Anatomy and physiology

Lesson 2/ finals
Endocrine system
The regulatory systems of the body, and aside from the endocrine
system, the nervous system is also one of the regulatory systems.
 Nervous and Endocrine Systems – are the 2 major regulatory
systems of the body. Together, they regulate and coordinate the
activities, and essentially, all bodies structures.
o Nervous System – function like a telephone messages that is
sent along many telephone wires to their specific destinations.
Primarily, they transmit information in the form of action
potentials along with the axons of your cells but in a form of
neurotransmitters that can called messengers.
 The neurotransmitters are released in the synapsis
between the neurons and cells they control.
o Endocrine System – more likely a satellite radio or a television Main regulatory functions of the endocrine
signal that broadcast widely that every radio or television system
with its receiver adjusted properly, can receive the signals. 1. Regulation of metabolism
 The endocrine system sends information to the cells 2. Control of food intake and digestion.
in the form of Chemical Messengers that is called 3. Modulation of tissue development
Hormones. The hormones are primarily released by 4. Regulation of ion levels
the endocrine glands. 5. Control of water balance
Chemical Messengers 6. Changes in heart rate and blood pressure
 Allow cells to communicate with each other to regulate body 7. Control of blood glucose and other nutrients
activities. 8. Control of reproductive functions.
 It is produced by specific collection of cells or by a gland. Exocrine glands
o An organ consisting of epithelial cells specialized in secretion –  This is the counterpart of the endocrine glands.
controlled release of chemical from a cell.  Exocrine glands have ducts that carry their secretions to the
Types of chemical messengers outside of the body, or into a hollow organ, such as the stomach or
1. Autocrine Chemical Messengers – a cell targets itself intestines.
 The signaling travels from itself  Examples of exocrine secretions are saliva, sweat, breast milk, and
2. Paracrine Chemical Messengers – a cell targets a nearby cell. digestive enzymes.
3. Neurotransmitters – it is a cell that targets a cell that is connected Comparison of the nervous and endocrine system
by a gap junction.  Similarities
4. Endocrine – a cell targets a distant cell through the blood stream. o They cooperate to regulate important processes.
THE MAIN DIFFERENCE BETWEEN THE DIFFERENT CATEGORIES OF THIS CHEMICAL  Regulate and coordinate the activities of essentially all body
MESSENGERS IS THE DISTANCE THAT THE SIGNALS TRAVELS THROUGH THE ORGANISM TO structures to achieve and maintain homeostasis.
REACH THE TARGET CELL. o Same molecule can be used as either a Neurotransmitter or a
Characteristics of the endocrine system Hormone.
 Composed of Endocrine Glands and Specialized Endocrine Cells o They share same structures in the brain.
o Secrete very small amounts of hormones into the bloodstream o Some neurons secrete hormones
to specific cites called target tissues, or effectors where they (neuropeptides/neurohormones)
stimulate a specific response. o They both have chemical messengers that bind to the same
receptor type.
 Differences
CATEGORY NERVOUS SYSTEM ENDOCRINE SYSTEM
Neurotransmitters
MODE OF
(directly onto their Hormone (bloodstream)
TRANSPORT
target cells)
SPEED OF RESPONSE Faster Slower
Longer-lasting effects
DURATION OF As long as there is
(Days/minutes/days/
RESPONSE Action Potential
weeks)
CHARACTERISTICS NERVOUS SYSTEM ENDOCRINE SYSTEM
MEDIATOR Neurotransmitters Hormones delivered to
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 Anatomy and physiology
Lesson 2/ finals
released locally in 1. Stability – they are longer lasting, and they have long lasting effects
tissues throughout
MOLECULES response to nerve unlike the nervous system because of stability.
body to blood.
impulses  Half-life (the amount of time it takes for 50% of the
Close to site of release, circulating hormone to be removed from the circulation and
Far from site of
at synapse; binds to excreted.)
SITE OF MEDIATOR release (usually); binds
receptors in 2. Communication – from a cell to a target cell
ACTION to receptor on or in
postsynaptic 3. Distribution
target cells
membrane.  Binding proteins (transport chaperone/protection)
Muscle (smooth,  Bound hormones (reservoir)
TYPES OF TARGET cardiac, and skeletal)  Free hormones in
Cells throughout body.
CELLS cells, gland cells, and
other neurons.
Typically, within Three types of stimuli regulate hormone release:
TIME TO ONSET OF milliseconds Seconds to hours or Control of Hormone Secretion
ACTION (thousandths of a days. 1. Humoral
second) 2. Neural
DURATION OF Generally, briefer Generally, longer 3. Hormonal
ACTION (milliseconds) (seconds to days) Control by humoral stimuli
 Differences according to the regulatory system in terms of  Exhibited by hormones that are sensitive to circulating blood levels
modulation. of certain molecules such as glucose or calcium
o Endocrine System – Amplitude-modulated system is about the o Metabolites and other molecules in the bloodstream that can
concentration of the hormone determines the strength of the directly stimulate the release of some hormones are referred
signal and the magnitude of the response. For most hormones, to as: Humoral stimuli.
a small concentration
of a hormone is a
weak signal and
produces a small
response whereas a
larger concentration is a
stronger signal and
results in a greater
response.
 Thereby, it determines the concentration of the THE HUMORAL STIMULI IN THIS FIGURE IS THE CALCIUM, THE ENDOCRINE CELLS ARE THE
hormone. ONE THAT RELEASE THE HORMONE. THE HUMORAL STIMULI ARE THE LEVEL OF THE
o Nervous System – Frequency modulated system is about the CALCIUM IN THE BLOODSTREAM. WHEN THE ENDOCRINE CELLS, DETECTS A LOW BLOOD
CALCIUM, THE ENDOCRINE CELL WILL RELEASE A HORMONE CALLED AS THE
strength of the signal depending on the frequency, not the size,
PARATHYROID HORMONE OR PTH. THIS PARATHYROID HORMONES ARE THE ONES WHO
of the action potentials. All action potentials are the same size
REGULATE THE CERUM CALCIUM TO ITS AFFECTS ON THE BONE, WITH THE USE OF
in a given tissue. A
OSTEOCLAST (WHICH IS KNOWN TO BE THE BONE RESORPTION. THE BONE RESORPTION IS
low frequency
THE NORMAL DESTRUCTION OF THE BONE. WHICH IS INDIRECTLY STIMULATED BY THE
of action
potentials is a PTH.) THEY USES THIS BONE RESOPTION IN ORDER TO ENCHANCE THE RELEASE OF THE
CALCIUM IN THE BLOOD STREAM. THAT IS WHY, ONES THE RELEASE OF THE CALCIUM IN
weak stimulus,
THE BLOODSTREAM INCREASES. THERE IS NOW AN INCREASE OF CALCIUM IN THE BLOOD
and a higher
STREAM.
frequency is a
stronger
stimulus. TO PROVIDE A CONTINUOUS HOMEOSTASIS:
IF THERE IS AN EXCESSIVE HIGH CALCIUM IN THE BLOOD STREAM THEN THE ENDOCRINE
Hormones CELL WILL NO LONGER SECRETE THE PARATHYROID HORMONE, THEN THERE IS NO
 Derived from the OSTEOCLAST ACTIVITY. THEREFORE, THERE IS NOW A DECREASE IN CALCIUM IN THE
Greek word Hormone (set into motion) BLOOD STREAM.
 Chemical messenger that is secreted into the blood, travels to a
Control by neural stimuli
distant target tissue, and binds to specific receptors to produce a
 Cause hormone
coordinated set of events in that target tissue.
secretion in direct
 Secreted by endocrine gland.
General characteristics of hormones

