Cytology Overview

Most commonly used slides:

Secondary Lysosomes (residual bodies) (2)
Golgi (1)
Marginal Heterochromatin (1)
Mitochondria (1)
Nuclear Pore/diaphragm (3)
Packaging/Hydroxylation (1)
Packaging/Sorting (1)
Peripheral Heterochromatin (2)
Rough ER (1)
Secretory/lysosomal proteins (2)
Polyribosomes

Important Figures:
Predominant Concepts:

Epithelium Overview
Most commonly used slides:
Basement Membrane (2)
Cilia/cilium/axoneme (5)
Desmosomes (1)
Endothelial Cell (1)
Keratinizing stratified squamous epithelium
Nonkeratinizing stratified squamous epithelium
Pseudostratified Columnar epithelium with goblet/cilia (2)
Simple columnar epithelium (3)
Simple cuboidal epithelium (1)
Simple squamous epithelium (1)
Stratified columnar epithelium (3)
Stratified Cuboidal epithelium (1)
Terminal Web (1)
Transitional Epithelium (3)
Zonula Occludens (tight junction) (3)

Important Figures:
Predominant Concepts:

Connective Tissue Overview:

Most commonly used slides:
Adipocytes (yellow/white) (3)
Adipocyte (brown)
Adipose Connective Tissue (1)
Basophil (1)
Dense Irregular Connective Tissue (3)
Dense Regular Connective Tissue (1)
Eosinophil (1)
Elastic Fibers (1)
Heparin/Histamine (2)
Internal Elastic Lamina (2)
Loose areolar Connective Tissue (2)
Mast cell (1)
Megakaryocyte (1)
Microtubules (1)
Microvillous (2)
Nuclephilic myelocyte (1)

Important Figures:
Predominant Concepts:

Cartilage Overview:
Most commonly used slides:
Cell Nest/Isogenous groups (1)
Chondrocytes (1) (*Reside in Lacuna)
Elastic Cartilage (3) (Will be stained for Visualization- black)
Fibrocartilage (2)
Fibroblast /Fibrocyte (3)
Hyaline Cartilage (2)
Perichondrium (3)

""Order of appearance in a slide: Perichondrium (B) (made of chondrogenic cells) -3

Hyaline Cartilage (A) fchondroblasts fC) to chondrocytes (D))
A. Chondroblasts B. Lacuna C. Isogenous Groups D. Territorial matrix (secreting
GAGs), E. Interterritorial Matrix

Elastic cartilage with no elastic fibers present in Perichondrium (A)

Fibrocartilage- chondrocytes in rows with thick collagen fiber bundles surrounding

No perichondrium

Important Figures:
Predominant Concepts:
MAIN CHARACTERISTICS: avascular, low metabolic rate, limited repair/continued
growth, no innervation
3 Main Components: Cells, fibers, amorphous ground substance
Perichondrium: surrounds cartilage not attached to bone; outer fibrous (fibroblastsj
& inner chondrogenic (chondrogenic cells) layers.
Chondroblast: secrete ground substance & fibers of cartilage

Hyaline Elastic Fibro

Where? fetal skeleton ear/epiglottis intervertebral
discs
Fiber Type Type II collagen Elastic Fibers, Type I Collagen
some type II coll
Perichondrium Yes, over surfaces Complete No perichondrium,
not attached to Perichondrium, its adherent to
bone buried in CT bone
Function Resilience Resistance

Articular Cartilage: subtype of hyaline with less ground substance, more fibers per
unit area; cannot regenerate due to insufficient vascularization.

Can damage cartilage regenerate? In children yes be of vascularization in adults not

as well be of lack of blood supply. After cartilage injury, the tissue is replaced with
bone through endochondral ossification.

