Download THE ENDOCRINE SYSTEM

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REV. 8/15/06
Dr. Vince Scialli
THE ENDOCRINE SYSTEM
TWO GREAT CONTROLLING SYSTEMS
Nervous System . . . . . . . . . . . . . . . . Endocrine System
1)
NERVOUS SYSTEM
Regulates activity via action potential impulses ~ AP’s
Impulses carried by specific sensory or motor neurons
Uses “synaptic communication” to carry message
Targets specific cells ~ for specific response
Response is immediate & usually short lasting
2)
ENDOCRINE SYSTEM
Controls cell activity by secreting hormones ~ EXCITE
Hormones = “Chemical Messengers”
Secreted into blood & transported throughout body
Generalized Widespread Response ~ Adrenalin or GH
Targeted specific cells:
TSH or FSH
Diverse or very specific effects:
Insulin ~ specific
Adrenaline ~ diverse
Response on target cells is delayed ~ due to circulation
Delayed, prolonged or continuous response
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ENDOCRINE SYSTEM ~ Controlling Spectrum
MAJOR processes controlled by hormone release
Reproduction
Testosterone
Estrogen
Follicle Stimulating Hormone
Leutenizing Hormone
Oxytocin ~ “Post Pit”
Growth & Development
Growth Hormone & Thyroid Hormone
Body Defense Mechanisms
Corticosteroids ~ Cortisone ~ Anti-inflammatory
Anti-Stress ~ Corticosteroids ~ Gluconeogenesis
Electrolyte, Water & Nutrient Balance
Aldosterone ~ Na+ retention ~ water retention
Anti-Diuretic Hormone ~ ADH
Cell Metabolism & Energy Regulation
Insulin & Thyroid Hormone
Digestive Processes
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TWO GLANDULAR SYSTEMS OF BODY
Exocrine Glands . . . . . . . Endocrine Glands
1.
EXOCRINE GLANDS ~ Merocrine . . . Apocrine . . . Holocrine
< PUREST ------------------------------ MESSY >
Secreted onto body surfaces ~ via ducts
Secretions are non-hormonal
Secreted & ACT LOCALLY in a target area only
DO NOT secrete into blood or lymphatics
Can be large in size or extensive in numbers ~ millions
Examples of Exocrine Glands
Secrete
Mucous Glands
Mucous
Sudoriferous Glands
Sweat
Sebaceous or Oil Glands
Sebum
Salivary Glands
Saliva
Mammary Glands
Milk
Liver
Bile
Enteric Glands
Digestion
Reproductive Glands
Several
Pancreas ~ Both Exocrine & Endocrine
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ENDOCRINE GLANDS
“Ductless Glands” ~ produce hormones ~ NO DUCTS
Secrete hormones most directly into blood
Surrounded by many capillaries ~ allows secretion into blood
Hormones travel through body ~ act on specific target organs
Can have a generalized effect or specific target effect
Effects can be short, prolonged or continuous lasting
Small Glands ~ very localized, & few in numbers ~ 12 groups
ENDOCRINE GLANDS
Pituitary Gland
Heart
Pineal Gland
Small Intestines
Thyroid Gland
Kidney
Parathyroid Gland
Pancreas
Thymus Gland
Gonads – ovaries &
testes
Adrenal Gland
Hypothalamus
Other Specialized Cells can produce hormones
Adipose Tissue . . . .Tumors or cancer cells
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CHEMISTRY OF HORMONES
Hormones ~ “chemical messengers” ~ “First Messengers”
Control other parts of body from where secreted
“Endocrine Communication” ~ NOT NEURAL
MOST Secreted into blood & circulatory system
Regulate functions of other cells somewhere else
Major Hormone Classifications
1.
Amino Acid Hormones ~ MOST COMMON
Most hormones are globular proteins or peptides
2.
Lipid Homones
Steroid Hormones ~ from cholesterol
Gonadal hormones ~ estrogen, testosterone
Adrenalcorticoids hormones ~ corticosteroids
Eicosanoids (eye cos an oids)
Increase inflammation & cause swelling
NON-CIRCULATING hormones ~ act locally only
Released from most cell membranes & have a
highly localized response
Prostaglandins ~ most common
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MECHANISM OF HORMONE ACTION
Hormones effect target cells ~ alter cell activity
Increase or decrease types & rates of cellular processes
Up-Regulation ~ increased sensitivity to hormone effects
Down-Regulation ~ less sensitive to hormone effects
Activity is very specific on a specific target cell
EG: Epinephrine causes blood vessel walls to contract
It will also cause an increase in heart rate
HORMONE EFFECTS ON TARGET CELLS
1.
Change plasma membrane permeability
2.
Change electrical charge of plasma membranes
3.
Stimulate secretory activity of cells
4.
Stimulate mitosis & cell division
5.
MOST
Stimulate Enzyme Activation or Deactivation ~ COMMON
Forms NEW proteins within cells
Amino Acid Hormones ~ cAMP Second Messenger
6.
