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Human Anatomy and Physiology
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Batangas State University ARASOF-Nasugbu – CONAHS Quick Notes

HUMAN ANATOMY AND PHYSIOLOGY
Stages of Long Bone Formation in an Embryo, Fetus and Young Child
Introduction
Bone is living tissue that is the hardest among other connective tissues in the body,
consists of 50% water. The solid part remainder consisting of various minerals, especially
76% of calcium salt and 33% of cellular material. Bone has vascular tissue and cellular
activity products, especially during growth which is very dependent on the blood supply as
basic source and hormones that greatly regulate this growth process. Bone-forming cells,
osteoblasts, osteoclast play an important role in determining bone growth, thickness of the
cortical layer and structural arrangement of the lamellae. This process of bone formation is
called osteogenesis or ossification. After progenitor cells form osteoblastic lines, they
proceed with three stages of development of cell differentiation, called proliferation,
maturation of matrix, and mineralization.
• Based on its embryological origin, there are two types of ossification, called:
o Intramembranous ossification that occurs in mesenchymal cells that
differentiate into osteoblast in the ossification center directly without prior
cartilage formation and:
o Endochondral ossification in which bone tissue mineralization is formed
through cartilage formation first.
• In intramembranous ossification, bone development occurs directly. In this process,
mesenchymal cells proliferate into areas that have high vascularization in embryonic
connective tissue in the formation of cell condensation or primary ossification centers.
This cell will synthesize bone matrix in the periphery and the mesenchymal cells
continue to differentiate into osteoblasts.
• After that, the bone will be reshaped and replaced by mature lamellar bone.

• Endochondral ossification will form the center of primary ossification, and the cartilage
extends by proliferation of chondrocytes and deposition of cartilage matrix.
• After this formation, chondrocytes in the central region of the cartilage start to proceed
with maturation into hypertrophic chondrocytes.
• After the primary ossification center is formed, the marrow cavity begins to expand
toward the epiphysis.
• After the primary ossification center is formed, the marrow cavity begins to expand
toward the epiphysis.
BONE CELLS AND MATRIX

• Bone is a tissue in which the extracellular matrix has been hardened to accommodate a
supporting function.
• The fundamental components of bone, like all connective tissues, are cells and matrix.
Although bone cells compose a small amount of the bone volume, they are crucial to the
function of bones.
• Four types of cells are found within one tissue:
▪ Osteoblasts
• The function is for bone formation. It is located at the growing portions of
bone, including periosteum and endosteum. It synthesizes the bone matrix
and are responsible for its mineralization. They are derived from
osteoprogenitor cells, a mesenchymal stem cell line.
▪ Osteocytes
• It maintains mineral concentration of matrix. It is inactive osteoblasts that
have become trapped within the bone they have formed.
▪ Osteogenic cells
• Develop in osteoblast. It is located at the deep layers of the periosteum and
the marrow.
▪ Osteoclasts
• It is break down bone matrix through phagocytosis. Predictably, they ruffled
border, and the space between the osteoblast and the bone is known as
Howship’s lacuna. It is located at the bone surfaces and at sites of old,
injured, or unneeded bone.

TWO TYPES OF OSSIFICATION
▪ INTRAMEMBRANOUS OSSIFICATION
• Intramembranous ossification mainly occurs during the formation of the flat bones of
the skull, as well as mandible, maxilla, and clavicles.
• The bones are formed from connective tissue such as mesenchyme tissue rather than
from cartilage.
• The four steps in intramembranous ossification are:
1. Mesenchymal cells group into cluster, differentiate into osteoblasts and ossification
centers form.
2. Osteoblasts become entrapped by the osteoid they secrete, transforming them to
osteocytes.
3. Trabecular matrix and periosteum form.
4. Compact bone develops superficial to the trabecular bone, and crowded blood
vessels condense into red bone marrow.

ENDOCHONDRAL OSSIFICATION
• Endochondral ossification begins with points in the cartilage called “primary ossification
centers.”
• They mostly appear during fetal development, though a few short bones begin their primary
ossification.
• These cartilage points are responsible for the formation of diaphysis of long bones, short
bones, and certain parts of irregular bones.
• Secondary ossification occurs after birth and forms the epiphyses of a long bones and
extremities of irregular and flat bones. The diaphysis and both epiphyses of a long bone
are separated by a growing zone of cartilage (the epiphyseal plate).
• When the child reaches skeletal maturity (18 to 25 years of age), all cartilage is replaced
by bone, fusing the diaphysis and both epiphyses together.
• The steps of endochondral ossification are:
• Mesenchymal cells differentiate into chondrocytes that produce a cartilage model
of the future bony skeleton.
• Blood vessels on the edge of the cartilage model bring osteoblasts the deposit a
bony collar.
• Capillaries penetrate cartilage and deposit bone inside cartilage model, forming
primary ossification center.
• Cartilage and chondrocytes continue to grow at ends of the bone while medullary
cavity expands and remodels.
• Secondary ossification centers develop after birth.
• Hyaline cartilage remains at epiphyseal (growth) plate and at joint surface as
articular cartilage.
BONE STRUCTURE
• Microscopic bone structure
-Long bones are composed of both cortical and cancellous bone tissue.

➢ The epiphysis is located at the end of the long bone and is the parts of the bone that
participate in joint surfaces.
➢ The diaphysis is the shaft of the bone and has walls of cortical bone and an underlying
network of trabecular bone.
➢ The epiphyseal growth plate lies at the interface between the shaft and the epiphysis and
is the region in which cartilage proliferates to cause the elongation of the bone.
➢ The metaphysis is the area in which the shaft of the bone joins the epiphyseal growth plate.
BONE GROWTH
• Bone growth occurs from the growth plate, and when a child is fully grown, the growth
plates harden into solid bone. An osteochondroma is an outgrowth of the growth plate and
is made up of both bone and cartilage.
• In the early stages of development, the size of a very small embryo can form a
chondroskeleton easily in which the further growth preparation occurs without internal
blood supply
• During the fourth month in the uterus, the development of vascular elements to the various
points of the chondrocranium(the other parts of the early cartilage of skeleton) becomes on
ossification center, where the cartilage changes into an ossification center and bones form
around the cartilage.

• Bone growths stop around the age 21 for males and the age of 18 for females when the
epiphyses and diaphysis have fused(epiphyseal plate closure)
• Normal bone growth is dependent on proper dietary intake of protein, minerals and
vitamins. A deficiency of vitamin D prevents calcium absorption from the GI tract resulting
in rickets (children) or osteomalacia (adults). Osteoid is produced but calcium salts are not
deposited, so bones soften and weaken.
❖ Oppositional bone growth

• At the length of the long bones, the reinforcement plane appears in the middle and at
the end of the bone, finally produces the central axis that is called the diaphysis and the
bony cap at the end of the bone is called the epiphysis. Between epiphyses and
diaphysis is a calcified area that is not calcified called the epiphyseal plate.
• Epiphyseal plate of the long bone cartilage is a major center for growth, and in fact,
this cartilage is responsible for almost all the long growths of the bones.
• Oppositional bone growth and remodeling. The epiphyseal plate is responsible for
longitudinal bone growth.
✓ Epiphyseal plate growth

• The cartilage found in the epiphyseal gap has a defined hierarchical structure,
directly beneath the secondary ossification center of the epiphysis.

• By close examination of the epiphyseal plate, it appears to be divided into five
zones
1. The resting zone: it contains hyaline cartilage with few chondrocytes, which
means no morphological changes in the cells.
2. The proliferative zone: chondrocytes with a higher number of cells divide
rapidly and form columns of stacked cells parallel to the long axis of the
bone.
3. The hypertrophic cartilage zone: it contains large chondrocytes with cells
increasing in volume and modifying the matrix, effectively elongating bone
whose cytoplasm has accumulated glycogen. The resorbed matrix is
reduced to thin septa between the chondrocytes.
4. The calcified cartilage zone: chondrocytes undergo apoptosis, the thin septa
of cartilage matrix become calcified.
5. The ossification zone: endochondral bone tissue appears. Blood capillaries
and osteoprogenitor cells (from the periosteum) invade the cavities left by
the chondrocytes. The osteoprogenitor cells form osteoblasts, which deposit
bone matrix over the three-dimensional calcified cartilage matrix.

❖ Appositional bone growth
• When bones are increasing in length, they are also increasing in diameter; diameter growth
can continue even after longitudinal growth stops. This is called appositional growth.
• Osteoblasts and osteoclasts play an essential role in appositional bone growth where
osteoblasts secrete a bone matrix to the external bone surface from diaphysis, while
osteoclasts on the diaphysis endosteal surface remove bone from the internal surface of
diaphysis.
• Osteoclasts resorb the old bone lining the medullary cavity, while osteoblasts through
intramembrane ossification produce new bone tissue beneath the periosteum. Periosteum
on the bone surface also plays an important role in increasing thickness and in reshaping
the external contour.
• Appositional bone growth is a bone deposit by osteoblast as bone resorption by osteoclast.
Summary
▪ Osteogenesis/ossification is the process in which new layers of bone tissue are placed by
osteoblasts.
▪ During bone formation, woven bone (haphazard arrangement of collagen fibers) is
remodeled into lamellar bones (parallel bundles of collagen in a layer known as lamellae)
▪ Periosteum is a connective tissue layer on the outer surface of the bone; the endosteum is
a thin layer (generally only one layer of cell) that coats all the internal surfaces of the bone

▪ Major cell of bone include: osteoblasts (from osteoprogenitor cells, forming osteoid that
allow matrix mineralization to occur), osteocytes (from osteoblasts; closed to lacunae and
retaining the matrix) and osteoclasts (from hemopoietic lineages; locally erodes matrix
during bone formation and remodeling.
▪ The process of bone formation occurs through two basic mechanisms:
• Intramembranous bone formation occurs when bone forms inside the mesenchymal
membrane. Bone tissue is directly laid on primitive connective tissue referred to
mesenchyme without intermediate cartilage involvement. It forms bone of the skull and
jaw; especially only occurs during development as well as the fracture repair.
• Endochondral bone formation occurs when hyaline cartilage is used as a precursor to
bone formation, then bone replaces hyaline cartilage, forms, and grows all other bones,
occurs during development and throughout life.
▪ During interstitial epiphyseal growth (elongation of the bone), the growth plate with zonal
organization of endochondral ossification, allows bone to lengthen without epiphyseal
growth plates enlarging zones include:
• Zone of resting.
• Zone of proliferation.
• Zone of hypertrophy.
• Zone of calcification.
• Zone of ossification and resorption.
▪ During appositional growth, osteoclasts resorb old bone that lines the medullary cavity,
while osteoblasts, via intramembranous ossification, produce new bone tissue beneath the
periosteum.
▪ Mesenchymal stem cell migration and differentiation are two important physiological
processes in bone formation.
▪
References:
https://courses.lumenlearning.com/boundless-ap/chapter/bone-development/
https://www.intechopen.com/books/osteogenesis-and-bone-regeneration/bone-development-and-
growth