Appositional vs. Interstitial growth:

Appositional growth=adding chondrocytes from chondroblasts in periphery
(periostium) (in old cartilage, throughout life) Occurs at the surface.
Interstitial growth=secretion of new matrix by chondroblasts within the mass (in
young cartilage)

Joints Overview:
Most commonly used slides:
Articular Cartilage (2)
Synovial Membrane
A. Articular cartilage B. Epiphyseal plate C. Synovial Cavity Arrow:Joint Capsule
D.Synovial Membrane E. Sharpeys Fibers F. Intra-Articular Disc
Type II B Cell- secretes Hyaluronic Acid (Increase rER-(A))

Important Figures: Synovial Joint

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Predominant Concepts:
Classification of synovial join: freely moveable
Components of Joint:
• Capsule: dense fibrous CT completely encloses joint
• Synovial Cavity: space between articulating surfaces, contains fluids
• IntraArticular Discs: pads of fibrocartilage or dense fibrous CT, facilitates
gliding
• Synovial Membrane: lined with simple epithelium on non-articulating
surfaces
Type II (B): secrete synovial fluid (fibroblast like) *Most abundant normally
Type I (A): keep synovial cavity free of debris (macrophage like)
3 tvoes of svnovial membranes
1. Areolar: overlies loose CT
2. Fibrous: overlies dense reg CT, tendons and ligaments
3. Adipose: overlies adipose tissue of superficial fascia
Sharpey's Fibers: capsule anchored to the bone;; collagen fibers insert from th<
capsule into the bone

Bones Overview:
Most commonly used slides:
Primary Center of Ossification/Diaphysis (3)
Bone Lining Cells (3)
Calcified Cartilage (1)
Canaliculi
Endochondral ossification/bone formation (3)
Epiphyseal Plate (1)
Howship's lacunae (3)
Haversian Canal
Intramembraneous Ossification (2)
Mineralized cartilage (1)
Maturation/hypertrophy/calcification zones (1)
Osteoblasts [3)
Osteoclasts (1)
Osteocyte (3)
Osteocyte Process (2)
Sarcomere (1)
Sharpey's Fibers (1)
Spongy/woven bone (1)
Volkraann's Canal (2)
Zone of proliferation (2)

Osteon formation via compaction

A. Spongy bone B. Osteocytes C. Parrallel Fibered Bone D.Osteoblasts E.Vessels
Difference between Epiphyseal [left side) and Diaphyseal fright side)bone structure:
at-** *•*:. - > ^idsssiaBss

Important Figures:
Crystallization: crystals develop at nucleation sites (hole zones) along collagen
fibrils

ENDOCHONDRAL OSSIFICATION DIAGRAM

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TRABECULAR REMODELING DIAGRAM

 Osteoclast
Mechanical events Resorption is Osteoblasts
precursor cells
on surface activate. terminated by complete cycle by
Adjacent cells fuse into combination of forming osteoid
stimulated by multinucleated local and systemic that mineralizes
signals from event.
osteoclast when factors leaving behind
BLCs release they attach to (osteoprotegerin- trapped
cytokines, localsurface, "clasts" matrix protein that osteocytes. Some
bone factors, release acids and inhibits "clasts") osteoblasts remain
initiate cascadeenzymes to Osteoprogenitors at surface and
leading to dissolve stimulated to form become BLCs,
differentiation of
mineralized matrix blasts via several which help
osteoclasts fromand PMLs help stimulatory factors regulate
precursor cells.degrade and (including growth subsequent
remove matrix.
Precursors attach factors) liberated remodeling cycles.
to bone surface. from matrix during
resorption.
COMPACT REMODELING DIAGRAM

