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Introduction to Anatomy and

Physiology II
Bio 132

Professor Peter Smith D.P.T, ATC


Smithpr@sunysuffolk.edu
http://www2.sunysuffolk.edu/smithpr/
Spring 2013

Overview of Anatomy and


Physiology
Anatomy The study of the structure of body
parts and their relationships to one another.
Physiology the study of the function of the
bodys structural machinery.
Understanding both the anatomy and physiology
of the human body is critical to all health care
providers.
You cant diagnose disease (Pathology) if you
dont understand both the underline anatomy
and physiology.

Homeostasis
A great deal of energy is spent trying to maintain
homeostasis.
the ability to maintain a relatively stable internal
environment in an ever-changing world.

The internal environment of the body is in a


dynamic state of equilibrium
Chemical, thermal, and neural factors interact to
maintain homeostasis
As we age these mechanisms become less efficient.
Makes us more susceptible to disease and less resilient
once we have one.

Negative Feedback
In negative feedback systems, the output shuts
off the original stimulus
This makes up 99% of the homeostatic
feedback loops.
Examples include regulation of : body
temperature, body pH, blood glucose levels,
blood pressure, body calcium levels.
Prevents large fluctuations and keeps the internal
environment relatively stable

Negative Feedback

Figure 1.5

Positive Feedback
In positive feedback
systems, the output
enhances or
exaggerates the
original stimulus.
Less than 1% of the
feedback loops.

Figure 1.6

Positive Feedback

Endocrine System: Overview


Endocrine system controlling system which
influences metabolic activities of cells by means
of hormones.
Hormones
chemical messenger secreted into bloodstream,
stimulates response in another tissue or organ

Endocrine glands produce hormones


pituitary, thyroid, parathyroid, adrenal, pineal, testes,
ovaries and the hypothalamus.
Other tissues and organs that produce hormones include:
adipose cells, cells in the walls of the small intestine,
kidneys, and heart.

Endocrine System

Hormones
Hormones:
Regulate the metabolic function of other cells
Alter plasma membrane permeability ( insulin)
Stimulate protein synthesis (GH)
Activate or deactivate enzyme systems
(GHRH,GHIH)
Induce secretory activity (Prolactin)
Stimulate mitosis (FSH)
Tend to have prolonged effects
Are classified as amino acid-based hormones, or steroids ( lipid
based)
Eicosanoids leukotrienes and prostaglandins

Amino Acid Based Hormones


Most hormones belong to this
class, including:
Glucagon, Insulin
are functional
polypeptides
Specificity of hormone is
determined by 3-D
configuration.
Polar molecules: water
soluble allowing them to be
transported in the blood.
They exert their effects on
extracellular receptors.

Steroids (Lipid Based Hormones)


Steroids derived from
cholesterol
Non polar molecules:
are hydrophobic
therefore require a
protein carrier to be
transported in the blood.
Adrenocortical hormones
Aldosterone
Gonadal
Estrogen,
Testosterone

Hormone Action
Hormones alter target cell activity by one of two
mechanisms
Second messengers involving:
Amino acidbased hormones cannot pass through
the membrane.
They attach to a specific regulatory G protein on
surface of cell membrane.
This sets off a series of steps that can activate or inhibit
numerous functioning enzymes in the cell.

Direct gene activation involving steroid hormones


Since steroid based hormones are lipophillic they
can diffuse through the cell membrane and enter
the nucleus where they can alter gene expression.

Amino Acid-Based Hormone Action: cAMP


Second Messenger

Figure 16.2a

Amino Acid-Based Hormone Action:


cAMP Second Messenger
1. Hormone (first messenger) binds to its
receptor, which then binds to a G protein
2. The G protein is then activated as it binds
GTP, displacing GDP
3. Activated G protein activates the effector
enzyme adenylate cyclase
4. Adenylate cyclase generates cAMP
(second messenger) from ATP
cAMP activates protein kinases, which then
cause cellular effects

Steroid Hormones

Figure 16..3

Steroid Hormones
1.

Steroid hormones and thyroid hormone are


hydrophobic, therefore require a carrier protein to
circulate in the blood.
To exert their effects they separate from their carrier
proteins and diffuse easily into their target cells.
Once inside, they bind and activate a specific
intracellular receptor
The hormone-receptor complex travels to the nucleus
and binds a DNA-associated receptor protein
This interaction prompts DNA transcription to produce
mRNA

2.
3.
4.
5.

The mRNA is translated into proteins, which bring about a


cellular effect.
Whats the significance of having both lipid and amino acid
based hormones.