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 Anatomy and physiology
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response to action potentials in neurons, as occurs during stress or
exercise.
 Hormones from the hypothalamus that cause the release of other
hormones called releasing hormones.
THE CONTROL OF THE NEURAL STIMULI IS ACT UPON BY THE NEURON AND BY THE
ACTION POTENTIALS. (1) AN ACTION POTENTIAL IN A NEURON INNERVATING AN
ENDOCRINE CELL STIMULATES SECRETION OF A STIMULATORY NEUROTRANSMITTERS.
WHEREIN THEY HAVE A DIRECT TARGET TISSUE, FROM A CELL TO A TARGET TISSUE.
THIS TYPE OF CHEMICAL MESSENGER, THEY ACT UPON DIRECTLY FROM CELL TO
ANOTHER CELL. (2) THE ENDOCRINE CELL SECRETES ITS HORMONE INTO THE BLOOD,
WHERE IT WILL TRAVEL TO ITS TARGET CELL/TISSUE. TO PROVIDE A HOMEOSTASIS, THE
STIMULATION OF THE ENDOCRINE CELL SHOULD BE INHIBIT/STOP. (3) AN ACTION
POTENTIAL IN THE NEURON STIMULATES SECRETION OF AN INHIBITORY
NEUROTRANSMITTER. WHEN IT IS ALREADY STIMULATED, IT WILL NOW ACT ON THE
ENDOCRINE CELLS. (4) THE ENDOCRINE CELL IS INHIBITED AND DOES NOT SECRETE ITS
HORMONE TO THE BLOOD.
Control by hormonal stimuli
 Hormonal stimulation of other hormone secretion is common in the
endocrine system.
 Hormones from the anterior pituitary that stimulate hormones from
other endocrine glands are called tropic hormones
ITSELF IN RELEASING THE RELEASING HORMONE. WHILE THE PARACRINE, WHERE THEY
RELEASE HORMONE TO STIMULATE A NEARBY HORMONE. BECAUSE THE HYPOTHALAMUS
RELEASES A RELEASING HORMONE TO ITS NEARBY TARGET TISSUE WHICH IS THE
ANTERIOR PITUITARY. WHICH IS THE ANTERIOR PITUITARY RELEASES TROPIC HORMONE.
WHILE FOR ENDOCRINE, BECAUSE THE TROPIC HORMONE IS RELEASE FROM THE
ANTERIOR PITUITARY GOES ONTO THE BLOOD STREAM.
Inhibition of hormone release
 Although the stimulus of hormone secretion is important, inhibition is
equally important.
1. Humoral substances can inhibit the secretion of hormones.
2. Neural stimuli can prevent hormone secretion.
3. Inhibiting hormones prevent hormone release.
Regulation of hormone levels in the blood
 Two processes regulate the overall blood levels of hormones.
1. Negative feedback. Prevents further hormone secretion once
a set point is achieved.
2. Positive feedback. Is a self-promoting system whereby the
stimulation of hormone secretion increases over time.
Negative feedback by hormones

1. The anteruir pituitary gland secretes a tropic hormone, which

travels in the blood to the target endocrine cells.
2. The hormone from the target endocrine cells travels to its target.
3. The hormone from the target endocrine cell also has a negative-
feedback effect on the anterior pituitary and hypothalamus.
(1)NEURONS IN THE HYPOTHALAMUS RELEASE STIMULATORY HORMONES CALLED Wherein it decreases the secretion of tropic hormone.
RELEASING HORMONES. RELEASING HORMONES NOW TRAVEL IN THE BLOOD TO THE
Positive feedback by hormones
ANTERIOR PITUITARY GLAND. (2) RELEASING HORMONES STIMULATE THE RELEASE OF
TROPIC HORMONES FROM THE ANTERIOR PITUITARY, WHICH TRAVEL IN THE BLOOD TO
THEIR TARGET ENDOCRINE CELL. THE TARGET CELL ARE LOCATED IN THE BLOOD, AND
WHEN THEY ARE STIMULATED. (3) THE TARGET ENDOCRINE CELL SECRETES ITS
HORMONE INTO THE BLOOD, WHERE IT TRAVELS TO ITS TARGET AND PRODUCES A
RESPONSE. (4) THE HORMONE FROM THE TARGET ENDOCRINE CELL ALSO INHIBITS THE
HYPOTHALAMUS AND ANTERIOR PITUITARY FROM SECRETING THE RELEASING HORMONE
AND THE TROPIC HORMONE. THIS IS NEGATIVE FEEDBACK. THE TARGET ENDOCRINE CELL
PROVIDES AN INHIBITORY STIMULATION TO THE PITUITARY GLAND TO THE
HYPOTHALAMUS. THE RELEASE OF THE HORMONES THAT THEY HAVE SECRETED, THE
RELEASING HORMONE AND THE TROPIC HORMONE WILL BE INHIBITED. THAT IS WHAT WE
1. The anterior pituitary gland secretes a tropic hormone, which
CALL NEGATIVE FEEDBACK. (5) IN SOME INSTANCES, THE HYPOTHALAMUS CAN ALSO
travels in the blood to the target endocrine cell.
SECRETE INHIBITING HORMONES, WHICH PREVENT THE SECRETION OF ANTERIOR PITUITARY
2. The hormone from the target endocrine cell travels to its target.
TROPIC HORMONES.
3. The hormone from the target endocrine cell has a positive-
feedback effect on the anterior pituitary and increases secretion
THE CHEMICAL MESSENGER THAT HAPPENS IN HERE ARE AUTOCRINE AND THE of the tropic hormone.
PARACRINE. THE NUMBER 5 STEP IS THE AUTOCRINE CHEMICAL MESSENGER, SINCE IT IT DEPENDS ON THE RESPONSE IN THE BODY IF IT STILL REQUIRES A RELEASE OF TROPIC
STIMULATE ITSELF. THE HYPOTHALAMUS HAS RELEASE A CHEMICAL AND ALSO INHIBITS HORMONES

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 Anatomy and physiology
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Endocrine Glands  3. In the posterior pituitary gland, action potentials cause the release
1. Pituitary Gland of neurohormones (blue circles) from axon terminals into the blood. 
2. Thyroid Gland 4. The neurohormones pass through the blood and influence the
3. Parathyroid Gland activity of their target tissues.
4. Adrenal Gland
5. Pancreas WE HAVE 2 DIFFERENT TYPES OF INPUT COMING FROM THE BRAIN, IT COULD BE
Pituitary Gland and Hypothalamus  STIMULATORY OR INHIBITORY. THE GREEN ARROW IN THE FIGURE ABOVE, REPRESENTS
 Both these structures integrate Nervous System and Endocrine THE STIMULATROY, WHICH MEANS THERE IS A STIMULI AND THERE SHOULD BE AN
System. INCREASE OF ACTIVITY. WHILE THE RED ARROW PERTAINS TO THE INHIBITORY, MEANS
 The pituitary gland secretes nine major hormones that regulate THAT THE STIMULI WOULD LIKE TO DECREASE THE ACTIVITY.
numerous body functions and the secretory activity of several
other endocrine glands. THESE INPUT COMING FROM THE HIGHER BRAIN CENTERS WILL BE RELAYED TO THE
 The hypothalamus regulates the secretory activity of the pituitary POSTERIOR PITUITARY GLAND VIA THE HYPOTHALAMIC NEURONS IN THE SUPRAOPTIC
gland in response to other hormones, sensory information, and NUCLEUS. WITH THIS HYPOTHALAMIC NEURONS IN THE SUPRAOPTIC NUCLEUS, THE
emotions. STIMULI WITHIN THE NERVOUS SYSTEM CAUSE THE HYPOTHALAMIC NEURONS TO EITHER
Pituitary gland  INCREASE OR DECREASE THEIR ACTION POTENTIAL FREQUENCY. THE POSTERIOR
 Located to the base PITUITARY GLAND IS REGULATED BY THE NERVOUS SYSTEM . THE AMPLIFICATION, IT IS
of the brain, inferior FREQUENCY-AMPLITUDE SYSTEM. THEY ARE DEPENDING TO THE ACTION POTENTIAL.
to hypothalamus
 Connected to the THE ACTION POTENTIAL ARE CONDUCTED BY THE AXONS OF THE HYPOTHALAMIC
hypothalamus by the NEURONS, AND THE SIGNALS THAT WILL PASS THROUGH VIA THE HYPOTHALAMOHYPO
infundibulum. PHYSIAL TRACT TO THE POSTERIOR PITUITARY GLAND. IN THE POSTERIOR PITUITARY
 Has 2 lobes: Anterior GLAND, THE ACTION POTENTIALS CAUSE THE RELEASE OF THE NEUROHORMONES (THE
Pituitary BLUE CIRCLES IN THE FIGURE, REPRESENTS THE NEUROHORMONES) FROM THE AXON
Gland(Adenohypophysi TERMINALS GOING TO THE BLOOD. THE NEUROHORMONES PASS THROUGH THE BLOOD,
s) and Posterior THEN INFLUENCE THE ACTIVITY OF THEIR TARGET TISSUE.
Pituitary Gland Posterior Pituitary Hormones  
(Neurohypophysis).  HORMONES TARGET TISSUE RESPONSE
Posterior pituitary Increased water
gland (Neurohypophysis) ANTIDIURETIC reabsorption (less
Kidneys
 continuous with the HORMONE (ADH) water is lost in the
hypothalamus in the form of urine)
brain Increased uterine
 forms from an contractions;
outgrowth of the increased milk
Uterus; Mammary
inferior part of the OXYTOCIN expulsion from
glands
brain (distal end of mammary glands;
infundibulum that unclear function in
enlarges) males.
 is a part of the nervous Antidiuretic Hormone (ADH) 
system 1. STIMULUS: CHANGE IN BLOOD OSMOLALITY(concentration of the
 its hormones are called blood) / BP CHANGES
neuropeptides, or 2. RECEPTORS: OSMORECEPTORS/ BARORECEPTORS to Central
neurohormones* Nervous System
o Will be stimulated - The receptors are the one that perceive the stimuli.
when the signal coming from the nervous system is received or 3. Receptors synapse with the ADH neurosecretory neurons in the
relayed by the hypothalamohypo physial tract. hypothalamus
Process of the secretion of the pituitary hormones 4. Stimulus (Increase in Blood osmolality/ Decrease in BP/Decreased
1. Stimuli within the nervous system cause hypothalamic neurons to Blood volume) will create INCREASE FREQUENCY INCREASE ACTION
either increase or decrease their action potential frequency.  POTENTIAL = ADH RELEASE
2. Action potentials are conducted by axons of the hypothalamic 5. TARGET TISSUE AND EFFECT: Kidney tubules retain water/ Blood
neurons through the hypothalamohypophysial tract to the posterior Vessels constrict
pituitary. The axon endings of neurons store neurohormones in the 6. RESPONSE: Increased blood volume OR Reduced blood osmolality/
posterior pituitary.  Increase in Blood Pressure

