Group 8

Ada Chua
Camille Roxas
Bamby Dio
Mervin Guevarra
Lianah Gutierrez
Edgar Sarmiento
Lyca Leviste
Jerika Abejo
Shahrukh Khan
Sydney Hoper

Mechanical barrier
Barrier against radiation
Immunologic barrier
Sensory modulation
Thermoregulation
-Sweat glands
-Blood vessels

Epidermis
-

Composed mainly of cells

Keratinocytes
The main cell type
They originate from the less well differentiated
basal cells in the basal layer
They provide a protective mechanical barrier

The arrows points

at the keratinocytes
in the epidermis

Melanocytes
-Neuroectodermal in origin
-Melanin - pigment produced by melanocytes
-Barrier against radiation
-Dendritic process - transfer melanin pigment to neighboring
keratinocytes via melanosomes
Melanin production
Transfer to keratinocyte Degradation of melanosomes

FACTORS THAT INCREASES MELANIN

PRODUCTION
-Genetically activated factors
-Estrogen
-Adenocorticotropic hormone
-Melanocyte stimulating hormone

Langerhans cells
-

Originate from the bone marrow

They function as skin macrophages

Immunologic surveillance against viral

infection, skin neoplasm, allograft
rejection

Basement Membrane:
-Anchors the epidermis and the dermis together
-Reservoir of growth factor
-Tissue organization
-Support for monolayer of cells during tissue development
-Semi-permeable selective barrier

Papillary Dermis:
-Thin arrangement of collagen fibers
-Functions:
Supplies nutrient to select layer in the epidermis
Regulates temperature
Both functions are accomplished by
extensive vascular network

Normal heat regulation

-

1/4 of the total blood volume is sent to the

skin surface for cooling

Heat regulation after strenuous physical activity

-

6 - 8 liters of blood flow to the skin surface

for cooling

Reticular Dermis:
-

Composed of densely packed mainly type 1

collagen and elastic fibers

Functions:
Gives strength and elasticity
Houses important structures such as glands,
nerves and hair follicles

Collagen:
-70% dry weight of the dermis
-Tropocollagen - collagen precursor
-Responsible for the tensile strength of the skin
-Types of collagen:
Type I - predominant type in adults
Type III - predominant type in fetal dermis

Elastic fibers
-They are branching protein that can be stretched
twice their resting length
-Allow the skin to regain its original shape after
distortion

Fibroblast
-Responsible for production and maintenance of
protein matrix

Ground Substance:
-

Glycosaminoglycans

Secreted by fibroblast

Constitute most of dermal volume

Cutaneous Receptors:
Pacinian Corpuscles
-Found in the palm of the hands and soles of the feet
-They are involve in the sensation of pressure

Ruffini's Endings
-Found in the subcutaneous tissue of fingers
-They modulate sensitivity to warm temperature

Krause's and Bulb

-They are involve in the sensation of cold temperature

Meisner's Corpuscles
-Found in the hands, feet, skin of lips
-They are involved in tactile sensation

Autonomic Fibers
-They synapse to sweat glands and receptors in the vascular
system

Sweat Secretion and Insensible Water

Loss
-

Eccrine Glands
Secretes aqueous secretion
Highest concentration on the palm
and soles, axilla and forehead

Sweat
Produced by sympathetic stimulation mediated by
acetylcholine
It is hypotonic but becomes isotonic with increased sweat
production
Sodium
-Less than in the plasma
Potassium
-Same as the plasma

Thermoregulation
-For every ml of water evaporated from the surface of the skin, 0.58
Kcal are removed from the body
-Insensible (evaporation) - skin, respiratory
Approximately 500 - 700 ml/day No electrolytes are lost Insensitive to
atropine
-Sensible
Up to 3 liters/hr Inhibited by atropine

Apocrine Gland/Pilosebaceous Unit

Pilosebaceous Unit:
-

Hair Follicle

Contains pluripotential stem cells

-

Limitless capability to replaced

injured cells

Restore epidermal continuity after

wound healing

Definition:
Inflammation of the hair follicle,
usually
secondary to Staphylococcus

Definition:
A folliculitis that progresses to form a
nodule that eventually becomes
fluctuant

Definition:
Deep seated infections with
multiple cutaneous draining sinuses

1. Non purulent cellulitis- No purulent

drainage, no exudate, no associated
abscess
-caused by Beta hemolytic
streptococci
2. Purulent cellulitis-Cellulitis
associated with purulent drainage or
exudate without a drainable abscess

Manifest as bullae, skin necrosis,

crepitus

Common sites

Genitalia Perineum Abdominal wall

Risk Factors:

Diabetes mellitus

Malnutrition

Obesity

Alcoholism

Renal failure

Steroid use

AIDS

Types of necrotizing infection according to org

involved

Type 1

Seen in immunocompromised host

Most common, gram+cocci, gram- rods and

anaerobes( bacteroides,clostridium)

