The Integumentary System: Anatomy and Functions

THE INTEGUMENTARY
SYSTEM
CREATEDBY: MRSPALLAVIPARBHATCHAUHAN

DEFINITIONS
 Disease- an abnormal condition of the
body or the mind that causes
dysfunction or discomfort.
 Disorder- a functional abnormality, or
disturbance.

ANATOMY AND PHYSIOLOGY OF THE
INTEGUMENTARY SYSTEM
 The skin is the largest sensory organ of the
body, with a surface area of 15-20 square feet
and a weight of about 9lb (4 kg).
 Layers of the skin –
 Epidermis: Consists of Melanocytes (melanin
production), Merkel Cells (Stimuli
Transmission), Langherhan Cells (Immunity)
 Dermis: Consists of Blood Vessels & nerves,
Lymph vessels, sweat and sebaceous glands.
 Hypodermis (subcutaneous fat)

 Epidermal appendages – Nails, Hair, Glands-
Sebaceous and sweat glands
 Functions-
 The skin is the first line of defense against infections.
 The skin protects underlying tissues and organs from
injury against chemicals, microbes, insect bites and
trauma through the presence of keratonocytes and
lipids.
 The skin receives stimuli from external environment,
detects touch, pressure, pain temperature and relays
information to nervous system because of presence of
nerve endings.
 The skin maintains normal body temperature through
conduction, convection and radiation.

 The skin excretes salts, water and organic wastes.
 The skin protects the body from excessive water loss through
evaporation (insensible perspiration = 600 ml/24 hours)
 The skin synthesizes Vitamin D3 by exposure to ultra-voilet
light, which converts to calciterol for normal calcium
metabolism.
 The skin stores nutrients

FUNCTIONS OF THE SKIN
•Immune Response Function
•Protection
•Sensation
•Temperature Regulation
•Excretion
•Vitamin D₃ synthesis
•Storage of nutrients

*Dermis layers
*
*
*Dermal papillae

NAILS
 Of hard keratin
 Corresponds to hooves and claws
 Grows from nail matrix

TERMINOLOGY
 Macule: A flat colored lesion, < 2cm, not raised above skin.
 Papule: Small solid lesion, < 0.5 cm, raised above skin and palpable.
 Nodule: Large (0.5 cm – 5 cm) firm lesion raised above the skin.
 Vesicle: Small, fluid-filled, < 0.5 cm, fluid is visible, raised above skin
and translucent.
 Pustule: Vesicle filled with leucocytes.
 Plaque: Large (> 1cm), flat-topped, raised lesion. Edges may be distinct
(e.g. in psoriasis) or gradually blend with surrounding skin (e.g. in
eczematous dermatitis)
 Excoriation: Linear, angular erosion that may be covered by crust and
caused by scratching.
 Fissure: Linear crack in the skin

 Scale: Excessive accumulation of stratum corneum.
 Wheal: Raised erythematous, edematous, papule or plaque usually representing
short-lived vasodilation or vaso-permeability.
 Bulla: Fluid-filled raised lesion, > 0.5 cm, translucent.
 Comedons: Small cysts formed in hair follicles due to blockage of follicular orifice
by retention of keratinous material and sebum. Inflammation can occur due to
activity of bacteria.
 Crust: Dried exudates of body fluids that may be yellow or red.
 Patch: Large (> 2 cm) flat lesion with the color different from surrounding skin.
Differs from macula only in size.
 Cyst: Soft, raised, encapsulated lesion filled with semi-solid or liquid contents.
 Scar: Change in skin secondary to trauma or inflammation. Site may be
erythematous, hypo-pigmented or hyper-pigmented.
 Paronchyia: Inflammation of skin folds surrounding finger nails.
 Frostbite: Damage to tissue caused by freezing.

ASSESSMENT OF INTEGUMENT SYSTEM
DESCRIPTION OF SKIN LESIONS
 Dermatologic conditions are usually described by
the types of lesions that appear on the skin, their
shape, and configuration. Types of lesions r:--
 Primary Lesions
 Secondary Lesions

PRIMARY LESIONS
 Macula : flat, circumscribed discoloration of skin; may have any size or shape.
 Papule : solid, elevated lesion less than 1 cm wide.
 Nodule : raised, solid lesion larger than 1 cm wide.
 Vesicle : circumscribed elevated lesion less than 1 cm, containing fluid.
 Bulla : a vesicle or blister larger than 1 cm wide.
 Pustule : circumscribed raised lesion that contains pus; may form as a result of purulent
changes in a vesicle.
 Wheal : elevation of the skin that lasts less than 24 hours, caused by edema of the dermis;
may be surrounded by erythematic or blanching.
 Plaque : solid, elevated lesion on the skin or mucous membrane, larger than 1 cm in diameter;
psoriasis is commonly manifested as plaques on the skin
 Cyst : soft or firm mass in the skin, filled with semisolid or with liquid material contained in a
sac.

SECONDARY LESIONS
 Secondary lesions involve changes that take place in primary lesions that modify
them.
 Scale : heaped-up, horny layer of dead epidermis; may develop as a result of
inflammatory changes.
 Crust : covering formed by the drying of serum, blood, or pus on the skin.
 Excoriation : linear scratch marks or traumatized areas of skin.
 Fissure : cracks in the skin, usually from marked drying and long-standing
inflammation.
 Ulcer : lesion formed by local destruction of the epidermis and by part or all of the
underlying dermis.
 Scar : new formation of connective tissue that replaces the loss of substance in the
dermis as a result of injury or disease.
 Atrophy : diminution in size or in loss of skin cells that causes thinning of the skin.

SHAPE AND CONFIGURATION
 After the type of lesion is identified, the shape, configuration or
arrangement (in relation to each other), and pattern of distribution
 Annular ring-shaped, Circinate circular, Confluent lesions run
together or join, Discoid disk-shaped, Discrete lesions remain
separate , Generalized widespread eruption, Grouped clustering of
lesions, Guttate drop like
 Herpetiform grouped vesicles, Linear in lines, Multiform more than
one kind of skin lesion, Nummular coin-shaped, Polymorphous
occurring in several or many forms

ASSESSMENT
HISTORY
 Obtaining a history of rash or other complaints related to
dermatologic conditions, you will understand characteristics of the
problem and their effects on the patient that will help in planning
care.
Characteristics of Rash
 When did the rash first occur? Was the onset sudden or gradual?
 What site was first affected? Describe the spread and its severity.
 What was the initial color and configuration of the rash? Has it
changed?
 Is there associated itching, burning, tingling, pain, or numbness?
 Has it been constant or intermittent?

Associated Factors
 What makes the rash worse or better? Is it seasonal? Is it affected by
stress?
 What medications are being taken? What topical products have been
used? What effect did they have?
 What skin products are used? What chemicals have come into
contact with the skin, such as laundry detergent, cleaning products,
insecticides?
 Has there been pet contact?
 What is the patient's occupation? Any hobbies, such as gardening or
hiking?
 What is the sexual history and chance of sexually transmitted
disease exposure?

Medical History
 Is there a history of hay fever, asthma, hives, eczema, or allergies?
 Has the patient had this particular rash or had other skin disorders in
the past?
 What is the family history of skin disorders?
 Are there any long-standing medical problems?

PHYSICAL EXAMINATION
 Focus your examination on the skin, hair, and nails.
Some dermatologic conditions affect other body systems.
 Ask the patient to show you the area of concern and
examine the skin surface under good lighting.
 Note the distribution and configuration of skin lesions.
Compare right and left sides of the body.
 Note the shape, border, texture, and surface of the
lesions.
 Palpate the lesions for texture, warmth, and tenderness.
 Use a metric ruler to determine size of lesions.
 Examine the scalp, nails, and oral mucosa.
 For dark-skinned persons, look for black, purple, or gray
lesions; palpate carefully to determine if rash is present.

DIAGNOSTIC TESTS
LABORATORY TESTS
TestsOf Microscopy And Culture.
Microscopy
 Sample taken by scraping, swabbing, or aspirating
a lesion is transferred to a glass slide for
observation or staining.
 Direct visualization of scrapings mixed with mineral oil to
detect scabies, mites, or lice nits that cling to hair.
 Gram stain may be performed to tentatively identify
bacteria in certain skin infections.

Nursing and Patient Care Considerations
 Use the side of a glass slide or a scalpel held at a 45-degree angle to
gently scrape the skin of a dry lesion or of an inflamed area.
 For moist or semi moist ulcerations or crusted lesions, roll a saline-
soaked cotton or Dacron-tipped swab over the lesion.
 For intact vesicles, aspirate fluid from the edge with a 25-gauge
sterile needle; if vesicle is partially broken, gently un roof with
forceps and obtain fluid on a swab.

Culture
 Drainage from lesions may be cultured on specific
media to detect causative organism and sensitivity to
antimicrobial therapy; also, portions of skin, hair, and
nails may be submitted for fungal culture.
 Usually takes 24 to 48 hours for results; fungal cultures
may take 4 to 5 weeks.
 Obtain specimen with cotton or Dacron-tipped swab and
send to laboratory in culturette or viral culture container;
refrigerate viral culture if laboratory pickup is delayed.
 To obtain specimen for fungal culture, scrape or clip the
affected skin, hair, or nails.

OTHER TESTS
Patch Testing
 Patch testing is an office procedure done in dermatology to
determine if patients are allergic to contact materials.
 Materials are applied in patches to the skin and checked for reaction
48 hours after application and possibly again later.
 Erythema, swelling, papules, and vesicles indicate an allergic
contact dermatitis rather than an irritant contact dermatitis or no
reaction.