Stimulate Gene Activation ~ COMMON
Lipid/Steroid Hormones ~ Form New Proteins
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EXAMPLES ~ MECHANISMS OF HORMONE ACTION
AMINO-ACID HORMONES (“PEPTIDES”) ~ MOST COMMON
Utilizes a Second Messenger System
Hormone ~ is the first messenger
Hormone CANNOT penetrate cell membrane ~ to big
Binds to “hormone receptor” site on target cell
Receptor binding ---> activates a “G-protein” --->
which activates an effector enzyme
Effector Enzyme = Adenylate cyclase
Adenylate cyclase generates Second Messenger ~ cAMP
cAMP activates protein kinase - - -> form NEW PROTEINS
inside cell
MANY reactions follow & cause specific cell activities
LIPID ~ STEROID HORMONES
Utilizes:
“from CHOLESTEROL”
Gene Activation ~ NO 2nd messenger system
Smaller & lipid soluble ~ can penetrate cell membrane
Once inside target cells ~ gene activation occurs
DNA is “transcribed” to messenger RNA ~ mRNA
mRNA ~ stimulates production of NEW proteins
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HORMONE TARGET CELL ACTIVATION & SPECIFICITY
Major hormones circulate in blood to all tissue
Specific hormones effect only specific tissue cells
Hormone Receptors ~ located on or in cells
Target Cells have specific hormone receptors on cell
membranes or inside target tissue that bind hormones
Receptor Binding is required for activity
SOME receptors are found only on/in SPECIFIC CELLS
Example: ACTH stimulates only the adrenal cortex
SOME receptors are found on/in MOST BODY CELLS
Example: Thyroxine stimulates most cells
Insulin affects all cells of body
Target Cell Activation Requirements
Adequate Hormone Blood Levels
Specific Receptor Binding Sites
Adequate Number of Receptors on or within cells
Specific Bonding Affinity between Hormone & Receptor
Any +/- Changes in any of the above results in:
Endocrine Dysfunction  Up Regulation OR
 Down Regulation
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ENDOCRINE DYSFUNCTION
Up-Regulation ~ Sensitization ~ Stimulation
Occurs when target cells form MORE receptors in
response to hormone presence
Down-Regulation ~ Desensitization ~ Inhibition
Occurs when prolonged exposure to high hormone
levels causes LOSS of receptors
Desensitizes target cells resulting in lower activity
Hormones also STIMULATE or INHIBIT other hormones
EG:
Estrogen stimulates Progesterone release
Progesterone antagonizes Estrogen action
DURATION OF HORMONAL ACTIVITY ~ “Half-Life”
Dependent on circulating blood levels of Hormone
1)
Rate of Release into the blood
2)
Speed of Inactivation & Removal from the body
Methods of Inactivation ~ Removal from body
1)
Degradation by enzymes in target cells
2)
Removed from blood via Kidney and Liver
3)
Excreted in Urine or Feces
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HALF-LIFE
Time required to reduce blood concentrations by 50%
Ranges from seconds to minutes to hours or longer
What is the Half-Life? . . . .If blood concentration is 20 units &
.....
15 units remain after 7 minutes
Answer
.....
.....
10 units remain after 14 minutes = HALF-LIFE
5 units remain after 21 minutes
Endocrine Reflexes ~ CONTROL HORMONE RELEASE
Blood levels are precisely controlled for optimal effects
1)
POSITIVE FEEDBACK MECHANISM
As hormone is released, target organ stimulates the
release of more hormone . . . more . . . more . . . more
EG:
2)
Oxytocin ~ Childbirth
MOST
NEGATIVE FEEDBACK MECHANISM ~ COMMON
As blood hormone levels rise, target organs inhibit
further hormone release ~ on . . . off . . . on . . . off
EG:
thermostat in a house
EG:
High blood sugar ---> insulin release --->
---> glucose uptake into cells ---> lower blood sugar
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TYPES OF ENDOCRINE GLAND RELEASE STIMULI
Endocrine Gland Reflexes
Stimulate glands to produce & release hormones
1) Humoral Stimuli ~ ions & chemicals
2) Neural Stimuli ~ nerve impulses
3) Hormonal Stimuli ~ other hormones
HUMORAL STIMULI
Hormones secreted in direct response to changing blood
levels of certain IONS & CHEMICALS
Examples:
Low blood Ca+ ---> parathyroid gland to secrete
parathyroid hormone (PTH) ---> higher blood Ca+ --->
reduced secretion of PTH
High blood sugar ---> pancreas to secrete insulin --->
lowering of blood sugar
NEURAL STIMULI
Nerve IMPULSES (AP’s) stimulate hormone release
EG:
Stress ---> Sympathetic NS activation
---> adrenal medulla secretes catecholamines
Adrenalin ~ norepinephrine & epinephrine
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HORMONAL “TROPIC” STIMULI ~ COMMON
Occurs when an endocrine gland releases hormones that
stimulate OTHER endocrine glands to release hormones
Hypothalamus ~ Highest level of endocrine control
Integrates activities of endocrine & nervous system
Produces Hormones that regulates Pituitary Gland
Pituitary produces other hormones that regulate
OTHER glands
Hypothalamic-Pituitary -Target Endocrine Gland
Feedback Loop
SEVERAL Hypothalamus “Regulating” Hormones
Thyrotropic Releasing Hormone (TRH)
Stimulates release of TSH from Ant. Pituitary
TSH stimulatesThyroid Hormone from Thyroid
Corticotropin Releasing Hormone (CRH)
Stimulates release of ACTH from Ant. Pituitary
StimulatesAdrenal Hormones from Adrenals
Gonadortophin Releasing Hormone (GnRH)
Stimulates release of FSH & LH from Ant. Pit.