Occurring in the perineum and trunk

Types of necrotizing infection

Type 2

Less common , monomicrobial w/ beta

hemolytic
strep or staph (40% MRSA)

Typically on the trunk and extremities

Associated with trauma

Types of necrotizing infection

Type 3

Rare, but fulminant

Usually due to V. Vulnificus of

traumatized
skin in sea divers

non infectious neutrophilic dermatosis

With sterile skin pustules which later ulcerates

Commonly affects the lower extremities

Commonly affects female in 3rd-6th decade of life

Linked to systemic disease such as

Inflammatory bowel disease
Rheumatoid arthritis
Hematologic disease
Monoclononal immunoglobin gammopathy

Extracutaneous manifestation:
Upper airway
Eye
Mucosa of genitalia
Lungs
Spleen

Treatment
Correction of underlying disorder
Systemic steroids Calcineurin inhibitors
Cyclosporine
Etarnercept Infliximab
Aggressive wound care and skin grafting

Chronic inflammatory disease due to follicular

obstruction characterized by multiple abscesses
with inter connected sinus tract due
With foul smelling exudate from draining sites
Inflammation extends to deep fascia

Common sites affected:

Axillary
Inguinal
Perineal
Mammary
Inframmary

Exacerbating factors
Poor hygiene
Smoking
Alcohol consumption
Bacterial infection

Treatment
Topical or systemic antibiotic
Ablation of hair follicles
Radiotx RFA
CO2 laser ablation

Treatment for refractory cases

Wide surgical debridement

Before

After

Formed as a result of penetration of congenital

coccygeal sinus by in grown hair
Common among males
Also called as Jeep Drivers Disease
-

Sweating and friction brought about by seating in

extended period of time-set stage for infection and
cyst formation

Before Shaving

After Shaving

Pre-op
excision
Markings

2 weeks post op

8 wks post op

4 wks post op

10 wks post op

Treatment:
-For Acute Pilonidal Abscess
I and D
-For Chronic Sinus Tract
Local excision and closure Fistulotomy
and marsupialization Cleft shaving,
personal hygiene

Staph Scalded Skin Syndrome:

-

Caused by the exotoxin produced

during a staphylococcal infection of the
nasopharynx or middle ear in pediatric
patients

Defect is in the granular layer of the

epidermis

Defect is at the dermoepidermal junction

Similar to 2nd degree burns
-Toxic Epidermal Necrolysis
30% total body involvement
-Steven Johnson Syndrome
Less than 10% total body involvement
With blisters in the oropharynx, anoderm and torso

Toxic Epidermal Necrolysis

Prodrome of URTI
Symmetrical macular eruption starting from
the face and trunks spreading to the
extremities
Macular rash evolve into blister

(a) Ellcltlng N lkolsky's sign on perlleslonal skin. Note the tangential

pressure,(b) Ellcltlng Nlkolsky's sign, peeling of skin revealing moist
erosion

Management
Early withdrawal of the drugs
Supportive
Temporary skin coverage

Management
IVIG (w/ anti FAS antibodies)
Plasmapharesis
Cyclosporine
Cyclophophamide
Anti tnf-a

Human papillomavirus
Human immunodeficiency virus

Common wart (verruca vulgaris)

Plantar warts (verruca plantaris)
Flat warts (verruca plana)
Venereal warts (condylomata acuminata)

Histology

Hyperkeratosis
Acanthosis
Papillomatosis
Koilocytes

Common wart
Fingers and toes
Rough, gray-brown surface
HPV 1, 2, AND 4

Plantar warts
Soles and palms
Resemble a common callus
HPV 1-4

Flat warts
Face, legs, and hands
Slightly raised and flat
HPV 3 AND 10

First line
Topical salicylic acid/silver nitrate

Second line
Cryotherapy

Recalcitrant
Electrodessication,cryoablation H2 antagonist,Zinc Sulfate

Venereal warts
One of the most common STD
Vulva, anus and penis
HPV types 6 and 11

Buschke-Lwenstein tumor
Multiple and large growths
HIV

Podophyllotoxin cream for small

Surgical excision for larger lesions

Significant risk of malignant transformation

Interferon, isotretinoin or vaccine recurrence

Immune response modifiers (Imiquimod)
HPV-induced lesions

Predispose to HPV 5 & 8

Multiple flat warts resembling
seborrheic keratosis
30-50% -Squamous cell CA

Delayed wound healing

Decreasing T-cell CD4+ count

Opportunistic infection
Low serum albumin
Poor nutrition

Poor collagen cross-linking and deposition

Prolonged, excessive pressure

1 hour of >30 mmHg pressure

Diminished cutaneous vascular flow

Muscle tissues are affected most

Debilitated patients
Age
Illness
Immobilization due to injuries

Paraplegics
Pressures as high 300 mmHg

ischial tuberosities

Bedridden individuals
Sacral pressure build to 150 mmHg

at the

Intact skin with nonblanchable redness

Partial thickness loss of dermis

May present as blister

Full thickness skin loss

Visible subcutaneous fat

No deeper structures exposed

Full thickness skin loss

Exposed bone, tendon or muscle

Multidisciplinary
Wound care

Debride, moist environment, relief of pressure

Host issues
Nutritional, metabolic and circulatory status

Pressure Ulcer
Prolonged excessive pressure (>30 or
60 mmHg) for 1 hour
Histological identifiable venous
thrombosis, muscle degeneration,
and tissue necrosis
Muscular tissues are affected most