Predominant Concepts: C,C*l/LC

Functions:
support weight, storage of minerals, structural reorg., highly vascular
Harder & More vascular than cartilage
Components:
Cells & ECM (Organic (osteoid)/Inorganic Matrix (hydroxyapatite/minerals))
Cells From UMCs: Osteoprogenitors->osteoblasts (can become osteocyte or BLC)
Function- bone deposition/maintenance
Cells from Monocytes/Macro: Osteoclasts
Function- bone breakdown & Calcium release
Organic Osteoid (35%)- collagen type I, glycoprotein's, GAGs, growth factors
Inorganic- (65%) hydroxyapatite, water hydration shell, minerals
 *Calcium phosphate= inorganic salt stored in bone
Osteoblasts: actively synthesize and secrete matrix & stimulate mineralization
*Become osteocytes or BLCs
Osteocytes: Mature bone cells trapped in matrix, found in lacunae, communicate via
canaliculi
Osteoclasts: multinucleated, fusion of macrophages, stimulates resorption, ruffled
border increases SA (provides active surface), creates resorption cavity, called
Howship's Lacuna (which contains hydrolytic enzymes & collagenase)
Lacunae & Canaliculi:
Caniculi are narrow fluid filled tunnels in matrix that surround processes and
interconnect lacunae of adjacent osteocytes. Processes communicate to neighboring
osteocytes via Gap junction.
*0steocytes communicate with each other through canaliculi & gap junctions
Bone fluid fills the space between osteocytes, its processes and surrounding bony
walls of lacunae and canaliculi.
*Function: allow diffusion of waste products and gas to maintain viability of
osteocytes & are a separate compartment controlling plasma calcium levels.
*BLCS regulate passage of material into and out of bone fluid
BONE RESORPTION:
Osteocytic osteolysis- rapid short term response to low circulating calcium levels.
Mainly dissolution of hydroxyapatite crystals with little involvement of collagen or
ground substance. Stimulated by PTH levels.
*PTH increases permeability of osteocytes and BLCs to Calcium.
Osteoclastic osteolysis- long term maintenance of calcium levels, occurs in
Howship's lacuna, release acids that breakdown minerals, acid hydrolases (like
collagenase), that breakdown proteins in the matrix. Phagocytosis. Occurs most
often in trabecular bone, but can occur in compact bone. Stimulated by PTH
(increases differentiation of osteoclasts & resorptive activity)
*2 steps of bone breakdown:
Focal decalcification under ruffled border
Extracellular digestion
BONE FORMATION:

Endochondral Intramembraneous
Where does this happen? Long Bones Flat bones (facial)
What is bone called? Woven/Spongy Bone
CT Model as template Cartilage (hyaline) Mesenchymal Membrane
Differentiation of Bone Chemical signals stimulate Osteoprogenitors-> Blasts
Cells in high 02 fusion of macrophages -> Cytes or BLCs
Hypertrophy of Osteoblasts secrete
chondrocytes in lacunae; osteoid (matrix) &
calcification of ECM stimulate mineralization
prevents diffusion of osteoid
Chondrocytes die & Monocyte/macrophages
lysosomal enzymes come in and remodel
 breakdown ECM, blood forming shape
vessels invade brining in
Monocytes &
osteoprogenitors
Osteoblasts & clasts, Composed of trabecula
calcified cartilage with intervening spaces
removed by OC's and filled with vessels &
osteoid deposited by marrow.
blasts, calcification of
osteoid to form bone.

Compaction: replacement of spongy bone tissue along the cortex, formed by

intramembraneous ossification. Spongy-> Compact
Blasts deposit osteoid in lamella around blood vessels, blasts become cytes
Laid down in concentric circles around vessel, called primary osteons.
Collagen fibers parallel within each lamella and in successive lamella (giving
the name Parrallel Fibered Bone forms primary osteons)
Once the deposition has caused intervening marrow spaces to be filled
compaction is complete.
In Compaction. Bone laid down in 2 ways:
1. Concentrically around axis
2. In Sheets at bone surface
2 Types of Primary Bone in Development: Both NonLamellar Bone
1. Woven bone trabeculae: trabecular around areas of CT
2. Parrallel fibered bone: from woven bone through Compaction
Cells of the Periosteum:
Outer Fibrous layer: fibroblasts, fibrocytes, collagen fibers, ground substance
Inner Osteogenic Layer: osteogenic cells, collagen fibers, ground substance
Bone Marrow: Red (hematopoiesis) & yellow (adipose, increases as you age)