SKIN BIOPSY
 Removal of a piece of skin by shave, punch, or excision technique to detect
malignancy or other characteristics of skin disorders.
 Types of biopsy.
 Shave biopsy : scalpel used to remove raised lesions, leaving lower layers of dermis
intact.
 Punch biopsy : special instrument used to remove round core of lesion, containing all
layers of skin. Core is usually closed with sutures.
 Excision biopsy : scalpel and scissors used to remove entire lesion; suturing required.
 Position the patient comfortably with the site exposed; explain that a local
anesthetic will be given.
 Check if the patient has any known allergies to local anesthetics.
 Ask the patient what current medication he or she is taking.
 Explain the procedure.
 Obtain written consent.
 After the biopsy, apply pressure to the site to stop bleeding if required and apply an
appropriate dressing. Pressure dressing may be required for larger wounds or
wounds that are bleeding.
 Place the biopsy specimen in a clearly labelled container with 10% formaldehyde
and transport it to the lab

WOUND COVERAGE: GRAFTS AND FLAPS
 Wound coverage, using grafts and flaps, is a type of
reconstructive (plastic) surgery performed to improve the
skin's appearance and function.
Skin graft
 A section of skin tissue is separated from its blood supply and
transferred as free tissue to a distant (recipient) site; it must
obtain nourishment from capillaries at the recipient site.
 In dermatology, skin grafting is used to repair defects that
result from excision of skin tumours and to cover areas of
denuded skin.

 Autografts grafts done with tissue transplanted from the
patient's own skin.
 Allografts involve the transplant of tissue from one
individual of the same species; these grafts are also
called allogenic or homografts.
 Xenograft or heterograft involve the transfer of tissue
from another species.

 Classification by thickness.
 Split thickness (thin, intermediate, or thick) graft that is cut at
varying thicknesses and is used to cover large wounds because
its total potential donor area is virtually unlimited.
 Full thickness graft consists of epidermis and all of the dermis
without the underlying fat; used to cover wounds that are too
large to close primarily. They are used frequently to cover facial
defects because they provide a better contour match and less
postoperative contracture

SKIN FLAPS
 A flap is a segment of tissue that has been left attached at one
end (called a base or pedicle); the other end has been moved
to a recipient area.
 It is dependent for its survival on functioning arterial and
venous blood supplies and on lymphatic drainage in its
pedicle or base.
 Free flap or free-tissue transfer one that is completely severed
from the body and is transferred to another site.
 Flaps may consist of skin, mucosa, muscle, adipose tissue,
and omentum.
 Used for wound coverage
 Flaps are classified according to the method of movement,
composition, location, or function.

Procedure for Skin Grafts
 Split-thickness skin graft is obtained by razor blade, skin-
grafting knife, electric, or air-powered dermatome/drum
dermatome. Most commonly obtained from the inner aspect of
the upper arm or outer thigh.
 A full-thickness skin graft is primarily excised, defatted, and
tailored to fit accurately over the defect area.
 Skin is taken from the donor or host site and applied to the
wound/defect site, called the recipient site or graft bed.
 Process of revascularization and reattachment of the skin
graft to the recipient bed is referred to as a take. A bolster
(pressure) dressing is applied to the graft to enhance the
survival of the skin graft by providing stable approximation of
the graft to the recipient bed.

 The bolster dressing is left in place for 1 week.
 The donor site is maintained clean and dry.
 If Scarlet Red (a single layer dressing impregnated with
epithelial growth promoter) is used on the donor site for
split-thickness grafts, it is left in place for 2 to 3 weeks to
allow the wound to heal.
 Occlusive dressings, such as Omniderm or Allevyn, may
also be used to decrease pain, alleviate frequent wound
care, and speed healing.
 Daily wound care and dressing change with an
antimicrobial ointment and nonstick dressing may also
be used.

 Preoperative Management and Nursing Care
 Aspirin and nonsteroidal anti-inflammatory drugs (NSAIDs)
and vitamin E are discontinued 14 days before the procedure.
Coumadin should be held for several days before the
procedure, and prothrombin time and International Normalized
Ratio (INR) should be measured before the procedure as
ordered.
 Efforts should be made to enhance wound healing several
months to several weeks before the procedure, such as
smoking cessation, alcohol avoidance, and proper nutrition.
 Medical history and examination should be evaluated,
particularly for latex sensitivity, cardiovascular problems
requiring endocarditis antibiotic prophylaxis, bleeding
problems, and high blood pressure.
 The procedure is usually done under local anesthetic, so no
meals are withheld.
 The operative site should be free from makeup.
 The patient should have someone available to drive home
after surgery unless otherwise notified.

Postoperative Management and Nursing Care
 Educate the patient with a skin graft on the following care:
 Initial pressure dressing will be left in place for 24 to 48 hours.
 If your wound begins to ooze apply firm pressure for 10 to 15 minutes
(without peeking). If bleeding persists, contact your surgeon.
 Do not take aspirin or aspirin-containing medication for pain. You may
take one to two acetaminophen tablets every 4 to 6 hours as needed.
 Most skin grafts are held in place by a bolster dressing (cotton ball or
foam). Do not remove the bolster dressing during the next week.
 You may clean site and apply ointment to the surrounding area of the
bolster dressing.
 Keep the graft edges moist with antibiotic ointment.
 Protect the graft from the sun. The sun will cause pigmentation changes
in the graft. A sunscreen may be used in 2 to 3 weeks.

 Skin grafts to the lower leg must be kept elevated because the
new capillary connections are fragile, and excess venous
pressure may cause rupture. Keep your leg elevated as much
as possible during the next week.
 Inspect the dressing daily. Report unusual drainage or signs of
an inflammatory reaction.
 After 2 to 3 weeks, any water-based moisturizer may be
applied to the skin donor site for split thickness skin grafts.
 Expect some loss of sensation in the grafted area for a time.
 Avoid strenuous exercise (jogging, lifting heavy objects).
Anything that causes your face to flush will raise your blood
pressure, cause bleeding, and impair healing.

AESTHETIC PROCEDURES
 Aesthetic procedures (cosmetic surgery) consist of reconstructive
(plastic) surgery performed to reconstruct or to alter congenital or
acquired defects or to restore or improve the body's appearance.
Types of Procedures
Rhytidectomy : Done through various techniques and incisions to alleviate
skin folds and wrinkles to improve the appearance of the aging face (face
lift).
 The correction can last as long as 10 years, but results vary with each
individual. Skin relaxes with time, and the muscles may also relax, but
seldom does the face revert to its preoperative condition.
 Surgical procedures include:
 Laser: The KTP (potassium-titanyl-phosphate) laser is now used in facial
plastic surgery.
Blepharoplasty: Removes loose skin, muscle and excess fat from upper or
lower eyelids. It will not remove lines at the lateral corners of the eyes.
 The procedure is generally done under local or general anesthetic or by
carbon dioxide laser

DERMABRASION, CHEMICAL PEEL, AND LASER
RESURFACING
 Patients with weathered skin, fine wrinkles (especially at the corner
of the eyes ), or acne pitting and scarring may benefit from these
procedures.
 The use of new carbon dioxide laser technology allows for a more
predictable result and eliminates the porcelain appearance from
chemicals such trichloroacetic acid. There is less risk of
hypopigmentation than with dermabrasion.
 Chemical peels using tretinoin cream (Retin-A) and AHA (Alpha-
hydroxy acids) result in the destruction of portions of the epidermis
and dermis, with subsequent regeneration of new tissues.
 Laser resurfacing is used for fine wrinkles, smoker lines, sun-
damaged skin, shallow acne scarring.

LIPOSUCTION
 Also called body contouring, liposuction reduces localized
deposits of fat, with a cannula aided by suction or fitted to a
syringe.
 May be done on the face, neck, breasts, abdomen, flanks, hips,
buttocks, and extremities.
Preoperative Management and Nursing Care
 Local or general anesthetic will be administered.
 No eating or drinking for several hours before surgery.
 Review patient's allergies and medication before surgery.
 Instruct patient to cleanse skin with antiseptic agent the night
before surgery, if prescribed.
 Explain procedure to the client.
 Make sure consent form is signed before any procedure.
 Make sure aspirin, warfarin (Coumadin), and NSAIDs have been
discontinued for 2 weeks before surgery, unless otherwise
indicated.

Liposuction, post-operative management.
 After liposuction, increased fluids are required.
 Aspirin and NSAIDs should be avoided for at least 1
week to prevent bleeding.
 Wear compression garment as instructed.
 Notify the surgeon if increased swelling develops; could
indicate development of a seroma.
 Keep sutured areas moist with ointment as instructed.
 Avoid jarring exercise as instructed.

