DISORDER OF

INTEGUMENTAR
Y SYSTEM
Ms. Mitali solanki,
Assistant professor,
MSC N, MSN,
ASSESSMENT:
CHIEF COMPLAINTS:
 ask the patients about itching, dryness,
rashes, lesion.
 any changes in skin, nails, hairs.

PAST HEALTH HISTORY:

 any previous history about trauma,
disease, surgery.
 skin allergy, food allergy, sun exposure
and radiation exposure.
 previous skin cancer, cosmatic history.
MEDICATION:
 ask about vitamins, minerals, hormonal,
antibiotics, corticosteroids drugs it may
cause skin changes.
 prescribed and over the counter drug
history.
NUTRITIONAL PATTERN, ELIMINATION
PATTERN, SLEEPING PATTERN,
EXERCISED PATTERN SHOULD BE
ASSESSED.
PHYSICAL EXAMINATION
 INSPECTION
I. COLOR: skin colour influenced by
many factors like temperature,
oxygenation, blood flow, exposure of
uv rays. Pallor can be caused by
decreased blood flow or anemia.
Cynosis or bluish discoloration due to
decreased tissue perfusion CVD or
respiratory diseases. Jaundice or any
liver disease may cause yellow
discoloration. Brown colour due to
excess production of melanine or
exposure of sun or pregnancy.
II. LESIONS

 Primary lesion:
1. Macules: it is flat, non palpable,
discolored skin area less than 1 cm.
2. Papules: It is solid elevation of skin with
no visible fluids, variable size seen from
pinhead to 1 cm. It can be brown,
purple, pink or red in color.
3. Pustules: these are elevated, pus filled
vesicle with circumscribed border
commonly seen in chest, back, neck or
face. Can seen after insect bite or
allergic reaction.
4. Cyst: sac like pocket of tissue that
contains fluid, air, other substances. Most
cyst are benign or non cancerous.
5. Nodules: it is growth that form under the
skin and it may filled with inflammed
tissue or mixture of tissue with fluid form
a lump.
6. Wheal: it is rounded, flat topped, pale red
papule that disappear within 24-48 hours.
Its seen after intra dermal injection.
7. Vesicle/ bulla: it is elevated, fluid filled,
round/oval shaped mass with thin,
circumscribed wall. Pin sized to 10 mm is
vesicles. After that it is known as blister
and when blister become larger than 1 cm
its called bulla.
2. SECONDARY LESION:
1. Ulcer: complete loss of epidermis ,
dermis and subcutaneous layer. In
ulcer necrosis tissue, bleeding and scar
tissue is present.
2. Fissure: it is cutaneous condition in
which linear like cleavage of skin
present. It is smaller than laceration.
Many fissure is known as cracked skin
and result from dry skin.
3. Scales: it is excess dead skin cell
white, grey or silver colour. Eg
dandruff, dry skin.
4. crust: it is deposition of dry blood,
serum, debris, pus with bacteria Over
the skin. Its can be brown, orange or
yellow.
5. scar: scar is flat, irregular area of
connective tissue left after a lesion or
wound has healed and made up of
fibrous tissue.
6. Keloids: it is elevated, irregular,
darkened area of excess scar tissue
caused by excessive collagen
formation during healing.
PALPATION:
 Palpate the skin to assess the
temperature, moisture, turgor, texture.
 Skin turgor: pinched the skin between
thumb and finger and released.
Normally it quickly it return back. Poor
skin turgor return take time and its
indicate dehydration and loss of skin
elasticity.
 Edema: when pressure applied from
finger leave an indentation its known as
pitting edema.
 1+ edema: 2 mm depth, slight pitting
 2+ edema : 4 mm depth, deep pit
 3+ edema: 6mm moderate pitting,
swallow extremities.
 4+ edema: 8mm indentation (depress)
last 2 to 3 min.
 Assess the hair color, texture, quality,
thickness.
 Assess the nail for color, shape,
thickness and abnormalities. Capillary
refill and clubbing of finger (nail 180+
degree angle) indicate respiratory,
cardio vascular disorder, liver disorder.
DERMATITIS
 Definition:
 Dermatitis is inflammation of upper layers
of skin, causing itching, blisters, redness,
swelling and often oozing, scabbing and
scaling.
TYPES OF DERMATITIS:
 Contact dermatitis
 Atopical dermatitis
 Seborrheic dermatitis
 Exfoliative dermatitis
CONTACT DERMATITIS
 Contact dermatitis: It is inflammation of skin
caused by direct contact with particular
substance such as jewellary, cleaning
product, perfumes and cosmetics.