Stimulates Testosterone, Estrogen &
Progesterone from Gonad
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12 MAJOR ENDOCRINE ORGANS
PITUITARY GLAND
Also called the “Hypophysis” ~ “Master Gland of Body”
Protected by sella turcica of the sphenoid bone
At the base of the brain ~ not a part of nervous system
Infundibulum ~ “stalk” ~ connects pituitary to hypothalamus
Two lobes:
Anterior Pituitary ~ “adenohypophysis”
Posterior Pituitary ~ “neurohypophysis”
HYPOTHALAMUS
Located above the brain stem ~ in diencephalon
Controls Autonomic Nervous System
Controls emotion ~ rage, fear, anger, pleasure
Body temperature regulation
Food intake regulation ~ appetite
Water balance & thirst regulation
Controls Endocrine System
Produces Hormones that “regulate” the Anterior Pituitary
Produces two hormones released by the Posterior Pituitary
ADH . . . . . . Oxytocin
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HYPOTHALAMUS
Produces “Releasing & Inhibiting” Regulating Hormones
Carried via “Hypophyseal Portal System” to Ant. Pit.
Vascular connection ~ hypothalamus & Ant. Pit
“Releasing” Hormones
Stimulate secretion of Anterior Pituitary Hormones
“Inhibiting” Hormones
Inhibit release of Anterior Pituitary Hormones
Produces 2 “Neuro-Hormones” for Posterior Pituitary
Paraventricular Nucleus
Supraoptic Nucleus
----> Oxytocin
----> Anti-diuretic Hormone ~ ADH
Carried via “Hypothalamic-Hypophyseal Tract”
by axons to posterior pituitary
Neuro-Hormones are secreted by Posterior Pituitary
“Hypophyseal Portal System”
Vascular connection ~ hypothalamus & anterior pituitary
“Hypothalamic-Hypophyseal Tract”
Neural connection ~ hypothalamus & posterior pituitary
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ANTERIOR PITUITARY ~ “Master Endocrine Gland”
Anterior Lobe ~ “Adenohypophysis”
Controlled by the hypothalamus via regulating hormones
Hypophyseal Portal System
Fenestrated Capillaries ~ vascular bed connections
Allows hypothalamic hormones to circulate
through the anterior pituitary
Regulating Hormones ~ regulate the secretions of
other hormones from anterior pituitary gland
Secretes 6 major hormones ~ ALL ARE PROTEINS
Instantaneous Response ~ NO storage in Anterior Pit.
Tropic Hormones: Hormonal Stimuli
Regulate the secretory action of OTHER endocrine
glands to release other hormones
TSH
ACTH
Thyroid Stimulating Hormone
Adrenal Corticotropic Hormone
FSH
LH
Follicle Stimulating Hormone
Leutenizing Hormone
Non-tropic Hormones: Effects NON-ENDOCRINE
glands
GH
PRL
Chapter 18 ~ Endocrine System ~ 05/02/17
Growth Hormone
Prolactin
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ANTERIOR PITUITARY - “TROPIC” HORMONES
THYROID STIMULATING HORMONE ~ TSH
TRH ~ Thyrotropin Releasing Hormone - Hypothalamus
Stimulates release of TSH from Anterior Pituitary
TSH (tropic) ~ stimulates Thyroid Gland to secrete
Thyroid Hormone
Negative Feedback “Shut Off” Mechanism
Rising blood levels of TH “shuts off” the Hypothalamus &
Anterior Pituitary to block further TSH release
Factors releasing TRH from Hypothalamus
Increased Energy Demands
Need to raise metabolic rate
Need to produce & release heat
EG:
Pregnancy
Cold temperatures
Exercise
Fever
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ANTERIOR PITUITARY - “TROPIC” HORMONES
ADRENOCORTICOTROPIC HORMONE ~ ACTH
CRH ~ Corticotropin Releasing Hormone - Hypothalamus
Stimulates release of ACTH from Anterior Pituitary
ACTH tropic action:
stimulates the adrenal cortex to
release several other hormones:
1)
Gluco-corticoids ~ corticosteroids ~ mostly
2)
Gonad-ocorticoids ~ androgens ~ small amount
3)
Mineralo-cortacoids ~ aldosterone
Negative Feedback “Shut Off” Mechanism
Rising blood levels of “corticoids” cause Anterior
Pituitary & Hypothalamus to block further CRH release
Factors stimulating CRH release:
fever
hypoglycemia
stress
dehydration . . . shock . . . blood loss . . . low blood
pressure
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ANTERIOR PITUITARY - “TROPIC” HORMONES
GONADOTROPINS
FSH ~ Follicle Stimulating Hormone
LH ~ Leuteinizing Hormone
GnRH ~ gonadotropin releasing hormone from Hypothalamus
Stimulates release of FSH or LH from Anterior Pituitary
FSH and LH ~ action is tropic
Stimulate gonad activity ~ ovaries & testes ~ at puberty
FSH
~ stimulates sperm & egg production
LH
~ cause ovarian follicle maturation & ovulation
~ causes release of Gonadal Hormones
Estrogen ~ Female ~ controls menstrual cycle
Progesterone ~ Female ~ maintains pregnancy
Testosterone ~ Male Testicular Hormone
Negative Feedback “Shut-Off” Mechanism
Rising blood levels of gonad hormones causes the
Hypothalamus to block GnRH release, & inhibits FSH &
LH release from Anterior Pituitary
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ANTERIOR PITUITARY - “NON-TROPIC” HORMONES
GROWTH HORMONE ~ GH ~ “Somatotropin”
“Anabolic Hormone” ~ stimulates most body cells
to increase in size and divide
GH targets bones & skeletal muscles
Stimulates epiphyseal plate & long bone growth
Increases skeletal muscle mass