Diseases in the
Integumentary System

COMMON SKIN DISORDERS
Infectious
disorders
Non-
infectious
disorders
Skin
cancers
Secretary
disorders
Eczematous
disorders

COMMON SKIN DISORDERS
 1. Infectious disorders – bacterial, viral, fungal and
parasitic
 2. Non-infectious disorders- Psoriasis
 3. Skin cancer- Benign skin tumors and malignant skin
tumors
 4. Secretary disorders
 5. Eczematous disorders
 6. Skin allergies

SKIN INFECTIONS
 Bacterial
 Impetigo
 Folliculitis
 Furuncle
 Carbuncle
 Cellulitis
 Acne
 Fungal /Parasitic
 Tinea Pedis
 Tinea Cruris
 Tinea Versicolor
 Tinea Corporis
 Toenail fungus
 Pediculosis
 Scabies

SKIN INFECTIONS
 Viral
 Herpes Simplex
 Herpes Zoster
 Verruca
 Molluscum Contagiosum
 Allergic/Irritation conditions
 Dermatitis
 Hives
 Eczema
 Psoriasis
 Sebacous Cysts
 Frostbite
 Other
 Skin checks - moles
 Sunburn
 Striae

BACTERIAL SKIN INFECTIONS
SKIN
DISORDER
DESCRIPTION MANAGEMENT
Impetigo
Streptococci or
Stapylococcus
aureus or both
Highly contagious
Lesions begin as vesicles or pustules
surrounded by edema and redness,
progresses to exudative & crusting stage
Oral antibiotics- Mupirocin
Systemic antibiotics-
Erythromycin or Dicloxacillin
Control of infections
Folliculitis,
furnuncles,
Carbanucles
Stapylococcus
aureus
Folliculitis- White pustules on forehead,
chest, upper back, neck, thighs , groin &
anxillae
Furuncles- Deeper inflamed nodules
Carbuncles – Interconnected furuncles &
often rupture, expelling purulent, foul-
smelling thick drainage
Folliculitis – warm
compresses, gentle washing
& topical antibiotics
Furnuncles- same as above
and Incision & drainage
Carbuncles – Systemic
antibiotics, I & D

CELLULITIS
 Cellulitis is acute bacterial infection of the skin and
subcutaneous tissue most often caused by
streptococci or staphylococci.

CELLULITIS
 Cellulitis is an inflammation of the deep dermal and subcutaneous
tissue that results from an infectious process.
Pathophysiology and Etiology
 Caused by infection with group A beta-hemolytic streptococci,
Staphylococcus aureus, Haemophilus influenzae, or other organisms.
 Usually results from break in skin that may be as simple as athlete's
foot.
 Infection can spread rapidly through lymphatic system.

SYMPTOMS OF CELLULITIS
 Fever
 Pain in the affected area
 Skin redness or inflammation
 Tight, "stretched" appearance of the skin

CLINICAL MANIFESTATIONS
 Tender, warm, erythematous, and swollen area.
 Possible fluctuant abscess
 or purulent drainage.
 Possible fever,
 chills,
 headache,
 malaise.

Diagnostic Evaluation
 Gram stain and culture of drainage.
 Blood cultures.

TREATMENT
 Topical antibiotics
 Oral antibiotics
 prompt treatment prevents the spread of infection to
the blood & vital organs

TREATMENT OF CELLULITIS
 Treatment is with antibiotics. For most patients, empiric
treatment effective against both group A streptococci and S.
aureus is used.
 Oral therapy is usually adequate with dicloxacillin 250 mg or
cephalexin 500 mg po qid for mild infections. Levofloxacin 500
mg po once/day or moxifloxacin
400 mg po once/day works well for patients who are unlikely to
adhere to multiple daily dosing schedules.
 For more serious infections, oxacillin or nafcillin 1 g is given IV
q 6 h.
 Immobilization and elevation of the affected area help reduce
edema; cool, wet dressings relieve local discomfort.

MANAGEMENT
 Oral antibiotics (penicillinase-resistant penicillins, cephalosporins,
or quinolones) may be adequate to treat small, localized areas of
cellulitis of legs or trunk.
 Parenteral antibiotics may be needed for cellulitis of the hands, face,
or lymphatic or widespread involvement
 Surgical drainage and debridement for suppurative areas.
Complications
 Tissue necrosis
 Septicaemia

IMPETIGO
 Superficial bacterial infection of the skin
 Most commonly Staph or Strep
 Thin vesicles with honey colored crusting
 Usually on face, hands, neck & extremities
 Spread occurs via contact from fingers, towels,
clothing
 Tx: Topical antibiotics

THE INCUBATION PERIOD IS THE TIME BETWEEN BEING EXPOSED
TO THE BACTERIA AND THE DEVELOPMENT OF SIGNS AND SYMPTOMS. THE
INCUBATION PERIOD IS USUALLY ONE TO THREE DAYS FOR STREPTOCOCCAL
AND FOUR TO 10 DAYS FOR STAPHYLOCOCCAL INFECTIONS.
INCUBATION PERIOD

IMPETIGO AND ECTHYMA
 Impetigo is a skin infection than can spread from
one person to another. It appears as sores on the
skin that are often covered by a thick dry honey-
colored crust. The sores don’t hurt, but may be
tender is touched. They may also be itchy. Any skin
area can be affected, but are usually on arms or
legs, the face, and sometimes on the scalp.
 Impetigo is a superficial skin infection with crusting
or bullae caused by streptococci, staphylococci, or
both.

DEFINITION
 Impetigo is the most common bacterial infection in
children. This acute, highly contagious infection of
the superficial layers of the epidermis is primarily
caused byStreptococcus
pyogenes or Staphylococcus aureus.

Ecthyma
 In this form of impetigo, painful fluid- or pus-filled sores
with redness of skin, usually on the arms and legs,
become ulcers that penetrate deeper into the dermis.
After they break open, they form hard, thick, gray-yellow
scabs, which sometimes leave scars. Ecthyma may be
accompanied by swollen lymph nodes in the affected
area.
Bullous impetigo
mainly seen in children younger
than 2 years, involves painless, fluid-filled blisters,
mostly on the arms, legs and trunk, surrounded by red
and itchy (but not sore) skin. The blisters may be large
or small. After they break, they form yellow scabs

Causes Impetigo
 Impetigo is usually caused by either streptococcus
or staphylococcus bacteria, which are normally
found on the skin and in the nose.
 When small cuts, scratches, or insect bites occur,
these bacteria can get under the skin surface and
cause infection.
 Infected are often reddish and puffy. Fluid or pus
oozes from the sore for a few days. The fluid dries
to form honey-colored crusts. As the bacteria
multiply, the sores increase in number and size.

Non-bullous impetigo is a
superficial skin infection that
manifests as clusters of
vesicles or pustules that
rupture and develop a honey-
colored crust.
Bullous impetigo is a superficial
skin infection that manifests as
clusters of vesicles or pustules that
enlarge rapidly to form bullae. The
bullae burst and expose larger
bases, which become covered with
honey-colored varnish or crust.
Impetigo (Bullous)Impetigo (Non-Bullous)

How is Impetigo Spread?
 Impetigo is very contagious. The bacteria are easily
passed to new areas of the skin by scratching or
touching the sore. It can be passed to other people
by unwashed hands, dirty fingernails, and clothing
or other objects that have touched the sores.

LAB. DIAGNOSIS
Specimen collection.
Suspected organisms
Impetigo: Group A
Streptococcus,
Staphylococcus
aureus
Skin biopsy
1. Skin swab

IMPETIGO
Treatment
 A mild infection may be treated
with a topical antibacterial such
as
 mupirocin(BACTROBAN )
 Fusidic acid (FUCIDIN)

IMPETIGO
 More severe cases may require oral antibiotics
such as Amoxycillin,
 Wash (do not scrub) the skin several times a day,
preferably with an antibacterial soap, to remove
crusts and drainage.

How Can Impetigo be Prevented?
 Bathe or shower daily with soap and water
 Wash hands regularly
 Always use your own person towel
 Keep fingernails short and clean
 Change and wash clothes frequently
 Keep infected children away from other children until
treatment has begun and child is no longer infectious
 Do not let your children play, or have other close
contact, with someone who may have impetigo
 If you or your children get a cut, scratch, or insect bite,
wash the wound with soap and water, apply an antibiotic
ointment, and cover the wound with a bandage. This will
minimize the chance of bacterial infection.

FOLLICULITIS
BY: NICOLE PITT
FOLLICULITIES

 Inflammation of follicles, primarily hair follicles.
 Folliculitis: inflammation of hair follicle from
 Infection
 Chemical irritation
 injury
 Infectious causes
 Staphylococcus aureus (most common)
 Streptococcus species
 Mixed bacterial infection
FOLLICULITIS

WHAT IS FOLLICULITIS?
 Small, white headed pimples
 Can result in hair loss or scarring
Two types:
 superficial folliculitis
 deep folliculitis

CAUSES
 Friction from shaving
 Excessive perspiration
 Inflammatory skin conditions
 Injuries to your skin
 Covering your skin with plastic dressings or adhesive tape
 Exposure to coal tar, pitch or creosote

RISK FACTORS
 Medical conditions that reduce your resistance to
infection
 A pre-existing skin condition
 Trauma to your skin from surgery
 Long-term antibiotic therapy for acne
 Topical corticosteroid therapy
 Obesity
 Living in a warm, humid climate

SYMPTOMS OF SUPERFICIAL
FOLLICULITIS
 Clusters of small red bumps
 Pus-filled blisters
 Itchy and tenderness

TYPES OF SUPERFICIAL FOLLICULITIS
 Staphylococcal folliculitis
 Pseudomonas folliculitis (hot tub folliculitis).
 Tinea barbae
 Pseudofolliculitis barbae
 Herpetic folliculitis

SYMPTOMS OF DEEP FOLLICULITIS
 Large swollen bumps
 Pus-filled blisters
 Lots of pain
 Possbile scars

TREATMENT
 Topical Antibacterial such as
 mupirocin (BACTROBAN ).
 Fusidic acid (FUCIDIN)
 More severe cases may require
oral antibiotics such as Amoxycillin

TREATMENT
 Antibiotic applied to the skin or taken orally
 For facial folliculitis : use an electric shaver, shaving
gel, moisturizing after-shave
 Good hygiene.