 Types:
1. irritant contact dermatitis
2. allergic contact dermatitis
1. irritant contact dermatitis:
80% person have this type occurs, when
chemical substances direct damage to the
skin. It is more painful than itchy.

Causes:
 soaps, chemical solvents, cosmetics and
skin products including deodorant.
 Irritated by body fluids.
2. allergic contact dermatitis:
it occurs when a substance to which
patient is sensitive trigers immune
response in skin.

CAUSES:
 Poison ivy
 Rubber
 Antibiotics, antihistamins
 Hair removing chemicals
 Deodorants
 After shave lotions
 Perfumes
 Perservatives and metals.
PATHOPHYSIOLOGY
Due to etiology

Activation of T cells

Inflammatory process begins

Release of cytokinease and other
chemical mediator

Icthing, swelling and pain

CLINICAL
MANIFESTATIONS:
 Red rash
 Swelling and large blister
 Dry, cracked, red patches
 Blister, draining fluids and crust
 Pain or tenderness

Diagnostic evaluation:
 History collection
 Physical examination
 Patch test
MANAGEMENT
 Medical management:
1. antihistamin: hydroxyzine,
diphenhydramine
2. corticosteroids: hydrocortisone
3. topical hydrocortisone application to
reduce the itching and inflammations
 Avoid contact with irritant or allergen
ATOPICAL DERMATITIS

 Atopical dermatitis is a common,

chronic, relapsing, pruritic, eczema that
begins in childhood.

 Etiology:
 Family history
 Environmental pollutants
 Overly sterile and modern lifestyle
 Harsh soap or detergent
 Weather change cold and dry
CLINICAL
MANIFESTATION:
 Redness
 Oozing
 Crusting rash
 Pruritus
 Itching
 Rashes on the extremities, back of
knees, neck, eyelids, back of the hands
MANAGEMENT
 hydrate the skin
 remove allergent
 Reduce inflammation
 Antibiotics
 antihistamins
SEBORRHEIC DERMATITIS
 It is a common, chronic inflammation of the
skin disorder generally confined the area of
skin regions with a high density od sebaceous
glands(face,scalps and upper trunk)

Causes:-
 Idiopathic
 Risk factors:
 Incresed androgen during puberty
 Law immunity
 Mood disorder
 Spinal injuries
CLINICAL
MANIFESTATION:
 Dry and greasy scaling of scalp
 Itching without hair loss
 Yellowish or reddish scaly pimple
 Redness, crusting of eyelids

DIAGNOSTIC EVALUATION:
 history collection
 Physical examination
MANAGEMENT
 Antifungal shampoo: ketoconazole
 Antiboitic cream: metronidazole
 Light therapy
EXFOLIATIVE DERMATITIS:
 It is a severe inflammation that cause
the entire skin surface to become red,
cracked and cover with scales.

Causes:
 Autoimmune cause
 Skin yeast
 Certain medication antibiotics,
antianxiety or depression medication
CLINICAL
MANIFESTATION:
 It start suddenly and spread
 Red and shiny skin
 Peeling of skin, loss of hair and nail
 Itching
 Enlarged lymph nodes
 Fever and chills

DIAGNOSTIC EVALUATION:
 history collection
 Physical examination
 Scartch test
MANAGEMENT
 Antibiotic medication
 IV fluids
 Nutritional supplementation
 Corticosteroids- prednisone 40-60 mg
 Topical corticosteroids(hydrocortisone
ointment)
COMMON VIRAL
INFECTION
 Warts
 Herpes simplex
 Herpes zooster
WARTS
 Wartsis a painless growth on the skin,
mucus membrane and genital area. It can
be sexually transmited.