Nervous / Endocrine System


Interrelationship
The nervous system modifies the stimulation of
endocrine glands and their negative feedback
mechanisms.
Nervous system is fast acting/short duration while the
endocrine is slow starting/long lasting.
The nervous system can override normal endocrine
controls.
For example, control of blood glucose levels are
normally maintained by the endocrine system.
Under stress when the body needs more glucose
the hypothalamus and the sympathetic nervous
system are activated to supply ample glucose.

Communication by the Nervous


and Endocrine Systems

Endocrine vs. Exocrine Glands


Exocrine glands
Ducts carry secretion to a surface or organ
cavity which exert extracellular effects.
(food digestion) Amylase is released to hydrolyze
polysaccharides into di and monosaccharides

Endocrine glands
no ducts, release hormones into tissue fluids
such as the blood.
Rich blood supply to distribute hormones.
intracellular effects, alter target cell metabolism

Control of Hormone Release


Blood levels of hormones:
Are controlled by negative feedback systems
Vary only within a narrow desirable range
Hormones are synthesized and released in response to
three basic mechanisms.
Humoral: changes and substances in the blood (glucose or
K+)
Neural: stimulation from the nervous system via
neurotransmitters.
Hormonal stimuli: organ or gland releases a hormone
that stimulates the release of another hormone from another
glands or organ.

Endocrine Organs

Hypothalamus
Controls many endocrine glands:
regulates the endocrine system through its direct
connection to the pituitary gland

The hypothalamus controls basic functions such


as:
body temperature, blood pressure, growth and
development ,reproduction, electrolyte balance and
water regulation.

It accomplishes this by producing both releasing


and inhibiting hormones that influence the
anterior pituitary gland.
Produces ADH and Oxytocin which are
transported to the posterior pituitary where they
will ultimately be released.

Pituitary Gland (Hypophysis)


Suspended from
hypothalamus by the
pituitary stalk
(infundibulum)
housed in sella turcica
of sphenoid bone
Adenohypophysis
(anterior pituitary)
arises from glandular
tissue
Neurohypophysis
(Posterior Pituitary)
arises from brain
(neural tissue)

Histology of Pituitary Gland

Neurohypophysis
Posterior Pituitary
Neurohypophysis
posterior lobe (neural
tissue) and the
infundibulum
Receives hormones
from the hypothalamus.
Hormones are stored,
and released
Oxytocin and ADH

Oxytocin
Oxytocin is a strong stimulant of uterine
contraction
During labor increasing levels leads to
increased intensity of uterine contractions.
Regulated by a positive feedback mechanism
PITOCIN is a synthetic form used to induce labor

Oxytocin triggers milk ejection (letdown reflex)


in women producing milk.
Baby suckling of breast causes ejection of
milk.
Its considered the pair bonding hormone

Oxytocin

Antidiuretic Hormone
AKA. Vasopressin is released in response to low
blood pressure, dehydration and high solute
concentration in the hypothalamus.
ADH helps to prevent dehydration by:
ADH stimulates thirst
ADH targets aquaporins in the kidney to
increase water permeability.
This will increase blood volume which increases
BP

Causes small arteries to constrict thus


increasing BP
Reduces secretory activity of sweat glands
preventing additional water loss

Antidiuretic Hormone (ADH)


Alcohol inhibits ADH release and causes
many unwanted trips to the bathroom.
Hang over symptoms primarily result of
dehydration .

Diabetes insipidus is a condition where


there is a hyposecretion of ADH
What effect will this have on urinary output
and hydration status?

Anterior Pituitary-Hypothalamic Connection:

Figure 16.5

Anterior Pituitary
Adenohypophysis anterior lobe, made up of
glandular tissue derived from the oral mucosa
during embryologic development.
Synthesizes and secretes a 6 major
hormones
There is a vascular connection via the
hypophyseal portal system
The vascular anatomical connection provides an a
means of delivering hypothalamic hormones directly
to the anterior pituitary.
Hypothalamic hormones avoid general circulation
allowing smaller amounts of hormones to be
delivered in a fraction of the time.