ENDOCHONDRAL OSSIFICATION-
PRENATAL EVENTS
Cartilage model formed
Bony collar along periphery (occurs by
intramembraneous ossification)
osteogenic->osteoblasts, which deposit
osteoid that becomes calcified
Chondrocytes hypertrophy in center
with associated changes in activity:
Increase alkaline phosphatase
Increase glycogen
Decrease Proteoglycans
ECM Calcified, leading to cessation of
POSTNATAL EVENTS
Secondary ossification centers develop
in epiphyseal cartilage, subsequent to
ingrowth of vessels
Primary and secondary ossification
centers grow and expand; calcification of
the extracellular bone matrix becomes
more extensive
Compaction of woven bone tissue occurs
along the cortex
Epiphyseal plate developes. This region
diffusion into the matrix of hyaline cartilage allows bone to
continue to grow in length.
Chondrocytes die, releasing lysosomal Epiphyseal plate exhibits zones that
enzymes and acids that begin to degrade represent the different stages of
extracellular cartilage matrix endochondral ossification
Periosteal Bud Develops, cluster of blood Modeling of the bone to determine
vessels that grow into and penetrate the correct shape and maintain marrow
matrix from the periosteum, bring cavity. Increase in length & girth, but
osteogenic cells which become blasts lesser increase in cortex thickness
and monocytes that become clasts
Primary ossification center develops in Remodeling of Bone to replace primary
center of diaphysis; blasts deposit bone with secondary bone (making it
osteoid along remnants of cartilage and stronger
develop into osteocytes Closure of epiphyseal plate during late
puberty, bone has completely replaced
cartilage; marrow cavity continuous
Osteoclasts breakdown cartilage Lifelong remodeling ensues; continuous
remnants and some of developing bone, resorption of old bone tissue and
creating the marrow cavity regeneration of new bone tissue

Stages visible at Epiphyseal plate:

1. Zone of reserve cartilage
2. Zone of Proliferation
3. Zone of Hypertrophy
4. Zone of Calcification/cell death
5. Zone of resorption & ossification

Mineralization: occurs in dentin and enamel of teeth

Pathological conditions associated with bone development:
Osteogenesis imperfecta: brittle bone disease; faulty synthesis of collagen I
Rickets: calcium, phosphate, vit C deficiency leads to insufficient bone
mineralization

FORMATION OF SECONDARY BONE TISSUE

Replace woven/parallel fibered bone with lamellar bone
Leads to correct bone shape
Releases calcium
Lifelong process

2 types of Secondary bone development:

1. Trabecular Remodeling
2. Compact Remodeling

"Trabecular Maturation/Development: Overview:

Begins at bony spicule (3 layers of spicule: l.BLCs 2.Lamina Lamitans S.Osteoid]
In response to hormonal/mechanical signals BLCs:
• become osteoid destructive, secreting collagenase and breaking down lamina
lamitans and osteoid.
• detach from bone surface, exposing it for resorption.
• Stimulate differentiation & activation of osteoclasts by releasing chem. sigs
Osteoclasts resorb bone tissue, PMLs phagocytose debris, osteoblasts differentiate
and deposit new bone tissue.
Mature trabecular bone: no blood vessels, nourished by marrow. Contain trabecular
packets composed of parallel sheets of lamella.
TRABECULLAR PACKET IS THE STRUCTURAL AND FUNCTIONAL UNIT OF SPONGY
BONE. Held together by cement lines that mark the beginning and end of a
remodeling cycle. Mature trabecular=lamellar secondary bone tissue. Collagen
fibers are parallel in lamella but perpendicular between adjacent lamella.