“Insulin-growth factor” ~ Somatomedins ~ enhance GH
Protein produced in liver & muscle stimulate growth
GH Actions
1)
Stimulates protein synthesis ~ anabolic ~ muscles
2)
Stimulates cartilage & bone development
3)
Stimulates fats for energy ~ increases glucose
4)
Converts glucose to glycogen stores for future
5)
Causes a “diabetogenic” effect
Causes glycogen breakdown & release of glucose
into blood causing ↑ blood sugar
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GROWTH HORMONE ~ GH ~ “Somatotropin”
Secretion of GH ~ NOT a feedback mechanism
GHRH – GH Releasing Hormone
Hypothalamic hormone - stimulates release of GH
GHIH – GH Inhibiting Hormone – Somatostatin
Hypothalamic hormone - inhibits release of GH
Growth Hormone Imbalances
Hyper-Secretion ~ giganticism or acromegaly
Gigantism ~ Abnormally large ~ normal proportions
Excess GH from early age ~ Andre the Giant
Acromegaly ~ Abnormally large ~ abnormal
proportions
Excess GH later in life
Hypo-Secretion ~ pituitary dwarfism ~ in children
Midget ~ Usually normal proportions
Corrected by GH replacement therapy as children
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ANTERIOR PITUITARY - “NON-TROPIC” HORMONES
PROLACTIN ~ PRL
PRL has direct action on non-endocrine mammary cells
Stimulates milk production by breast (not release)
PRL is controlled by Hypothalamus
PRH ~ Prolactin “Releasing” Hormone = seratonin
Causes prolactin release from Ant. Pituitary
PIH ~ Prolactin “Inhibiting” Hormone = dopamine
Prevents prolactin secretion from Ant. Pituitary
PRL Levels fluctuates in females with ESTROGEN
Low Estrogen stimulates PIH ---> LESS Prolactin
High Estrogen levels stimulates PRH ---> MORE PRL
Menstruation ~ HIGH Estrogen ---> PRH ---> MORE PRL
Breast swelling & tenderness ~ temporary
Generally NO milk production
Pregnancy ~ cause HIGH levels of PRH near term
Infant Suckling ~ stimulates PRH ---> MORE PRL
PRL Hyper-Secretion ~ occurs in nursing mothers
PRL Hypo-Secretion – only occurs in heavy nursers
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POSTERIOR PITUITARY
Neurohypophysis ~ Posterior Lobe + Infundibulum
Neural Portion (axons) is an extension of the Hypothalamus
Stores two “neurohormones” produced in the hypothalamus
1)
Oxytocin ~ effects uterus & mammaries
2)
Antidiuretic Hormone ~ ADH ~ retains water
Neurohormones released into capillary beds of posterior
pituitary in response to neural stimulation ~ Humoral
OXYTOCIN ~ “Post pit”
PRODUCED in hypothalamus ~ Paraventricular Nuclei
Uterus & Cervic Stretching during childbirth stimulates
Released from Posterior Pituitary ~ Positive Feedback
Effects: Stimulates uterus muscle contraction
Stimulates mammaries to release & “let-down”
Stimulates sexual arousal & organism
Promotes nurturing & cuddling ~ “nesting”
Highest Concentrations ~ during childbirth & nursing
Synthetic Drug ~ induces labor & stimulates milk “letdown”
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POSTERIOR PITUITARY
ANTIDIURETIC HORMONE ~ ADH
What is “Diuresis”???
=
Excess Urine Production
ADH = “Anti-Urine Hormone” = AGAINST DIURESIS
“Vasopressin” ~ causes vasoconstriction & elevates BP
PRODUCED in hypothalamus ~ Supra Otic Nuclei
Stimulated by need to retain fluids
Dehydration ~ Excess sweating ~ no fluid intake
Hemorrhage ~ Blood Loss
Low blood pressure & Shock
Released from Posterior Pituitary into blood
Effects:
Targets Kidneys ----> Water Retention
Prevents urine formation ----> water retention
Reabsorbs water back into blood in kidneys
Increases blood pressure ~ due to vasoconstriction
& retained fluid volume in blood
Controlled by Negative feedback “Shut-Off” Mechanism
Inhibited by High Blood Volume . . . High Blood
Pressure. . . Fluid Retention . . . Over-Hydration
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ADH INHIBITORS ~ BLOCK ADH ~ “Diuretics”
Stimulate urine production & fluid loss
Results in copious urine production & output
Flushes water from body ~ Dehydration
Morning after dry mouth & intense thirst ~ drinking
Decreases Blood Fluid Volume ----> lowers BP
Examples of ADH Inhibitors ~ ALL act as DIURETICS
Drinking excessive fluid & Alcoholic beverages
Diuretic Drugs ~ Diet Pills ~ Dexetrene
Hypertension Drugs ~ to lower blood pressure
ADH Hypo-Secretion ----> Diuresis & Fluid Loss
CANNOT retain water ~ CANNOT concentrate urine
----> fluid loss, HIGH urine output, low blood volume
“Diabetes Insipitus” ~ NO ADH
Excess urine ~ polyuria ~ intense thirst ~ fluid loss
Caused by head injury to hypothalamus or Pituitary
Treated by Re-Hydration & fluid therapy
ADH Hyper-Secretion ~ uncommon ~ trauma, tumor, drugs
Fluid retention, LOW urine output, high blood volume
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THYROID GLAND
Largest “pure” endocrine ONLY gland in body ~ “Butterfly”
On the trachea . . . Anterior throat area . . . below the larynx
Two lateral lobes connected by a median isthmus
Blood Supply ~ via thyroid artery off common carotid artery
Extremely vascular ~ Surgery very difficult
Internal Thyroid Tissue Histology
1.