Stages of Bone Fracture Healing
Introduction
• Bones are made of a combination of compact bone tissue for strength and spongy bone
tissue for compression in response to stresses. It is remodeled through the continual
replacement of old bone tissue as a person grows and gets old, as well as repaired when
fractured.
• Fracture is any crack or break of bones happens because of several cases like car accident,
injuries in sports or even because of simple falls. Basically, there are two types of fractures
in the bone:
1) Closed or simple fracture- the broken bone does not penetrate the skin
2) Open or compound fracture- any fracture which the bone punctures or penetrates
the skin
• So, the bone takes at least 6-8 weeks to be fully healed from being fractured. Within this
time frame, the bone undergoes 4 stages of repair or healing processes:

• 4 Stages of Repair or Healing Processes:
a) The Formation of Hematoma at the break
• Blood vessels in the broken bone tear and hemorrhage, resulting in the formation
of clotted blood, or a hematoma, at the site of the break.
• The severed blood vessels at the broken ends of the bone are sealed by the clotting
process.
• Bone cells deprived of nutrients begin to die.
• Usually happens over days 1 to 5 after the fracture.
b) Formation of a Fibrocartilaginous Callus

• Within days of the fracture, capillaries (blood vessels) grow into the hematoma,
while phagocytic cells begin to clear away the dead cells because of the bone cells
being deprived of nutrients.
• Through fragments of the blood clot may remain, fibroblasts and osteoblasts
enter the area and begin to reform bone.
• Fibroblasts produce collagen fibers that connect the broken bone ends, while
osteoblasts start to form spongy bone.
• The repair tissue between the broken bone ends, the fibrocartilaginous callus, is
composed of both hyaline and fibrocartilage.
• Some bone spicules may also appear at this point.
• Usually happens days 5 to 11 of the healing process of the bone.
c) Formation of a Bony Callus

• The fibrocartilaginous callus is converted into a bony callus of spongy bone.
• It takes about two months for the broken bone ends to be firmly joined together
after the fracture.
• This is similar to the endochondral formation of bone when cartilage becomes
ossified; osteoblasts (a cell that secretes the matrix for bone formation),
osteoclasts (large cells that dissolve the bone) , and bone matrix (composite
material consisting of organic, which is almost compromised by collagen, and
inorganic components) are present.

• Mostly happens from days 11 to 28 of bone repair.
d) The Remodeling and Addition of Compact Bone

• The bony callus is then remodeled by osteoclasts and osteoblasts, with excess
material on the exterior of the bone and within the medullary cavity being
removed.
• Compact bone is added to create bone tissue that is like the original, unbroken
bone.
• This remodeling can take many months; the bone may remain uneven for years.
• Most probably begins in the middle of the formation of bony callus, especially to
day 18 onwards, which lasts for months to years before fully remodeled.
References:
https://courses.lumenlearning.com/boundless-biology/chapter/bone/
https://www.ncbi.nlm.nih.gov/books/NBK551678/

Events at the Neuromuscular Junction
Introduction
Skeletal muscle cell contraction occurs after a release of calcium ions from internal
stores, which is initiated by a neural signal. Each skeletal muscle fiber is controlled by a motor
neuron, which conducts signals from the brain or spinal cord to the muscle.
• The following list presents an overview of the sequence of events involved in the
contraction cycle of skeletal muscle:
o The action potential travels down the neuron to the presynaptic axon
terminal.
o Voltage-dependent calcium channels open and Ca2+ ions flow from the
extracellular fluid into the presynaptic neuron’s cytosol.
o The influx of Ca2+ causes neurotransmitter (acetylcholine)-containing
vesicles to dock and fuse to the presynaptic neuron’s cell membrane.
o Vesicle membrane fusion with the nerve cell membrane results in the
emptying of the neurotransmitter into the synaptic cleft; this process is
called exocytosis.
o Acetylcholine diffuses into the synaptic cleft and binds to the nicotinic
acetylcholine receptors in the motor end-plate.
o The nicotinic acetylcholine receptors are ligand-gated cation channels, and
open when bound to acetylcholine.

o The receptors open, allowing sodium ions to flow into the muscle’s cytosol.
o The electrochemical gradient across the muscle plasma membrane causes a
local depolarization of the motor end-plate.
o The receptors open, allowing sodium ions to flow into and potassium ions
to flow out of the muscle’s cytosol.
o The electrochemical gradient across the muscle plasma membrane (more
sodium moves in than potassium out) causes a local depolarization of the
motor end-plate.
o This depolarization initiates an action potential on the muscle fiber cell
membrane (sarcolemma) that travels across the surface of the muscle fiber.
o The action potentials travel from the surface of the muscle cell along the
membrane of T tubules that penetrate into the cytosol of the cell.
o Action potentials along the T tubules cause voltage-dependent calcium
release channels in the sarcoplasmic reticulum to open, and release
Ca2+ ions from their storage place in the cisternae.
o Ca2+ ions diffuse through the cytoplasm where they bind to troponin,
ultimately allowing myosin to interact with actin in the sarcomere; this
sequence of events is called excitation-contraction coupling.
o As long as ATP and some other nutrients are available, the mechanical
events of contraction occur.
o Meanwhile, back at the neuromuscular junction, acetylcholine has moved
off of the acetylcholine receptor and is degraded by the enzyme
acetylcholinesterase (into choline and acetate groups), causing
termination of the signal.
o The choline is recycled back into the presynaptic terminal, where it is used
to synthesize new acetylcholine molecules.
• Anatomy of the Neuromuscular Junction

o We stimulate skeletal muscle contraction voluntarily. Electrical signals from the
brain through the spinal cord travel through the axon of the motor neuron.
o The axon then branches through the muscle and connects to the individual muscle
fibers at the neuromuscular junction. The folded sarcolemma of the muscle fiber
that interacts with the neuron is called the motor end-plate; the folded
sarcolemma increases surface area contact with receptors.
o The ends of the branches of the axon are called the synaptic terminals, and do
not actually contact the motor end-plate. A synaptic cleft separates the synaptic
terminal from the motor end-plate, but only by a few nanometers.
o Communication occurs between a neuron and a muscle fiber through
neurotransmitters. Neural excitation causes the release of neurotransmitters from
the synaptic terminal into the synaptic cleft, where they can then bind to the
appropriate receptors on the motor end-plate.
o The motor end-plate has folds in the sarcolemma, called junctional folds, that
create a large surface area for the neurotransmitter to bind to receptors.
o Generally, there are many folds and invaginations that increase surface area
including junctional folds at the motor endplate and the T-tubules throughout the
cells.

• Physiology of the Neuromuscular Junction
o The neurotransmitter acetylcholine is released when an action potential travels
down the axon of the motor neuron, resulting in altered permeability of the
synaptic terminal and an influx of calcium into the neuron. The calcium influx
triggers synaptic vesicles, which package neurotransmitters, to bind to the
presynaptic membrane and to release acetylcholine into the synaptic cleft by
exocytosis.
Reference:
https://courses.lumenlearning.com/cuny-csi-ap-1/chapter/neuromuscular-junctions-and-muscle-
contractions/

Sliding Filament Theory
Introduction
▪ What causes filaments to slide?
▪ Calcium ions (Ca2+) bind regulatory proteins on thin filaments and expose myosin-
binding sites, allowing the myosin heads on the thick filaments to attach
▪ Each cross bridge pivots, causing the thin filaments to slide toward the center of
the sarcomere
▪ Contraction occurs, and the cell shortens
▪ During a contraction, a cross bridge attaches and detaches several times
▪ ATP provides the energy for the sliding process, which continues as long as calcium
ions are present

• Schematic representation of contraction mechanism: the sliding filament theory.
▪ In a relaxed muscle fiber, the regulatory proteins forming part of the actin myofilaments
prevent myosin binding. When an action potential (AP) sweeps along its sarcolemma
and a muscle fiber is excited, calcium ions (Ca2+) are released from intracellular storage
areas (the sacs of the sarcoplasmic reticulum).
▪ The flood of calcium acts as the final trigger for contraction, because as calcium binds
to the regulatory proteins on the actin filaments, the proteins undergo a change in both
their shape and their position on the thin filaments. This action exposes myosin-binding
sites on the actin, to which the myosin heads can attach, and the myosin heads
immediately begin seeking out binding sites.
▪ The free myosin heads are “cocked,” much like an oar ready to be pulled on for rowing.
Myosin attachment to actin causes the myosin heads to snap (pivot) toward the center
of the sarcomere in a rowing motion. When this happens, the thin filaments are slightly
pulled toward the center of the sarcomere. ATP provides the energy needed to release
and recock each myosin head so that it is ready to attach to a binding site farther along
the thin filament.
• Contraction of a Skeletal Muscle as a Whole
▪ Graded responses
▪ Muscle fiber contraction is “all-or-none,” meaning it will contract to its fullest
when stimulated adequately
▪ Within a whole skeletal muscle, not all fibers may be stimulated during the
same interval
▪ Different combinations of muscle fiber contractions may give differing
responses
▪ Graded responses—different degrees of skeletal muscle shortening
▪ Graded responses can be produced in two ways
▪ By changing the frequency of muscle stimulation
▪ By changing the number of muscle cells being stimulated at one time
▪ Muscle response to increasingly rapid stimulation
▪ Muscle twitch

▪ Single, brief, jerky contraction
▪ Not a normal muscle function
▪ In most types of muscle activity, nerve impulses are delivered at a rapid
rate
▪ As a result, contractions are “summed” (added) together, and one
contraction is immediately followed by another
▪ When stimulations become more frequent, muscle contractions get
stronger and smoother
▪ The muscle now exhibits unfused (incomplete) tetanus
▪ Fused (complete) tetanus is achieved when the muscle is stimulated so
rapidly that no evidence of relaxation is seen
▪ Contractions are smooth and sustained
▪ Muscle response to stronger stimuli
▪ Muscle force depends upon the number of fibers stimulated
▪ Contraction of more fibers results in greater muscle tension
▪ When all motor units are active and stimulated, the muscle contraction is as
strong as it can get
▪ ATP
▪ Only energy source that can be used to directly power muscle contraction
▪ Stored in muscle fibers in small amounts that are quickly used up
▪ After this initial time, other pathways must be utilized to produce ATP
Summary
The basic unit controlling changes in muscle length, scientists proposed the sliding
filament theory to explain the molecular mechanisms behind muscle contraction. Within
the sarcomere, myosin slides along actin to contract the muscle fiber in a process that
requires ATP.