 Abscess or boil
 Usually starts as folliculitis
 Deep folliculitis-spreads to deeper tissue
 Walled-off nodule of purulent infection
 Painful
 Firm or fluctuant
 Fever is uncommon
 Can be at any site
 Most often in areas of friction
FURUNCLE

FURUNCLE (BOIL)
 Deep extension of superficial folliculitis into the
dermis and subcutaneous tissue
 Cause – Staph
 1-5 cm red/tender nodule which may contain pus
 Tx:
 Simple lesions- warm compress
 Severe infections – drainage & antibiotics

 Carbuncles involve a coalition of furuncles
 Deeper, more extensive involvement
 Require greater degree of debridement
 Furuncles and carbuncles uncommon in children
 Very painful and may have fever, chills
 Occur in areas with thick dermis (back of neck,
lateral aspect of thigh
CARBUNCLES

CARBUNCLE
 Large deep abscess that is a progression of a
furuncle
 May be 3-10 cm in size
 Can present c fever/chills
 Tx: drainage & antibiotics

ACNE IS A COMMON SKIN CONDITION THAT
MAINLY APPEARS DURING YOUR TEENAGE
YEARS, WHEN HORMONE LEVELS ARE CHANGING

ACNE IS CAUSED BY:
 family/genetic history
 oily cosmetics
 stress
 diet
 hot weather
 exposure to some chemicals
 Vitamin A and Vitamin E deficiency
 poor hygiene
 use of anabolic steroids
 puberty and menstrual cycles

ACNE
 Obstruction of sebaceous follicles (oil glands)
 Open comedones or closed comedones
 Usually on the face, chest, back
 Causes:
 Stressful events (hormonal changes)
 Friction acne
 Oil based cosmetics
 NO correlation between chocolate, chips or colas
 Tx: topical +/or oral antibiotics

ACNE USUALLY OCCURS
ON THE FACE,
ARMS,
CHEST,
NECK
AND BACK
Photos taken from Wikipedia

SOMETIMES ACNE CAN BE
CLEARED BY REGULAR
WASHING AND SPECIAL ACNE
TREATMENTS.
Images from Clipart

1-ACNE (VULGARIS)
 Acne is a disorder of pilosebaceous follicles
causing comedones,papules and pustules on the
face ,chest and upper back
 Affects many adolescents, about 80% between the
ages of 12 – 15.
 Result of hormonal changes that occur at puberty
 SEBACEOUS GLANDS increase secretion of
SEBUM, the oily fluid that is released through the
hair follicles.

TYPES OF ACNE
MILD/ Comedonal
MODERATE/ Papulopustular
SEVER/ Nodulocystic

Pathophysiology
 Acne develops as a result of blockages in the follicles.
 excessive deposition of the protein keratin
 oily sebum in the hair follicle resulting in the formation of a plug
 enlargement of the sebaceous glands and increases sebum production.
 A microcomedo may enlarge to form an opencomedo (blackhead) or closed comedo.
 The dark color of a blackhead occurs due to oxidation of the skin pigment melanin
 Comedones result from the clogging of sebaceous glands with sebum, a naturally
occurring oil, and dead skin cells.
 inflammation within and around the follicle,
 leading to inflammatory lesions (papules, infected pustules, or nodules) in
the dermis around the microcomedo or comedone,
 which results in redness and may result in scarring or hyperpigmentation.
 Severe acne isinflammatory, but acne can also be noninflammatory.

CLINICAL MANIFESTATIONS:
 Closed comedone (whitehead) - a clogged follicle. Whiteheads
usually appear on the skin as small, round, white bumps.
 Open comedone (blackhead) - a plugged follicle that opens and
turns dark at the surface of the skin. Blackheads do not indicate the
presence of dirt.
 Papules - inflamed lesions that appear as small, pink bumps on the
skin.
 Pustules (pimples) - inflamed pus filled lesions that are red at the
base.
 Cysts and nodules - large, inflamed, pus filled lesions deep under
the skin that can cause pain and scarring.

COMEDONAL ACNE
Closed comedones (whiteheads) If duct
blocked by dirt or dead cells, the sebum
accumulates, causing a whitehead
Open comedones (blackheads)Sebaceous
accumulation at the surface becomes
oxidized and turns black, causing a
blackhead
 Non-inflammatory
Topical retinoids-isoTretinoin (ISOTREX) or
benzyl peroxide (BREVOXYL)

PAPULOPUSTULAR ACNE
Papules/Pustules
 Once propionibacterium acnes (that’s
always present on the skin)enters the
broken skin, pus forms and a pimple or
pustule results.
 Squeezing the pimple spreads the
infection
 Topical retinoids alone usually insufficient
 Consider topical retinoids plus Topical
antibiotics (erythromycin,clindamycin)
ISOTRIXIN(isotretnoin+erythromycin)

NODULOCYSTIC ACNE
 Soft nodules that are secondary
comedones from repeated
ruptures and reencapsulations
 Painful and disfiguring
 Treatment consists of topical
agents (benzyl
peroxide,retinoids) + oral
antibiotics or oral isotretinoin
alone

DIAGNOSIS
 Complete history
 Pay attention to endocrine function
- Rapid appearance with virilization/menstrual
irregularity
 Complete medication list
 Physical exam:
- Location - scarring
- Lesion type - keloid
- pigmentation

TREATMENT
The goals of pharmacotherapy for acne vulgaris are to reduce
morbidity and to prevent complications.
Medication: Benzoyl Peroxide Antibiotics,Topical and Oral
retinoids
Benzoyl Peroxide :
Benzoyl peroxide is a first-line treatment for mild and
moderate acne vulgaris due to its effectiveness and mild side-
effects

ANTIBIOTICS:
 Topical and systemic antibiotics used in the treatment of
acne vulgaris are directed at Propionibacterium acnes.
They also have anti-inflammatory properties.
 Minocycline
 Doxycycline
 Tetracycline

RETINOIDS:
 These agents decrease the cohesiveness of abnormal hyperproliferative
keratinocytes, and they may reduce the potential for malignant degene-
ration. They also modulate keratinocyte differentiation.
 isotretinoin
 Tretinoin topical
 Adapalene
 Tazarotene

Management
 Treatment of acne vulgaris should be directed toward the known pathogenic
factors, including follicular hyperproliferation, excess sebum, P acnes, and
inflammation. The most appropriate treatment is based on the grade and severity
of the acne.
Pharmacotherapy
 Retinoid-like agents (eg, topical tretinoin, adapalene, tazarotene, isotretinoin)
 Antibiotics (eg, tetracycline, minocycline, doxycycline,
trimethoprim/sulfamethoxazole, clindamycin, topical clindamycin, topical
erythromycin, daptomycin)
 Selective aldosterone antagonists (eg, spironolactone)
 Estrogen/progestin combination oral contraceptive pills (eg, ethinyl estradiol,
drospirenone, and levomefolate; ethinyl estradiol and norethindrone; ethinyl
estradiol and norgestimate; ethinyl estradiol and drospirenone)
 Acne products (eg, erythromycin and benzoyl peroxide, clindamycin and tretinoin,
clindamycin and benzoyl peroxide, azelaic acid, benzoyl peroxide)
 When a topical or systemic antibiotic is used, it should be used in conjunction with
benzoyl peroxide or topical retinoid to reduce the emergence of resistance.

Nonpharmacotherapy
 Diet therapy, such as a low-glycemic diet and
avoidance of “junk foods,” has been suggested as a
nonpharmacologic measure to manage acne
vulgaris.
Procedures
 Manual extraction of comedones
 Intralesional steroid injections
 Superficial peels that use glycolic or salicylic acid

ALTERNATIVE TREATMENTS
 Phototherapy with blue and red light emitted from special
fluorescent lights, LEDs, lasers, or dichroic bulbs.
 Photodynamic therapy involving intense blue or violet light,
 zinc, teat tree oil, heat therapy, salt water therapy are all
used for treating acne.

VIRAL SKIN INFECTIONS (CONTD…)
SKIN DISORDER DESCRIPTION MANAGEMENT
Herpes simplex: herpes
simplex virus
Vesicles preceded by sensation
of itching or burning; clear
exudate from vesicles, followed
by crusting; common to nose,
lips, cheeks, ears and genitalia
Analgesics, steroids, oral or
systemic antiviral agents like
acyclovir, valacyclovir or
famicyclovir
Avoid sunburns , sexual
intercourse
Universal precautions

HERPES SIMPLEX
 Viral infection either Type I OR Type II
 “You can’t kill it and it won’t kill you”
 Clear papules c superficial ulcerations/erosions
 May cause fever, lymph node enlargement, burning
pain
 Lesions will crust over in 5-14 days
 Tx: analgesic for pain, oral antiviral (acyclovir)

VIRAL SKIN INFECTIONS
 Most common viruses cause cold sores & warts
 COLD SORES --Herpes Simplex
 WARTS --Human Papillomavirus (HPV)

1-COLD SORES
 Cold sores are small, blister-like lesions that usually
appear around the mouth.
 They are caused by the herpes simplex viruses.
The strain that usually causes them around the
mouth is herpes simplex type 1 (HSV-1).

TREATMENT OF COLD SORES
The current FDA-approved
medications used in the
treatment of herpes simplex
virus in adults are
acyclovir(Zovirax),
valacyclovir(Valtrex),

VIRAL SKIN INFECTIONS
SKIN DISORDER DESCRIPTION MANAGEMENT
Herpes zoster
(Shingles):Varicella
zoster virus
Acute viral infection of the dorsal nerve
root ganglion,
Characterized by unilaterally clustered
skin vesicles along peripheral sensory
nerves on the trunk, thorax or face
accompanied by pain, fever, burning,
neuralgia, pruritus & parasthesia
Analgesics, steroids, oral or
systemic antiviral agents
like acyclovir, valacyclovir
or famicyclovir
Isolation of patient
Universal precautions when
handling blisters

HERPES ZOSTER
 Herpes zoster (shingles) is an inflammatory
condition in which reactivation of the chickenpox
virus produces a vesicular eruption along the
distribution of the nerves from one or more dorsal
root ganglia. The prevalence increases with age.