Etiology:
 Human papillomavirus

Clinical Manifestation:
 Smooth flat surface
 Sometime painful
Management:
1. chemical: salicylic acid, tretonoin
2. Freezing: liquid nitrogen spray or
topical application through cotton
3. Burning and cutting: laser or electrical
current used for burning. it is painful
and leaving scar.
HERPES SIMPLEX
 Herpes simplex is a common skin infection.
There are two types of the causative virus,
which are identified by viral typing. Generally,
herpes simplex type 1 occurs on above waist
lips, face and mouth and type 2 in the genital
area.
MODES OF TRANSMISSION:
 Direct contact
 Respiratory droplet
 Salivary secretions
Clinical manifestation:
 Burning and tingling sensation
 Area become erythmatous and swallon
 Redness
 Lesion may burn, itch and painful
 Vesicle become pastule, ulcer and crusting
healing take place in 10 to 14 days
 Fever, sore throat
 Lesions appear as grouped vesicles on an
erythematous base initially involving the
vagina, rectum, or penis.
Diagnostic evaluation:
 History collection
 Physical examination(lesion assessment)
 Tzanck smear test- with blunt scalpel blade
scrape the base of lesion and take smear on
slide
 Vesicle fluid culture

Management
 Antiviral medication – acyclovir orally or
ointment
200 mg of acyclovir administered five times
each day for 5 days
famciclovir
 Sunscreen
HERPLES ZOSTER
 Herpes zoster, also called shingles, is an
infection and acute inflammation
caused by the varicella-zoster virus
characterized by a painful vesicular
eruption along the area of distribution of
the sensory nerves from one or more
posterior ganglia.
Etiology:
 Varicella zoster virus
 Old age
 Patient on immunosupresant agent
 Law immunity
 Radiotherapy or chemotherapy
 After organ transplant
 Cranial nerve and spinal injuries
PATHOPHYSIOLOGY
due to etiology

herpes virus infection in ganglia near

brain and spinal cord

virus travel by peripheral nerve to skin

multiplication and formation of blister

Clinical manifestation:

 eruption is usually accompanied or preceded by

pain
 pain may be burning, lancinating (ie, tearing or
sharply cutting), stabbing, or aching.
 Some patients have no pain, but itching and
tenderness may occur over the area.
 malaise and gastrointestinal disturbances
 patches of grouped vesicles appear on the red
and swollen skin.
 The early vesicles, which contain serum, later
may become purulent, rupture, and form crusts.
 .
CONTI..
 The blisters are usually confined to a narrow
region of the face or trunk
 The clinical course varies from 1 to 3 weeks.
 If an ophthalmic nerve is involved, the patient
may have eye pain.
 The healing time varies from 7 to 26 days
Diagnostic evaluation:
 History collection
 Physical examination
 Blood test

Management
 oral antiviral agents such as acyclovir
(Zovirax), valacyclovir (Valtrex), or
famciclovir (Famvir) are administered
within 24 hours of the initial eruption.
 Analgesic to reduce pain
FUNGAL INFECTION
TINEA PEDIS: ATHLETE’S
FOOT
 Tinea pedis (ie, athlete’s foot) is the
most common fungal infection. It is
especially prevalent in those who use
communal showers or swimming pools

Etiology:
 Trichophyton rubrum
Clinical manifestation:
 Soles of one or both feet have scaling and mild
redness
 More acute infections may have clusters of clear
vesicles on dusky base.
 Bad smelling
 Thick, abnormal toenails
 Peeling, cracking and scaling of feet