Common locations:
Ischial tuberosity (28%)
Trochanter (19%)
Sacrum (17%)
Heel (9%)

Classification of Pressure Ulcers

Stage I: Non-blanching erythema
Stage II: Partial thickness injury with
blister or crater
Stage III: Full thickness extending to
but not including the fascia
Stage IV: Full thickness with necrosis
of muscle and bone

Treatment:
Relief of Pressure
Air flotation mattress, gel cushioned seats
Debridement of all necrotic tissues and
irrigation
Optimization of nutrition
Shallow ulcers may be allowed to close by
secondary intention, but deeper wounds
with involvement of the underlying bone
require surgical dbridement and coverage

Degloving injury
Skin and subcutaneous tissue are separated
from musculo-fascial layer
Treatment
Clean
Debridement
Place back the degloved skin
Antibiotic

Gram +
Staphylococcus aureus or Streptococcus
viridans
Eikenella corrodens, Haemophilus
influenzae, and beta-lactamase-producing
bacteria
Treatment: 1st Gen Cephalosporin in
combination with penicillin or Ampicillin in
combination with clavulanic acid

Pasteurella multocida,
Staphylococcus species, alphahemolytic streptococci, E.corrodens,
Actinomyces, and Fusobacterium.

Treatment:
Should not be closed primarily.
Selected facial wounds may be closed
primarily after very thorough cleansing;
Initiation of antibiotic therapy.
should be approached via drainage,
copious irrigation, dbridement of
necrotic material, antibiotic therapy,
extremity immobilization, and
elevation.

Acid Exposure:
Coagulative Injury
-Initial Treatment
Copius skin irrigation with saline or water for 30 minutes
-Hydrofluoric Acid
Continue to injure tissues until neutralized by calcium
May cause cardiac arrhythmia
Treatment:
-Quaternary ammonium compounds
-Calcium carbonate/ topical/ IV / intrarterial

Alkali
Liquefaction Injury:
-Saponification of fat
Facilitates tissue penetration and increases tissue
damage Produces longer and more sustained
injury
-Treatment:
Continuous water irrigation for at least 2 hours

Mild
Emollient and oral analgesic 2nd degree
burns
Debridement and silvadene
Severe injury ( muscles, vessels, bones)
Liposuction and saline infusion

IV Fluid Extravasation:
Considered a chemical burn
Dorsum of the hands
-Most common site
Injury is produced by:
-Chemical toxicity
-Osmotic toxicity
-Pressure effect of a closed environment

Most Common Substances:

Cationic Solutions
-K ion, calcium ion Osmotically Active Chemicals
-Hypertonic glucose, TPN solutions
Antibiotic/Cytotoxic drugs
-Doxorubicin - DNA Complex
Prevents the release of cytokines and growth factor

Mechanism:
-Direct cellular injury to the blood vessels
-Microvascular thrombosis
-Decrease tensile strength Treatment:
-Rapid rewarming
-Elevation and splinting
-Daily hydrotherapy
-Serial debridement

Hypertrophic Scars:
-Thick red raised scar that do not outgrow their original
border
Keloids:
-They are much bulkier, their nodularity and firmness
extend beyond the wounds
-Common among dark skinned individual

HYPERTROPHIC SCARS
Usually develop within 6 weeks of trauma
Risk increases if epithelialization takes longer than 21 days
Rarely elevated more than 4mm
They usually occur across areas of tension and flexor surface
at right angle to the joints or skin creases

KELOIDS
Tend to occur 3 months to a year after the initial insult
They don't extend into underlying subcutaneous tissues
Areas of the body with higher incidence of keloid formation
Earlobe
Deltoids Parasternal
Upper back regions

Keratinocytes
Express human leukocyte antigen 2 Intercellular adhesion molecule-1
Keloids
Higher deposition of Immunoglobulin G and IgM
Antinuclear antibody against fibroblast
HTS
Higher T lymphocyte and Langerhan cells
Larger number of mast cells in both HTS and keloids

Treatment:
1.
2.
3.
4.

Intradermal injection of
triamcinolone
Mechanical pressure or
radiation
Topical application of silicone
sheets
Excision of keloids E hypertropic
scar