Cerebrospinal Fluid Flow
 Cerebrospinal fluid (C.S.F.) is a clear, colorless bodilly fluid the occupies the sub-
arachnoid space or the space between Arachnoid membrane and the Pia mater
 C.S.F. supplies nutrients to the cortex and deeper structure in the brain rather than the
blood flow that supplies the surface region.
 Total Volume:
 Adults: 140-170 mL
 Children: 10-60 mL
 50% to 70% of C.S.F. is produced in the brain by modified ependymal cell in Choroid
plexus

 Two components can be distinguished in C.S.F. circulation
 Bulk flow - C.S.F. is produced by Choroid plexus and absorbed by Arachnoid
granulation, and
 Pulsatile flow - C.S.F. flow is pulsatile and results from pulsations related to
cardiac cycle.
CEREBROSPINAL FLUID FLOW PROPER

 C.S.F. is produced by Choroid Plexus that covers the flow of Lateral ventricle (Cerebral
cortex) and the roof of the Third ventricle.
 C.S.F. flows from Choroid plexus through the body and tail of Lateral ventricle via
Interventricular foramen (Foramen of Monro). .
 C.S.F. then flows to the 4th Ventricle via Cerebral aqueduct (Aqueduct of Sylvius) and
existing via Lateral aperture ( Foramen of Luschka).
 The C.S.F. that exits from Lateral aperture flows to the Pontine cistern on the ventral
surface of the brain stem, while the flow from the Medial aperture (Foramen of Magendie)
enters the Cerebello-medullary cistern anf follows one to two paths.
 First path flows around the Cerebellum, draining into the Superior cistern from
where it flows into the Interpeduncular cistern
 Second path flows down the sub-dural space around the Spinal cord down to the
Lumbar Cistern. It is where the fluid is taken from lumbar puncture.
 C.S.F. then flows back up to the Spinal cord and it joins the flow from 4th ventricle and
the Superior cistern.
 For the Ventral cistern, C.S.F. flows across the Cortical surface in the sub-arachnoid space
draining into the Superior sagittal sinus via Arachnid granulation.
 C.S.F. then flows now to the posterior surface towards the Confluence of the Sinuses where
it joints the Venous blood flowing from sub-cortical regions via straight sinus.

 C.S.F. Flows Mnemonics
 Little Infants Try Crying For Food Sorry All Done
 Lateral ventricle
 Interventricular Foramen
 Third ventricle
 Cerebral aqueduct
 Fourth ventricle
 Foramen of Luschka and Magendie
 Sub-arachnoid space
 Arachnoid granulation
 Dural venous sinus.

ORGANIZATION OF NERVOUS SYSTEM

Nervous System is the network of nerve cells and fibers which transmit nerve impulses
between parts of the body. The Nervous System coordinates voluntary and involuntary actions in
the body by sending and receiving information.
It is comprised of an enormous number of cells (over 100 billion), primarily of two types:
neurons (the signaling units) and glial cells (the supporting units). The function of the nervous
system is mostly a story of the neuron. The neuron is the functional unit of the nervous system and
is designed to transmit information between cells.
 The nervous system can be divided into two

major parts: The Central Nervous System (CNS)
and The Peripheral Nervous System (PNS).
Central Nervous System consists of neurons

associated with central processing and which are located
in the brain and spinal cord.
 The Brain is the center of the nervous system and

the spinal cord sense signal to and from the brain,
to and from the rest of the body.
 Sensory information  Visceral Information
 are things whereas the brain collects  Is to relay information
from our senses that give us information to the other parts of our
about the world around us. Body from our brain.
 Sensory (afferent) neurons transmit impulses from skin and other sensory organs or from
various places within the body to the CNS.
Different Types of Sensory Neurons
 Unipolar - Is a neuron in which only one process, called a neurite, extends from the cell
body. The neurite then branches to form dendritic and axonal processes.
 Bipolar - Is a type of neuron that has two extensions (one axon and one dendrite). They
are part of the sensory pathways for smell, sight, taste, hearing, touch, balance and
proprioception.
 Pseudounipolar - Is a type of neuron which has one extension from its cell body. This
type of neuron contains an axon that has split into two branches; one branch travels to the
peripheral nervous system and the other to the central nervous system.
 Multipolar - Is a type of neuron that possesses a single axon and many dendrites (and
dendritic branches), allowing for the integration of a great deal of information from
other neurons.
 Through sensory input (Afferent),
sensory and visceral neurons
form.
 These are
the neurons that monitor
stretching, temperature, chemical
changes and irritation. The
cerebral cortex in the brain
interprets these sensations as
things such as hunger, fullness,
pain, nausea, gas, cramping, etc.
 Visceral afferents transmit

conscious sensation and unconscious visceral sensation.
Ex: gut distention and cardiac ischemia, blood pressure and chemical composition
of the blood). Their most important function is to initiate autonomic reflexes at the local,
ganglion, spinal, and supra spinal levels.
 Sensory afferent are the nerve cells that are activated by sensory input from the
environment.
Ex: Touching a hot surface with your fingertips, the sensory neurons will be the ones
firing and sending off signals to the rest of the nervous system about the information they
have received.
)
Peripheral Nervous System consists of neurons associated with sensory input
(afferent) and motor output (efferent) and function to connect the central nervous system
to all other parts of the body.
 Nerves of the PNS are classified in three ways:
1. PNS nerves are classified by how they are connected to the CNS. Cranial nerves
originate from the terminate in the brain, while spinal nerves originate from or
`terminate at the spinal cord.
2. Nerves of the PNS are classified by the direction of the nerve propagation.
 Motor (efferent) neurons transmit impulses from the CNS to effector
(muscles or glands)
3. Third, motor neurons are further classified according to the effectors they target.
 The Somatic Nervous System (SNS) directs the contraction of skeletal muscles.
 The Autonomic Nervous System (ANS) controls the activities of organs, glands, and
various involuntary muscles, such as cardiac and smooth muscles.
The Autonomic Nervous System has two divisions:
 Sympathetic Nervous System is
involved in the stimulation of
activities that prepare the body for
action, such as increasing the heart
rate, increasing the release of
sugar from the liver into the blood,
and other activities generally
considered as fight or flight
responses.
 Parasympathetic Nervous
System activates tranquil
functions, such as stimulating the
secretion of saliva or digestive
enzymes into the stomach and
small intestine.
Generally, both Sympathetic and Parasympathetic systems target the same organs, but
often work antagonistically and each system is stimulated appropriately to maintain
homeostasis.
ROUTE OF SOUNDWAVES THROUGH EAR
Human ear, organ of hearing and equilibrium that detects and analyzes sound by
transduction or the conversion of sound waves into electrochemical impulses and maintains the
sense of equilibrium.
The human ear, like that of the other mammals, contains sense organs that serve two
quite different functions that of hearing and that of postural equilibrium and coordination of head
and eye movements.
Anatomically, the ear has three distinguishable parts: the outer, middle, and inner ear.
The outer ear consists of the visible portion called the auricle, or pinna which projects from the
side of the head, and the short external auditory canal, the inner end of which is closed by the
tympanic membrane, commonly called the eardrum. The function of the outer ear is to collect
sound waves and guide them to the tympanic membrane. The middle ear is narrow air-filled
cavity in the temporal bone. It is spanned by a chain of three tiny bones, the malleus (hammer),
incus (anvil), and stapes (stirrup), collectively called the auditory ossicles. This ossicular chain
conducts sounds from the tympanic membrane to the inner ear, which has been known since the
time of Galen (2nd century CE) as the labyrinth. It is complicated system of fluid-filled passages
and cavities located deep within the rock-hard petrous portion of the temporal bone. The inner
ear consists of two functional units: the vestibular apparatus, consisting of the vestibule and
semicircular canals, which contains the sensory organ of hearing. These sensory organs are
highly specialized endings of the eight cranial nerve, also called the vestibulocochlear nerve.

 The sound waves arrive at the pinna (auricle), the only visible part of the ear.
 Once the sound waves have passed the pinna, they move into the auditory canal (external
acoustic meatus) before hitting the tympanic membrane (eardrum)
 Once the sound waves reach the tympanic membrane, it begins to vibrate and they enter
into the middle ear
 The vibrations are transmitted further into the ear via three bones (ossicles): malleus
(hammer), incus (anvil), and the stapes (stirrup). These three bones form a bridge from
the tympanic membrane to the oval window.
 Once sound passes through the oval window, it enters into the cochlea in the inner ear.
 Hair cells in the organ of Corti (within the cochlea) are stimulated which in turn
stimulates the cochlear branch of the vestibulocochlear nerve.
 The cochlear nerve then transmits electrical impulses to the auditory region of the brain
in the temporal lobe.

Nerve Impulse
NERVE IMPULSE
 Nerve impulse is the way nerve cells (neurons) communicate with one another.
 Also known as action potential.
 Nerve impulses are mostly electrical signals along the dendrites to produce a nerve
impulse.
 The action potential is the result of ions moving in and out of the cell.
 Specifically, it involves potassium (K+) and sodium (Na+) ions.
 The ions are moved in and out of the cell by potassium channels, sodium channels and
the sodium-potassium pump.
1. Resting membrane is polarized. In the resting

state, the external face of the membrane is
slightly positive; its internal face is slightly
negative. The chief extracellular ion is sodium
(Na+), whereas the chief intracellular ion is
potassium (K+). The membrane is relatively
impermeable to both ions.
 The plasma membrane at rest is inactive (polarized)

 Fewer positive ions are inside the neuron’s plasma membrane than outside
 K+ is the major positive ion inside the cell
 Na+ is the major positive ion outside the cell
 As long as the inside of the membrane is more negative (fewer positive ions) than
the outside, the cell remains inactive.

2. Stimulus initiates local depolarization. A
stimulus changes the permeability of a local
“patch” of the membrane, and sodium ions
diffuse rapidly into the cell. This changes the
polarity of the membrane (the inside becomes
more positive; the outside becomes more
negative) at that site.
 A stimulus changes the permeability of the neuron’s membrane to sodium ions.

 Sodium channels now open, and sodium (Na+) diffuses into the neuron.
 The inward rush of sodium ions changes the polarity at that site and is called
depolarization.
3. Depolarization and generation of an action

potential. If the stimulus is strong enough,
depolarization causes membrane polarity to be
completely reversed, and an action potential is
initiated.
 A graded potential (localized depolarization) exists where the inside of the

membrane is more positive and the outside is less positive.
 If the stimulus is strong enough and sodium influx great enough, local
depolarization activates the neuron to conduct an action potential (nerve impulse).

