Integumentary System Castroverde, Bacsa, Tababa

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Integumentary

system

BACSA, CASTROVERDE, TABABA


TOPIC OUTLINE

1. Structure 2. Functions 3. Portal of entry 4. Defense mechanism 5. Response to injury


1. Structure
• The skin is the
largest organ in
the body and has
haired and
hairless portions.
• The skin consists
of epidermis,
dermis, sub cutis
and adnexa (hair
follicles and
sebaceous,
sweat, and other
glands).
• The haired skin is
thickest over the
dorsal aspect of
the body and on
the lateral aspect
of the limbs and
is thinnest on the
ventral aspect of
the body and the
medial aspect of
the thighs.
Quick note!

• The skin of large animals are generally thicker than the skin of small animals.
• The basale stratum is the only layer capable of cell division 'pushing up' cells to
replenish the outer layer which is constantly shedding dead cells.
• The Epidermis contains the pigment melanin which gives skin colour and allows
the skin to tan, uneven distribution of melanin causes 'freckles'.
EPIDERMIS

• Melanocytes produces melanin pigment, giving skin and hair their color.
• Langerhans cells are bone marrow-derived cells of monocyte-macrophage
lineage that process and present in the basal, spinous, and granular layers of
the epidermis but have a preference for a suprabasal position.
• Merkel cells are located in haired and hairless skin, particularly in regions of
the body with high tactile sensitivity (digits and lips) and in the outer portion
of hair follicles.
• The epidermis of
haired skin
consists of four
basic layers:
stratum corneum,
stratum
granulosum,
stratum spinosum
and stratum
basale.
• The outermost
layer of the
epidermis is the
stratum
corneum, which
consists of many
sheets of
flattened,
keratinized cells
termed
corneocytes.
• The next layer is
the stratum
granulosum,
which consists of
effete cells with
basophilic
keratohyalin
granules.
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• Deep to the
stratum
granulosum is the
stratum spinosum,
a layer of
polyhedral-shaped
cells attached to
one another by
desmosomes.
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• The innermost
layer of the
epidermis is the
germinal layer or
stratum basale,
which consists of a
single layer of
cuboidal cell
resting on a
basement
membrane.
BASEMENT MEMBRANE
• The epidermis and dermis are separated by a basement
membrane.
• The basement membrane zone is composed of hemidesmosomes
of basal cell, the lamina Lucida and the lamina densa, which also
serve to anchor the epidermis to dermis.
DERMIS

• The dermis (corium) consisting of collagen and elastic fibers in a


glycosaminoglycan ground substance, supports hair follicles, glands, vessels,
and nerves.
• The dermis is generally subdivided into superficial and deep layers that blend
together without a clear line of demarcation.
TWO LAYERS OF DERMIS

• The Papillary layer is the upper layer of the dermis, it has ridges and valleys
causing finger prints. It contains receptors which communicate with the Central
Nervous System, these include touch, pressure, hot, cold and pain receptors.

• The reticular layer is made of dense elastic fibers (connective tissue), this
houses hair follicles, nerves, and certain glands.
DERMIS

• Smooth muscle fibers of the arrector pili muscle attach the connective tissue
sheath of the hair follicle to the epidermis and are responsible for causing the
hair to stand erect.
• Skeletal muscle fibers from the cutaneous muscle extend into the lower
dermis and are responsible for voluntary skin movement.
IMPORTANT GLANDS

• The sebaceous glands located near the hair follicles


secrete oil to keep skin and hair soft and moist.
• The sudoriferous glands secrete sweat to regulate
temperature and are located under the dermis with
ducts to the surface.
• The ceruminous glands secrete wax to stop dust
entering the ear.
VESSELS AND NERVE

• Cutaneous arteries give rise to three


vascular plexus: deep, middle and
superficial.
• The deep plexus supplies the sub cutis
and deep portions of follicles and
apocrine glands;
• The middle plexus supplies the
sebaceous gland, mid portion of follicles,
and aRrector pili muscles, and the
• Superficial plexus supplies the superficial
portions of the follicles and epidermis.
SUBCUTIS (PANNICULUS,
HYPODERMIS)
• • The subcutis attaches the dermis
to subjacent muscle or bone and
consists of adipose tissue and
collagenous and elastic fibers,
which provide flexibility.
• Adipose tissue insulates against
temperature variation and in the
case of paw pads, serves in shock
absorption.
ADNEXIA (HAIR FOLLICLE)