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 Anatomy and physiology
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 PREGNANT WOMEN: During childbirth, milk-let down
 NON-PREGNANT WOMEN: DURING MENSTRUATION: Rid uterine wall
lining; AFTER SEXUAL ACTIVITY: Movement of sperm cell 
Control of oxytocin secretion
1. Stretch of the uterus and the uterine cervix or mechanical
stimulation of the breasts’ nipples increases action potentials in
axons of oxytocin-secreting neurons. 
2. Action potentials are conducted by sensory neurons from the
uterus and breast to the spinal cord and up ascending tracts to the
hypothalamus. 
3. Action potentials are
conducted by axons of
Flow of the ADH oxytocin-secreting
neurons in the
THE STIMULI COULD EITHER BE CHANGES IN THE BLOOD OSMOLALITY OR A CHANGE IN
hypothalamohypophysial
BLOOD PRESSURE. THE OSMORECEPTOR OR THE RECEPTORS ARE THE ONE THAT
tract to the posterior
PERCEIVED IN THE CHANGES IN THE STIMULI. FOR THE OSMORECEPTORS, THEY ARE THE
pituitary, where they
ONE THAT DETECTS THE CHANGES IN THE BLOOD OSMOLALITY. WHILE THE
increase oxytocin
BARORECEPTORS, THEY ARE THE ONE THAT DETECTS THE CHANGES IN THE BLOOD
secretion. 
PRESSURE. BOTH OF THEM, IF THERE IS A CHANGE IN THE STIMULI, THE FREQUENCY OF
THE ACTION POTENTIALS WILL ALSO CHANGE AND THE ACTION POTENTIALS WILL
4. Oxytocin enters the
PROCED OR DELIVER THE INFORMATION TO THE VAGOS NERVE GOING TO THE circulation, increasing
HYPOTHALAMUS. contractions of the
uterus and milk letdown
AN INCREASE IN THE OSMOLALITY AND A DECREASE IN THE BLOOD PRESSURE, from the lactating breast
INCREASE NOW THE ACTION POTENTIAL IN THE ADH SECRETING NEURON. THE ACTION
POTENTIALS ARE CARRIED BY THE AXONS OF THE ADH SECRETED NEURONS THROUGH THIS EVENT IS WHAT WE CALL AS POSITIVE FEEDBACK MECHANISM, SINCE THERE IS AN
THE HYPOTHALAMOHYPO PHYSIAL TRACT TO THE POSTERIOR PITUITARY. IN THE CONTINUOUS STIMULATION OF THE RELEASE OF THE OXYTOCIN.
POSTERIOR PITUITARY, ACTION POTENTIALS CAUSE THE RELEASE OF ADH FROM THE Anterior pituitary gland (Adenohypophysis) 
AXON TERMINALS INTO THE BLOOD. INCREASING ADH ACTS ON THE KIDNEY TUBULES TO  develops as an
INCREASE WATER REABSORPTION, RESULTING IN REDUCED URINE VOLUME, INCREASED outpocketing of the roof of the
URINE OSMOLALITY, AND DECREASED BLOOD OSMOLALITY AND INCREASE BLOOD embryonic oral cavity called the
VOLUME AND BLOOD PRESSURE. THIS HELPS MAINTAIN BLOOD OSMOLALITY AND pituitary diverticulum, or Rathke
VOLUME. pouch.
1. Osmoreceptors in the hypothalamus detect changes in blood  Hormones secreted
osmolality, and baroreceptors detect changes in blood pressure and from the anterior pituitary are
change the frequency of action potentials in axons of the vagus traditional hormones, not
nerve to the hypothalamus.  neurohormones.
2. An Increase in osmolality and a decrease in blood pressure increase
action potentials in ADH-secreting neurons.
3. Action potentials are carried by axons of ADH- secreting neurons
through the hypothalamohypophysial tract to the posterior I N THE FIGURE ABOVE SHOWS THE
pituitary.  DEVELOPMENTAL PROCESS OF THE
4. In the posterior pituitary, action potentials cause the release of ADH PITUITARY GLAND STARTING FROM THE AN EMBRYO TO THE 4 TH WEEKS. WHERE IT
from the axon terminals into the blood.  SHOWS (IN THE FIGURE) THE NEUROHYPOPHYSIAL BUD AND THE PITUITARY DIVERTICULUM
5. Increasing ADH acts on the kidney tubules to increase water THAT IS STATED. ON THE 8TH WEEKS, WHEREIN THE HYPOPHYSIAL POUCH IN THE
reabsorption, resulting in reduced urine volume, increased urine NEUROHYPOPHYSIAL BUD CONNECTS WITH EACH OTHER. WITHIN THE 16TH WEEK, THESE
osmolality, and decreased blood osmolality. This helps maintain blood ARE NOW CALLED AS THE PITUITARY GLAND SEPARATED WITH THE ANTERIOR AND
osmolality and volume and increase blood volume and blood pressure. POSTERIOR.
Oxytocin 
 SECRETED BY: oxytocin-secreting neurons in the hypothalamus WHEREIN THE ANTERIOR GLOBE OF THE PG, ADENOHYPOPHYSIS. HORMONES THAT ARE
SECRETED IN THE ANTERIOR PITUITARY ARE TRADITIONAL HORMONES, NOT A
 STIMULUS: UTERINE STRETCH, CERVIX MECHANICAL STIMULATION
NEUROHORMONES, IN COMPARE TO THE HORMONES SECRETED BY THE POSTERIOR
and BREAST NIPPLE STIMULATION
 EFFECT: smooth muscle contraction
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 Anatomy and physiology
Lesson 2/ finals
PITUITARY GLAND. BECAUSE THE HORMONE SECRETED BY THE POSTERIOR PITUITARY
GLAND IS CALLED AS NEUROHORMONE.