Pathophysiology and Etiology
 Caused by a varicella-zoster virus, which is a
member of a group of deoxyribonucleic acid
viruses.
 Virus is identical to the causative agent of varicella
(chickenpox). After the primary infection, the
varicella-zoster virus may persist in a dormant state
in the dorsal nerve root ganglia. The virus may
emerge from this site in later years, either
spontaneously or in association with
immunosuppression, to cause herpes zoster.

CLINICAL MANIFESTATIONS
 Eruption may be accompanied or preceded by fever, malaise,
headache, and pain; pain may be burning, lancinating, stabbing,
or aching.
 Inflammation is usually unilateral, involving the cranial, cervical,
thoracic, lumbar, or sacral nerves in a bandlike configuration.
 Vesicles appear in 3 to 4 days.
 Characteristic patches of grouped vesicles appear on erythematous,
edematous skin.
 Early vesicles contain serum; they later rupture and form crusts; scarring
usually does not occur unless the vesicles are deep and they involve the
dermis.
 If ophthalmic branch of the facial nerve is involved, patient may have a
painful eye. (This can be a medical emergency.)
 In healthy host, lesions resolve in 2 to 3 weeks.
 A susceptible person can acquire chickenpox if he or she comes
in contact with the infective vesicular fluid of a zoster patient. A
person with a history of chickenpox or has received the
immunization is immune and thus is not at risk from infection
after exposure to zoster patients.

 Diagnostic Evaluation
 Usually diagnosed by clinical presentation.
 Culture of varicella-zoster virus from lesions or
detection by fluorescent antibody techniques,
including viral detection that uses monoclonal
antibodies (MicroTrak) or by electron microscopy, to
confirm diagnosis.

Management
 Antiviral drugs, such as acyclovir (Zovirax), famciclovir
(Famvir), and valacyclovir (Valtrex), interfere with viral
replication; may be used in all cases, but especially for
treatment of immunosuppressed or debilitated patients. Must
be started within 72 hours of onset.
 Corticosteroids early in illnessâ€”given for severe herpes
zoster if symptomatic measures fail; given for anti-
inflammatory effect and for relief of pain. Controversial.
 Pain management; aspirin, acetaminophen, NSAIDs,
opioidsâ€”useful during the acute stage, but not generally
effective for postherpetic neuralgia. If treated early (48 to 72
hours), may decrease risk of postherpetic neuralgia.

PEMPHIGUS
 Pemphigus is a serious autoimmune disease of the skin and of the
mucous membranes, characterized by the appearance of flaccid
blisters (bullae) of various sizes on apparently normal skin and
mucous membranes (mouth, esophagus, conjunctiva, vagina).
 Familial benign chronic pemphigus (Hailey-Hailey disease) is a
familial type of pemphigus that appears in adults, affecting
particularly the axillae and groin.

 Pathophysiology and Etiology
 The etiologic agent causing pemphigus is unknown.
 Certain drugs, other autoimmune diseases, and
genetics may play a role in its development.
 Many variants of pemphigus exist.

 Clinical Manifestations
 Initial lesions may appear in oral cavity; flaccid blisters (bullae)
may arise on normal or erythematous skin.
 The bullae enlarge and rupture, forming painful, raw, and
denuded areas that eventually become crusted.
 The eroded skin heals slowly; eventually, widespread areas of the
body may become involved.
 In the mouth, the blisters are usually multiple, of varying size and
irregular shape, painful, and persistent. Oral lesions may appear
initially, with lesions of the mucous membranes of the pharynx
and esophagus; the conjunctivae, larynx, urethra, cervix, and
rectum may become affected as well.
 An offensive odor may emanate from the bullae due to infection.
 Positive Nikolsky's signâ€”separation of epidermis when minimal
pressure is applied to the skin. Downward pressure on a bulla will
cause it to expand laterally.

 Skin biopsies of blisters and surrounding
skinâ€”demonstrate acantholysis (separation of
epidermal cells from each other).
 Immunofluorescence of skin cells shows antibodies
that bind to the epidermis in a lacy pattern network.
(pemphigus antibodies).

 Management
 Corticosteroids in large doses to control the disease and keep
skin free from blisters.
 Immunosuppressive agents, such as cyclophosphamide
(Cytoxan) and azathioprine (Imuran), are used alone or in
combination with steroids, for immunosuppressive and
steroid-sparing effect.
 Plasmapheresisâ€”reinfusion of specially treated plasma cells;
temporarily decreases serum level of antibodies.
 Treatment of denuded skin.
 Complications
 Infections (skin, pneumonia, septicemia).
 Adverse effects from acute and chronic corticosteroids; GI
bleeding, secondary infection, psychosis, hyperglycemia, and
others.

VIRAL SKIN INFECTIONS (CONTD…)
SKIN
DISORDER
Warts : human
papillomavirus
Rough, fresh or grey- colored skin
protrusion
Electrodessication or
cryosurgery, intra-lesional
injections of cytotoxic agents

2-WARTS
 Warts are small, usually painless growths on the skin
caused by a virus called human papillomavirus (HPV).
Mostly harmless.
 Warts can be disfiguring and embarrassing.
 Sometimes they itch or hurt (particularly on the feet).
 Keratinocytes proliferate making the surface
rough

PLANTAR WARTS
 Plantar warts are found on the soles of the feet.
They can be very painful and cause difficulty in
walking or running.

FLAT WARTS
 Flat ("plane") warts may arise on the face, legs,
and other body parts, often in large numbers.

SUBUNGUAL AND PERIUNGUAL WARTS
 Subungual(under) and periungual (around)
warts appear under and around the fingernails or
toenails.
 Genital Warts– very serious & difficult to remove

TREATMENT FOR COMMON WARTS
Salicylic-acid preparations
Treatment for common
skin warts has long
been based upon the
use of products
containing salicylic acid.
(DUOFILM LIQUID)

 Salicylic acid is a keratolytic medication, which means it
dissolves the protein (keratin), which makes up most of
the wart and the thick layer of dead skin.
 Freezing the wart (cryotherapy) to remove it
 Burning the wart to remove it

FUNGAL SKIN INFECTIONS
SKIN
DISORDE
R
Candidiasis:
Candida
albicans
Appearance depends on
location;
in mouth, infection is called
thrush, Skin lesions, Vaginal
thrush
Eliminate or control pre-disposing factors –
antibiotics (which alter flora), malnutrition,
diabetes, immune suppression, pregnancy
or birth control pills
Use topical antifungal powders& creams

FUNGAL SKIN INFECTIONS (CONTD…)
SKIN
DISORDER
Tinea :
Ringworm
infections
Tinea corporis
Tinea capitis
Tinea cruris (jock itch)
Tinea pedis (athlete’s foot)
Anti-fungal solutions & creams
Wet dressings, keratolytic agents
Cleaning & drying of the skin, Wearing
absorbent undergarments, wearing open
shoes during warm weather

FUNGAL SKIN INFECTIONS
DERMATOPHYTES
(FUNGI) – live on the
dead, top layer of the
skin
 Symptoms may or may
not appear

RINGWORM (TINEA)
 caused by many different fungi
 Symptoms
 Itchy, red, scaly patches which may look like a ring
because redder from outside and are normal inside

CLASSIFICATION OF RINGWORM
Classified by its location on the body
 TINEA CORPORIS –Body ringworm
 On smooth areas, arms, legs, body

TINEA PEDIS :”ATHLETES FOOT”
 on soles, between toes, toenail

• Athlete's foot, also called tinea pedis, is a fungal infection of
the foot. It causes peeling, redness, itching, burning, and
sometimes blisters and sores.
• Athlete's foot is a very common infection.
•The fungus grows best in a warm, moist environment such as
shoes, socks, swimming pools, locker rooms, and the floors of
public showers. It is most common in the summer and in warm,
humid climates.
• It occurs more often in people who wear tight shoes and who use
community baths and pools.
TINEA PEDIS
(Athlete’s Foot)

•Athlete's foot is caused by a microscopic fungus that lives on dead
tissue of the hair, toenails, and outer skin layers.
•There are at least four kinds of fungus that can cause athlete's
foot. The most common of these fungi is trichophyton rubrum.
•Trichophyton rubrum is a fungus that is the most common cause
of athlete's foot, jock itch and ringworm.
•This fungus was first described by Malmsten in 1845.
CAUSATIVE AGENT OF ATHLETE’S FOOT

From person to person
•Athlete's foot is a communicable disease caused by a parasitic fungus
in the genus Trichophyton, either Trichophyton
rubrum or Trichophyton mentagrophytes.
•It is typically transmitted in moist environments where people
walk barefoot, such as showers, bath houses, and locker rooms.
•It can also be transmitted by sharing footwear with an infected
person, or less commonly, by sharing towels with an infected person.
MODE OF TRANSMISSION

CONTINUATION...
To other parts of the body
• The various parasitic fungi that cause athlete's foot can also
cause skin infections on other areas of the body, most often
under toenails (onychomycosis) or on the groin (tinea cruris).