4. Propagation of the action potential.
Depolarization of the first membrane patch
causes permeability changes in the adjacent
membrane, and the events described in step
2 are repeated. Thus, the action potential
propagates rapidly along the entire length of
the membrane.
 If enough sodium enters the cell, the action potential (nerve impulse) starts and is
propagated over the entire axon.
 All-or-none response means the nerve impulse either is propagated or is not.
 Fibers with myelin sheaths conduct nerve impulses more quickly.
5. Repolarization. Potassium ions diffuse out of

the cell as the membrane permeability changes
again, restoring the negative charge on the
inside of the membrane and the positive charge
on the outside surface. Repolarization occurs in
the same direction as depolarization.
 Membrane permeability changes again—becoming impermeable to sodium ions

and permeable to potassium ions.
 Potassium ions rapidly diffuse out of the neuron, repolarizing the membrane.
 Repolarization involves restoring the inside of the membrane to a negative charge

and the outer surface to a positive charge.
6. Initial ionic conditions restored. The

ionic conditions of the resting state are
restored later by the activity of the
sodium-potassium pump. Three sodium
ions are ejected for every two potassium
ions carried back into the cell.

 Initial conditions of sodium and potassium ions are restored using the sodium-
potassium pump.
 This pump, using ATP, restores the original configuration.
 Three sodium ions are ejected from the cell while two potassium ions are returned
to the cell.
 Until repolarization is complete, a neuron cannot conduct another nerve impulse.

Structure of Heart
➢ The heart has four valves, one for each chamber of the heart. The valves keep blood moving
through the heart in the right direction.
➢ These valves include the mitral valve, tricuspid valve, pulmonary valve and aortic valve.
Each valve has flaps (leaflets or cusps) that open and close once during each heartbeat.
How do the heart valves function?

• As the heart muscle contracts and relaxes, the valves open and shut, letting blood flow into
the ventricles and atria at alternate times. The following is a step-by-step illustration of
how the valves function normally in the left ventricle:
• After the left ventricle contracts, the aortic valve closes and the mitral valve opens, to allow
blood to flow from the left atrium into the left ventricle.
• As the left atrium contracts, more blood flows into the left ventricle.
• When the left ventricle contracts, the mitral valve closes and the aortic valve opens, so
blood flows into the aorta.

➢ To better understand your valve condition and what your health care provider will discuss, it helps
to know the role each heart valve plays in healthy blood circulation. Every part of the circulatory
system must work together to deliver blood, oxygen and nutrients to all tissues.
➢ Atrioventricular valves: The tricuspid valve and mitral (bicuspid) valve.
➢ The Semilunar valves are pocketlike structures attached at the point at which the
pulmonary artery and the aorta leave the ventricles.
● Tricuspid valve: located between the right atrium and the right ventricle.
▪ Has three leaflets or cusps.
▪ Separates the top right chamber (right atrium) from the bottom right chamber (right
ventricle).
▪ Opens to allow blood to flow from the right atrium to the right ventricle.
▪ Prevents the back flow of blood from the right ventricle to the right atrium.

● Pulmonary valve: located between the right ventricle and the pulmonary artery.
▪ Has three leaflets.
▪ Separates the right ventricle from the pulmonary artery.
▪ Opens to allow blood to be pumped from the right ventricle to the lungs (through
the pulmonary artery) where it will receive oxygen.
▪ Prevents the back flow of blood from the pulmonary artery to the right ventricle.
● Mitral valve: located between the left atrium and the left ventricle.
▪ Has two leaflets.
▪ Separates the top left chamber (left atrium) from the bottom left chamber (left
ventricle).
▪ Opens to allow blood to be pumped from the lungs to the left atrium.
▪ Prevents the back flow of blood from the left ventricle to the left atrium.
● Aortic valve: located between the left ventricle and the aorta.
▪ Has three leaflets, unless it's abnormal from birth, i.e., bicuspid aortic valve.
▪ Separates the left ventricle from the aorta.
▪ Opens to allow blood to leave the heart from the left ventricle through the aorta and
the body.
▪ Prevents the backflow of blood from the aorta to the left ventricle.

INTRINSIC CONDUCTION SYSTEM OF THE HEART
▪ Cardiac muscle contracts spontaneously and independently of nerve impulses
▪ Spontaneous contractions occur in a regular and continuous way
▪ Atrial cells beat 60 times per minute
▪ Ventricular cells beat 20−40 times per minute
▪ Need a unifying control system—the intrinsic conduction system (nodal system)
▪ Two systems regulate heart activity
▪ Autonomic nervous system
▪ Intrinsic conduction system, or the nodal system
➢ Sets the heart rhythm

➢ Composed of special nervous tissue
➢ Ensures heart muscle depolarization in one direction only (atria to ventricles)
➢ Enforces a heart rate of 75 beats per minute
▪ Components include:
▪ Sinoatrial (SA) node
▪ Located in the right atrium
▪ Serves as the heart’s pacemaker
▪ Atrioventricular (AV) node is at the junction of the atria and ventricles
▪ Atrioventricular (AV) bundle (bundle of His) and bundle branches are in the
interventricular septum
▪ Purkinje fibers spread within the ventricle wall muscles

▪ The sinoatrial node (SA node) starts each heartbeat
▪ Impulse spreads through the atria to the AV node
▪ Atria contract
▪ At the AV node, the impulse is delayed briefly
▪ Impulse travels through the AV bundle, bundle branches, and Purkinje fibers
▪ Ventricles contract; blood is ejected from the heart
▪ Tachycardia—rapid heart rate, over 100 beats per minute
▪ Bradycardia—slow heart rate, less than 60 beats per minutes

• Cardiac Cycle
• The cardiac cycle refers to one complete heartbeat, in which both atria and ventricles
contract and then relax
▪ Systole = contraction
▪ Diastole = relaxation
▪ Average heart rate is approximately 75 beats per minute
▪ Cardiac cycle length is normally 0.8 second
▪ A healthy human heart beats 72 times per minute which states that there are 72
cardiac cycles per minute.
• Cardiac Cycle Physiology

▪ The human heart consists of four chambers, comprising left and right halves.
▪ Two upper chambers include left and right atria; lower two chambers include right
and left ventricles.
▪ Right ventricle is to pump deoxygenated blood through the pulmonary arteries and
pulmonary trunk to the lungs.
▪ Left ventricle is responsible for pumping newly oxygenated blood to the body
through the aorta.

• Cardiac Cycle Phases
• Atrial diastole (ventricular filling)
o Heart is relaxed
o Pressure in heart is low
o Atrioventricular valves are open
o Blood flows passively into the atria and into ventricles
o Semilunar valves are closed
• Atrial systole
o Ventricles remain in diastole
o Atria contract
o Blood is forced into the ventricles to complete ventricular
filling.
• Isovolumetric Contraction:
o Ventricles begin to contract.
o The atrioventricular valves, valve, and pulmonary artery
valves close, but there won’t be any transformation in
volume.
• Ventricular Ejection:
o Here ventricles contract and emptying.
o Pulmonary artery and aortic valve close.
• Isovolumetric Relaxation:
o No blood enters the ventricles and consequently
o pressure decreases
o ventricles stop contracting and begin to relax
o Now due to the pressure in the aorta – pulmonary artery
and aortic valve close.

• Ventricular Filling Stage:
o In this stage, blood flows from atria into the ventricles.
o It is altogether known as one stage (first and second stage).
o After that, they are three phases that involve the flow of blood to the pulmonary
artery from ventricles.
• Duration of Cardiac Cycle

▪ In a normal person, a heartbeat is 72 beats/minute. So, the duration of one cardiac
cycle can be calculated as:
▪ 1/72 beats/minute=.0139 minutes/beat
▪ At a heartbeat 72 beats/minute, duration of each cardiac cycle will be 0.8 seconds.
• Duration of different stages of the cardiac cycle:
▪ Atrial systole: continues for about 0.1 seconds

▪ Ventricular systole: continues for about 0.3 seconds
▪ Atrial diastole: continues for about 0.7 seconds
▪ Ventricular diastole: continues for about 0.5 seconds
• Heart Sounds
▪ Heart murmurs: A sound made by backflow of

blood through either set of valve that cannot close
or open properly.
▪ Heart murmurs sound like a “whoosh” or “slosh”
▪ Lub: The first heart tone, or S1, caused by the
closure of the atrioventricular valves (mitral and
tricuspid) at the beginning of ventricular
contraction or systole.
▪ Dub: The second heart tone, or S2 (A2 and P2),
caused by the closure of the aortic valve and pulmonary valve at the end of
ventricular systole.

▪ The heart tone “lub,” or S1, is caused by the closure of the mitral and tricuspid
atrioventricular (AV) valves at the beginning of ventricular systole.
▪ The heart tone “dub,” or S2 ( a combination of A2 and P2), is caused by the closure
of the aortic valve and pulmonary valve at the end of ventricular systole.
▪ S3 and S4 are a “ta” sound that indicates ventricles that are either too weak or too
stiff to effectively pump blood.
▪ They can occur in normal persons or be associated with pathological processes.
▪ Because of their cadence or rhythmic timing S3 and S4 are called gallops.
▪ Gallops are low frequency sounds that are associated with diastolic filling.
▪ A common aid in distinguishing these sounds auditorily, is to remember that S3 has
the same cadence as the word "Kentucky" and S4 sounds like "Tennessee".

Circulatory Pathways
➢ The blood vessels of the body are functionally divided into two distinctive
circuits: pulmonary circuit and systemic circuit.
✓ The pump for the pulmonary circuit, which circulates blood through the lungs, is
the right ventricle.
✓ The left ventricle is the pump for the systemic circuit, which provides the blood
supply for the tissue cells of the body.
Pulmonary Circuit
▪ Pulmonary circulation transports oxygen-poor blood from the right ventricle to the lungs,
where blood picks up a new blood supply. Then it returns the oxygen-rich blood to the
left atrium.

Systemic Circuit
▪ The systemic circulation provides the functional blood supply to all body tissue.
▪ It carries oxygen and nutrients to the cells and picks up carbon dioxide and waste products.
▪ Systemic circulation carries oxygenated blood from the left ventricle, through the arteries,
to the capillaries in the tissues of the body. From the tissue capillaries, the deoxygenated
blood returns through a system of veins to the right atrium of the heart.
❖ The coronary arteries are the only vessels that branch from the ascending aorta.
❖ The brachiocephalic, left common carotid, and left subclavian arteries branch from
the aortic arch.
❖ Blood supply for the brain is provided by the internal carotid and vertebral arteries.
❖ The subclavian arteries provide the blood supply for the upper extremity.
❖ The celiac, superior mesenteric, suprarenal, renal, gonadal, and inferiormesenteric arteries
branch from the abdominal aorta to supply the abdominalviscera.
❖ Lumbar arteries provide blood for the muscles and spinal cord.
❖ Branches of the external iliac artery provide the blood supply for the lower extremity.
❖ The internal iliac artery supplies the pelvic viscera.