• Horses and cattle have been distributed simple follicles with one large follicle,
usually with sebaceous and apocrine glands and arrector pili muscles.
• Pigs have simple follicle grouped in clusters.
• Goats, dogs and cats have compound follicles that consists primarily follicles
and smaller secondary follicles.
• Sheep have simple follicles in hair-growing areas and compound follicles in
wool-growing areas.
STAGES OF HAIR GROWTH

• In the anagen stage of the hair cycle, mitotic activity and growth occur.
• The catagen stage is transitional phase during which cellular proliferation
ceases.
• Then enters the resting stage, Telogen, after which mitotic activity and new hair
production resumes.
• The exogen stage is the phase in which the hair is shed.
SWEAT
GLANDS
• Apocrine glands are located
throughout haired areas of
skin in domestic animals and
are tubular or saccular coiled
glands. Thus this gland is also
called epitrichial glands.

• Eccrine glands are merocrine


in secretion and in contrast
to ducts of apocrine glands,
the ducts open directly onto
the surface of the epidermis.
Thus the eccrine glands are
also called atrichial glands
SEBACEOUS GLAND

• Sebaceous glands are simple, branched, or compound alveolar glands that


undergo holocrine secretion, with ducts opening into hair follicles except at
some mucocutaneous junctions where the glands open on the surface of the
skin.
SPECIES DIFFERENCES

• Well developed sebaceous glands are found in the supracaudal gland of dogs
and cats;
• Infraorbital, inguinal, and interdigital regions of sheep;
• The base of the horn of goats;
• The anal sac glands of cats;
• The preputial glands of horses;
• And the submental organs of cats.
2. FUNCTIONS

• Provides a protective barrier against fluid loss, microbiologic agents, chemicals,


and physical injury
• Absorptive surface
• Produces vitamin D
• Regulates temperature and blood pressure
• Participates in innate and adaptive immunity and inflammation and repair
• Stores nutrients
• Acts as sensory organ
3. PORTALS OF ENTRY

• The skin only becomes an efficient portal of entry for microorganisms when the
barrier is damaged by trauma, excessive moisture, heat or cold or by
disruption of the normal flora of the integument.
PORTALS OF ENTRY

• UV radiation (UVR) can damage the skin by direct exposure if the body’s
natural defenses, such as the hair coat and melanin pigments, are not present
or inadequate.
• The dermal capillaries can be a portal of entry to the skin via the
hematogenous route. Embolization of infectious agents, such as bacteria or
fungi can damage the skin via this route during hematogenous dissemination.
• The hematogenous route is also most often the delivery system for drugs and
toxins.
PORTAL OF ENTRY (EPIDERMIS)

• Absorption through stratum corneum and epidermis


• Direct contact with heat, cold, irritants, caustic substances and
microbiologic agents
• Penetrating of ultraviolet or ƴ-radiation
• Penetrating trauma, including injection form exterior
PORTAL OF ENTRY (ADNEXIA)

• Penetration through follicular openings


• Rupture of follicle, gland, or other structure (anal sac)
PORTAL OF ENTRY (DERMIS
AND PANNICULUS VESSELS)
• Drugs or toxins
• Leukocyte trafficking
• Embolism
• Location within capillary beds
PORTALS OF ENTRY (NERVE)

• Migration from ganglion along sensory nerves via axonal flow to


epithelial cells
4. DEFENSE MECHANISMS

• The most critical defense is the barrier derived from the more superficial layers
of the skin, which include the stratum corneum, epidermis, basement
membrane and superficial dermis. Without these outer layers of the skin,
animals cannot survive.
DEFENSE MECHANISMS

• One of the most important cells in the skin is the keratinocytes.