Follicular Cells - spherical cells ~ surround lumen
Produce thyroglobulin ~ glycoprotein
2.
Lumen of follicle ~ stores colloid
Colloid = thyroglobulin + attached iodine
“Iodinated Thyroglobulin”
Precursor for Thyroid Hormone ~ T3 or T4
3.
Parafollicular Cells ~ around & between the follicle
Endocrine cells that produce calcitonin
Calcitonin ~ lowers blood calcium levels
Thyroid Gland is Unique . . .
Only endocrine gland that stores hormones in
large quantities ~ in colloid
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THYROID HORMONE ~ TH
“Body’s major “metabolic hormone”
Thyroid Hormone is two Iodine containing hormones
T4 Thyroxine ~ STORED FORM ~ NOT ACTIVE
90% of TH ~ secreted by follicle cells
T3 Triiodothyronine ~ NOT stored ~ “ACTIVE”
Formed at target tissues by conversion of
T4 (STORED)
>>>
T3 (“Active)
Thyroid Hormone affects most cells except:
Brain . . . Spleen . . . Testes . . . Uterus . . . Thyroid
Effects of Thyroid Hormone
1.
Stimulates carbohydrate, lipid & protein metabolism
Glucose & fat catabolism ~ energy produced
Protein & cholesterol synthesis ~ growth
2.
Increases basal metabolic rate & O2 consumption
Calorigenic Effect ~ burn calories ~ body heat
Promotes normal oxygen use by cells
3.
Regulates tissue growth, development, & function
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Thyroid Hormone Release ~ “Negative Feedback”
1.
Falling blood levels of thyroxin (T4) ----> Hypothalamus to
release thyrotropic releasing hormone (TRH)
2.
TRH ----> anterior pituitary to release thyroid stimulating
hormone (TSH) into blood
3.
TSH ----> Thyroid to release thyroxin (T4 & T3) into blood
4.
Thyroxin (T4 & T3) is carried to target organ receptors
T3 is formed at the target tissue by conversion of T4
5.
T3 or T4 actively exert effects on the target tissue
6.
Rising blood levels of T3/T4 “shuts off” hypothalamus -->
inhibits release of TRH (hypothalamus) & TSH (Ant. Pit)
Factors Triggering TSH release from anterior pituitary:
Any conditions increasing body energy requirements
Pregnancy ~ requires energy for fetus
Prolonged Cold ~ requires body heat
Extensive Exercise ~ requires energy & O2
Factors Inhibiting TSH release:
Somatostatin ~ growth hormone inhibitor ~ less energy
Rising levels of glucocorticoids ~ high blood sugar
High blood iodine concentration ~ Stimulates excess TH
----> shuts off Hypothalamus
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THYROID GLAND DISFUNCTION ~ Common
Hypo-Thyroidism ~ “Under-activity of Thyroid Gland”
Thyroid Gland Defects ----> LOW TRH or TSH secretion
Symptoms:
Myxedema – mucous area swelling
Low metabolic rate – weight gain
Feeling chilly
Thick dry skin ~ hair thins & loss
Lethargy & sluggishness
Cretinism ~ severe hypothyroidism in infants
Short, disproportionate body, thick tongue & neck,
mental retardation ~ irreversible
Cause unknown ~ genetic deficiency ???
Prevented by TH replacement therapy
Goiter ~ enlarged thyroid due to lack of iodine ~ common
Follicle cells produce colloid but cannot iodinate
colloid (CANNOT MAKE THYROID HORMONE)
-----> Low blood TH ~ NONE produced
NO negative feedback “shut-off” of TSH
-----> Continuous release of TSH
Unusable colloid accumulates in thyroid gland
Treatment:
Removal of Thyroid Gland ~thyroidectomy
Oral TH tablets & Dietary Iodine ~Thyroxin
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THYROID GLAND DISFUNCTION
Hyper-Thyroidism ~ thyrotoxicosis
“Overactivity of Thyroid Gland”
“Graves” Disease
Cause:
“Autoimmune disease” ~ against self
Body produces antibodies ~ mimic TSH
Causes continuous production of TH
Symptoms:
Elevated metabolic rate
Sweating
Rapid, irregular heartbeat
Nervousness
Weight loss, even with adequate
food intake
Treatment:
Surgical removal of thyroid
To stop excessive TH release
Oral controlled thyroxin
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THYROID GLAND HORMONES
CALCITONIN
Produced by parafollicular cells of Thyroid
Protein hormone ~ lowers blood Ca++
Direct antagonist to parathyroid hormone
Mode of Action:
1. Targets skeletal tissue & bone
2. Inhibits osteoclast activity & bone resorption
3. Inhibits release of ionic calcium from bone
4. Stimulates calcium uptake into bone
Stimulates osteoblast activity in bone
Calcitonin Secretion Stimuli:
Cycles up & down with parathryroid hormone
Excessive blood levels of calcium -----> “calcitonin”
release ~ to lower blood calcium
Part of “negative feedback” system with “parathyroid
hormone” from parathyroid gland
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PARATHYROID GLAND
Very tiny ~ on posterior side of thyroid gland . . . two pairs,
one on each side ~ numbers can vary
Function is antagonistic to thyroid gland
Thyroid ~ calcitonin lowers blood Ca++
Parathyroid ~ parathyroid hormone raises blood Ca++
Histology of Parathyroid Tissue
1.
Chief Cells – round and dark stained
Produce “Parathyroid Hormone” ~ PTH
2.
Oxyphil Cells – function unknown ~ egg whites
3.