Major Systemic Arteries
▪ All systemic arteries are branches, either directly or indirectly, from the aorta. The aorta
ascends from the left ventricle, curves posteriorly and to the left, then descends through the
thorax and abdomen.
▪ This geography divides the aorta into three portions: ascending aorta, arotic arch,
and descending aorta. The descending aorta is further subdivided into the thoracic arota
and abdominal aorta.
Major Systemic Veins
▪ After blood delivers oxygen to the tissues and picks up carbon dioxide, it returns to the
heart through a system of veins. The capillaries, where the gaseous exchange occurs, merge
into venules and these converge to form larger and larger veins until the blood reaches
either the superior vena cava or inferior vena cava, which draininto the right atrium.
Fetal Circulation
▪ Most circulatory pathways in a fetus are like those in the adult but there are some notable
differences because the lungs, the gastrointestinal tract, and the kidneys are not functioning
before birth. The fetus obtains its oxygen and nutrients from the mother and also depends
on maternal circulation to carry away the carbon dioxide and waste products.
▪ The umbilical cord contains two umbilical arteries to carry fetal blood to the placentaand
one umbilical vein to carry oxygen-and-nutrient-rich blood from the placenta to the fetus.
The ductus venosus allows blood to bypass the immature liver in fetal circulation.
The foramen ovale and ductus arteriosus are modifications that permit blood to bypass the
lungs in fetal circulation.

Pulmonary Circulation and Systemic Circulation: The Routes and Function of Blood Flow
Circulatory system
The circulatory system consists of the heart and the arteries and veins that convey blood throughout
the body. Blood must always circulate to sustain life. It carries oxygen from the air we breathe to
cells throughout the body. The pumping of the heart drives this blood flow through the arteries,
capillaries, and veins. One set of blood vessels circulates blood through the lungs for gas exchange.
The other vessels fuel the rest of the body. Read on to learn more about these crucial circulatory
system functions.
1. There Are Two Types of Circulation: Pulmonary Circulation and Systemic Circulation
Pulmonary circulation moves blood between the heart and the lungs. It transports deoxygenated
blood to the lungs to absorb oxygen and release carbon dioxide. The oxygenated blood then flows
back to the heart. Systemic circulation moves blood between the heart and the rest of the body. It
sends oxygenated blood out to cells and returns deoxygenated blood to the heart.

2. The Heart Powers Both Types of Circulation
The heart pumps oxygenated blood out of the left ventricle and into the aorta to begin systemic
circulation. After the blood has supplied cells throughout the body with oxygen and nutrients, it
returns deoxygenated blood to the right atrium of the heart. The deoxygenated blood shoots down
from the right atrium to the right ventricle. The heart then pumps it out of the right ventricle and
into the pulmonary arteries to begin pulmonary circulation. The blood moves to the lungs,
exchanges carbon dioxide for oxygen, and returns to the left atrium. The oxygenated blood shoots
from the left atrium to the left ventricle below, to begin systemic circulation again.

3. The Circulatory System Works in Tandem with the Respiratory System
The circulatory and respiratory systems work together to sustain the body with oxygen and to
remove carbon dioxide. Pulmonary circulation facilitates the process of external respiration:
Deoxygenated blood flows into the lungs. It absorbs oxygen from tiny air sacs (the alveoli) and
releases carbon dioxide to be exhaled. Systemic circulation facilitates internal respiration:
Oxygenated blood flows into capillaries through the rest of the body. The blood diffuses oxygen
into cells and absorbs carbon dioxide.

4. The Pulmonary Loop Only Transports Blood Between the Heart and Lungs
In the pulmonary loop, deoxygenated blood exits the right ventricle of the heart and passes through
the pulmonary trunk. The pulmonary trunk splits into the right and left pulmonary arteries. These
arteries transport the deoxygenated blood to arterioles and capillary beds in the lungs. There,
carbon dioxide is released and oxygen is absorbed. Oxygenated blood then passes from the
capillary beds through venules into the pulmonary veins. The pulmonary veins transport it to the
left atrium of the heart. The pulmonary arteries are the only arteries that carry deoxygenated blood,
and the pulmonary veins are the only veins that carry oxygenated blood.

5. The Systemic Loop Goes All Over the Body
In the systemic loop, oxygenated blood is pumped from the left ventricle of the heart through the
aorta, the largest artery in the body. The blood moves from the aorta through the systemic arteries,
then to arterioles and capillary beds that supply body tissues. Here, oxygen and nutrients are
released and carbon dioxide and other waste substances are absorbed. Deoxygenated blood then
moves from the capillary beds through venules into the systemic veins. The systemic veins feed
into the inferior and superior venae cavae, the largest veins in the body. The venae cavae flow
deoxygenated blood to the right atrium of the heart.

Hepatic Portal System
Hepatic Portal System

 It is also called portal venous system.
 It is the venous system that returns blood from the digestive tract and spleen to the liver.
 It is a series of veins that carry blood from the capillaries of the stomach, intestine,
spleen, and pancreas to capillaries in the liver.
 The portal system begins in the capillaries and venules of the digestive system.
 It connects venous blood from the lower esophagus, stomach, duodenum, jejunum, ileum,
colon, spleen, and delivers it to portal vein.
 Not all gastrointestinal tracts are part of this system.
 Normal hepatic circulation is a high flow – low resistance system.
 Portal hypertension is a condition in which the blood pressure of the portal venous
system is too high
o It is often the result of cirrhosis of the liver.
Functions of the Hepatic Portal System

 Its main function is to deliver de – oxygenated blood to the liver to be detoxified before it
returns to the heart.
 To rid the body of toxins.
Four vessels that make up the Hepatic Portal System:

 Hepatic Portal Vein – this is the main vein located to the liver and it connects to
the capillaries.
 Inferior mesenteric vein – this vein takes blood from the colon and rectum and
connects with the portal vein.
 Superior mesenteric vein – this drain blood from small intestine and connects
with hepatic portal vein.
 Gastrosplenic vein – it is formed by the union of the splenic vein from the spleen
and the gastric vein from the stomach.
Why Hepatic Portal System is important?

 It transports one product of one region directly to another region.
 Between the two regions, if the heart were involved, those product will spread in the rest
of the body.

Gastrointestinal tract Processes and Controls
The Essential processes of the GI tract

There are 6 essential processes of GI tract;
1. Ingestion—placing of food into the mouth
2. Propulsion—movement of foods from one region of the digestive system to another

▪ Peristalsis—alternating waves of contraction and relaxation that squeeze food along
the GI tract.
▪ Segmentation—movement of materials back and forth to foster mixing in the small
Intestine.
3. Food breakdown: mechanical breakdown

Example of mechanical breakdown:
 Mixing of food in the mouth by the tongue
 Churning of food in the stomach
 Segmentation in the small intestine

 Mechanical digestion prepares food for further degradation by enzymes
4. Food breakdown: Digestion
 Digestion occurs when enzymes chemically break down large molecules into their
building blocks
▪ Each major food group uses different enzymes
 Carbohydrates are broken down to monosaccharides (simple sugars)
 Proteins are broken down to amino acids
 Fats are broken down to fatty acids and glycerol
5. Absorption
 End products of digestion are absorbed in the blood or lymph
 Food must enter mucosal cells and then move into blood or lymph capillaries
6. Defecation
 Elimination of indigestible substances from the GI tract in the form of feces

SWALLOWING
Swallowing
Sometimes called deglutition in scientific contexts, is the process in the human or animal
body that allows for a substance to pass from the mouth, to the pharynx, and into the esophagus,
while shutting the epiglottis.
 Swallowing
 It is the process by which food is transported from the mouth to the stomach.
 It is an important part of eating and drinking. If the process fails and the
material (such as food, drink, or medicine) goes through the trachea, then
choking or pulmonary aspiration can occur. In the human body the automatic
temporary closing of the epiglottis is controlled by the swallowing reflex.
 The portion of food, drink, or other material that will move through the neck in one
swallow is called a bolus.
To Understand Swallowing,

Recall that the digestive system is made up of organs that can be classified into two groups, the
alimentary canal (or gastrointestinal tract), and accessory digestive organs. All of these organs
have a particular function, and work together to process food.
There are Three (3) Phases;

 Each phase is controlled by a different neurological mechanism.
1. The Oral Phase - It is a voluntary process. It is also commonly known as the buccal
phase. It involves the contraction of the tongue to push the bolus up against the soft
palate and then posteriorly into the oropharynx by both the tongue and the soft palate.
2. The Pharyngeal Phase - It is a involuntary process. It is under autonomic control of the

swallowing center located in the lower pons and medulla oblongata of the brainstem.
More specifically, the nucleus ambiguus in the reticular formation is part of the
swallowing center, and it is responsible for generating general somatic efferent signals.
3. The Esophageal Phase - This process is involuntary. The food bolus is forced inferiorly
from the pharynx into the esophagus after the sequential contraction of the three
pharyngeal constrictor muscles (the superior, middle and inferior constrictor muscles),
which together make up the external circular layer of the pharynx.

Peristaltic Waves in Stomach
 A mixing wave initiated in the body of the stomach progresses toward the
pyloric sphincter.
 The more fluid part of the chyme is pushed toward the pyloric sphincter
(blue arrows) whereas the more solid center of the chyme squeezes past the
peristaltic constriction back towards the body of the stomach. (Pink arrows).
 Peristaltic waves move in the same way as the mixing waves but are
stronger.

 Again, the more fluid part of the chyme is pushed toward the pyloric region
(blue arrows) whereas the more solid center of chyme squeezes past the
peristaltic constriction back toward the body of the stomach. (Pink arrows)
 Peristaltic contractions force a few milliliters of the most fluid chyme

through the pyloric opening into the duodenum (small blue arrows). Most of
the chyme, including the more solid portion, is forced back toward the body
of the stomach for further mixing. (pink arrows)

Pathway of Renal Blood Vessels
⚫ The artery supplying each kidney is the renal artery.

⚫ As the renal artery approaches the hilum, it divides into segmental arteries, each of which
gives off several branches called interlobar arteries, which travel through the renal columns
to reach the cortex.
⚫ At the cortex-medulla junction, interlobar arteries give off the arcuate (ar′ku-at) arteries,
which arch over the medullary pyramids.
⚫ Small cortical radiate arteries then branch off the arcuate arteries to supply the renal cortex.
⚫ Venous blood draining from the kidney flows through veins that trace the pathway of the
arterial supply but in a reverse direction—cortical radiate veins to arcuate veins to
interlobar veins to the renal vein, which emerges from the kidney hilum and empties into
the inferior vena cava. (There are no segmental veins.)

The 3 Major Renal Processes in urine formation
• Glomerular filtration. Water and solutes smaller than proteins are forced through the
capillary walls and pores of the glomerular capsule into the renal tubule.
• The glomerulus acts as a filter. The filtrate that is formed is essentially blood plasma
without blood proteins. Both proteins and blood cells are normally too large to pass through
the filtration membrane, and when either of these appear I the urine, there is some problem
with the glomerular filters.
• As long as the systemic blood pressure is normal, filtrate will be formed.
• If the arterial blood pressure drops too low, the glomerular pressure becomes inadequate
to force substances out of the blood into the tubules, and filtrate formation stops.
• Tubular reabsorption. Water, glucose, amino acids, and needed ions are transported out
of the filtrate into the tubule cells and then enter the capillary blood.
• Tubular secretion. Hydrogen, potassium, creatinine, and drugs are removed from the
peritubular blood and secreted by the tubule cells into the filtrate.