• The keratinocytes produce keratin filaments, desmosomes, and
hemidesmosomes, providing structural integrity to the cytoplasm's and an
interconnecting network that anchors the keratinocytes to each other and the
basement membrane.
DEFENSE MECHANISMS
• Defensins are small cysteine-rich cationic proteins found in both vertebrates
and invertebrates. They have also been reported in plants. They are, and
function as, host defense peptides
• Cathelicidin-related antimicrobial peptides are a family of polypeptides
primarily stored in the lysosomes of macrophages and polymorphonuclear
leukocytes (PMNs).
• Cathelicidins serve a critical role in mammalian innate immune defense against
invasive bacterial infection.
• Neuropeptides are small protein-like molecules (peptides) used by neurons to
communicate with each other
• Most eicosanoids are produced from arachidonic acid, which is a
polyunsaturated fatty acid that you get from eating foods like animal fats.
NORMAL SKIN VS. DISRUPTED
SKIN
5. RESPONSE TO INJURY

• Numerous endogenous and exogenous factors can potentially cause injury of


the skin. Determining a definitive diagnosis of a skin disorder depends on
obtaining a complete history, including age, breed and sex of the animal.

• Patterns of responses to injury are illustrated by changes in the epidermis,


dermis, adnexa and panniculus
ALTERATIONS IN EPIDERMAL
GROWTH
• In the normal epidermis, balance is established between the rate of
proliferation of the basal cells (germinal cells) and the rate of loss of
differentiated cells (squamous epithelial cells) from the surface, resulting in the
constant thickness of the epidermis and each of the layers.
• The orderly proliferation, differentiation and cornification of epidermal cells is
regulated by cytokines, hormones and nutritional factors such as protein, zinc,
copper, fatty acids and vitamin A and B vitamins.
DISORDERS OF CORNIFICATION

• A disorder of cornification called hyperkeratosis is characterized by an increase


in the thickness of the stratum corneum and occurs in two forms;
orthokeratotic and parakeratotic hyperkeratosis.
DISORDERS OF CORNIFICATION

• In orthokeratotic hyperkeratosis
(also referred to as
hyperkeratosis), squamous
epithelial cells are anuclear
DISORDERS OF CORNIFICATION

• Parakeratotic hyperkeratosis (also


referred to as parakeratosis), the
squamous epithelial cells have
nuclei.
RESPONSE TO INJURY
RESPONSE TO INJURY

 Apoptotic keratinocytes
have the morphologic features
of dyskeratotic cells.
EPIDERMAL ATROPHY

• Cutaneous atrophy can


affect the epidermis, follicles,
sebaceous glands and
dermal collagen and occurs
in response to hormonal
imbalances such as
hyperadrenocorticism in
dogs and cats, partial
ischemia and severe
malnutrition.
RESPONSE TO INJURY

• Intracellular fluid
accumulation limited to the
basal layer of the epidermis
is termed hydropic or
vacuolar degeneration and
can result in the formation of
intrabasilar vesicles.
FEATURES OF PRIMARY
AND SECONDARY SKIN
LESIONS
ALTERATION IN EPIDERMAL
PIGMENTATION
• Melanin is produced by melanocytes located in the basal and
lower spinous layers of the epidermis, in the external root sheath
and hair matrix of follicles, and perivascularly in the dermis.
ALTERATION IN EPIDERMAL
PIGMENTATION
Hyperpigmentation
• results from an increased production of melanin from existing melanocytes or an
increase in the number of melanocytes.
Hypopigmentation
• can be congenital or hereditary and develops because of a lack of melanocytes,
failure of melanocytes to produce melanin, or failure of transfer of melanin to
epidermal cells.
Pigmentary incontinence
• refers to the loss of melanin pigment from the basal layer of the epidermis or
outer root sheath or bulb of the hair follicles caused by damage to the cells of the
basal layer or of the follicular components and the accumulation of the pigment in
macrophages in the upper dermis or perifollicular regions, respectively.
ALTERATIONS IN DERMAL GROWTH,
DEVELOPMENT OR TISSSUE MAINTENANCE

Dermal Atrophy
• results from a decrease in the quantity of collagen fibrils and
fibroblasts in the dermis and leads to a decrease in the thickness
of the dermis noted clinically by thin, translucent skin with more
visible vasculature.

• Severe dermal atrophy can also be caused by repeated topical


application of glucocorticoids.
ALTERATIONS IN DERMAL GROWTH,
DEVELOPMENT OR TISSSUE MAINTENANCE

Fibrosis
• Fibrosis (fibroplasia)
develops in response to
various injuries, particularly
ulceration of the epidermis.
It consists of proliferation of
fibroblasts and newly formed
collagen fibrils (extracellular
matrix).
ALTERATIONS IN DERMAL GROWTH,
DEVELOPMENT OR TISSSUE MAINTENANCE

Collagen Dysplasia
• is generally an inherited
abnormality of collagen that results
in decreased tensile strength and
an increased ability of the skin to
stretch beyond normal limits.