FOR THE ANTERIOR PITUITARY GLAND, THEY ARE THE TYPICAL OR TRADITIONAL OF
HORMONES.
Hormones of anterior pituitary
HORMONES TARGET TISSUE RESPONSE
Increased growth in
tissues 
- Increased amino
acid uptake and
protein synthesis 
- increased Control growth Hormone (GH) secretion
breakdown of lipids 1. Stress and decreased blood glucose levels increase of growth
GROWTH HORMONE and release of fatty hormone-releasing hormone (GHRH), and decrease the release of
(GH), OR Most tissues acids from cells  growth hormone-inhibiting hormone (GHIH), from the hypothalamus.
SOMATOTROPIN - Increased glycogen 2. GHRH and GHIH through the hypothalamohypophysial portal system to
synthesis and the anterior pituitary.
increased blood 3. Increased GHRH reduced GHIH act on the anterior pituitary and result
glucose levels. in increased GH secretion.
- increased 4. GH Acts on target tissues.
somatomedin 5. Increasing GH and somatomedins have a negative-feedback effect
production on the hypothalamus, resulting in decreased GHRH and increased
GHIH release.
THYROID-STIMULATING Increased thyroid  GH in target tissues:
Thyroid gland
HORMONE (TSH) hormone secretion o Increases protein synthesis and decreases protein
Increased breakdown.
ADRENOCORTICOTROPIC
Adrenal cortex glucocorticoid o Increases tissue growth
HORMONE (ACTH)
hormone secretion. o Increases lipid breakdown
GROWTH HORMONE: DIRECT EFFECTS o Increases glucose synthesis and reduces glucose usage
 determining how tall a person becomes o Increases somatomedin secretion
 It also regulates metabolism.
THERE ARE 2 TYPES OF GROWTH HORMONE, GHIH AND GHRH, WHICH ARE ACTIVATED
o GH plays an important role in regulating blood nutrient levels BY THE STIMULUS. THE STIMULUS CAN EITHER BE LOW BLOOD GLUCOSE OR ORTHER
after a meal and during periods of fasting. STRESSORS. FOR THE GREEN ARROW, REPRESENTS THE STIMULATION. WHILE RED
 Slows protein breakdown ARROW, REPRESENTS INHIBITORY.
 Use of lipids to promote growth and protein synthesis
o Increases lipolysis FOR THE STRESS AND DECREASE BLOOD GLUCOSE LEVELS INCREASE THE RELEASE OF
o Increase release of fatty acids from adipocytes into blood GROWTH HORMONE RELEASING HORMONE AND DECREASE THE GROWTH HORMONE
 Increase glucose synthesis by liver INHBITING HORMONE. FROM THE HYPOTHALAMUS. THE GHIH AND GHRH TRAVELS TO
GROWTH HORMONE: INDIRECT EFFECTS THE HYPOTHALAMOHYPOPHYSIAL PORTAL SYSTEM TO THE ANTERIOR PITUITARY. THE
 Increases PRODUCTION OF SOMATOMEDINS INCREASED GHRH AND REDUCED GHIH ACT ON THE ANTERIOR PITUITARY AND RESULT
o best-known are insulin-like growth factors (IGFs) TO AN INCREASE GROWTH HORMONE SECRETION. THE GROWTH HORMONE ACTS ON THE
 stimulate growth in cartilage and bone and increase TARGET TISSUES 5. INCREASING GH AND SOMATOMEDINS HAVE A NEGATIVE-
the synthesis of protein in skeletal muscles. FEEDBACK EFFECT ON THE HYPOTHALAMUS, RESULTING IN DECREASED GHRH AND
GROWTH HORMONE INCREASED GHIH RELEASE.
 Two neurohormones released from the hypothalamus regulate the
secretion of GH THE INCREASE IN GROWTH HORMONE AND SOMATOMEDIN RESULTS TO THE NEGATIVE
FEEDBACK MECHANISM TO MAINTAIN HOMEOSTASIS.
o growth hormone–releasing hormone (GHRH)
 Low blood glucose levels and other stressors GROWTH DISORDERS
o growth hormone–inhibiting hormone (GHIH)  PITUITARY DWARFISM
 high blood glucose level o chronic hyposecretion, or insufficient secretion, of GH in
infants and children

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o Delayed bone growth – short stature HORMONES OF ANTERIOR PITUITARY

 N bone shape HORMONES TARGET TISSUE RESPONSE
 N intelligence Increased lipid
 Mild Obesity LIPOTROPINS Adipose tissues
breakdown
 Delayed development of adult reproductive functions Analgesia in the brain;
Chronic hypersecretion, or excessive secretion of GH Brain, but not all
inhibition of
 GIGANTISM B ENDORPHINS target tissues are
gonadotropin-releasing
known
o before the epiphyseal plates have ossified causes hormone secretion
exaggerated and prolonged growth in long bones Increased melanin
 ACROMEGALY MELANOCYTE-
Melanocytes in the
production in
o AFTER the epiphyseal plates have ossified causes STIMULATING melanocytes to make
skin
exaggerated and prolonged growth in long bones HORMONE (MSH) the skin darker in
o No height increase color
Ovulation and
progesterone
production in ovaries;
LUTEINIZING Ovaries in females;
testosterone
HORMONE (LH) testes in males
synthesis and support
for sperm cell
production in testes
• Follicle maturation
and estrogen
FOLLICLE- Follicles in ovaries ni secretion in
STIMULATING females; seminiferous ovaries;
CHRONIC HYPERSECRETION OF GH
HORMONE (FSH) tubules in males • sperm cell
The influence of GH on soft tissues results in
production in
o a bulbous or broad nose,
testes
o an enlarged tongue, • Milk production in
o thickened skin, lactating women;
o sparse subcutaneous adipose tissue. • increased
o Nerves are frequently compressed as a result of the Ovaries and mammary response of
proliferation of connective tissue. PROLACTIN
glands ni females follicle to LH and
o chronic hyperglycemia - leading to Diabetis Melitus and severe FSH;
atherosclerosis.’ • unclear function in
TREATMENT males
o surgical removal or irradiation of a GH- producing tumor. PROLACTIN
THYROID STIMULATING HORMONE (TSH)  Milk production by the mammary glands of lactating females is
aka THYROTROPIN particularly because of the release of hormone prolactin.
 stimulates the synthesis and secretion of thyroid hormones from  Can enhance progesterone secretion by the ovaries after ovulation.
the thyroid gland  No role for this hormone has been clearly established in males.
 TSH secretion is controlled by two mechanisms.  REGULATED BY 2 NEUROHORMONES OF HYPOTHALAMUS:
o Thyrotropin-releasing hormone, TRH (Hypothalamus) o prolactin-releasing hormone (PRH),
 stimulates TSH secretion. o prolactin-inhibiting hormone (PIH).
o Thyroid hormones - inhibit TSH secretion ANTERIOR PITUITARY GLAND AND HYPOTHALAMUS
ADRENOCORTICOTROPIC HORMONE (ACTH) Communication of Anterior Pituitary gland and hypothalamus:
 stimulates secretion of the hormone cortisol from the adrenal  Release of anterior pituitary hormones is stimulated by releasing
cortex hormones and suppressed by inhibiting hormones from the
o principal hormone that regulates chronic stress. hypothalamus.
 STIMULUS: Environmental stress IF THE DO NOT RELEASE HORMONES SUCH AS THE RELEASING HORMONES AND
 ADDISON DISEASE - chronic adrenocortical insufficiency, the INHIBITING HORMONES, THE REGULATION OF THE RELEASING OF THE HORMONES COMING
adrenal cortex degenerates, usually due to an autoimmune condition FROM THE ANTERIOR PITUITARY GLAND WILL NOT HAPPEN.
HYPOTHALAMUS IS ESSENTIAL IN RELEASING THE HORMONES OF ANTERIOR PITUITARY.

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Gonadotropin- Anterior pituitary cells
Increased secretion
 Via hypothalamohypophysial Portal system releasing hormone that secrete LH and
of LH and FSH
o From the floor of the hypothalamus to the anterior pituitary. (GnRH) FSH
The signal will be transported to the anterior pituitary. Anterior pituitary cells
Prolactin- releasing Increased prolactin
o Neurohormones enter from hypothalamus to anterior that secrete
hormone (PRH) secretion
pituitary prolactin
Anterior pituitary cells
Prolactin- inhibiting Decreased prolactin
that secrete
hormone. (PIH) secretion
prolactin