Ribcage and Diaphragm Position during Breathing (Inspiration/Expiration)
• At the end of normal inspiration: Chest is expanded laterally, rib cage is elevated, and
diaphragm is depressed and flattened. Lungs are stretched to the larger thoracic volume
causing the interpulmonary pressure to fall and air to flow into the lungs.
• At the end of normal expiration: Chest is depressed and the lateral dimension is reduced, rib
cage is descended, and diaphragm is elevated and dome-shaped. Lungs recoil to smaller
volume, intrapulmonary pressure rises and air flows out of the lungs.

External and Internal Respiration
EXTERNAL RESPIRATION
• The exchange of gases between the
alveoli and the blood (pulmonary gas exchange)
• Oxygen is loaded into the blood
o oxygen diffuses from the air of
o the alveoli into the more oxygen-poor blood of the pulmonary capillaries
• Carbon dioxide is unloaded out of the blood
o Carbon dioxide diffuses from the blood of the pulmonary capillaries into the alveoli
and flushed out of the lungs during expiration.

• Relatively speaking, blood draining from the lungs into the pulmonary veins is rich in
oxygen and poor in carbon dioxide.
INTERNAL RESPIRATION
• The exchange of gases between the blood and the tissue cells.
• The opposite of what occurs in the lungs.
• In this process, oxygen leaves and carbon dioxide enter the blood.
• The partial pressure of carbon dioxide is lower in the blood than it is in the tissue, causing
carbon dioxide to diffuse out of the tissue, cross the interstitial fluid, and enter the blood
(called loading).
• The partial pressure of oxygen in the blood is about 100 mm Hg, creating a pressure
gradient that causes oxygen to diffuse out of the blood, cross the interstitial space, and
enter the tissue (called unloading) .

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lyandar
e
coor
dinat
edov
era22–32daycy
cle,
wit
hanav
eragel
engt
hof28day
s.
• Thef
ir
sthal
foft
heov
ari
ancy
clei
sthef
oll
i
cul
arphaseshowni
nFi
gur
e1.
Bat
angasSt
ateUni
ver
sit
yARASOF-
Nasugbu–CONAHSQui
ckNot
es
• Sl
owl
yri
singl
evel
sofFSHandLHcauset
hegr
owt
hoff
oll
i
clesont
he
sur
faceoft
heov
ary
.Thi
spr
ocesspr
epar
est
heeggf
orov
ulat
ion.Ast
he
f
oll
i
clesgr
ow,
theybegi
nrel
easi
ngest
rogensandal
owl
evel
of
pr
ogest
erone.
Fi
gur
e2.Thi
smat
ureeggf
oll
i
clemayr
upt
ureandr
eleaseanegg.(
credi
t:scal
e-bardat
a
f
rom Mat
tRussel
l
)
• Pr
ogest
eronemai
ntai
nst
heendomet
ri
um t
ohel
pensur
epr
egnancy
.The
t
ri
pthr
ought
hef
all
opi
ant
ubet
akesaboutsev
enday
s.Att
hisst
ageof
dev
elopment
,cal
l
edt
hemor
ula,
ther
ear
e30-
60cel
l
s.
• I
fpr
egnancyi
mpl
ant
ati
ondoesnotoccur
,thel
i
ningi
ssl
oughedof
f.Af
ter
aboutf
iveday
s,est
rogenl
evel
sri
seandt
hemenst
rual
cycl
eent
erst
he
pr
oli
fer
ati
vephase.
• Theendomet
ri
um begi
nst
ore-gr
ow,
repl
aci
ngt
hebl
oodv
essel
sand
Bat
angasSt
ateUni
ver
sit
yARASOF-
Nasugbu–CONAHSQui
ckNot
es
gl
andst
hatdet
eri
orat
eddur
ingt
heendoft
hel
astcy
cle.
• Justpr
iort
othemi
ddl
eoft
hecy
cle(
appr
oxi
mat
elyday14)
,thehi
ghl
evel
ofest
rogencausesFSHandespeci
all
yLHt
ori
ser
api
dly
,thenf
all
.The
spi
kei
nLHcausesov
ulat
ion:
themostmat
uref
oll
i
cle,
li
ket
hatshowni
n
Fi
gur
e2,
rupt
uresandr
eleasesi
tsegg.Thef
oll
i
clest
hatdi
dnotr
upt
ure
degener
ateandt
hei
reggsar
elost
.Thel
evel
ofest
rogendecr
easeswhen
t
heext
raf
oll
i
clesdegener
ate.
• Fol
l
owi
ngov
ulat
ion,
theov
ari
ancy
cleent
ersi
tsl
uteal
phase,
il
lust
rat
edi
n
Fi
gur
e1andt
hemenst
rual
cycl
eent
ersi
tssecr
etor
yphase,
bot
hofwhi
ch
r
unf
rom aboutday15t
o28.
• Thel
uteal
andsecr
etor
yphasesr
efert
ochangesi
nther
upt
uredf
oll
i
cle.
Thecel
l
sint
hef
oll
i
cleunder
gophy
sical
changesandpr
oduceast
ruct
ure
cal
l
edacor
pusl
uteum.
• Thecor
pusl
uteum pr
oducesest
rogenandpr
ogest
erone.The
pr
ogest
eronef
aci
l
itat
est
her
egr
owt
hoft
heut
eri
nel
i
ningandi
nhi
bit
sthe
r
eleaseoff
urt
herFSHandLH.
• Theut
erusi
sbei
ngpr
epar
edt
oacceptaf
ert
il
izedegg,
shoul
ditoccur
dur
ingt
hiscy
cle.Thei
nhi
bit
ionofFSHandLHpr
event
sanyf
urt
hereggs
andf
oll
i
clesf
rom dev
elopi
ng,
whi
l
ethepr
ogest
eronei
sel
evat
ed.
• Thel
evel
ofest
rogenpr
oducedbyt
hecor
pusl
uteum i
ncr
easest
oa
st
eadyl
evel
fort
henextf
ewday
s.
Bat
angasSt
ateUni
ver
sit
yARASOF-
Nasugbu–CONAHSQui
ckNot
es
• I
fnof
ert
il
iz
edeggi
simpl
ant
edi
ntot
heut
erus,
thecor
pusl
uteum
degener
atesandt
hel
evel
sofest
rogenandpr
ogest
eronedecr
ease.
• Theendomet
ri
um begi
nst
odegener
ateast
hepr
ogest
eronel
evel
sdr
op,
i
nit
iat
ingt
henextmenst
rual
cycl
e.Thedecr
easei
npr
ogest
eroneal
so
al
l
owst
hehy
pot
hal
amust
osendGnRHt
otheant
eri
orpi
tui
tar
y,r
eleasi
ng
FSHandLHandst
art
ingt
hecy
clesagai
n.
• Fi
gur
e3v
isual
l
ycompar
est
heov
ari
anandut
eri
necy
clesast
he
commensur
atehor
monel
evel
s.
Fi
gur
e3.Ri
singandf
all
i
nghor
monel
evel
sresul
tinpr
ogr
essi
onoft
heov
ari
anand
menst
rual
cycl
es.
(
credi
t:modi
fi
cat
ionofwor
kbyMi
kael
Häggst
röm)
Bat
angasSt
ateUni
ver
sit
yARASOF-
Nasugbu–CONAHSQui
ckNot
es
OLOGY
● Embr
yoni
cDev
elopment
● Theembr
yoi
sanear
lydev
elopment
alst
ageofani
mal
s.I
nhumanst
heembr
yo
begi
nst
odev
elopaboutf
ourday
saf
teraneggi
sfer
ti
li
zed.Appear
ingi
nit
ial
l
yas
at
inymassofcel
l
s,i
tev
ent
ual
l
ygi
vesr
iset
othef
etus,
anobv
ioushumanf
orm.
● Embr
yodev
elopmenti
sal
soknownas“
embr
yogenesi
s,
”whi
chi
sthepr
ocess
t
hatoccur
saf
terf
ert
il
izat
ion.
 Fer
ti
li
zat
ioni
sthesper
m cel
lcomi
ngt
oget
herwi
tht
hiseggcel
l
andt
hisact
,thi
sist
heconcept
ionofwhathast
hepot
ent
ialt
otur
n
i
ntoar
eal
organi
sm,
int
hiscase,
ahumanbei
ng.
Bat
angasSt
ateUni
ver
sit
yARASOF-
Nasugbu–CONAHSQui
ckNot
es
 Fer
ti
li
zat
ioni
sacompl
exmul
ti
-st
eppr
ocesst
hati
scompl
etei
n24
hour
s.
 Thesper
mfr
om amal
emeet
sanov
um f
rom af
emal
eandf
ormsa
zy
got
e
● Thef
ert
il
izedeggcel
lwi
l
ldi
vi
det
ofor
mthe“
mor
ula,
”abal
l
-l
ikest
ruct
urewi
th16
cel
l
s.I
tthendi
vi
desi
ntowhati
scal
l
eda“
blast
ula.
”
SI
GNI
FICANCEOF
FERTI
LIZATI
ON:
● St
imul
atest
hesecondar
yoocy
tet
ocompl
etei
tsmat
urat
iont
ofor
m hapl
oid
ov
um.
● Rest
orest
hedi
ploi
dnumberofchr
omosomesi
nthezy
got
e.
● Act
ivat
est
heeggt
odev
elopi
ntoanewi
ndi
vi
dual
byr
epeat
edmi
tot
icdi
vi
sions.
● Eggbecomesmet
abol
i
cal
l
ymor
eact
ive.
● Combi
nes char
act
ers oft
wo par
ent
s.Thi
s causes v
ari
ati
ons and hel
ps i
n
ev
olut
ion.
● Cl
eav
age,i
n embr
yol
ogy
,thef
ir
stf
ew cel
l
ulardi
vi
sionsofa
zygot
e (
fer
ti
li
zed
egg)
.
o I
nit
ial
l
y,t
hezy
got
espl
i
tsal
ongal
ongi
tudi
nal
plane.
o Theseconddi
vi
sioni
sal
sol
ongi
tudi
nal
,butat90degr
eest
othepl
aneof
t
hef
ir
st.
o Thet
hir
ddi
vi
sioni
sper
pendi
cul
art
othef
ir
stt
woandi
sequat
ori
ali
n
posi
ti
on.