Solar elastosis
• is caused by chronic exposure of
the skin to the UV spectrum of
sunlight.
ABNORMAL DEPOSITS IN
DERMIS
Amyloid
• is an abnormal proteinaceous
substance that can be deposited in
a localized site in the body (organ
limited) or can be “systemic” where
multiple organs are involved.
• Clinical lesion vary from papules
and plaques to nodules that
usually are covered by a normal
hair coat.
• Histologic lesions include nodular
to diffuse granulomatous
dermatitis and panniculitis with
deposition of amyloid, an
eosinophilic hyaline material
ABNORMAL DEPOSITS IN
DERMIS
Mucin
• Mucin, a normal component of the
ground substance of the dermis,
consists of protein bound to
hyaluronic acid and can be deposited
in increased quantity in focal areas or
diffusely.
• puffy appearance.
• In histologic sections, much of the
water is lost and mucin appears as
fine amphophilic granules or fibrils
that separate dermal collagen.
ABNORMAL DEPOSITS IN
DERMIS
Calcium Deposits
 Mineralization is a general term for the deposition of insoluble,
inorganic minerals in the cutaneous tissue and usually consists of
calcium in combination with phosphate or carbonate.
FOUR BASIC FORM OF
MINERALIZATION
• Dystrophic mineralization can also occurs as a result of injury or
degeneration of cellular and extracellular components of the skin, with normal
serum calcium levels, and without abnormalities in calcium metabolism.
• Metastatic calcification may be the result of increased extracellular calcium
levels and the failure of the cells normal ability to strictly regulate
intracellular calcium with result accumulation within mitochondria.
• Idiopathic mineralization it occurs in the absence of tissue injury or
abnormalities in calcium or phosphorus metabolism.
• Iatrogenic mineralization develops via direct exposure to calcium salts such
as occurs with topical exposure to calcium chloride deicing solutions.
HOST DEFENSE
MECHANISM TO INJURY
ANGIOGENESIS

• Endothelial cells form tubular structures


that become blood vessels and
reestablish blood flow
WOUND CONTRACTION AND
COLLAGEN PRODUCTION
• Fibroblasts produce collagen and contractile microfilaments that
link to matrix Newly formed collagen bundles link to each other
and to collagen bundles at wound edge to contract the wound
Inflammation, edema, and vascularity gradually disappear.
REEPITHELIALIZATION

• Epithelial cells produce proteases to dissect between viable and


nonviable tissue, migrate and proliferate to cover wound, and
reestablish basement membrane
CONDITIONS IN
DIFFERENT SPECIES
EQUINE
PIGMENTARY DISORDER

Waardenburg-like syndrome
• can cause hearing loss and changes in coloring of the hair, skin,
and eyes. Although most with Waardenburg syndrome have
normal hearing, moderate to profound hearing loss can occur in
one or both ears. The hearing loss is present from birth
(congenital).
PIGMENTARY DISORDER

• Mutations in any of these


Mutations; genes disrupt the normal
• EDN3 - endothelin 3 development of melanocytes,
• EDNRB – endothelin receptor leading to abnormal
type B pigmentation of the skin,
hair, and eyes and problems
• MITF -melanocyte inducing with hearing.
transcription factor.
• PAX3 - transcription factors.
• SNAI2 -maintain the normal
function of cells after birth.
• SOX10 -transcription factors
PIGMENTARY DISORDER
BOVINE
EPITHELIOGENESIS
IMPERFECTA (APLASIA CUTIS)
• Epithelium is present on the right
(normal area) (arrow) but is
abruptly missing on the left. The
lack of germinal epithelium results
in the failure of the epidermis,
adnexa, or mucosae to develop
completely. Skin, adnexa, and oral
mucosa can be affected in this
disease.
OVINE
ALOPECIA/HY
POTRICHOSIS
• Animals with hypotrichosis
are susceptible to extremes
of temperature, and the
skin is more likely to
sustain traumatic injury
and secondary infection
because of the lack of the
protective hair coat.
PORCINE
ALOPECIA
• Mexican hairless and
German pigs, presumed
autosomal dominant Other
breeds, presumed
autosomal recessive
FELINE
PIGMENTARY DISORDER