Flow of the hypothalamic control of the anterior

pituitary
1. Stimuli within the nervous system regulate the secretion of
releasing hormones (green circles) and inhibiting hormones (red
circles) from neurons of the hypothalamus.
2. Releasing hormones and inhibiting hormones pass through the
hypothalamohypophysial portal system to the anterior pituitary.
3. Releasing hormones and inhibiting hormones (green and red circles)
leave capillaries and stimulate or inhibit the release of hormones THYROID GLAND
(yellow squares) from anterior pituitary cells.  The butterfly-shaped located just inferior to the larynx (voice box).
4. In response to releasing hormones, anterior pituitary hormones  It is composed of right and left lateral lobes, one on either side of
(yellow squares) travel in the blood to their target tissues (green the trachea, that are connected by an isthmus anterior to the
arrow), which in some cases are other endocrine glands. trachea
THE RELEASING HORMONES AND THE INHIBITING HORMONES PASS THROUGH THE  About 50% of thyroid glands have a small third lobe, called the
HYPOTHALAMOHYPOPHYSIAL PORTAL SYSTEM GOING TO THE ANTERIOR PITUITARY. pyramidal lobe.
RELEASING HORMONES AND INHIBITING HORMONES LEAVE CAPILLARIES AND STIMULATE  20 g, darker red
OR INHIBIT THE RELEASE OF HORMONES FROM ANTERIOR PITUITARY CELLS. IN
RESPONSE, THERE IS A STIMULATION OF THE RELEASE OF HORMONES IN THE
CAPILLARIES. IN RESPONSE TO RELEASING HORMONES, ANTERIOR PITUITARY HORMONES
TRAVEL IN THE BLOOD TO THEIR TARGET TISSUES. WHICH IN SOME CASES ARE OTHER
ENDOCRINE GLANDS
Hormones TARGET TISSUE RESPONSE
Growth hormone– Anterior pituitary cells
Increased growth
releasing hormone that secrete growth
hormone secretion
(ghrh) hormone
Growth hormone– Anterior pituitary cells  contains numerous THYROID FOLLICLES
Decreased growth o Center of each follicle is called: COLLOID, which is composed of
inhibiting hormone that secrete growth
hormone secretion THYROGLOBULIN, a precursor to thyroid hormones, also serves
(ghih), or somatostatin hormone
Increased thyroid- as storage of thyroid hormones
Anterior pituitary cells o PARAFOLLICULAR CELLS
Thyrotropin- releasing stimulating hormone
that secrete thyroid-
hormone (trh) secretion  delicate network of loose connective tissue contains
stimulating hormone
numerous capillaries between follicles
Anterior pituitary cells  Secrete CALCITONIN
Corticotropin- Increased
that secrete o plays a role in reducing the concentration of calcium in
releasing hormone adrenocorticotropic
adrenocorticotropic the body fluids when calcium levels become elevated.
(CRH) hormone secretion
hormone
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 Anatomy and physiology
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HISTOLOGY OF THYROID GLAND Reduced activity of sweat and Copious sweating; warm, flushed
sebaceous glands; dry, cold skin skin
Reduced heart rate, reduced blood Rapid heart rate, elevated blood
pressure, dilated and enlarged pressure, abnormal
heart electrocardiogram
Weak skeletal muscles that exhibit
Weak, untoned skeletal muscles;
tremors, quick movements with
sluggish movements
exaggerated reflexes
Constipation Bouts of diarrhea
THYROID GLAND Hyperactivity, insomnia,
 A basement membrane surrounds each follicle. Apathy, somnolence restlessness, irritability, short
 Inactive follicular cells = shape is low cuboidal to squamous attention span
 But if the inactive follicular cells has been under the influence of
Coarse hair; rough, dry skin Soft, smooth hair and skin
TSH = Active follicular cellsin secretion = from cuboidal to low
columnar in shape. Decreased iodide uptake Increased iodide uptake
 The follicular cells produce two hormones: Possible goiter (enlargement of the
o tetraiodothyronine or T4 (thyroxine) thyroid gland) due to loss of Almost always a goiter
o triiodothyronine or T3 negative feedback
HORMONES OF THE THYROID Gland Myxedema (swelling of the face Exophthalmos (protruding eyes) as
HORMONES TARGET TISSUE RESPONSE and body) as a result of a result of connective tissue
SECRETED BY THYROID FOLLICLES subcutaneous mucoprotein proliferation and other deposits
Increased metabolic deposits behind the eye
rate; increased REGULATION OF THYROID HORMONES
THYROID HORMONES protein synthesis; TH is regulated by:
Most cells of the body
(T3,T4) essential for normal  Thyrotropin-releasing hormone (TRH) from the hypothalamus
growth and  TSH from the anterior pituitary gland
maturation  STIMULUS:
SECRETED BY PARATHYROID FOLLICLES o Release TH: Stress and exposure to cold
Decreased rate of o Decrease TH: Prolonged fasting
bone breakdown by  Increased TH inhibits Thyrotropin Releasing Hormones and Thyroid
osteoclasts; Stimulating Hormone secretion
CALCITONIN Bone  Decreased TH or removal of thyroid gland: Thyroid Stimulating
prevention of a
large increase in Hormone levels increased: GOITER
blood ca2+ levels Regulation of thyroid hormone secretion
MECHANISM OF ACTION OF THYROID HORMONES 1. Stress and hypothermia cause TRH to be released from neurons
 lipid-soluble hormones within the hypothalamus. It passes through the
hypothalamohypophysial portal system to the anterior pituitary.
 they can bind to nuclear receptors in their target tissues and
2. TRH causes cells of the anterior pituitary to secrete TSH, which
STIMULATE PROTEIN SYNTHESIS
passes through the general circulation to the thyroid gland.
EFFECTS OF THYROID HORMONES
3. TSH causes increased synthesis
 normal rate of metabolism for an individual depends on an adequate
and release of T3 and T4 into the
supply of thyroid hormone at which glucose, lipids, and protein are
general circulation.
metabolized.
4. T3 and T4 act on target tissues to
o Adequate Thyroid hormones = Normal body temperature
produce a response.
o INCREASED METABOLIC RATE = HEAT PRODUCTION 5. T3 and T4 also have an inhibitory
 growth of bone, hair, teeth, connective tissue, and nervous tissue effect on the secretion of TRH
o No T3,T4 = Growth Hormone don’t work! from the hypothalamus and TSH
EFFECTS OF HYPOSECRETION AND HYPERSECRETION OF from the anterior pituitary.
THYROID HORMONES THE STIMULUS HERE IS THE HYPOTHERMIA OR
HYPOTHYROIDISM HYPERTHYROIDISM OTHER STRESSORS.
Decreased metabolic rate, low
Increased metabolic rate, high body  T3 and T4 in target tissues:
body temperature, cold
temperature, heat intolerance  Increase metabolism
intolerance
 Increase body temperature
Weight gain, reduced appetite Weight loss, increased appetite
 Increase normal growth and development
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 Anatomy and physiology
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THYROID GLAND DISORDERS
 GOITER HYPERTHYROIDISM
o abnormal enlargement of the thyroid gland Characterized by goiter and exophthalmos;
o can result from either hypothyroidism or hyperthyroidism Apparently an autoimmune disease; most patients have a
 TOXIC GOITER GRAVES DISEASE TSH-like immunoglobulin, called thyroid-stimulating
 secretes excess T3 and T4, and it can result from immunoglobulin (tsi), in their plasma
 elevated TSH secretion or elevated TSH-like *Hypersecretion
immunoglobulin TUMORS -
 Exophthalmos often accompany hyperthyroidism. BENIGN Result in either normal secretion or hypersecretion of
HYPOTHYROIDISM ADENOMA OR thyroid hormones (rarely hyposecretion)
 CAUSES OF DECREASED SECRETION OF THYROID HORMONES CANCER
o IODINE DEFICIENCY (Dietary intake of iodine is low = not THYROIDITIS—
enough to synthesize T3/T4) Produces painful swelling of the thyroid gland with
A VIRAL
o taking certain drugs Normal or slightly increased t3 and t4 production
INFECTION
o being exposed to chemicals that inhibit T3 and T4 synthesis
ELEVATED TSH
o inadequate secretion of TSH Result from a pituitary tumor
LEVELS
o autoimmune disease that depresses thyroid hormone
function Sudden release of large amounts of t3 and t4; caused by
o surgical removal of the thyroid gland THYROID STORM
surgery, stress, infections, or other, unknown factors
CAUSE DESCRIPTION
REGULATION OF CALCITONIN
Causes inadequate T3 and T4 synthesis, which
results in elevated thyroid-stimulating hormone  STIMULUS: elevated blood Ca2+ levels
IODINE DEFICIENCY (TSH) secretion; thyroid gland enlarges (goiter)  RESPONSE: Bone deposition
as a result of TSH stimulation; T3 and T4 o Decreased blood calcium and phosphate levels
frequently remain in the low to normal range o Decrease osteoclast activity
GOITROGENIC (GOITER- Inhibit T3 and T4 synthesis ; found in certain o Lengthen osteoblast lifespan
CAUSING) drugs and in small amounts in certain plants, PARATHYROID GLANDS
SUBSTANCES such as cabbage  Partially embedded in the
Caused by maternal iodine deficiency or posterior part of each
NEONATAL congenital errors in thyroid hormone synthesis; lobe of the thyroid gland
HYPOTHYROIDISM results in developmental delay and a short,  are made up of two cell
malformed appearance types:
Results from lack of TSH secretion; often o Chief Cell- secrete
PITUITARY
associated with inadequate secretion of other parathyroid hormone
INSUFFICIENCY
anterior pituitary hormones (PTH)
PITUITARY Autoimmune disease in which thyroid hormone o Oxyphils
INSUFFICIENCY secretion can be normal or depressed  Funtion is
Partial or complete surgical removal or drug- unknown
LACK OF THYROID induced destruction of the thyroid gland as a  Typically associated with thyroif cancer and stain.
GLAND treatment for Graves disease REGULATION OF PTH
(hyperthyroidism).  STIMULUS to RELEASE: decreased blood Ca2+ levels
HYPERTHYROIDISM  STIMULUS to INHIBIT: increased blood Ca2+ levels
Hypersecretion of T3 and T4 can result from:  RESPONSE: increased blood Ca2+ levels (Bone Resorption)
 Synthesis of an immunoglobulin that stimulates TSH receptors o Bone: Bone breakdown (Increased osteoclast activity)
and acts like TSH. o Small intestine – increased absorption of Ca2+
 TSH-secreting tumors of the pituitary gland o Kidneys – Increased reabsorption of Ca2+: less Ca2+ in
 thyroid tumors urine and Active Vitamin D synthesis
 GRAVES DISEASE: Most common cause PTH - Increased vitamin D synthesis - increased rate of Ca2+ and
 EXOPTHALMOS: COMMON phosphate reabsorption in the intestine - Increase blood ca2+ levels
PTH - phosphate release from bone and absorption in small intestine and
excretion in kidney – decrease blood phosphate levels