Capillaries - extensive network
Parathyroid Hormone ~ PTH ~ “Parathormone”
Most important hormone controlling blood calcium levels
PTH Secretion & Release Stimuli
Low blood calcium levels (hypo-calcemia) ---->
Stimulate Parathyroid Hormone release
High blood calcium levels (hyper-calcemia) ---->
inhibits Parathyroid Hormone release
Main Effect of PTH ~ increases blood calcium ion levels
Direct antagonist to calcitonin (lowers blood Ca++ )
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Parathyroid Hormone ~ PTH
Blood Calcium Balance ~ needed for many body functions
Nerve impulse transmission
Muscle contraction
Blood clotting
Bone development & maintenance
Mode of Action ~ Parathyroid Hormone
1.
Skeletal Tissue ~ stimulates bone cells (osteoclasts)
to release calcium from bone into blood
2.
Kidney ~ enhances reabsorption of calcium into blood
3.
Kidney ~ activates Vitamin D -----> increases intestinal
absorption of Ca++
Parathyroid Gland Dysfunction
Hyper-parathyroidism ~ Rare ~ Parathyroid Gland Tumor
Hypo-parathyroidism ~ Parathyroid Hormone Deficiency
Causes: Parathyroid trauma
Thyroid gland removal with parathyroid
Symptoms:
Hypocalcemia ~ low blood calcium
Loss of nerve function
Muscle twitches
Convulsions . . . Respiratory paralysis . . .
Death
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ADRENAL GLAND ~ the “Stress Gland”
Paired ~ pyramid shaped ~ On top of each kidney
“suprarenal glands” ~ above the kidney
Each adrenal gland ~ two distinct glands in one
Adrenal Medulla – smaller interior part
Adrenal Cortex – larger portion surrounds medulla
Each produces different types of hormones
BOTH are stimulated in response to stressful situations
Adrenal Cortex
Zona glomerulosa
Hormones
Mineralocorticoids
(Aldosterone)
Zona fasciculata
Gluco-corticoids
Cortico-steroids
Cortisone
Cortisol)
Zona reticularis
Gonado-corticoids
(Androgen)
Function
Mineral &
water balance
Na+ retention
Gluconeogenesis
Energy Metabolism
Anti-inflammatory
Immune Supression
Sex Hormones
Adrenal Medulla
Hormones
Function
Adrenal Medulla
Hormones
Catecholamines
Adrenalin
Epinephrine
Nor-Epinephrine
Increases BP
Increases HR
Dilates Bronchioles
Decrease Peristalsis
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ADRENAL CORTEX
MINERALOCORTICOIDS ~ Aldosterone
Aldosterone ~ 95% of mineralo-corticoids
Produced in Zona Glomerulosa
Regulate Na+ concentration in body fluids & blood
Retains Na+ ~ most vital ion causing fluid retention
Sodium retention causes fluid retention ~ EDEMA
Retains water & fluid ~ same effect as ADH
Aldosterone Effects
Reduces Na+ excretion from body
Retains Na+ from urine in kidney tubules
Retains Na+ from perspiration & saliva
Water follows sodium > > > fluid retention
Aldosterone Secretion Stimuli
Anything Requiring Fluid Retention
Decreased Na+ blood levels
Decreased blood volume
Shock
Dehydration
Blood Loss
Decreased blood pressure
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Aldosterone Release Mechanisms
Renin-Angiotensin-Aldosterone Mechanism ~ MAJOR
1.
Low blood pressure or lost blood volume is sensed
by juxtaglomerular apparatus in kidney
2.
Kidney releases Renin into blood
3.
Renin ----> Angiotensin I in blood
Angiotensin I ----> Angiotensin II in blood
4.
Angiotensin II stimulates adrenal cortex to release
Aldosterone which ----> Na+ retention in the kidney
5.
Na+ & water retained in the blood ---->increasing
blood volume & blood pressure ~ decreased urine
Other Aldosterone Release Mechanisms ~ MINOR
ACTH ~ adrenocorticotropic hormone
Severe stress ----> hypothalamus secretes
corticotropin releasing hormone ----> anterior
pituitary to secrete ACTH ----> release of
Aldosterone ----> Sodium Retention Effects
Atrial Natriuretic Peptide ~ ANP ~ inhibits aldosterone
Increased blood pressures stimulates heart to
release ANP which inhibits the renin-angiotensin
mechanism
----> Na+ & water excretion & lower blood pressure
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ADRENAL CORTEX HORMONES
GLUCOCORTICOIDS ~ “Cortisone”
Produced in Zona Fasciculata
Cortisol ~ hydrocortisone ~ most significant
Cortisone ~ produced in liver from cortisol
Glucocorticoid Effects ~ MANY
1.
Reduces stress ~ prepares body for crisis
Thru gluconeogenesis & glycogenoslysis
“Diabetogenic” Effect ~ ↑ blood sugar
Converts glycogen to glucose
Converts fats to glucose
2.
Stimulates protein breakdown to amino acids
3.
Anti-Inflammatory ~ reduces swelling ~ “cortisone”
4.
Supresses immunity ~ organ transplants
5.
Stimulates appetite ~ “cortisol”
6.