THE INCUBATION PERIOD DIFFERS:
1. TINEA CORPORIS HAS AN INCUBATION PERIOD OF FOUR TO TEN DAYS
2. TINEA CAPITIS HAS AN INCUBATION PERIOD OF 10–14 DAYS
3. THE INCUBATION PERIOD OF TINEA PEDIS AND TINEA UNGUIUM IS PROBABLY
WEEKS BUT EXACT LIMITS ARE UNKNOWN.
INCUBATION PERIOD

 Fungal culture
 Biposy
LABORATORY EXAMINATIONS
REQUIRED

AS THE INFECTION PROGRESSES, THE SKIN GROWS SOFT AND THE
CENTER OF THE INFECTION BECOMES INFLAMED AND SENSITIVE TO THE
TOUCH. GRADUALLY, THE EDGES OF THE INFECTED AREA BECOME MILKY
WHITE AND THE SKIN BEGINS TO PEEL. A SLIGHT WATERY DISCHARGE ALSO
MAY BE PRESENT.
1. ITCHING, STINGING AND BURNING BETWEEN YOUR TOES
2. ITCHING, STINGING AND BURNING ON THE SOLES OF YOUR FEET
3. ITCHY BLISTERS
4. CRACKING AND PEELING SKIN, ESPECIALLY BETWEEN YOUR TOES AND ON
THE SOLES OF YOUR FEET
5. EXCESSIVE DRYNESS OF THE SKIN ON THE BOTTOMS OR SIDES OF THE
FEET
6. TOENAILS THAT ARE THICK, CRUMBLY, RAGGED, DISCOLORED OR PULLING
AWAY FROM THE NAIL BED
SIGNS AND SYMPTOMS

1. KEEP YOUR FEET CLEAN, DRY, AND COOL.
2. WHENEVER POSSIBLE, TAKE OFF YOUR SHOES TO "AIR OUT" YOUR
FEET.
3. CLEAN YOUR FEET DAILY WITH SOAP AND WATER.
4. ALWAYS DRY WELL BETWEEN YOUR TOES.
INTERVENTION
Nursing Management

CONTINUATION...
5. Use an absorbent powder such as talcum powder or
aluminum chloride powder.
6. Wear absorbent socks (e.g., made out of cotton or wool).
7. Avoid tight-fitting footwear, since sweaty feet provide
ideal conditions for fungal growth.
8. Change your socks after exercising or after any excess
sweating.

INTERVENTION
medical Management
•Topical anti-fungals (creams, solutions, gel, and lotions), either
over-the-counter or prescription, are usually effective for
uncomplicated cases of athlete's foot. When these topical agents
don't work, antifungal pills are often prescribed.
•Some medications used to treat athlete's foot contain both an
antifungal and antibacterial ingredient to help speed up healing. In
addition, special aluminum acetate wet dressings may be helpful
when applied to vesiculated or macerated lesions. Shoes may also
be treated with antifungal powders.
•A foot condition that doesn't clear up after appropriate treatment
may not be due to a fungal or bacterial infection. The symptoms
may be caused by some other type of skin disease. That's why it's
important to see your doctor to confirm the presence of athlete's
foot.

 TINEA CAPITIS – “SCALP” ringworm.
 HIGHLY CONTAGIOUS
 TINEA CRURIS – groin ringworm (jock itch)

PARASITIC SKIN INFECTIONS
SKIN
DISORDER
Pediculosis :
Pediculus
humanus,
Phithirus pubis
Pediculosis capitis – head lice
Pediculosis corporis- body lice
Pediculosis pubis – pubic lice
Intense itching: scratch marks
may be evident
Application of pediculicides (Permethrin
rinse)
Head lice- Application of shampoo into
dry hair, use of fine-toothed comb
Body lice- Pediculocide lotion into the
involved areas
Clothing should be washed & dried in
hot cycles or dry cleaned
Family members, close contacts &
sexual partners should also be treated

PARASITIC SKIN INFECTIONS (CONTD…)
SKIN
DISORDER
Scabies :
Sarcoptes scabei
Multiple straight or wavy
thread-like lines beneath
the skin, itching
Topical application of scabicide- lindane,
crotamiton, permethrin 5% with re-treatment
in 1 week to kill residual eggs
All clothing & linen should be washed and
dried in hot cycles or dry cleaner.
Family members, close contacts & sexual
partners should also be treated

SCABIES
 Scabies is a HIGHLY CONTAGIOUS skin problem
caused by a mite.
 A female mite lays eggs under the skin of a human and
stays inside until she dies.

SYMPTOMS
 Scabies only affects the skin, outside the body.
 Sever pruritus is the hallmark of scabies.
 extreme itching, which can worse at night and after
bathing

WHERE SCABIES IS MAINLY
FOUND
 In between the fingers
 Around the head and neck
 Groin areas
 Itching a scabies rash can make the infection worse.
 Scabies is passed from one person to another

TREATMENTS
 Permethrin 5% (Nedax)
 Permethrin is a neurotoxin
that causes paralysis and
death in parasites.
 Most common treatment
used today for scabies.

NON-INFECTIOUS DISORDERS- PSORIASIS
DESCRIPTION CAUSES CLINICAL
MANIFESTATIONS
Chronic, non-infectious skin
inflammation involving
keratin synthesis resulting in
psoriatic patches
Stress, Trauma,
Infection, Changes in
climate, certain
medications
Pruritis; Shedding , silvery, white
scales on a raised, reddened, round
plaque that usually affects scalp,
knees, elbows, extensor surfaces of
arms & legs & sacral regions; Yellow
discoloration, pitting & a thickening
of nails, psoriatic arthritis

BACKGROUND.
 ‘’Psoriasis vulgaris’’
 Psoriasis is a chronic, noncontagious, multisystem,
inflammatory disorder.
 Skin lesions vary from localized patches to entire
body coverage.
 Affects 2-4% of general population.
 Occur at any age. Commonly in 15-25 years. M-F –
1:1.
 5 types – plaque*, guttate, inverse, pustular and
erythrodermic.

Psoriasis is a common skin condition that causes
skin redness and irritation. It is characterized by
red, scaly skin patches which are usually found on
the scalp, elbows and knees, and may be
associated with severe arthropathy.

CAUSES.
 Genetics
 1/3 psoriasis patients report a family history.
 PSORS1 to PSORS9.
 Lifestyle
 Chronic infections, stress, climate (temperate
countries).
 HIV
 Advanced HIV. More severe in patients with HIV along
with psoriatic arthritis.
 Medication
 Beta blockers, calcium channel blockers, statins,
NSAIDS, Lithium, terbinafine, steroid withdrawal.

PLAQUE PSORIASIS.
 85-90% of people with psoriasis.
 Raised areas of inflamed skin covered with silvery-
white scaly skin.
 Elbows, knees, scalp & back.
 Uncontrolled plaque psoriasis -> psoriatic
eythroderma.
 Severe itching, swelling and pain.
 Often occurs from abrupt withdrawal of
glucorticosteroids.
 Fatal – affects the function of skin – temperature
and barrier functions.

PUSTULAR PSORIASIS.
 Raised bumps filled with noninfectious pus.
 Skin around the pustules is red and tender.
 Usually localized to hands and feet - palmoplantar
pustulosis.
 Generalized pustular psoriasis (von Zumbusch) –
rare psoriasis during pregnancy.
 Annular pustular psoriasis – rare form. Seen during
childhood.

INVERSE PSORIASIS.
 Flexural psoriasis.
 Smooth, inflamed patches of skin.
 Affects skin folds – around genitals, armpits,
overweight patients ( panniculus), intergluteal cleft
and under breasts.

GUTTATE PSORIASIS.
 Numerous small, scaly, red/pink, ‘teardrop’ shaped
lesions.
 Primarily appears on the trunk but also limbs and
scalp.
 Usually preceded by a streptococcal infection –
streptococcal pharyngitis.

OTHER.
 Seborrheic-like psoriasis – red plaques with greasy
scales usually on scalp, forehead, skin folds close
to the nose, around mouth and trunk.
 Psoriatic arthritis –
 painful inflammation of joints and connective tissue –
fingers and toes – sausage shaped – dactylitis.
 Can also affect hip, knees, spine and sacroiliac joint.
 30% psoriasis affect individuals will develop psoriatic
arthritis.

o Red patches of skin covered with
silvery scales.

o Dry, cracked skin that may bleed.

o Itching, burning or soreness.

o Thickened, pitted or ridged nails.

MEDICAL SIGNS
 Other than clinical presentation.
 Auspitz’s sign – pinpoint bleeding when scale is
removed.
 Koebner phenomenon – psoriatic skin lesions
induced by trauma.
 Itching and pain localized to papules/ plaques.

Researchers feel that psoriasis is an immune
system disorder but also think that genetics and
the environment contribute to flare-ups. There are
several triggers that can make psoriasis worse.

o Topical medications such as lotions,
ointments, creams, and shampoos.
o Body-wide (systemic) medications,
which are pills or injections that affect
the whole body, not just the skin
o Phototherapy, which uses light to
treat psoriasis.

DIAGNOSIS.
 Clinical presentation!
 Scaly, erythematous plaques, papules, patches –
painful + itchy.
 DDx – discoid eczema, seborrheic eczema.
 Skin biopsy – histological – stratum granulosum
layer often missing or severely decreased –
prematuration.

TREATMENT.
 Topical agents.
 Corticosteroids – continuously 8 weeks.
 Moisturizers – Calcipotriol & coal tar.
 Phototherapy.
 311-313 nanometers. UV-B lamps. UV-A tanning beds.
PUVA.
 Systemic agents – methotrexate, ciclosporin,
retinoids. – immune suppressants & regulate
epithelial cell growth.
 Alternatives- Sea baths – balneotherapy &
fish oils.

MANAGEMENT OF PSORIASIS
•Topical Corticosteroids
•Topical non-steroids
•Coal tar products
•Medicated Shampoo
•Intra-lesional therapy
•Systemic therapy
•Photochromotherapy

PROGNOSIS.
 Most people experience mild lesions that can be
treated with topical therapies.
 -ve impact on quality of life – physical, aesthetic
discomfort.
 Linked with low self esteem & depression.
 Increased risk of diabetes & HTN, Crohn’s disease
& Ulcerative colitis.

