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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
http://e.hormone.tulane.edu/learning/images/chem_strucs/signaling/paracrine.gif
AUTOCRINE GLAND
http://edrv.endojournals.org/content/24/2/152/F4.large.jpg
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
www.emc.maricopa.edu
HORMONE TYPES
STEROID/THYROID
ADRENAL CORTEXTHYROID
SEX HORMONESAMINES NEURONS
ADRENAL MEDULLAPEPTIDE POSTERIOR PITUITARY
HYPOTHALAMUS
PROTEIN PARATHYROIDANTERIOR PITUITARY
GLYCOPROTEIN ANTERIOR PITUITARY
STEROID HORMONES
www.emc.maricopa.edu
HORMONE STRUCTURE
www.emc.maricopa.edu
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
www.emc.maricopa.edu
STEROID HORMONE ACTION PART 2
www.emc.maricopa.edu
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
www.emc.maricopa.edu
NON-STEROID HORMONE ACTION 2
www.emc.maricopa.edu
NON-STEROID HORMONE ACTION 3
www.emc.maricopa.edu
NON-STEROID HORMONE ACTION 4
www.emc.maricopa.edu
AMPLIFICATION ??
STEROID NON-STEROID
NOT MUCH A LOT
NEGATIVE FEEDBACK ??
www.emc.maricopa.edu
NEGATIVE FEEDBACK
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ENDOCIRNE SYSTEM
www.emc.maricopa.edu
HYPOTHALAMUS
• LINKS NERVOUS SYSTEM TO ENDOCRINE SYSTEM BY THE PITUITARY
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HYPOTHALAMUS
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HYPOTHALAMUS/ PITUITARY
www.emc.maricopa.edu
ANTERIOR/POSTERIOR PITUITARY
www.emc.maricopa.edu
HYPOTHALAMUS/PITUITARY CONTROL
www.emc.maricopa.edu
PITUITARY HORMONES
www.growtall.com
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
www.unomaha.edu
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
www.complab.nymc.edu
ADRENAL GLANDS
www.emc.maricopa.edu
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
www.bing.com/images/search?q=NEGATIVE+FEEDBACK+OF+INSULIN+PRODUCTION&view=detail&id=AFF3A8A0FD15705C197FD8561D310C1FBE152481&first=61&FORM=IDFRIR
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