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PARATHYROID HORMONE Neuromuscular system
HORMONE TARGET TISSUE RESPONSE less excitable; possible
PARATHYROID Bone, Increased rate of breakdown of muscular weakness
HORMONE kidneys, bone by osteoclasts. Increased force of
(PTH) small increased reabsorption of Ca2+ in contraction of cardiac
intestine kidneys. muscle; at very high blood
Increased absorption of Ca2+ Ca2+ levels, possible
from the small intestine; cardiac arrest during
increased vitamin D synthesis. contraction
increased blood Ca2+ levels SECONDARY caused by
MAJOR REGULATOR OF BLOOD CALCIUM, PHOSPHATE AND MAGNESIUM HYPER conditions
LEVELS PARATHYROIDISM that reduce
HYPOCALCEMIA blood Ca2+ Neuromuscular system less
 INACTIVE PARATHYROID GLAND levels, such excitable; possible muscular
 ABN LOW LEVELS OF CA2+ IN BLOOD as: weakness
 DECREASE EXTRACELLULAR CALCIUM = INCREASE Na channels Inadequate Increased force of
OPEN = Na+ diffuses into cells and causes depolarization Ca2+ in the contraction of cardiac
 SYMPTOMS diet, muscle; at very high blood
o nervousness
inadequate Ca2+ levels, possible cardiac
o muscle spasms
levels of arrest during contraction.
o cardiac arrhythmia
vitamin D
o convulsions.
pregnancy, or
 Extreme cases may lead to tetany of skeletal muscles, including the lactation
respiratory muscles, which can cause death.
 The blood calcium level directly controls the secretion of both
Causes and Symptoms of Hyposecretion and calcitonin and parathyroid hormone via negative feedback loops
Hypersecretion of PTH that do not involve the pituitary gland.
CAUSE SYMPTOMS ADRENAL GLANDS
HYPO Accidental Hypocalcemia  AKA suprarenal glands
PARATHYROIDISM removal Increased neuromuscular  LOCATION: lies superior to each kidney in the retroperitoneal space,
during excitability, possible tetany,  SHAPE: flattened pyramidal shape.
thyroidectomy laryngospasm, and death  SIZE: 3–5 cm in height, 2–3 cm in width, and a little less than 1 cm
from asphyxiation thick, with a mass of 3.5–5 g, only half its size at birth.
Flaccid heart muscle; possible o HAS 2 REGIONS
cardiac arrhythmia  ADRENAL CORTEX
Diarrhea o ZONA GLOMERULOSA – secretes
PRIMARY a result of Hypercalcemia or normal mineralcorticoids
HYPER abnormal blood Ca2+ levels; calcium o ZONA FASCICULATA – secrets glucocorticoids
PARATHYROIDISM parathyroid carbonate salts may be o ZONA RETICULATA – secretes androgens
function deposited throughout the  ADRENAL MEDULLA – secretes epinephrine and
Adenomas of the body, especial y in the norepinephrine
- parathyroid renal tubules (kidney
gland (90%) stones), lungs, blood
- idiopathic vessels, and gastric
(unknown cause) mucosa
hyperplasia of Bones weakened as a
parathyroid cells result of reabsorption;
(9%) some cases are first
- carcinomas (1%) diagnosed when a
radiograph is taken of a
broken bone

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 Anatomy and physiology
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o Increase the release of fatty acids from adipose tissue into the
HORMONES OF THE ADRENAL MEDULLA blood.
 The adrenal medulla is a modified sympathetic nervous system o Increase heart rate
ganglion. o Decrease blood flow through blood vessels of most internal
 In response to stimulation by sympathetic neurons organs.
STIMULUS: Emotional excitement, injury, stress, exercise, and low blood o Increase blood flow through blood vessels of skeletal muscle and
glucose levels the heart.
 AM secretes two major hormones: o Increase blood pressure
o EPINEPHRINE/ADRENALINE (80%) o Decrease the function of visceral organs.
o NOREPINEPHRINE/ NORADRENALINE (20%) ADRENAL CORTEX
o Secretion of adrenal medullary hormones prepares the  The adrenal cortex produces steroid hormones
individual for physical activity and to sustain it.  COMPLETE LOSS of adrenocortical hormones - death
o EFFECTS: SHORT-LIVED 3 LAYERS
HORMONES OF ADRENAL MEDULLA o ZONA GLOMERULOSA – MINERALOCORTICOIDS
TARGET o ZONA FASCICULATA – GLUCOCORTICODS
HORMONE TISSUE
RESPONSE
o ZONA RETICULATA – ANDROGEN
• Increased cardiac output; HORMONES OF ADRENAL CORTEX
• increased blood flow to skeletal TARGET
Heart, HORMONE RESPONSE
muscles and to the heart TISSUE
blood Increased Na+ reabsorption and
EPINEPHRINE • vasoconstriction of blood vessels, MINERALOCORTIC
vessels,
PRIMARILY; especial y in the viscera and skin; OIDS Kidney K+ and H+ excretion; enhanced
liver, (ALDOSTERONE)
NOREPINEPHRINE • increased release of glucose and water reabsorption
adipose
fatty acids into the blood; Increased protein and lipid
cells
• in general, preparation for breakdown; increased glucose
physical activity GLUCOCORTICOIDS Most
(CORTISOL) production; inhibition of immune
tissues
REGULATION OF ADRENAL MEDULLA SECRETIONS response and decreased
inflammation
Of minor importance in males.
Many in females, development of some
ANDROGENS
tissues secondary sex characteristics,
such as axil ary and pubic hair
MINERALOCORTICOIDS
 MINERAL HOMEOSTASIS
 Aldosterone is the major mineralocorticoid
o ADJUST BP and BLOOD VOLUME
 promotes excretion of H in the urine
 Increase Na blood levels
 Decrease K blood levels
 Renin–angiotensin–aldosterone or RAA pathway controls secretion
1. Stress, physical activity, and low blood glucose levels act as stimuli to of aldosterone
the hypothalamus, resulting in increased sympathetic nervous  Returns Blood Pressure to its (N) range through modulation of
system activity. kidney function
2. An increased frequency of action potentials conducted through the  STIMULUS: Low BP
sympathetic division of the autonomic nervous system stimulates  RESPONSE: Increase BP
the adrenal medulla to secrete epinephrine and some  TARGET TISSUE: KIDNEY
norepinephrine into the blood.  MECHANISM OF ACTION:
3. Epinephrine and norepinephrine act on their target tissues to o INCREASE NA REABSORPTION IN KIDNEYS – INCREASE NA
produce responses. BLOOD LEVELS - INCREASE BLOOD VOLUME - INCREASE
 Epinephrine and norepinephrine in the target tissues: BLOOD PRESSURE
o Increase the release of glucose from the liver into the blood. o INC K+ excretion into the urine- DEC. K+ BLOOD LEVELS

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 Anatomy and physiology
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o INC RATE OF H+ SECRETION into the urine - DEC. PH of body
fluids