What Is Dermatitis ?
DERMATITIS IS THE INFLAMMATION OF
THE SKIN CAUSED BY FACTORS SUCH
AS:
1.ALLERGIES
2.IRRITANTS
3.ULTRAVIOLET LIGHT
4.FOODS
5.MEDICATIONS
6.HEREDITARY

ECZEMA
 The term Eczema and dermatitis are often used
interchangeably
 Dermatitis simple mean the inflammation of the skin
 where as Eczema is a general term for many types of
acute conditions.

TYPES OF DERMATITIS
 SEBORRHEIC DERMATITIS [Skin eruptions on
face, scalp, and trunk of body. This symptoms
will produce greasy, dry scales and will appear
reddish.]
 CONTACT DERMATITIS [The appearance of
skin vesicles that burn, itch , sting or scale. ]
 ATOPIC DERMATITIS [There will appear
lesions on the face, neck, knees, elbows, trunk
of body.]

SEBORRHEIC DERMATITIS
 affect the areas rich in sebaceous glands
 Fungal infection:
 Malassezia globosa ,
 Malassezia restricta
 Genetic,
 environmental,
 hormonal, and
immune-system factors
have been shown to be involved in the
manifestation of seborrhoeic dermatitis

Antifungals
Over-the-counter
Dermol
betadine
zinc pyrithione
salicylic acid
selenium disulfide
Ketoconazole
Prescription
ciclopiroxolamine
sodium sulfacetamide
terbinafine
Fluconazole
Ketoconazole
Antihistamines
loratadine
cetirizine
fexofenadine
diphenhydramine
chlorpheniramine
Other medications
Coal tar
Lithium gluconate
Lithium succinate
Vitamin B6 ointment
Topical steroid

Contact dermatitis:
Definition:
Contact dermatitis is a term for
a skin reaction (dermatitis)
resulting from
exposure to
•ALLERGENS (ALLERGIC
CONTACT DERMATITIS)
OR
•IRRITANTS(IRRITANT CONTACT
DERMATITIS).
•Phototoxic dermatitis occurs when
the allergen or irritant is activated
by sunlight.

CONTACT DERMATITIS
 Dermatitis/Contact dermatitis is a non-contagious
inflammatory skin disorder in which the skin becomes
red, sore, or inflamed after direct contact with a
substance
 Skin inflammation caused by factors such as:
 Allergies
 Irritants
 Ultraviolet light
 Foods

Contact
dermatitis
IRRITANT
CONTACT
DERMATITIS
ALLERGIC
CONTACT
DERMATITIS
PHOTOTOX
IC
DERMATITI
S

Irritant contact dermatitis:
It is a form of contact dermatitis that can be
divided into forms caused by chemical
irritants and those caused by physical
irritants.
Irritant contact
dermatitis
Chemical irritant
contact dermatitis
Detergents,
surfactants, extremes
of pH, and organic
solvents
Plant poisons
Physical irritant
contact dermatitis
Various env.
conditions
(like excss temp.
humidity)

IRRITANT CONTACT DERMATITIS
 Most common form of dermatitis
 It is a cutaneous inflammation resulting from a direct
cytotoxic effect of a chemical or physical agent
 Commonly seen in occupational accidents
 Most frequent irritants are acids and alkaline solutions

Red or brown lesions that will itch. itching and
burning are prominent features
Scrating of lesion lead to broken skin which result
in weepy lesion
Lesions restricted to the area where the irritant
damaged the tissue
SYMPTOMS

ALLERGIC CONTACT DERMATITIS (ACD)
 Allergic contact dermatitis results from a delayed
reaction to some allergen, such as metal or a
chemical to which an individual has been
previously sensitized

SYMPTOMS
 Present in same manner as irritant CD however can
also be noticed on skin areas distant from where
the allergen was in direct contact

 Allergic contact
dermatitis to leather
shoes.

CONTACT DERMATITIS
 Contact dermatitis with
Nickel.
 Reddish marking and
itching will occur.

TREATMENT
 The goals for the treatment of eczema/dermatitis
are to prevent itching, inflammation, and
worsening of the condition.
 Treatment of eczema may involve both lifestyle
changes and the use of medications.
 avoid the cause

TREATMENT
 Emollients
 Lactic acid LACTICARE
 Liquid paraffin OILATUM
 Topical corticosteroids
 Clobetasol (Dermovate)
 Betamethasone (Betnovate,)
 Fluticasone (Cutivate)

TREATMENT
 If itching is severe, oral antihistamines
(diphenhydramine) may be prescribed.
 antibiotics (for infections)

SKIN CANCERS – BENIGN TUMORS
•Cysts
•Warts
•Angiomas
•Pigmented nevi (Moles)
•Keloids

SKIN CANCERS – MALIGNANT TUMORS
MALIGNANT
TUMORS
DESCRIPTION
Basal cell
carcinoma
The most common type- basal cell cancers arises from the basal cells
contained in the epidermis.
Squamous cells It is a tumor of the epidermal keratinocytes and can infiltrate surrounding
structures, metastasize to lymph nodes & be subsequently fatal.
Malignant
melanoma
Cancer of the melanocytes can metastasize to brain, lungs, and bone,
liver and skin and ultimately fatal.

RISK FACTORS FOR SKIN CANCER
•Fair-skinned, fair-haired, blue-eyed people
•People who sustain sunburn or who do not tan
•Long time sun exposure
•Exposure to chemical pollutants
•Elderly people and sun-damaged skin
•History of X-ray therapy for acne or benign lesions
•Scars from sunburns
•Immune-suppression
•Genetic factors

BENIGN TUMORS
 Benign tumors are common skin growths. Most do
not require any treatment but are important to
recognize to differentiate from malignant lesions.

 Characteristics and Management
 Seborrheic Keratoses
 Tumors are benign, wartlike lesions of varying size and color, ranging
from light tan to black that may appear to be stuck on; they are the most
common skin tumors in middle-aged and older people.
 Treatment is usually unnecessary, but lesions can be removed by liquid
nitrogen cryotherapy.
Actinic (Solar) Keratoses
 Premalignant skin lesions appearing as rough, scaly patches with
underlying erythema, which develop as a consequence of prolonged
exposure to ultraviolet rays.
 Develop in areas of body that experience prolonged sun exposure; may
gradually transform into squamous cell carcinoma.
 Many topical treatments are available, including the antineoplastic
fluorouracil (Efudex), the immune response modifier imiquimod (Aldara),
liquid nitrogen cryosurgery, and curettage.

Verrucae (Warts)
 Common, benign skin tumors caused by human papillomavirus.
 Often disappear spontaneously, so may not need treatment.
 Treatment options:
 Freezing with liquid nitrogenâ€”destroys wart and spares rest of skin.
 Area may be treated surgically with curettage or electrodesiccation.
 Application of salicylic acid, topical fluorouracil, topical vitamin A acid, or other
irritants may be helpful, especially for flat warts.
Hemangiomas
 Hemangiomas are benign tumor of the capillaries, which presents shortly
after birth.
 They grow rapidly for 6 to 18 months, followed by stabilization and
subsequent regression. Most hemangiomas resolve by age 9.
 Surgery is reserved for complicated hemangiomas that may be
obstructing the airway.
 Hemangiomas blocking the visual axis or compressing against the eye
are treated with high doses of corticosteroids or interferon.
 For hemangiomas that do not threaten vision or life, no intervention is
preferred.
 Lasers can be used for ulcerated hemangiomas.

Pigmented Nevi (Moles)
 Common skin tumors of various sizes and shapes, ranging from
yellowish to brown to black; may be flat, macular lesions, elevated
papules, or nodules that occasionally contain hair.
 Most pigmented nevi are harmless; however, in rare cases, malignant
changes supervene and a melanoma develops at the site of the nevus.
 Nevi at sites subject to repeated irritation from clothing or jewelry can be
removed for comfort.
 Nevi that show change in size, shape, or color become symptomatic (itch
or bleed), or develop notched borders should be removed to determine if
malignant changes have occurred. This is especially true for nevi with
irregular borders or variations of red, blue, and blue-black.
Keloids
 Benign overgrowths of connective tissue expanding beyond the site of
scar or trauma in predisposed individuals.
 More prevalent among dark-skinned individuals.
 Usually asymptomaticâ€”may cause disfigurement and cosmetic
concern.
 Managementâ€”intralesional corticosteroid therapy, surgical removal,
radiation or silicone gel sheeting

CANCER OF THE SKIN
 Skin cancer is the most common malignancy. Basal
cell carcinomas (BCCs) are easily curable because
of early diagnosis and slow progression. These
cancers are locally invasive and tend not to
metastasize. Squamous cell carcinomas (SCCs)
are less common than BCCs and have an
increased potential for metastasis. Conversely,
malignant melanomas are least common and have
a higher risk of metastasize.

 Pathophysiology and Etiology
 Most basal and squamous cell carcinomas are located on sun-
exposed areas and are directly related to ultraviolet radiation.
Sun damage is cumulative.
 Risk factors for skin cancer include:
 Fair complexion, blue eyes, blond or red hair.
 Working outdoors.
 Older people with sun-damaged skin.
 History of X-ray treatment of skin conditions.
 Exposure to certain chemical agents (arsenicals, nitrates, tar and pitch,
oils, and paraffins).
 Burn scars, damaged skin in areas of chronic osteomyelitis, fistulae
openings.
 Long-term immunosuppressive therapy.
 Genetic susceptibility.
 Multiple dysplastic neviâ€”moles that are larger, irregular, more
numerous, or variable colorsâ€”or family history of dysplastic nevi.
 Congenital nevi that are large (more than 20 cm in size)
 Types of skin cancer:
 Basal cell carcinomaâ€”arises from basal layers of the epidermis or hair
follicle; most common type, rarely metastasizes.
 Squamous cell carcinomaâ€”arises from the epidermis; metastasis occurs
more commonly than with basal cell carcinoma.
 Malignant melanomaâ€”arises from nevocytic cells in the epidermis
metastasize.