Used as a synthetic drug ~ allergy & inflammation
Cortisone . . . Prednisone . . . Hydrocortisone
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Glucocorticoid Hormone Release - stimulated by stress
Physical & Emotional trauma . . . Hemorrhage . . . Illness
Severe stress ----> hypothalamus secretes corticotropin
releasing hormone ----> anterior pituitary to secrete
ACTH ----> stimulates release of Cortisol & Cortisone
GLUCOCORTICOID DYSFUNCTION
Hyper-Secretion of Cortisone ~ Cushing’s Syndrome
Caused By: Over usage of cortisone ~ MOST
ACTH tumor of the anterior pituitary
Symptoms: Persistent Hyperglycemia ~ high
blood sugar
Wasting Away ~ Lost muscle mass
Na+ & H2O retention ~ excessive thirst
High Blood Pressure
Severe edema ~ moon faced
Poor wound healing ~ anti-inflammatory
Susceptible to infection ~ Immune
Supression
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GLUCOCORTICOID DYSFUNCTION
HYPO-Secretion of Cortisone ~ Addison’s Disease
Caused By: Deficiency of both glucocorticoids &
mineralocorticoids ~ aldosterone
Symptoms: Low blood glucose ~ hypoglycemia
Weight loss ~ no glucose for energy
Na+ loss ~ cannot retain fluid
Dehydration (cannot retain fluid)
Hypotension ~ loss of fluid volume
“Polyuria” ~ excess urine production
GONADOCORTICOIDS ~ Sex Hormones
Produced in Zona Reticularis of Adrenal Cortex
Mainly Androgen ~ male sex hormone ~ Testosterone
Some Estrogen ~ female sex hormone
Lower concentrations than ovaries & testis
Significant levels ~ up to puberty ~ between ages of 7-13
Hyper-secretion could cause masculinization in children
Early hair ~ beard
Deeper voice
Sexual aggressiveness
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ADRENAL MEDULLA
Centrally located in adrenal gland ~ Smaller portion
Secretes CATECHOLAMINES - effects Sympathetic NS
80% Epinephrine & 20% Norepinephrine
Release:
= Adrenaline
Stress stimulates the sympathetic
nervous system ~ prepares body for crisis
Immediate Response ~ “short acting”
Sympathomimetic Effects:
Blood sugar rises
Heart beats faster
Blood pressure increases
Bronchioles dilate ~ more air
Pupils dilate ~ more light
Digestion & Peristalsis Slows
Visceral Vasodilation & Peripheral Vasoconstriction
diverts Blood to where it is needed
From skin & digestive organs to brain, heart & skeletal
muscle
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MAJOR ENDOCRINE ORGANS
PANCREAS
Large, soft, triangular - posterior to stomach
Mixed gland:
Endocrine & Exocrine function
Exocrine Pancreas ~ 99%
Ascinar Cells ~ epithelial cells ~ 99% of gland
Digestive enzymes ducted into small intestine
Amylase
~ carbohydrate breakdown
Lipase
~ lipid breakdown
Protease
~ protein breakdown
Endocrine Pancreas ~ 1%
Islets of Langerhans~ 1% of Gland
Tiny island cluster cells among Ascinar cells
Alpha cells ~ secrete Glucagon
Beta cells ~ secrete Insulin
Both regulate blood glucose ~ effects are opposite
Glucagon ~ raises blood glucose ~ hyper-glycemic
Insulin ~ lowers blood glucose ~ hypo-glycemic
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GLUCAGON
Protein produced in alpha cells ~ (islets of langerhans)
Potent hyper-glycemic effects:
 Blood Sugar
Glucagon Secretion ~ Humoral Stimuli
Stimulated by:
Falling blood sugar levels
Inhibited by:
Rising blood sugar levels
Effects of Glucagon ~ Glucagon  Blood Sugar
1.
Breaks down glycogen to glucose ~ glycogenolysis
2.
Stimulates Glucose Synthesis from fats & amino
acids
“gluconeogenesis”
3.
Stimulates Release of glucose from liver into blood
 blood sugar
4.
Stimulates breakdown of protein to Amino Acids
“Catabolic Effect”
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INSULIN
Small protein ~ made in beta cells ~ islets of langerhans
Potent hypoglycemic effects
 Blood Sugar
Insulin Secretion ~ Humoral Stimuli
Stimulated by:
Rising blood sugar levels
Eating a meal
Other hyperglycemic hormones
Glucagon
Thyroxin
Adrenalin
Inhibited by:
Growth Hormone
Glucocorticoids
Lower blood sugar levels
Major Effects of Insulin ~ opposite of glucagon
1.
Enhances glucose uptake & utilization by all cells
2.
Stimulates glycogen storage in muscle & liver
Inhibits Glycogenolysis ~ lowers blood sugar
3.
Inhibits conversion of fats & amino acids to glucose
Inhibits Gluconeogenesis ~ lowers blood sugar
4.
Stimulates protein synthesis from amino acids
“Anabolic Effect”
5.