*Compact Maturation/Development Overview:

Osteoclasts form cutting cone, boring tunnel through bone tissue and osteoblasts
follow behind creating CLOSING CONE, that fills in the tunnel with layers of new
bone tissue. Lamella deposited from outside to inside. SECONDARY OSTEON
STRUCTURAL AND FUNCTIONAL UNIT OF COMPACT BONE. Central Haversian canal
with concentric lamellae of bone tissue; has osteocytes with long processes
extending through called canaliculi.
3 types of osteons: 1. Static (intact) 2. Metabolic (resorbing) 3. Rebuilt (rebuilding)

Appositional growth: width growth from new osteons being created within the
existing circumferential lamella. New circumferential lamella deposited by
intramembraneous ossification from UMCs in inner layer of periosteum.

Time Table: 20-60 yrs old. Total remodeling takes 6-7 months
Osteoclast resorption = 1 week
PML resorption phage = 1 month
Deposition of osteoid = 3-4 weeks
Mineralization of osteoid= 4-5 months

REPAIR: Broken vessels at fracture site cause bleeding/clot formation, signals

fibroblasts and new capillaries from periosteum to move in forming granulation
tissue. Strong repair tissue, called calluses, form uniting broken fragments. External
periosteal callus (around ends) & internal endosteal callus (between ends). In well
oxygenated environments UMCS->osteoblasts, in non oxygenated environments
UMCs-> chondroblasts (*cartilage and bone help calluses repair broken bone)
Periosteal buds invade callus leading to endochondral ossification. Followed by
remodeling

TRANSPLANT: autogenic: from self, use spongy bone be of high osteogenic cells
allogenic: from donor use compact bone preferred

REGULATION OF GROWTH & REMODELING:

Growth Hormone: anterior pituitary secreted, stimulates liver to make:
Insulin like growth factors: stimulate chondrocyte proliferation in epiphyseal
plate
Gonadal hormones: induce growth spurt at puberty & cessation when epiphyseal
plate closes
*Estrogen facilitates bone formation, inhibits resorption, inhibits apoptosis ol
osteoblasts, lengthening deposition phage. Rapid decline in estrogen at
menopause can cause osteoporosis.
Vitamin D: increases calcium absorption from small intestine increasing bone
density
PARATHYROID SIGNALS:
PTH: stimulates resorption increasing blood Ca levels
Calcitonin: inhibits resorption decreasing blood Ca levels

Muscle Overview:
Most commonly used slides:
A Band (2)
Actin Myofilaments
Cardiac Muscle
Contracted Smooth Muscle (2)
Intercalated Discs (2)
Skeletal Muscle (2)
Smooth Muscle (4)
Triad
Endomysium
Heart
Purkinje fibers

Cardiac Muscle X-Secction

Skeletal Muscle- X section then longitudinal
Structural components: Skeletal muscle Fibers (£-€<? \oo\ j 1)3 )

Cell specializations at Intercalated Discs.

Smooth muscle Myosin (type II)

*Calcium dependent phosphorylation of myosin regulatory light chains is
responsible for contraction of smooth muscle.
Cytosolic Calcium induces binding of calmodulin to myosin light chain kinase, active
complex phosphorylates myosin light chain, inactive myosin converted to active
myosin that then binds to F-actin myofilament.
Troponin not being involved in contraction distinguishes smooth muscle from
other types of muscle.
Predominant Concepts:
Muscle Cells & Connective tissue= MUSCLE TISSUE
Specialized for contraction, function=movement
Layers of Connective tissue in Muscle:
Entire muscle covered by dense CT called EPIMYSIUM
CT partition inwards dividing muscles into fascicles by PERIMYSIUM
Partitions of loose CT covering each individual fiber= ENDOMYSIUM
3 Types of Muscle Cells: Cardiac, Skeletal, Smooth
SKELETAL MUSCLE:
Multinucleated, peripherally located in sarcoplasm striated muscle cells.
SARCOMERE: structural and functional unit of Skeletal Muscle
Bounded by Z lines
A Band: dark (actin and myosin)
I Band: light (actin only)
H band in the middle: myosin only
M line in the middle of H band: crosslinked myosin
Sliding actin farther into the middle of sarcomere between myosin causes
contraction. Actin pull on Z lines bringing them closer together.
*I band obliterated during muscle contraction
Troponin & Tropomyosin make skeletal muscle sensitive to calcium.
Troponin I: inhibits myosin binding to actin
Troponin C: binds calcium
Troponin T: binds troponin complex to tropomyosin
Calcium binding to C, causes tropomyosin to be pushed further into F actin groove
exposing the active site for the myosin head. ATP binds myosin, is hydrolysed giving
the energy required to cause the myosin head to contract. Myosin detaches from
actin and the cycle is repeated.