Typical basal cell below
lower lip

Classic presentation
of basal cell

Classic superficial
basal cell

 Clinical Manifestations
 Basal Cell Carcinoma
 Lesions typically begin as small nodules with a
rolled, pearly, translucent border with
telangiectasia, crusting, and occasionally ulceration
 Appear most frequently on sun-exposed skin,
frequently on face between hairline and upper lip.
 If neglected, may cause local destruction,
hemorrhage, and infection of adjacent tissues,
producing severe functional and cosmetic
disabilities.

 Squamous Cell Carcinoma
 Appears as reddish rough, thickened, scaly lesion
with bleeding and sorenessâ€”may be
asymptomatic; border may be wider, more
indurated, and more inflammatory than BCC (see
Figure 33-5B).
 May be preceded by leukoplakia (premalignant
lesion of mucous membrane) of the mouth or
tongue, actinic keratoses, scarred or ulcerated
lesions.
 Seen most commonly on lower lip, rims of ears,
head, neck, and backs of the hands.

Typical squamous cell cancer on
the ear

Typical squamous cell cancer on the face and scalp

SQUAMOUS CANCER OF THE LOWER LIP

More advanced squamous cell cancer
on the finger

 Malignant Melanoma
 Melanoma in situ. Earliest phase, difficult to recognize because clinical changes are minimal.
 Superficial spreading melanoma (most common).
 Circular, with irregular outer portions; the margins may be flat, or elevated and palpable.
 Has combination of colorsâ€”hues of tan, brown, and black mixed with gray, bluish black, or white.
 May be dull pink-rose color in a small area within the lesion.
 Occurs anywhere on body; usually affects middle-aged persons.
 Nodular melanoma.
 Spherical blueberry-like nodule with relatively smooth surface and relatively uniform blue-black,
blue-gray, or reddish blue color.
 May be polypoidal and elevated, with smooth surface of rose-gray or black color.
 Occurs commonly on torso and extremities.
 Invades directly into the subjacent dermis (vertical growth) and hence has a poorer prognosis.
 Lentigo malignant melanoma.
 First appears as tan, flat maculeâ€”malignant degeneration is manifested by changes in color,
size, and topography.
 Evolves slowly; occurs on exposed skin surfaces of persons in their 40s or 50s.
 Acrolentiginous melanoma (uncommon).
 Irregular pigmented macules, which develop nodules; may become invasive early.
 Occurs commonly on palms, soles, nail beds, and rarely on mucous membranes.
 Most common type of melanoma in Blacks and Asians

VARIETY OF MELANOMA SKIN LESIONS

Superficial
spreading
melanomas in all
stages of
development.
The small early
lesions have
irregular borders,
irregular
pigmentation,
and small white
areas indicating
regression. The
largest tumors
show an
accentuation of
all of these
features.

Superficial Spreading Melanoma

 Excisional biopsy (for histopathologic diagnosis)
and microstaging determination of thickness and
level of invasion; helps determine treatment and
prognosis.

 Management
 BCC and SCC
 Method of treatment depends on tumor location, cell type (location and depth),
history of previous treatment, and whether it is invasive, or if metastasis has
occurred.
 Curettage followed by electrodesiccationâ€”usually done on small tumors of basal
or squamous cell type (less than 1 cm).
 Surgical excision for larger lesions or for those in areas more likely to recur
(around nose, eyes, ears, lips); may be followed by simple closure, flap, or graft.
 Mohs' surgery, a microscopically controlled excision, with immediate examination
of frozen or chemically fixed sections for evidence of cancer cells. Layers are
removed until a reasonable cancer-free margin is achieved.
 Radiation therapyâ€”can be done for cancer of eyelid, tip of nose, in or near vital
structures, such as facial nerve or where tissue sparing is difficult with other forms
of treatment; also used for extensive malignancies where goal is palliation, or
when other medical conditions contraindicate other forms of therapy.
 Other therapeutic regimensâ€”topical fluorouracil, interferon, retinoids,
photoradiation.

Radiation for Skin Cancer
Electron beam for large areas. Daily (Mon-Fri)
for 3 – 6 weeks

Side Effects of Skin Radiation
The treated skin will get red, itchy and sunburned.
There are a number of good creams than can be
used including Aloe, Aquaphor, Sween, Biafine.
The skin reaction may show up in a delayed manner
(worse at 1-2 weeks) and may develop slight,
superficial ulceration or crusting, but heals quickly (1-
2 weeks) except the shin which heals more slowly

 Melanoma
 Complete excision of lesion. If depth is between 1 and 4
mm, or there is ulceration present, sentinel lymph node
biopsy may be done at the time of reexcision. Margins of
1 cm are required on reexcision. Close subsequent
follow-up is necessary.
 Systemic chemotherapyâ€”generally used for
recurrence of metastasis or palliation; may be combined
with autologous bone marrow transplantation or several
agents used in combination.
 Early detection has a 5-year survival rate approaching
95% for thin (< 0.75 mm) in primary melanoma. The 8-
year

ASSESSMENT OF SKIN CANCERS
•Change in color, size or shape of pre-existing lesion
A waxy nodule
An irregular, circular, bordered lesion
with hues of tan, black or blue
A small, red, nodular lesion
An oozing, bleeding or crusting lesion
•Pruritus
•Local soreness

MANAGEMENT OF SKIN CANCERS
•Surgical management
•MOHS’ Micrographic
Surgery
•Electro surgery
•Cryosurgery
•Radiation therapy

SECRETARY DISORDERS
SKIN
DISORDER
Seborrheic
Dermatoses
Seborrhea is excessive production of
sebum (secretions of sebaceous glands)
It can be oily(moist or greasy) or dry(flaky
desquamation-dandruff)
Skin hygiene
Proper aeration of the skin
Topical corticosteroids
Anti-seborrhea shampoo-
Containing selenium sulfide
suspension, zinc pyrithione,
salicylic acid etc.

SECRETARY DISORDERS (CONTD…)
SKIN
DISORDER
Acne vulgaris It is a common follicular disorder
affecting hair follicles. It is
characterized by comedones ),
both closed comedones and
open comedones
Nutritional therapy
Skin hygiene
Topical pharmacologic therapy - Benzyl
peroxide, topical antibiotics
Systemic pharmacologic therapy –
Antibiotics, Oral retinoids, Hormonal
therapy (corticosteroids, anti-
androgens,oral contraceptives)
Surgical – Extraction of comedo
contents, drainage of pustules and
cysts, excision of sinus tracts & cysts,
intra-lesional corticosteroids,
cryotherapy

ECZEMATOUS DISORDERS- TYPES
• Allergic contact dermatitis
• Irritant dermatitis
• Nummular eczema
• Seborrheic dermatitis
• Stasis dermatitis
• Atopic dermatitis

ECZEMATOUS DISORDERS
ASSESSMENT MANAGEMENT
Redness, Itching, Minute papules and
vesicles, Weeping, oozing or crusting of
lesions
•Avoid irritants.
•Skin hydration and skin
hygiene
•Cool, wet compresses to
soothe the skin
•Minimize scratching
•Anti-histamines and topical
corticosteroids

SKIN ALLERGIES
Inappropriate and often
harmful immune system
response to substances that
are normally harmless.
Skin allergies are usually
characterized by pruritus,
erythema, redness, urticaria,
respiratory, gastro-intestinal
symptoms.

DIAGNOSTIC TESTS
•SKIN BIOPSY
•SKIN CULTURES
•WOODS’ LIGHT EXAMINATION
•PATCH TESTING
•SKIN SCRAPINGS

TREATMENT MODALITIES FOR SKIN CONDITIONS
1.Dressings
2.Topical preparations
3.Intra-lesional therapy
4.Systemic therapy
5.Surgical treatment

ASSESSMENT
•Family History
• Personal history
skin allergies
 allergic reaction to food, medications
chemicals, previous skin problems
skin cancer
skin turgor

ASSESSMENT (CONTD…)
Physical Assessment
•Exposure to chemical & environmental pollutants
•Exposure to radiation
•Exposure to sun
•Personal hygiene habits
•Cosmetics and harsh soaps
•Medications
•Nutritional deficiencies
•Emotional stress
•Infection
•Developmental changes and ageing

Macule
Papule
Nodule
Vesicle Pustule

Excoriation
Scales
Ulcer
Fissure
Scar
Cyst
Wheal

•Assess hair and nails
for color, texture,
distribution, hair loss
Frost bite
ParonychiaPsoriasis of
Nails

Psychosocial Assessment
•Changes in body image and
decreased self-esteem
•Social isolation and fear of rejection
•Restrictions in physical activity
•Pain
•Disruption or loss of employment
and financial constraint

NURSING DIAGNOSIS
Impaired skin integrity
r/t
changes in the barrier function
of the skin

NURSING DIAGNOSIS
Sleep pattern disturbances
r/t
pruritus

NURSING DIAGNOSIS
Body image disturbance
r/t
unsightly skin appearance

NURSING DIAGNOSIS
Knowledge deficit
about
skin care & methods of
treating skin ailments

NURSING DIAGNOSIS
Potential risk for infection

Prepared by: MRS PALLAVIPARBHAT CHAUHAN

The Integumentary System: Anatomy and Functions

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