 Pr ogr
essingthr
ough2- cell
,4-
cell
,8-
cel
land16cel lstages.
 Af ourcellembryoisshownher e.Thecell
sincleavagestageembry
osare
knownas blast
omer es.
Notethattheblastomeresinthisembryo,andtheeight-
cellembryobel
ow,ar
e
di
sti
nct l
yround
● Af
tert
hef
ormat
ionoft
hebl
ast
ula,“
dif
fer
ent
iat
ion”occur
s.Di
ff
erent
iat
ioni
sthe
pr
ocesswher
einonecel
lget
sdi
ff
erent
iat
edf
rom t
heot
hercel
l
s,whi
chgi
vesus
Bat
angasSt
ateUni
ver
sit
yARASOF-
Nasugbu–CONAHSQui
ckNot
es
av
ari
etyofcel
l
s.
● Thecel
lmassdi
ff
erent
iat
edcel
l
swi
l
lthenr
equi
renut
ri
ti
on.So,i
mpl
ant
ati
on
occur
s.Thi
siswher
ethebl
ast
ocy
stconnect
sit
sel
fint
heut
erust
ogetpr
oper
nut
ri
ti
onf
rom t
hemot
her
’sbody
.
Bl
ast
ocy
st.–chr
oni
cl
evesi
cle
 I
nnercel
lmass-whi
chi
sfat
edt
obecomet
heembr
yo.
Lay
ersofcel
l
s
 Fi
rstl
ayeri
sthe
endoder
m,a sheetofcel
l
sthat
di
spl
acest
hehy
pobl
astandl
i
esadj
acentt
othey
olk
sac.
 Thesecondl
ayerofcel
l
sfi
l
lsi
nast
hemi
ddl
elay
er,
or
mesoder
m.
 The cel
l
s oft
he epi
blastt
hatr
emai
n(nothav
ing
mi
grat
ed t
hrough t
he pr
imi
ti
ve st
reak) become
t
he
ect
oder
m
 Tr
ophobl
ast
s-(
trophe=“
tof
eed”or“
tonour
ish”
)Thecel
l
sthatf
ormt
he
out
ershel
l
.
Thesecel
l
swi
l
ldev
elopi
ntot
hechor
ioni
csacandt
hef
etal
por
ti
onof
t
he
placent
a (
theor
ganofnut
ri
ent
,wast
e,andgasexchangebet
weenmot
herandt
he
dev
elopi
ngof
fspr
ing)
.
 Ast
hebl
ast
ocy
stf
orms,
thet
rophobl
astexcr
etesenzy
mest
hatbegi
ntodegr
ade
t
hezonapel
l
uci
da.I
napr
ocesscal
l
ed“
hat
chi
ng,
”theconcept
usbr
eaksf
reeof
t
hezonapel
l
uci
dai
npr
epar
ati
onf
ori
mpl
ant
ati
on.
 The bl
ast
ocy
stcomes i
n cont
actwi
tht
he ut
eri
ne wal
land adher
es t
oit
,
embeddi
ngi
tsel
fint
heut
eri
nel
i
ningv
iat
het
rophobl
astcel
l
s.Thusbegi
nst
he
pr
ocessof
i
mpl
ant
ati
on,whi
chsi
gnal
stheendoft
hepr
e-embr
yoni
cst
ageof
dev
elopment
I
mpl
ant
ati
on
Canbeaccompani
edbymi
norbl
eedi
ng.Thebl
ast
ocy
stt
ypi
cal
l
yimpl
ant
sint
he
f
undusoft
heut
erusoront
hepost
eri
orwal
l
.
 Thi
stakespl
aceabout5t
o7day
saf
terov
ulat
ion.
Bat
angasSt
ateUni
ver
sit
yARASOF-
Nasugbu–CONAHSQui
ckNot
es
Dev
elopmentoft
hePl
acent
a
 Dur
ingt
hef
ir
stsev
eralweeksofdev
elopment
,thecel
l
soft
heendomet
ri
um
r
efer
redt
oasdeci
dual
cel
l
snour
isht
henascentembr
yo.
 Dur
ingpr
enat
alweeks4–12,t
hedev
elopi
ngpl
acent
agr
adual
l
ytakesov
ert
he
r
oleoff
eedi
ngt
heembr
yo,
andt
hedeci
dual
cel
l
sar
enol
ongerneeded.
 Themat
urepl
acent
aiscomposedoft
issuesder
ivedf
rom t
heembr
yo,
aswel
las
mat
ernal
tissuesoft
heendomet
ri
um.
Pl
acent
aconnect
stot
heconcept
usv
iat
he
umbi
l
ical
cor
d,whi
chcar
ri
es
o deoxy
genat
edbl
ood
o wast
esf
rom t
hef
etust
hrought
woumbi
l
ical
art
eri
es
o nut
ri
ent
s
o oxy
genar
ecar
ri
edf
rom t
hemot
hert
othef
etust
hrought
he
si
ngl
eumbi
l
ical
vei
n.
 Pl
acent
adev
elopst
hroughoutt
heembr
yoni
cper
iodanddur
ingt
hef
ir
stsev
eral
weeksoft
hef
etal
per
iod.
 Pl
acent
ati
on
i
s compl
ete byweeks 14–16.As a f
ull
ydev
eloped or
gan,t
he
pl
acent
apr
ovi
desnut
ri
ti
onandexcr
eti
on,
respi
rat
ion,
andendocr
inef
unct
ion.
Bat
angasSt
ateUni
ver
sit
yARASOF-
Nasugbu–CONAHSQui
ckNot
es
SYNOPSI
S
Ast
hezy
got
etr
avel
stowar
dtheut
erus,i
tunder
goesnumer
ouscl
eav
agesi
nwhi
ch
t
henumberofcel
l
sdoubl
es(
blast
omer
es)
.Uponr
eachi
ngt
heut
erus,t
heconcept
ushas
become a t
ight
lypacked spher
e ofcel
l
s cal
l
ed t
he mor
ula,whi
ch t
hen f
orms i
ntoa
bl
ast
ocy
stconsi
sti
ng ofan i
nnercel
lmass wi
thi
naf
lui
d-f
il
led cav
itysur
rounded by
t
rophobl
ast
s.Thebl
ast
ocy
sti
mpl
ant
sint
heut
eri
newal
l
,thet
rophobl
ast
sfuset
ofor
ma
sy
ncy
tiot
rophobl
ast
,andt
heconcept
usi
senv
elopedbyt
heendomet
ri
um.Fourembr
yoni
c
membr
anesf
ormt
osuppor
tthegr
owi
ngembr
yo:t
heamni
on,
they
olksac,
theal
l
ant
ois,
and
t
hechor
ion.Thechor
ioni
cvi
l
lioft
hechor
ionext
endi
ntot
heendomet
ri
um t
ofor
mthef
etal
por
ti
on oft
he pl
acent
a.The pl
acent
a suppl
i
es t
he gr
owi
ng embr
yo wi
th oxy
gen and
nut
ri
ent
s;i
tal
sor
emov
escar
bondi
oxi
deandot
hermet
abol
i
cwast
es.
Fol
l
owi
ng i
mpl
ant
ati
on,embr
yoni
c cel
l
s under
go gast
rul
ati
on,i
n whi
ch t
hey
di
ff
erent
iat
eandsepar
atei
ntoanembr
yoni
cdi
scandest
abl
i
sht
hreepr
imar
yger
mlay
ers
(
theendoder
m,mesoder
m,andect
oder
m).Thr
ought
hepr
ocessofembr
yoni
cfol
ding,t
he
f
etusbegi
nst
otakeshape.Neur
ulat
ionst
art
sthepr
ocessoft
hedev
elopmentofst
ruct
ures
oft
hecent
ralner
voussy
stem andor
ganogenesi
sest
abl
i
shest
hebasi
cpl
anf
oral
lor
gan
sy
stems.
OLOGY
Bat
angasSt
ateUni
ver
sit
yARASOF-
Nasugbu–CONAHSQui
ckNot
es
St
agesofLabor
● Laborbegi
nswi
thut
eri
necont
ract
ionswhenf
etusi
sin“
ful
lter
m,”whi
chi
swhen
t
hef
etusi
sini
ts37-
42weeksofgest
ati
on.
● Laborcanbebr
okendowni
nto3st
ages.
o 1stSt
age:
▪ Di
vi
dedi
nto2phases:
● Ear
lyorLat
entPhase
o Last
sunt
ilcer
vixdi
l
atesi
nto6cm.
o I
tbegi
ns wi
th 30s i
rr
egul
arcont
ract
ions ev
ery 5-
30mi
ns.Then,r
egul
arcont
ract
ions occurev
ery3-
Bat
angasSt
ateUni
ver
sit
yARASOF-
Nasugbu–CONAHSQui
ckNot
es
5mi
nswi
theachcont
ract
ionl
ast
ingf
orami
nut
eor
mor
e.
● Act
ivePhase
o Cer
vixdi
l
atesf
rom 6-
10cm.
o I
ntense60-
90scont
ract
ionsoccurev
ery0.
5-2m r
est
i
nbet
ween.
o Amni
oti
csacr
upt
uresher
eifi
thasn’
tal
ready
.
nd
o 2 St
age:
Pushi
ngSt
age
▪ Occur
saf
tert
hecer
vixi
scompl
etel
ydi
l
ated.
▪ St
rongandf
orcef
ulcont
ract
ionsoccurur
gingt
hewomani
nlabor
t
o“push.
”
▪ Theur
get
opushmaynotbeasov
erwhel
mingwhent
hewoman
hashadanepi
dur
al.
▪ Lengt
hoft
hisst
agei
sdependentonhow manyt
imest
heonei
n
l
aborhasgi
venbi
rt
handt
heposi
ti
onandsi
zeoft
hebaby
.
▪ Womenar
eir
ri
tabl
edur
ingt
hisst
age.
o 3rdSt
age:
▪ Ut
eruscont
ract
s
▪ Pl
acent
asepar
atesf
rom t
heut
eri
newal
landcar
eful
l
yremov
ed
Bat
angasSt
ateUni
ver
sit
yARASOF-
Nasugbu–CONAHSQui
ckNot
es
OLOGY
Ci
rcl
eofWi
l
li
s
 TheCi
rcl
eofWi
l
li
sisaci
rcul
ator
yanast
omosi
sthatsuppl
i
esbl
oodt
othebr
ain
andsur
roundi
ngst
ruct
uresi
nrept
il
es,
bir
dsandmammal
s,i
ncl
udi
nghumans.
 The ci
rcl
e ofWi
l
li
s(cer
ebr
alar
ter
ialci
rcl
e orci
rcul
us ar
ter
iosus)i
s an
anast
omot
icr
ingofar
ter
iesl
ocat
edatt
hebaseoft
hebr
ain.
 Thi
sar
ter
ialanast
omot
icci
rcl
econnect
sthet
womaj
orar
ter
ialsy
stemst
othe
br
ain,t
hei
nter
nalcar
oti
dar
ter
iesandt
hev
ert
ebr
obasi
l
ar(
ver
tebr
alandbasi
l
ar
ar
ter
ies)sy
stems.
 I
tisf
ormedbyf
ourpai
redv
essel
sandasi
ngl
eunpai
redv
esselwi
thnumer
ous
br
anchest
hatsuppl
ythebr
ain.
 Theci
rcl
eofWi
l
li
sisani
mpor
tantj
unct
ionofar
ter
iesatt
hebaseoft
hebr
ain.
Thest
ruct
ureenci
rcl
est
hemi
ddl
ear
eaoft
hebr
ain,i
ncl
udi
ngt
hest
alkoft
he
pi
tui
tar
ygl
andandot
heri
mpor
tantst
ruct
ures.
Bat
angasSt
ateUni
ver
sit
yARASOF-
Nasugbu–CONAHSQui
ckNot
es
 Twoar
ter
ies,
cal
l
edt
hecar
oti
dar
ter
ies,
suppl
ybl
oodt
othebr
ain.Theyr
unal
ong
ei
thersi
deoft
heneckandl
eaddi
rect
lyt
otheci
rcl
eofWi
l
li
s.
 Eachcar
oti
dar
ter
ybr
anchesi
ntoani
nter
nalandext
ernalcar
oti
dar
ter
y.The
i
nter
nalcar
oti
dar
ter
ythenbr
anchesi
ntot
hecer
ebr
alar
ter
ies.Thi
sst
ruct
ure
al
l
owsal
loft
hebl
oodf
rom t
het
woi
nter
nalcar
oti
dar
ter
iest
opasst
hrought
he
ci
rcl
eofWi
l
li
s.
 Theci
rcl
eofWi
l
li
siscr
it
ical
,asi
tist
hemeet
ingpoi
ntofmanyi
mpor
tantar
ter
ies
suppl
yi
ngbl
oodt
othebr
ain.Thei
nter
nalcar
oti
dar
ter
iesbr
anchof
ffr
om her
e
i
ntosmal
l
erar
ter
ies,
whi
chdel
i
vermuchoft
hebr
ain’
sbl
oodsuppl
y.
 Theci
rcl
eofWi
l
li
spl
aysani
mpor
tantr
ole,
asi
tal
l
owsf
orpr
operbl
oodf
lowf
rom
t
hear
ter
iest
obot
hthef
rontandbackhemi
spher
esoft
hebr
ain.Thear
ter
iest
hat
st
em of
ffr
om t
heci
rcl
eofWi
l
li
ssuppl
ymuchoft
hebl
oodt
othebr
ain.
 Theci
rcl
eofWi
l
li
sal
soser
vesasasor
tofsaf
etymechani
sm wheni
tcomest
o
bl
oodf
low.I
fabl
ockageornar
rowi
ngsl
owsorpr
event
sthebl
oodf
low i
na
connect
edar
ter
y,t
hechangei
npr
essur
ecancausebl
oodt
ofl
ow f
orwar
dor
backwar
dint
heci
rcl
eofWi
l
li
stocompensat
e.
 Thi
smechani
sm coul
dal
sohel
pbl
oodf
low f
rom onesi
deoft
hebr
aint
othe
ot
heri
nasi
tuat
ioni
nwhi
cht
hear
ter
iesononesi
dehav
ereducedbl
oodf
low.I
n
anemer
gency
,suchasast
roke,t
hismayr
educet
hedamageoraf
ter
eff
ect
sof
t
heev
ent
.
 I
mpor
tant
ly,t
heci
rcl
eofWi
l
li
sdoesnotact
ivel
ycar
ryoutt
hef
unct
ion.I
nst
ead,
t
henat
uralshapeoft
heci
rcl
eandt
hewayt
hatpr
essur
eact
sint
hear
easi
mpl
y
al
l
owf
orbi
dir
ect
ional
bloodf
lowwhennecessar
y.
 Thest
ruct
ureandf
unct
ionoft
heci
rcl
eofWi
l
li
smaypr
otectagai
nstst
rokei
n
peopl
ewhohav
eacompl
eteci
rcl
eofWi
l
li
s.Thecompl
eteci
rcl
eal
l
owsbl
oodt
o
gof
rom onesi
deoft
hebr
aint
otheot
her
,ev
enwhenbl
ockagesort
hinni
ng
v
essel
soccur
.
 Theant
eri
orci
rcul
ati
onoft
hebr
ainder
ivesf
rom t
hebi
l
ater
alI
CAs,br
anchesof
t
hecommoncar
oti
dar
ter
ies(
CCA)
.Thepost
eri
orci
rcul
ati
onder
ivesf
rom t
he
bi
l
ater
alVAs,
branchesoft
hesubcl
avi
anar
ter
ies.
 Ther
eisnoev
idencet
odat
esuppor
ti
ngt
heexi
stenceofconv
ent
ionall
ymphat
ic
Bat
angasSt
ateUni
ver
sit
yARASOF-
Nasugbu–CONAHSQui
ckNot
es
v
essel
swi
thi
nthecent
ral
ner
voussy
stem (
CNS)
.
 Recentr
esear
ch,howev
er,hasdescr
ibedf
unct
ionall
ymphat
icv
essel
sint
he
dur
alsi
nusesoft
heCNSandaper
ivascul
arnet
wor
kofgl
i
alcel
l
s(t
hegl
ymphat
ic
net
wor
k)t
hatact
stoel
i
minat
ewast
eanddi
str
ibut
emol
ecul
est
hroughoutt
he
br
ain.
 Theci
rcl
eofWi
l
li
sli
esatt
hebaseoft
hebr
ain,
nearsev
eral
crani
alner
ves.
 Theopt
icchi
asm l
i
esi
ntheant
eri
orpor
ti
onoft
heci
rcl
e,bet
weent
heI
CA-
MCA
j
unct
ionandt
hebi
l
ater
alACAs.
 Theocul
omot
or(
CN3)andt
rochl
ear(
CN4)ner
vesbot
hfl
ow post
eri
orl
ytot
he
PCA.
 Acompl
eteCi
rcl
eofWi
l
li
sispr
esenti
nami
nor
it
yoft
hepopul
ati
on,wi
thmany
phy
siol
ogi
cvar
iant
scont
aini
ngdupl
i
cat
ed,f
enest
rat
ed,hy
popl
ast
ic,orabsent
v
essel
sincer
tai
nregi
onsoft
her
ing.