Fiber type attributed to myoglobin & mitochondrial content

RED FIBERS: small diameter, lots of myoglobin, sustain contractions over long
periods of time- slow twitch motor units
WHITE FIBERS: larger fibers with less myoglobin, fast twitch units that contract
faster for shorter bursts of activity, fatique easily. (Rapid contraction & precise fine
movement)
INTERMEDIATE FIBERS: structurally and functionally between red and white

Allow rapid delivery and removal of Calcium:

T-Tubules- enter skeletal muscle at AI Junction in triad
Sarcoplasmic Reticulum: terminal cisternae + sarcotubules (calcium reservoir)
TRIAD: 2 terminal cisternae + an intervening T Tubule

Neuromuscular Junction: motor neuron has swollen terminal portion of axon called
terminal boutons that contact muscle fiber at motor end plate. Intracellular gap
between boutons & muscle called Synaptic Cleft. Sarcolemma has junctional folds
that increase surface area of synaptic cleft. Motor unit=a neuron with a specific
muscle cell it innervates.
*Muscles capable of most delicate movements have fewest muscle cells per motor
neuron ratio.

Afferent Nerve Endings:

Each muscle spindle (sense the degree of tension in a muscle) has 3-12 Intrafusal
Fibers of 2 types; modified neuron terminals enclosed in a CT Capsule.
2 types intrafusal fibers:
1. Nuclear Bag Fiber: aggregation of nuclei in an expanded midregion
2. Nuclear Chain Fiber: numerous nuclei arranged in a chain.
Primary afferent (sensory) neurons: spiral around nuclear regions of both fiber
types and make contact with nuclear chain fibers. Both types receive motor
(efferent) innervation by GAMMA EFFERENT FIBERS, that regulate the sensitivity oi
the receptor.

Tendons only contain Afferent Fibers (sensory)- they can't move

Growth and regeneration of muscle tissue

Cannot divide, but can be replaced by new cells, called satellite cells.
"These cells reside between the sarcolemma of the fiber and the basal lamina.
After injury these cells proliferate forming new myoblasts. As long as basal lamina
remains intact, myoblasts fuse to form new myotubules, which can mature into
muscle fibers. *Basal lamina disruption can result in adjacent fibroblasts from
endoperimysium repairing the injury site with scar tissue. Major muscle
damage=fibrous scar tissue

Exercise= leads to muscle hypertrophy (growth in myofibril number)

Inactivity (disuse or loss of motor innervation)= leads to atrophy

Pathology: myasthenia gravis= autoimmune characterized by muscle weakness. acH

receptors blocked by antibodies to the receptor protein, reduces functional receptor
sites so fiber can't respond to nerve stimulus.

CARDIAC MUSCLE:
Involuntary, striated, single central nucleus (can be 2), branching & anastomosing.
Cardiac muscle joined by Intercalated Discs at the Z Line. Each is composed of 2 cell
membrane specializations:
Gap Junctions: allow electrical communication
Desmosomes: physical adhesion
**T Tubules insert at Z line, not AI Junction; terminal cisternae only form DIAD

*Cardiac muscle cannot be replaced or repaired, no mitosis & no satellite cells

Purkinje fibers: specialized to conduct impulse for contraction; comprise the Bundle
of His (components of conduction system of the heart that extend through the
ventricular walls!
SMOOTH MUSCLE
Involuntary, found in hollow organs and blood vessels. Layers, innervated by ANS
Short spindle shaped with single rod nucleus in central portion of cell. No Striations.
Secrete their own endomysium (composed of Reticular Fibers)
*No defined epimysium
Sarcoplasm is thick myosin and thin actin + intermediate filaments (desmin,
vimentin)
Actin & Myosin insert into cytoplasmic and sarcolemma associated structures rich in
a-actinin called dense bodies/attachment plaques. (Z line counterpart) Bundles
streth from one dense bod to another forming cable like harnass system.