Activity of the Adenophypophysis


The hypothalamus sends a chemical stimulus to
the anterior pituitary in the form of releasing
hormones :
Releasing hormones stimulate the synthesis
and release of hormones from the anterior
pituitary.
example TRH (Thyrotropin Releasing
Hormone) causes the production and
release of TSH( Thyroid Stimulating
Hormone)
Inhibiting hormones shut off the synthesis and
release of hormones.
PIL( Prolactin inhibiting Hormone)
inhibits the synthesis and release of
Prolactin

Metabolic Action of Growth Hormone


Releasing hormone (GHRH) from the hypothalamus
stimulates GH release in response to low blood sugar,
increased levels of stress i.e. exercise and increases in levels
of some amino acids.
GH: causes cells in the liver, muscle, cartilage, bones and
other tissues to release (IGFs):
Insulin like growth factors. (Anabolic)
Skeletal muscle: increase uptake of A.A to build more
protein and inhibits protein catabolism.
Facilitates bone and cartilage growth by absorbing
building blocks such as sulfur.( i.e. glucoseamine sulfate,
Chondroitin sulfate)
Promotes sodium, potassium and chloride retention by the
kidneys and enhances calcium absorption by the small
intestine.

Metabolic Action of Growth


Hormone
Anti-insulin effects include
Liver: reduces the formation of glycogen and
promotes lipolysis of adipose cells. (the
hydrolysis triglycerides for energy).
Decreased rate of glycogen production in
the liver makes more available for
structures rely on sugar exclusively. (brain)
:Growth hormoneinhibiting hormone (GHIH)
inhibits GH release

Gigantism
Excessive growth
hormone before the
growth plates fuse.
Good for basketball
Bad for horse racing.

Acromegaly
To much GH usually
after the growth
plates have fused.
Results in great
wrestlers.

Beware the Pituitary


Tumor.

Dwarfism
Hyposecretion of GH
May require GH
replacement therapy

Thyroid Gland
The largest endocrine
gland, located in the
anterior neck, consists of
two lateral lobes
connected by a median
tissue mass called the
isthmus
Its rich blood supply reflect
its importance.

Thyroid Stimulating Hormone

Triggered by hypothalamic secretion of thyrotropinreleasing hormone (TRH )


TSH stimulates the normal development and secretory
activity of the thyroid gland (Thyroxin)
Rising blood levels of thyroid hormones act on the
pituitary and hypothalamus to block the release of TSH

Thyroid Gland
Thyroid follicles
lined with simple cuboidal epithelial (follicular
cells) that secretes two hormones, T3 and T4
T4 : 98% and relatively inactive.
T3 :cells convert T4 into this form which is much
more active.

Colloid: incorporates iodine and thryoglobulin to


produce thyroid hormone
thyroid hormone is stimulated by conditions that
increase the bodies need for ATP.
A in body temperature, hypoglycemia, high altitude
and pregnancy all increased thyroid hormone

Synthesis of Thyroid Hormone

Figure 16.8

Thyroid Hormone
Thyroid hormone (TH) action is like turning up the
thermostat.
TH causes:
bodys metabolic rate and O2 consumption
Calorigenic effect - heat production with increased ATP
consumption.
heart rate, contraction strength blood pressure and
respiratory rate
by enhancing norepinephrine and epinephrine
actions.

stimulates many things necessary for growth and


devolvement.
in appetite and breaking down of CHO, lipids and
proteins for energy

Endemic goiter

Goiter = enlarged thyroid


gland
results from dietary iodine
deficiency.
Cant produce TH,
no feedback to Pituitary
TSH
This causes hypertrophy of
the thyroid gland.

Toxic goiter (Graves disease)


Antibodies mimic TSH
causing d TH to be
released,
Excessive Thyroxin levels
elevated metabolism
heart rate
weight loss
nervousness
exophthalmos (bulging
eyes)
ANS induced sweating.

Thyroid Histology

Calcitonin
Parafollicular cells produce calcitonin:

blood Ca2+ and promotes Ca2+ deposition in bone.

Calcitonin:
Inhibits osteoclast activity (breaks down bone
releasing calcium from the bone matrix)
Stimulates calcium uptake and incorporation
into the bone matrix by increasing osteoblast
activity.
Regulated by a blood (calcium ion concentration
in the blood) negative feedback mechanism
Antagonist to parathyroid hormone (PTH)

Parathyroid Glands
Tiny glands
embedded in the
posterior aspect of
the thyroid
Chief (principal) cells
secrete PTH
(parathyroid hormone)
PTH regulates calcium
balance in the blood

Effects of Parathyroid Hormone

Figure 16.11

Adrenal Cortex

Figure 16.12a

Adrenal (Suprarenal) Glands


Adrenal glands paired, pyramid-shaped
organs on top of the kidneys structurally and
functionally they are two glands in one.
Adrenal Cortex releases a variety of hormones
that allow the body to deal stress blood pressure
changes with development of secondary sex
characteristics.
Adrenal medulla nervous tissue that is the
hormonal branch of the sympathetic nervous
system (fight/flight)

Adrenal Cortex
Different corticosteroids are produced in
each of the three layers
Zona glomerulosa mineralocorticoids
(chiefly aldosterone)
Zona fasciculata glucocorticoids
(chiefly cortisol)
Zona reticularis gonadocorticoids
(chiefly androgens) testosterone in males and
estrogen in females

Adrenocorticotropic Hormone
(ACTH) (Corticotropin)
Produced by the Anterior Pituitary.
Triggered by hypothalamic corticotropinreleasing hormone (CRH)
Stimulates the adrenal cortex to release
corticosteroids and mineralocorticoids.

