEGATIVE FEEDBACK

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ENDOCIRNE SYSTEM


HYPOTHALAMUS

• LINKS NERVOUS SYSTEM TO ENDOCRINE SYSTEM BY THE PITUITARY

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HYPOTHALAMUS

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HYPOTHALAMUS/ PITUITARY


ANTERIOR/POSTERIOR PITUITARY


HYPOTHALAMUS/PITUITARY CONTROL


PITUITARY HORMONES

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ANTERIOR PITUITARY

• 5 TYPES OF EPITHELIAL CELLS AROUND BLOOD VESSELS

• CONTROL BY HORMONES (RELEASING FACTORS) RELEASED BY THE HYPOTHALAMUS

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

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

PITUICYTES

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THYROID

• ISTHMUS www.growtall.com

FOLLICLES

• FOLLICULAR CELLSwww-medlib.med.utah.edu

EXTRAFOLLICULAR CELLS

THYROGLOBULIN

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

• CALCITONIN– BY EXTRAFOLLICULAR CELLS– DIRECTLY: BLOOD CALCIUM LEVELS;

DIGESTIVE HORMONES

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

PARATHYROID

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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

ADRENAL GLAND

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• LOCATED BEHIND THE PERITONEUM, 12TH THORACIC VERTEBRAE, BENEATH ADIPOSE TISSUE

• TWO PARTS:– CORTEX– MEDULLA

ADRENAL MEDULLA

• MEDULLA: MODIFIED POSTGANGLIONIC NEURONS

• TIED TO SYMPATHETIC ns– EPINEPHRINE/ADRENALIN– NOREPINEPHRINE

• AMINE• CONVERTED FROM NOREPINEPHRINE• STORED IN CHROMAFFIN GRANULES

(VESSICLES)

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

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

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

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

SEX HORMONES

• ZONA RETICULARIS• MALE ADRENAL ANDROGENS/ SOME

CONVERTED TO ESTROGEN OF FEMALES

• SUPPLEMENT SEX HORMONES FROM GONADS EARLIER IN LIFE

ADRENAL GLAND

1. CONNECTIVE TISSUE2. CORTEX3. MEDULLA

4.ZONA FASCICULATA5. ZONA RETICULARIS6. MEDULLA

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ADRENAL GLANDS


PANCREAS

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PANCREAS

• EXOCRINE AND ENDOCRINE ??• ATTACHED TO DUODENUM• PANCREATIC ISLETS/ ISLETS OF

LANGERHANS– ALPHA CELLS: GLUCAGON– BETA CELLS: INSULIN– DELTA CELLS: SOMATOSTATIN

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

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ISLETS OF LANGERHANS

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NEGATIVE FEEDBACK ???

NEGATIVE FEEDBACK???

http://physiology-11.wikispaces.com/file/view/blood_glucose.jpg/197617660/blood_glucose.jpg

• SOMATOSTATIN (ALSO SECRETED BY HYPOTHALAMUS)– INHIBITS BOTH HORMONES

PINEAL GLAND

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• 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)

THYMUS

• http://homepage.smc.edu/wissmann_paul/physnet/anatomynet/anatomy/endocrinesystem.html

THYMUS

• SHRINKS WITH AGE• SECRETE THYMOSINS

– PRODUCTION AND DIFFERENTIATION OF SOME WHITE BLOOD CELLS

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

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

KIDNEYS:ERYTHROPOIETIN ??

STRESS

• STRESSOR: ??• STRESS ??

– CONDITION IN BODY• INCREASES ACTIVITY OF

SYMPATHETIC NS AND ADRENAL CORTEX

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

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??

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

• 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???

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

• 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

CHAPTER 13 ENDOCRINE SYSTEM. COMPARISON??? .

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