HYPOSECRETION HYPERSECRETION
Removal of gland or loss
Tumor in gland or
of function or Addison
CAUSE aldosteronism
disease (low levels of
aldosterone and cortisol)
Hyponatremia
(low blood levels of Na)
Slight hypernatremia
Hyperkalemia
Hypokalemia Alkalosis 1. Corticotroponin-releasing hormone (CRH) is released from
(high blood levels of K)
High BP hypothalamic neurons in response stress or low blood glucose and
Acidosis
SYMPTOMS Weakness of skeletal passes, by way of the hypothalamohypophysial portal system to the
Low BP
muscles anterior pituitary.
Tremors and tetany of
Acidic urine 2. In the anterior pituitary, CRH binds to and stimulates cells that
skeletal muscles
Polyuria secrete adrenocorticotropic hormone (ACTH)
3. ACTH binds to membrane-bound receptors on cells of the adrenal
GLUCOCORTICOIDS cortex, primarily the Zona fasciculata, and stimulates the secretion
 help to provide energy for cells by stimulating the increased use of of glucocorticoids, primarily cortisol.
lipids and proteins. 4. Cortisol acts on target tissues, resulting in increased lipid and protein
breakdown, increased glucose levels, and anti-inflammatory effects.
 Most abundant is CORTISOL
5. Cortisol has a negative-feedback effect because it inhibits CRH
 STIMULUS OF CRH: Stress and Hypoglycemia
release from the hypothalamus and ACTH secretion from the
 Adrenocorticotropic Hormone (ACTH) is necessary to maintain the anterior pituitary.
secretory activity of the adrenal cortex.  Cortisol in the target tissues:
 Corticotropin-releasing hormone (CRH) released from the o Increases lipid and protein breakdown
hypothalamus stimulates the anterior pituitary to secrete ACTH - o Increases blood glucose
Zona fasciculata is very sensitive to ACTH - increasing cortisol o Has an anti-inflammatory effect.
secretion. GLUCOCORTICOIDS
 ACTH is inhibited by high cortisol level in the blood HYPOSECRETION HYPERSECRETION
 ACTH and cortisol inhibit CRH through Negative Feedback Removal of gland or Tumor in gland or Cushing
TARGET TISSUE RESPONSE CAUSE loss of syndrome (high
PERIPHERAL TISSUES: - INHIBIT GLUCOSE USE function cortisol and androgens)
- SKELETAL - GLUCONEOGENESIS (from amino acids Hyperglycemia (high blood glucose
MUSCLE and from lipids – liver) Hypoglycemia (low levels; adrenal diabetes; leads to
- LIVER = ELEVATED BLOOD GLUCOSE LEVELS blood glucose levels) diabetes mellitus) Depressed
- ADIPOSE - GLYCOGEN SYNTHESIS IN CELLS Depressed immune immune system
TISSUE - INCREASE LIPOLYSIS system Destruction of tissue proteins,
- DECREASE PROTEIN SYNTHESIS Unused proteins and causing muscle atrophy and
IMMUNE TISSUES Anti-inflammatory; depress antibody, WBC lipids from diet, weakness, osteoporosis, weak
production, and the release of inflammatory resulting in weight capillaries (easy bruising), thin
components in response to injury; loss skin, and impaired wound
suppress the immune system SYMPTOMS
Loss of appetite healing; mobilization and
TARGET CELLS FOR Receptor molecules for epinephrine and nausea, vomiting redistribution of lipids, causing
EPINEPHRINE norepinephrine decrease without adequate Bronzing of skin due depletion of adipose tissue from
amounts of glucocorticoid to increased limbs and deposition
pigmentation (if in face (moon face), neck
Regulation of corticol secretion ACTH levels are (buffalo hump), and abdomen
elevated) (Cushing syndrome)
Emotional effects, including
euphoria and depression

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 Anatomy and physiology
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 SIZE: ~12.5–15 cm (5–6 in.) in length, 85-100 grams
 LOCATION: between the greater curvature of stomach and
duodenum

ANDROGENS
 males and females: small amounts of weak androgens ACINI MAKE UP THE EXOCRINE PORTION OF THE PANCREAS, WHICH SECRETES ENZYMES
 The major androgen secreted by the adrenal gland is THAT MOVE THROUGH THE DUCTS TO THE SMALL INTESTINE. WHERE THEY ARE
dehydroepiandrosterone (DHEA). After puberty in males, the RESPONSIBLE IN DIGESTING OUR FOOD.
androgen testosterone is also released in much greater quantity by PANCREATIC HORMONES
the testes  regulating the concentration of glucose and amino acids.
 In females, however, adrenal androgens play important roles.  GLUCAGON
o stimulate pubic and axillary hair growth and sex drive in  INSULIN
females.  SOMATOSTATIN
o prepubertal growth spurt
o After menopause
CELLS IN HORMONE TARGET TISSUE RESPONSE
HYPOSECRETION HYPERSECRETION
ISLETS
Undescended
testes, loss of ALPHA Glucagon Primarily liver Glycogen breakdown;
CAUSE testes, Tumor in gland or release glucose in the
complications adrenogenital syndrome blood
following
mumps BETA Insulin Especialy liver, Increased uptake and use
In women, hirsutism (excessive skeletal muscle, of glucose and amino acids
In women, adipose tissue
facial and body hair), acne,
SYMPTOM reduction of DELTA Somatostatin Alpha and beta cells Inhibition of insulin and
increased sex drive,
S pubic and glucagon secretion
regression of breast tissue, and
axillary hair
loss of regular menstruation
PANCREAS
 ENDOCRINE and EXOCRINE GLAND INSULIN
BOTH ENDOCRINE AND EXOCRINE. SINCE PANCREAS HAS THE ABILITY TO SECRETE  FUNCTION: lower blood glucose levels by stimulating glucose
CHEMICALS TO THE BLOOD STREAM AND EXOCRINE BECAUSE IT SECRETE ITS PRODUCT transport into body cells.
INTO A DUCT.  STIMULUS: Elevated Blood glucose (After a meal)
o ACINI – pancreatic juice to the small intestine  RESPONSE: Increased ability of taking up and use of glucose and
IT IS THE FUNCTIONAL UNIT OF THE PANCREAS, THE PANCREATIC ACINER. IT IS amino acids
RESPONSIBLE FOR THE SYNTHESIS, STORAGE AND SECRETION OF ENZYMES IN THE  TOO LITTLE TO NO INSULIN: INCREASE BLOOD GLUCOSE
DIGESTION OF THE SMALL INTESTINE. PRIMARILY, PANCREATIC JUICE. o POLYPHAGIA – an intense sensation of hunger
ACINI – RESPONSIBLE FOR THE EXOCRINE ACTIVITY. o POLYURIA – increased urine volume and loss of water in the
o PANCREATIC ISLETS(ISLETS OF LANGERHANS)– responsible in urine.
secreting hormones in the pancreas; resposible for the o POLYDIPSIA – increased sensation of thirst
endocrine activity.  TOO MUCH INSULIN: DECREASE BLOOD GLUCOSE
 alpha (α) cells (20%) – secrete glucagon o HAS AN EFFECT TO THE NS
 beta (β) cells (75%) – secrete insulin TARGET TISSUE RESPONSE
 delta (δ) cells – secrete somatostatin, SKELETAL MUSCLE, Increased glucose uptake and glycogen
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 Anatomy and physiology
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CARDIAC MUSCLE,
CARTILAGE, BONE,
synthesis; increased uptake of certain
FIBROBLASTS,
amino acids
LEUKOCYTES, AND
MAMMARY GLANDS
LIVER Increased glycogen synthesis; increased use
of glucose for energy (glycolysis)
ADIPOSE CELLS Increased glucose uptake, glycogen
synthesis, lipid synthesis, and fatty acid
uptake; increased glycolysis
NERVOUS SYSTEM Little effect, except increased glucose
uptake in the satiety center

