CHAPTER13b

Report
CHAPTER 13
ENDOCRINE
SYSTEM
COMPARISON???
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ENDOCRINE
NERVOUS
CHEMICAL/
HORMONE
BLOOD
IMPULSE
TIME
SLOWER/
USUALLY
FASTER
CONTROLS
MORE LONG
TERM
EFFECTS
MORE SHORT
TERM
EFFECTS
HOMEOSTASIS
RAPID, PRECISE
CONTROL
MESSENGER
PATHWAY
NERVES
GLAND TYPES
EXOCRINE
SECRETES INTO A
DUCT
ENDOCRINE
DUCTLESS,
SECRETES INTO
BLOOD STREAM
AFFECTS
NEIGHBORING CELLS
PARACRINE
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
www.heartinfo.org/
•
ORGANS
www.parathyroid.com
HOW HORMONES TRAVEL
www.emc.maricopa.edu
HORMONE STRUCTURE
www.emc.maricopa.edu
HORMONE TYPES
STEROID/
THYROID
AMINES
ADRENAL CORTEX
THYROID
SEX HORMONES
NEURONS
ADRENAL MEDULLA
PEPTIDE
POSTERIOR PITUITARY
HYPOTHALAMUS
PROTEIN
PARATHYROID
ANTERIOR PITUITARY
ANTERIOR PITUITARY
GLYCOPROTEIN
STEROID HORMONES
www.emc.maricopa.edu
HORMONE STRUCTURE
www.emc.maricopa.edu
PARACRINE SECRETIONS
PROSTAGLANDINS
LEUKOTRIENES
LIVER, KIDNEYS,
LUNGS, HEART,
THYMUS, PANCREAS,
BRAIN
REPRODUCTIVE
ORGANS
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
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STEROID HORMONE ACTION
PART 2
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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
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NON-STEROID HORMONE
ACTION 2
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NON-STEROID HORMONE
ACTION 3
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NON-STEROID HORMONE
ACTION 4
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AMPLIFICATION ??
STEROID
NON-STEROID
NOT MUCH
A LOT
NEGATIVE FEEDBACK ??
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NEGATIVE FEEDBACK
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ENDOCIRNE SYSTEM
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HYPOTHALAMUS
www.growtall.com
• LINKS NERVOUS SYSTEM TO
ENDOCRINE SYSTEM BY THE
PITUITARY
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
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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
www.unomaha.edu
THYROID
• ISTHMUS
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FOLLICLES
THYROGLOBULIN
www-medlib.med.utah.edu
• FOLLICULAR CELLS
EXTRAFOLLICULAR CELLS
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 ->
SEX HORMONES
• ZONA RETICULARIS
• MALE ADRENAL ANDROGENS/ SOME
CONVERTED TO ESTROGEN OF
FEMALES
• SUPPLEMENT SEX HORMONES FROM
GONADS EARLIER IN LIFE
ADRENAL GLAND
www.complab.nymc.edu
1. CONNECTIVE TISSUE
2. CORTEX
3. MEDULLA
4.ZONA FASCICULATA
5. ZONA RETICULARIS
6. MEDULLA
ADRENAL GLANDS
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PANCREAS
en.wikipedia.org
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/endocrinesy
stem.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

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