Stimulates Glucose conversion to fat for storage
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PANCREATIC DYSFUNCTION
HYPO-GLYCEMIA ~ low blood sugar
Causes:
Glucagon Deficiency
Insulin overdose - very common
Symptoms: Persistent low blood sugar
Anxiety - - - > Nervousness - - - > Tremors
- - - > Weakness - - - > Convulsions - - - >
Diabetic Coma - - - > Unconscious - - - > Death
Treatment:
dietary sugar . . . candy bar . . . orange
juice
HYPER-GLYCEMIA ~ high blood sugar ~ COMMON
Causes: Insulin Deficiency ~ “Diabetes Mellitus”
Cells cannot utilize glucose
Symptoms: Nausea & Anxiety
Glucosuria ~ high urine sugar spill over
Ketouria ~ ketones in urine from FA
Ketoacidosis ~ drop in blood pH → ↑ H+
Rapid breathing ~ blow off carbon dioxide
to increase blood pH ~ Hyperpnea
Severe depression, coma, death
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Three Cardinal Signs of Diabetes Mellitus ~ “3 P’s”
1)
Polyuria ~ excessive urine output
High glucose in blood causes spill over into acts as
diuretic ~ Draws water into urine
Concentrated urine ~ high Specific Gravity > 1.035
Decreased blood volume & dehydration ~ fluid loss
2)
Polydipsia ~ excessive thirst
Severe dehydration due to fluid loss ---->
Stimulates hypothalamus thirst centers
------->>> Excessive thirst
3)
Polyphagia ~ excessive appetite
Body cannot utilize glucose ~ thinks it’s starving
Excessive hunger & food intake
Treatment of Diabetes Mellitus:
Type I ~ Juvenile ~ Insulin Dependent Diabetic ~ 10% of
cases
Treat with Synthetic Insulin
Type II ~ Non-Insulin Dependent ~ 90% of cases
Treat with Proper Diet, Weight Loss & Exercise
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OTHER ENDOCRINE ORGANS
PINEAL GLAND
Tiny pine cone shaped . . . in epithalamus of diencephalon
Soft tissue landmark ~ pineal sand/calcium for brain X-rays
Endocrine function is a mystery ~ biorythms/sleep-wake/temp
MELATONIN ~ pineal gland hormone
Peak levels at night make us drowsy
Stimulation of pineal gland related to visual light
Influences sleep/wake cycle, body temperature, &
appetite ~ biorythms
THYMUS
Large in infants & children ~ provides immunity in children
Located deep to sternum in upper thorax at base of heart
Becomes adipose tissue & connective tissue with age ~ scars
Secretes hormones:
Thymopoitens
Thymosins
Effect: Normal development of T-lymphocytes ~ T-cells
Important in the immune response ~ infant & young
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OTHER ENDOCRINE ORGANS
GONADS
Male Gonads ~ Testis
Female Gonads ~ Ovaries
Produce more sex hormones than the adrenal cortex . . .
Release regulated by FSH & LH gonadotropins from pituitary
OVARIES ~ Two oval shaped . . . Posterior abdominal cavity
Produce ova or eggs for fertilization
Produce female ovarian hormones
ESTROGEN ~ release influenced by FSH
Released from follicle cells of ovaries
Causes maturation of reproductive organs
Female secondary sex characteristics ~ puberty
Menstrual cycle ~ uterus cyclic changes
PROGESTERONE ~ release influenced by LH
Released from corpus luteum ~ old follicle
Maintains pregnancy ~ secreted for months
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TESTES
Two ~ Located in “extra-abdominal” sac ~ scrotum
Produce sperm (influenced by FSH) & male sex hormone
Testicular Hormones ~ male hormone ~ androgens
TESTOSTERONE ~ release influenced by LH
Produced in interstitial cells of testis
Causes maturation of male reproductive organs
Male secondary sex characteristics & sex drive
Necessary for normal sperm production
OTHER HORMONE PRODUCING STRUCTURES
Not really endocrine glands . . . but have other endocrine cells
HEART
Atrial wall stretched by excess fluid volume & pressure
Releases:
Atrial Natriuretic Peptide ~ ANP
Effects of ANP:
Inhibits Aldosterone release by adrenal cortex
Inhibits sodium & fluid retention
Reduces blood volume & lowers blood pressure
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GASTROINTESTINAL TRACT (GIT) ORGANS
Several Hormones Released to aid digestion
Hormone
Source
Target Organ & Effect
Gastrin
Stomach
Stomach HCL release
Serotonin
Stomach
Stomach contraction
Intestinal
Gastrin
Duodenum
Inhibits stomach HCL
Slows GI Motility
Secretin
Duodenum
Inhibits gastric secretions
Release bicarbonate from
pancreas & liver
Cholecystokinin
Duodenum
Pancreatic juices & bile
Amylase ~ CHO
Lipase ~ Fats
Protease ~ Proteins
KIDNEY
Erythropoietin ~ EPO
Influences bone marrow to
produce more RBC’s
Renin
Stimulates Aldosterone
SKIN
Cholicalciferol
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Precursor to Vitamin D3
Intestine absorb of Ca++
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HORMONES INVOLVED IN GROWTH
Involves coordination of several endocrine organs
Important Hormones:
Growth Hormone
Thyroid Hormone
Insulin
Parathyroid Hormone
Calcitrol ~ for Ca++ absorption
Reproductive Hormones
HORMONES INVOLVED IN AGING
Few functional changes with age ~ most work untill death
Major changes involve decline of reproductive hormones
Decline in Growth Hormone
Other changes due to disease processes ~ i.e., diabetes
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HORMONES INVOLVED IN STRESS
Stress Activates the General Adaptation Syndrome
Involves:
Hypothalamus . . . Adrenal Gland . . . Organs
General Adaptation Syndrome Phases
Alarm Phase ~ immediate fight or flight ~ adrenaline
Neural Stimulation ~ immediate ~ short acting
Catecholamines:
Epinephrine & Nor-epinephrine
Sympathetic Effects: ↑ BP . . . ↑ HR . . . ↓ Digestion
Resistance Phase ~ longer term response
Involves several endocrine organs
Anterior Pituitary ~ ACTH ~ stimulates adrenals
Growth Hormone ~ mobilizes energy reserves
Kidney releases Renin ~ stimulates aldosterone
Gluconeogenesis ~ ↑ glucose for energy
Na+ & fluid retention ~ ↑ Blood Pressure
Exhaustion Phase ~ organ & TOTAL system failure
it’s over !!!
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