• Waardenburg-like syndrome, autosomal dominant with complete penetrance


for the loss of pigmentation, and an incomplete penetrance for the inner ear
degeneration
• Chédiak-Higashi syndrome, Persian cats, autosomal recessive Maltese coat color
dilution, autosomal recessive, melanophilin (MLPH) gene deletion
CANINE
ALOPECIA
• Hair loss (alopecia) is a common
disorder in dogs which causes
the animal to have partial or
complete hair loss. It can affect a
dog's skin, its endocrine system,
its lymphatic system, and its
immune systems.
TYPES OF ALOPECIA

• Multiple areas of hair loss — This is often accompanied by the reddening of the skin and mild scaling. A
fungus such as ringworm or bacterial infections are generally associated with this type of hair loss. Another
common cause includes scleroderma, a skin condition that develops from scar tissue or as a result of a recent
vaccination.

• Symmetrical hair loss — There are several known causes for this, including excessive levels of steroids in the
dog's body produced by the adrenal glands, low thyroid levels, increased levels of estrogen, low levels of
female hormone secretion, and testosterone-related hair loss (occurring when the levels are lowered suddenly
in the dog).

• Patchy to generalized hair loss — Mange is one of the most familiar causes of this type of hair loss. Other
causes include bacterial infections and ringworm. It is is accompanied with redness of the skin and
inflammation.
PATCHY TO
GENERALIZED
HAIR LOSS
Patchy to generalized hair
loss — Mange is one of the
most familiar causes of this
type of hair loss. Other
causes include bacterial
infections and ringworm. It is
is accompanied with redness
of the skin and inflammation.
SYMMETRICA
L HAIR LOSS
Symmetrical hair loss — There
are several known causes for
this, including excessive levels of
steroids in the dog's body
produced by the adrenal glands,
low thyroid levels, increased
levels of estrogen, low levels of
female hormone secretion, and
testosterone-related hair loss
(occurring when the levels are
lowered suddenly in the dog).
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ACRAL
MUTILATION
SYSNDROME
• Acral Mutilation Syndrome
leads to lesions on distal
extremities caused by self-
mutilation, loss of
sensitivity to pain on distal
limbs may cause a
tendency to lick or bite
their own pads which could
result in an auto-
amputation of claws, digits
and footpads in severe
cases, no limping.
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MUCINOSIS
AND SHAR-PEI
FEVER
The mucinoses are a diverse group
of disorders which have in common
the deposition of basophilic, finely
granular and stringy material
(mucin) in the connective tissues of
the dermis (dermal mucinoses), in the
pilosebaceous follicles (follicular
mucinoses) in the epidermis and
tumors derived therefrom (epithelial
mucinoses). 
SEBACEOUS
ADENITIS
Sebaceous adenitis is a rare type of
inflammatory skin disease that
affects the skin glands of young and
middle age dogs. This condition
most commonly affects Poodles,
Akitas, and Samoyeds, although
other breeds - and some cats (rarely)
- can also be infected.

Symptoms and Types

• There are two primary types of


sebaceous adenitis. One type occurs
in long-coated animals, and the
other type occurs in short-coated
breeds.
ZINC-
RESPONSIVE
DERMATOSIS
• A rare scaling skin
disorder, zinc-responsive
dermatosis is the result of
zinc deficiency, zinc
malabsorption or
incorrect utilization of
zinc.
• When zinc deficiency
occurs, certain immune
responses are reduced
(those handled by T cells)
and antibody production
is decreased.
TYPES OF ZINC-RESPONSIVE
DERMATOSIS
• Syndrome I - Usually only found in northern breeds like Siberian Huskies and
Alaskan Malamutes; this condition is inherited and results in something going
awry in the absorption or metabolization of zinc.
• Syndrome II - Occurs in quickly growing puppies of a larger breed that ingest a
diet that is high in phytate and deficient in zinc or a diet that has parts that can
inhibit zinc being absorbed Generic Dog Food Disease - Scaling and crusting as
developed in some dogs after being fed a generic dog food for two to four
weeks.
CAUSES OF SYNDROME I AND
SYNDROME II
• Syndrome I is the result of a genetic defect in your dog’s intestinal absorption.
• Syndrome II occurs when large-breed puppies consume a diet that is high in
phytate and deficient in zinc.
Pathologic basis of diseases
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