HOMEOSTASIS THAT HAS BEEN DISTURBED AND HOMEOSTASIS

RESTORED
FOR EXAMPLE, IN THE NORMAL RANGE OF THE SUPPOSEDLY NORMAL RANGE OR GLUCAGON
CONCENTRATION OF GLUCOSE IN THE BLOOD, IF THERE IS A DISTURBANCE THAT RESULTS  stimulated when blood glucose levels decline
TO AN INCREASE BLOOD GLUCOSE LEVEL IN THE BLOOD, OUR ORGAN WILL REACT INTO  RELEASE GLUCOSE from intracellular stores
IT. THE FOLLOWING STIMULUS IN RESPONSE IN THE INCREASE OF BLOOD GLUCOSE TARGET TISSUE RESPONSE
LEVEL, THE PANCREAS, THE PANCREATIC ISLETS DETECT AN INCREASE IN BLOOD SKELETAL MUSCLE, CARDIAC
GLUCOSE AND SECRETE INSULIN. SECONDLY, THE INTESTINE, WHICH DIGESTIVE HORMONE MUSCLE, CARTILAGE, BONE,
Little effect
SUCH AS GASTRIN, SECRETIN, CHOLECYSTOKININ, STIMULATES INSULIN SECRETION. FIBROBLASTS, LEUKOCYTES,
LASTLY, AUTONOMIC NERVOUS SYSTEM, WHICH IS A PARASYMPATHETIC STIMULATION AND MAMMARY GLANDS
OF PANCREAS PROMOTES INSULIN SECRETION. ALL OF THIS STIMULUS REACTS IN THE Glycogenolysis and release of glucose into
SECRETION OF THE INSULIN WHEN THEY DETECT IN THE INCREASE OF THE LEVEL OF the blood; Gluconeogenesis from amino
GLUCOSE IN THE BLOOD. THEN, THE RESPONSE BECAUSE OF THE SECRETION OF THE LIVER acids and, to some degree, from lipids;
INSULIN, THE INSULIN NOW STIMULATES THE GLUCOSE UPTAKE BY MOST TISSUES AND increased metabolism of fatty acids,
PROMOTES GLYCOGEN STORAGE IN SKELETAL MUSCLE AND LIVER. THE EXCESS GLUCOSE resulting in more ketones in the blood
IS CONVERTED TO ADIPOSE TISSUE. THIS RESPONSES WILL NOW LEADS TO DECLINE OF Lipolysis; probably unimportant under
ADIPOSE CELLS
AMOUNT OF GLUCOSE IN THE BLOOD. BECAUSE THE GLUCOSE IS NOW CONVERTED INTO most conditions
GLYCOGEN WHICH WILL BE USED BY OUR MUSCLE AND OUR LIVER AS WELL AS THE NERVOUS SYSTEM No effect
ADIPOSE TISSUE IN PERFORMING PHYSICAL ACTIVITY OR TO PROVIDE GLYCOLYSIS. NOW, HORMONES OF THE REPRODUCTIVE SYSTEM
HOMEOSTASIS IS RESTORED.  Gonads are the organs that produce gametes— sperm in males
and oocytes in females.
HOW ABOUT WHEN THERE IS A DECREASE IN BLOOD GLUCOSE?  Secretes reproductive hormones
THERE IS STILL A DISTURBANCES IN THE HOMEOSTASIS, SO THERE IS ALSO A STIMULUS o Reproduction
THAT WILL HAPPEN. THE SAME ORGANS STATED ABOVE ARE RESPONSIBLE. WHICH IS o Puberty
THE PANCREAS, WHERE THE PANCREATIC ISLETS DETECTS A DECREASE IN BLOOD
o Menstruation
GLUCOSE AND WILL NO SECRETE INSULIN. SECONDLY, THE INTESTINE WHERE THE
o Gamete formation
INACTIVITY OF THE INTESTINE DECREASE INSULIN SECRETION. LASTLY, THE AUTONOMIC
o Pregnancy
NERVOUS SYSTEM WHERE THE SYMPATHETIC STIMULATION OF THE PANCREAS INHIBITS
INSULIN SECRETION, INCLUDING DURING EXERCISE. AND IN RESPONSE, THE DECREASE OF  depend on the secretion of FSH and LH from the anterior pituitary
INSULIN REACTS IN DECREASED GLUCOSE UPTAKE, INCREASED GLYCOGEN BREAKDOWN gland
BY THE LIVER AND SKELETAL MUSCLE, AND INCREASED GLUCOSE SYNTHESIS IN THE
TESTES
LIVER. BECAUSE OF THIS IT COULD RESULT NOW INTO BLOOD GLUCOSE LEVEL
HORMONE TARGET RESPONSE
INCREASES, TO RESTORE THE HOMEOSTASIS.
TISSUE
Aids in spermatogenesis,
DIABETES MELLITUS development of genitalia,
 inadequate secretion of insulin or the inability of tissues to respond maintenance of functional
to insulin. TESTOSTERONE MOST CELLS
reproductive organs,
 Type 1 Diabetes Mellitus Insulin-dependent diabetes mellitus (IDDM) secondary sexual characteristics,
o destruction of the pancreatic islets (VIRAL) and sexual behavior
 Type 2 Diabetes Mellitus Noninsulin-dependent diabetes mellitus INHIBIN APG Inhibits FSH secretion
(NIDDM) OVARIES
HORMONE TARGET RESPONSE
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TISSUE
Aids in uterine and mammary gland
development and function, maturation of
genitalia,
ESTROGEN Most cells
secondary sex characteristics, sexual
behavior,
menstrual cycle
Aids in uterine and mammary gland
development and function, maturation 1. Light entering the eye stimulates neurons in the retina to initiate
PROGESTERONE Most cells of genitalia, action potentials.
secondary sex characteristics, 2. Action potentials are transmitted to the hypothalamus.
menstrual cycle 3. Action potentials from the hypothalamus are transmitted through
INHIBIN APG Inhibits FSH secretion the sympathetic division to the pineal gland.
Increases the flexibility of connective 4. A decrease in light (an increase in darkness) results in increased
Connective
RELAXIN tissue in the pelvic area, especial y the sympathetic stimulation of the pineal gland and increased melatonin
tissue cells
symphysis pubis secretion. An increase light results in decreased sympathetic
PINEAL GLAND stimulatioin of pineal gland and decreased melatonin secretion.
 LOCATION: PART OF THE EPITHALAMUS, attached to the roof of 5. Melatonin inhibits GnRH secretion from the hypothalamus and may
the third ventricle of the brain at the midline. help regulate sleep cycles by enchancing the tendency to sleep.
 MASS: 0.1–0.2 g TO SUMMARIZE, IF THERE IS AN INCREASE IN LIGHT RAYS THAT IS DETECTED BY YOUR
 The gland consists of masses of neuroglia and secretory cells called EYES. IT COULD RESULT TO A DECREASE IN MELATONIN, SO THAT THE INDIVIDUAL WILL
pinealocytes NOT FEEL OR NOT HAVE A TENDENCY TO SLEEP. BUT IF THERE IS A DARKNESS OR
 FUNCTION: secretes hormones that act on the hypothalamus and DECREASE LIGHT, IT CAN RESULT TO AN INCREASE OF SECRETION OF MELATONIN
the gonads to inhibit reproductive functions, such as by inhibiting RESULTING TO SLEEPYNESS.
the secretion of certain reproductive hormones. THYMUS
o MELATONIN  important for immune function.
o ARGININE VASOTOCIN  It is in the neck and superior to the heart in the thorax.
PINEAL GLAND  The thymus secretes the hormone thymosin
HORMONE TARGET TISSUE RESPONSE  TARGET TISSUE: Immune tissues
MELATONIN At least the Inhibition of GnRH secretion,  RESPONSE: Development and maturation of the immune system
hypothalamus thereby inhibiting THE STRESS RESPONSE
reproduction; significance is  It is impossible to remove all of the stress from our everyday lives.
not clear in humans.  Some stress, called eustress, prepares us to meet certain
May help regulate sleep- challenges and thus is helpful.
wake cycles  Other stress, called distress, is harmful.
ARGININE Possibly the Possible inhibition of GnRH  Any stimulus that produces a stress response is called a stressor.
STRESSOR
VASOTOCIN hypothalamus secretion
 A stressor may be almost any disturbance of the human body
THYMUS o heat or cold
 important for immune function. o environmental poisons
 It is in the neck and superior to the heart in the thorax. o toxins given off by bacteria
 The thymus secretes the hormone thymosin o heavy bleeding from a wound or surgery
 TARGET TISSUE: Immune tissues o a strong emotional reaction.
 RESPONSE: Development and maturation of the immune system o The responses to stressors may be pleasant or unpleasant,
REGULATION OF MELATONIN SECRETION FROM THE PINEAL
GLAND and they vary among people and even within the same
person at different times. Your body’s homeostatic
mechanisms attempt to counteract stress. When they are
successful, the internal environment remains within normal
physiological limits.

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Organs of the endocrine system

SOON AFTER A MEAL: BLOOD LEVELS OF NUTRIENTS, SUCH AS GLUCOSE, AMINO ACIDS,
AND FATTY ACIDS, INCREASE. BECAUSE OF THE HAPPENINGS INSIDE OF THE STOMACH.
FROM THE STOMACH, THE NUTRIENTS ENTERS THE BLOOD. THE PARASYMPATHETIC
STIMULATION AND INCREASING BLOOD GLUCOSE LEVELS CAUSE ELEVATED INSULIN
SECRETION FROM THE PANCREAS. AFTER THIS THE NUTRIENTS NOW MOVE TO THE
CELLS, FOR THEM TO BE ABLE TO UTILIZE THE NUTRIENTS. AFTER UTILIZING THE
NUTRIENTS, WITHIN 1-2 HOURS AFTER A MEAL, NUTRIENTS LEVELS DECLINE. THIS
RESULTS NOW TO THE FOLLOWING: THE LOWERED BLOOD GLUCOSE LEVELS AND
INCREASING SYMPATHETIC STIMULATION CAUSE INSULIN SECRETION TO DECLINE. THE
LOWERED BLOOD GLUCOSE LEVELS AND INCREASING SYMPATHETIC STIMULATION CAUSE
ELEVATED GLUCAGON SECRETION. LOWERED BLOOD NUTRIENT LEVELS PROMOTE GH
SECRETION. LOWERED BLOOD NUTRIENT LEVELS PROMOTE CORTISOL SECRETION. THESE
RESPONSES, PARTICULARLY IN THE NUTRIENT LEVEL DECLINE, TARGETS THE FOLLOWING:
MOST OF THE CELLS, THE GLUCOSE UPTAKE DECREASES AND SWITCHES TO LIPID AND
PROTEIN METABOLISM. TO THE LIVER, THE RELEASE GLUCOSE, KETONES AND
TRIGLYCERIDES INTO THE BLOOD. AND TO THE ADIPOSE TISSUE, THE RELEASE FATTY
ACIDS INTO THE BLOOD.
REGULATION OF BLOOD NUTRIENT LEVELS AFTER A MEAL

REGULATION OF BLOOD NUTRIENT LEVELS DURING EXERCISE

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THE PROLONGED EXERCISE ARE THE PATHOPHYSIOLOGY OR PHYSIOLOGICAL RESPONSES IN

PERFORMING A PROLONGED EXERCISE IN COMPARE TO SHORT TERM EXERCISE.

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