ACTH is stimulated by
fever,
hypoglycemia,
various stressors

Mineralocorticoids
Regulate the electrolyte concentrations of
extracellular fluids
Aldosterone most important mineralocorticoid
Maintains Na+ balance by reducing excretion of Na+
from the body while increasing K+ excretion.
Aldosterone secretion is stimulated by:
Rising blood levels of K+
Low blood Na+
Decreasing blood volume or pressure

Glucocorticoids (Cortisol)
Stress on body causes hypothalamus to release
CRHACTH targets adrenal cortex to release
Cortisol: Cortisol
targets liver and muscle cells:
Increases levels of the following in the blood to
ensure there is enough available fuel to deal with
stress.
glucose
fatty acids
amino acids
Gluconeogenesis (formation of glucose from noncarbohydrates)
Inhibit inflammation
Depressed the immune system

Cushing Disease
Cushing Disease :hyper secretion of ACTH or Cortisol
Results in moon face hunch back appearance.
Muscle wasting
Hyperglycemia
Depress cartilage and bone formation
Promote diseases of the cardiovascular, nervous and
gastrointestinal systems.
Increased blood pressure
Often medically induced as a result of patient given high dose
corticosteroids
For treatment of inflammatory, autoimmune and allergic medical
condition.

Cushing Disease

Cushing Disease

Adrenal Medulla
The adrenal medulla functions as an extension
of the sympathetic nervous system.
Under periods of stress a neuron from the
hypothalamus directly stimulates as the adrenal
medulla.
Since this is a direct neural connection the
adrenal medulla can release the catecholamines
(epinephrine and norepinephrine) immediately.
Catecholamines are the hormonal portion of the SNS
Functionally their effects on the body are the same.

Stress and the Adrenal Gland

Figure 16.15

Addison's Disease
Results from a
hyposecretion of ACTH or
an autoimmune disease
that damages the
adrenals.
Results in decreased
glucocorticoids and
mineralocorticoid release.
Results in hypotension
and hypoglycemia
Corticosteroid
replacement therapy

A patient 16 y/o male with complaints of tunnel vision


and HA comes into your office. He is 6ft 11inches in
height and weighs 295 lbs. The patients parents are
both over 6 feet. What is a possible diagnosis for his
condition.

A. A tumor causing increased thyroid function.


B. Genetic ( follow up with ophthalmologist for
tunnel vision.)
C. A hyperactive pancreas
D. A pituitary tumor
E. Under active hypothalamic secretions

Clinical Question
What actions would be appropriate.
A) Order a head CT to observe any anomalies in
the cranium.
B) Blood work to look at levels of GH, LH,
insulin, ETC
C) Send him to an ophthalmologist for further
examination.
D) Set him up with your 6ft 2 sister and tell him
not to walk into any walls.
E) All of the above.

A 48 female presents to the doctor with the


following complaints. She reports excessive
fatigue recent weight gain and depression.
She has recently been loosing her hair and
has become very forgetful.
Is this an endocrine problem?
If so what hormone might explain these
symptoms.

A patient was in a car accident five years


ago. Since then he has been in chronic pain
managed by opiate painkillers. The patient
reports that the medication is no longer
working. The doctor responds by increasing
the dose.
Why did the patient require a higher dose of
medication to get the same therapeutic
effect?

Hormones and Target Cell Sensitivity

Cells respond to hormonal levels of stimulation differently. When signaling is


low the target cell will make more receptors. When stimulation is high the cell
will reduce the number of receptors.
What is the clinical applications to the cells intrinsic homeostatic
mechanisms?

Endocrine Screen

Hyperglycemia / Hypoglycemia
Poly /glucosurea
Temp. intolerance (hot vs. cold)
Changes in heart rate / palpitations
Changes in physical features
Skin changes, excessive abnormal hair growth, Body Fat
distribution

Deep Rapid Breathing


Changes in Body WT.
Fatigue /weakness
Goiter
Irradiation exposure

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