Underdeveloped SR with no T Tubules. Have CAVEOLAE instead (primitive T Tube

counterpart)

Smooth muscle cells linked by gap junctions, permitting synchronized contraction

Can undergo mitosis & hyperplasia. Regeneration can occur from UMCs called
pericytes.

CONTRACTION- Smooth Muscle

Actin & myosin not organized into sarcomeres
No troponin (does have tropomyosin)
Calcium required to initiate contraction derived from outside cell via caveolae
Myosin light chain kinase responsible for calcium sensitivity

Vessels Overview:
Most commonly used slides:
Arteriole (2)
Polychromatic Erythroblasts (1)
Tunica adventitia
Tunica Intima
Vein
AORTA- Elastic Vessel
A. Tunica Media
B B. Lumen
C. Tunica Intima
D. Tunica Adventitia
WA-S?*-{& V A.
B.
Internal Elastic Lamina
External Elastic Lamina
C. Tunica Media
D. Tunica Adventitia

A. Arteriole
B. Venule

Important Figures:

Predominant Concepts:
Layer Tunica Intima Tunica Media Tunica Adventitia
Cells Endothelium Muscle & Elastin Loose CT (can have
own vasculature-
vasa vasorum)
Name in Heart Endocardium Myocardium Epicardium

Elastic vs. Muscular arteries.

Elastic: (ex: aorta) media made of elastin, always has vasa vasorum
Muscular: internal elastic lamina present and visible, media is elastin with smooth
muscle (the amount of elastin decreases with distance from aorta)
Arterioles= 1-2 cells thick
No Vasa Vasorum
Low pressure

Capillaries: partial tunica intima, an endothelial cell, and BM

Endothelial cells held together by tight junctions that don't completely seal, except
for in the brain where it is continuous and constitutes the blood/brain barrier

Capillaries have 2 ways to transfer things through the cell:

1. diffusion across cytoplasm
2. shuttling of pinocytotic vesicles

2 types of Capillaries: Continuous (type I) pinocytotic and fenestrated (type II)

*Basement membrane continuous under fenestrae

In type I: Pericytes: scattered along the length of vessels in adventitial region,

potential source for further smooth muscle development
Type II predominant in kidneys & dental pulp

Metarterioles: a thoroughfare channel, tiny arteriovenous shunt (walls have a

discontinuous layer of smooth muscle cells) *Serve as low resistance channels for
increased blood flow for thermoregulation.

Postcapillary venules: increasing number of pericytes, leakiest part of vascular

system *where tissue fluid leaving the blood vessel and percolating through the
tissue beds to deliver nutrients and remove wastes is formed. Also the site where
majority of WBCs leave the peripheral circulation to enter the connective tissue and
being their primary roles.

VEINS: small: T Media is thinner and less muscular

Large: thicker layer of subendothelial CT, hardly any smooth muscle fibers in media
Adventitia thickets region, collagen and elastic fibers. *Large veins have vasa
vasorectum.

LYMPHATIC CAPILLARIES: incomplete basal lamina, drainage not obstructed

One end of capillary ends blindly.
No pericytes
Can be much wider
NO RED BLOOD CELLS PRESENT

Anchoring filaments: extend from lymphatic capillaries to hold them open.

LYMPHATIC VESSELS: difficult to distinguish from veins (except for absense of

blood cells) have valve leaflets that ensure unidirectional flow under low pressure.
Begin at blind end called lacteals m the intestinal villi, absorb emulsified fat. Main
function is to remove tissue fluid and large waste macromolecules.