Fenest
rat
ionsoccurwhenasi
ngl
evessel
’
slumendi
vi
desi
ntot
wochannel
sthat
l
aterf
usebackt
oget
her
.
 Dupl
i
cat
ionoccur
swhent
woar
ter
ieswi
thdi
sti
nctor
igi
nsf
usei
ntoasi
ngl
e,
downst
ream segment
.
 Fenest
rat
ionsanddupl
i
cat
ionsar
emor
ecommoni
ntheant
eri
orci
rcul
ati
on;t
he
mostcommonl
yinv
olv
edar
ter
yist
heACom.
 Hy
popl
ast
icar
ter
iesar
ethemostcommonanomal
i
esseeni
ntheCoW,most
f
requent
lyaf
fect
ingt
hePCom orACom.
Bat
angasSt
ateUni
ver
sit
yARASOF-
Nasugbu–CONAHSQui
ckNot
es

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Quick Notes

Kareen C. Aclan, PTRP

Batangas State University ARASOF-Nasugbu – CONAHS Quick Notes

Stages of Long Bone Formation in an Embryo, Fetus and Young Child

Batangas State University ARASOF-Nasugbu – CONAHS Quick Notes

BONE CELLS AND MATRIX

Batangas State University ARASOF-Nasugbu – CONAHS Quick Notes

Batangas State University ARASOF-Nasugbu – CONAHS Quick Notes

Batangas State University ARASOF-Nasugbu – CONAHS Quick Notes

Batangas State University ARASOF-Nasugbu – CONAHS Quick Notes

❖ Oppositional bone growth

✓ Epiphyseal plate growth

Batangas State University ARASOF-Nasugbu – CONAHS Quick Notes

Batangas State University ARASOF-Nasugbu – CONAHS Quick Notes

Batangas State University ARASOF-Nasugbu – CONAHS Quick Notes

Batangas State University ARASOF-Nasugbu – CONAHS Quick Notes

Stages of Bone Fracture Healing

Batangas State University ARASOF-Nasugbu – CONAHS Quick Notes

b) Formation of a Fibrocartilaginous Callus

c) Formation of a Bony Callus

Batangas State University ARASOF-Nasugbu – CONAHS Quick Notes

d) The Remodeling and Addition of Compact Bone

Batangas State University ARASOF-Nasugbu – CONAHS Quick Notes

Events at the Neuromuscular Junction

Batangas State University ARASOF-Nasugbu – CONAHS Quick Notes

• Anatomy of the Neuromuscular Junction

Batangas State University ARASOF-Nasugbu – CONAHS Quick Notes

Batangas State University ARASOF-Nasugbu – CONAHS Quick Notes

Sliding Filament Theory

Batangas State University ARASOF-Nasugbu – CONAHS Quick Notes

Batangas State University ARASOF-Nasugbu – CONAHS Quick Notes

Batangas State University ARASOF-Nasugbu – CONAHS Quick Notes

Cerebrospinal Fluid Flow

Batangas State University ARASOF-Nasugbu – CONAHS Quick Notes

CEREBROSPINAL FLUID FLOW PROPER

Batangas State University ARASOF-Nasugbu – CONAHS Quick Notes

Batangas State University ARASOF-Nasugbu – CONAHS Quick Notes

ORGANIZATION OF NERVOUS SYSTEM

 The nervous system can be divided into two

Central Nervous System consists of neurons

 The Brain is the center of the nervous system and

 are things whereas the brain collects  Is to relay information

about the world around us. Body from our brain.

 Visceral afferents transmit

ROUTE OF SOUNDWAVES THROUGH EAR

Batangas State University ARASOF-Nasugbu – CONAHS Quick Notes

Batangas State University ARASOF-Nasugbu – CONAHS Quick Notes

1. Resting membrane is polarized. In the resting

 The plasma membrane at rest is inactive (polarized)

Batangas State University ARASOF-Nasugbu – CONAHS Quick Notes

 A stimulus changes the permeability of the neuron’s membrane to sodium ions.

3. Depolarization and generation of an action

 A graded potential (localized depolarization) exists where the inside of the

Batangas State University ARASOF-Nasugbu – CONAHS Quick Notes

5. Repolarization. Potassium ions diffuse out of

 Membrane permeability changes again—becoming impermeable to sodium ions

 Repolarization involves restoring the inside of the membrane to a negative charge

6. Initial ionic conditions restored. The

Batangas State University ARASOF-Nasugbu – CONAHS Quick Notes

Batangas State University ARASOF-Nasugbu – CONAHS Quick Notes