Diagnostic evaluation:
 History collection
 Physical examination
Medical Management
 soaks of potassium permanganate solutions
are used to remove the crusts, scales, and
debris and to reduce the inflammation.
 Topical antifungal agents (eg, miconazole,
clotrimazole) are applied to the infected
areas. Topical therapy is continued for several
weeks because of the high rate of recurrence.
TINEA CAPITIS:
RINGWORM OF THE SCALP
 Ringworm of the scalp is a contagious
fungal infection of the hair shafts and a
common cause of hair loss in
children(toddler and school age
children).
Causes:
 Microsporum canis and tricophyton
verrucosum. It can spread by close
contact with person and pet. Increase
risk with sharing towel, haircomb, hats
of infected person
Clinical manifestation:
 Hair loss
 Scaly scalp
 Itchy scalp
 Black dots on scalp
 Patches slowly enlarge
 Brittle or fragile hair
 Tender or painful area on scalp
 Temporary hair loss
 Medical Management
 Griseofulvin, an antifungal agent, is
prescribed for patients with tinea capitis.
 Topical agents do not provide an effective
cure because the infection occurs within
the hair shaft and below the surface of the
scalp.
 However, topical agents can be used to
inactivate organisms already on the hair.
This minimizes contagion and eliminates
the need to clip the hair.
 The hair should be shampooed two or three
times weekly, and a topical antifungal
preparation should be applied to reduce
dissemination of the organisms.
Nursing Management
 Because tinea capitis is contagious, the
patient and family should be instructed
to set up a hygiene regimen for home
use.
 Each person should have a separate
comb and brush and should avoid
exchanging
hats and other headgear.
 All infected members of the family must
be examined because familial infections
are relatively common. Household pets
should also be examined.
TINEA CORPORIS
 Tinea corporis is ringworm of infection of
the trunk,legs and arms and
characterized by red circular rashes with
clearer skin in the middle.
Causes:
 Ringworm is fungal infection caused by
dermatophytosis mold like parasites.
 Directed contact with infected peson
and animal. heat and humidity increase
the chances of spreading infection
 Crowding
 Sharing clothing, bedding or towel with
fungal infected person
 Sports like wrestling
 Wear tights and restricted clothing
 Law immunity.
Clinical manifestation:
 Red ring shaped patches
 Affected skin may contain blisters,
bumps, or scabs.
 Itching, burning

Diagnostic evaluation:
 History collection
 Physical examination
 Scraping skin test
Management:
 Topical antifungal drugs: clotrimazole,
terbinafine
 Oral antifungal drugs: itraconazole,
terbinafine.
TINEA CRURIS
 Jock itch is fungal infection that affect the
skin of genital, inner thighs and buttocks.
Causes:
 Dematophytes
 Overweight man
 Tight clothing
 Hot, humid weather
 Law immunity
 Man who play more sports
 Sharing towel, comb, toilet seat.
 Clinical manifestation:
 Inflammation of groin, anal region and
upper thigh
 Patches
 Sharp border
 Redness
 blisters
MANAGEMENT
 Antifungal cream, powder, or lotion:
clotrimazole, miconazole application for
2- 3 weeks
 Wear loose cloth and underwear
 Showers after exercises
 Wash clothes after uses
 Separate towel and cloth
 Use talcum powder
TINEA UNGUIUM
 It is fungal or yeast infection affect the
nail and causes brittle and thick nails.
Causes:
 Trichophyton species or candidia albicans
 Tight footwear
 Humid and moist environment
 Wear shoes and socks that not absorb
sweating
 Athlete’s foot
 Minor trauma
 AIDS and DM
Clinical manifestation:
 Pain and discomfort
 Nails is brittle, thickened and dull
 Debris accumulation under nails
 Surrounding skin infection cellulitis

Diagnostic evaluation:
 History collection
 Scraping nail and microscopic
examination
 Nail culture
 Management:
 Oral antifungal medication: teribinafine
and itraconazole
 Antifungal nailpaints: ciclopirox
 Surgical nail removal
PEDICULOSIS
 Pediculosis is infestation of the hairy
parts of the skin or clothing with eggs,
larvae or adults of lice
 Lice are called ectoparasites because
they live on the outside of the host’s
body. They depend on the host for their
nourishment, feeding on human blood
approximately five times each day. They
inject their digestive juices and
excrement into the skin, which causes
severe itching..
PEDICULOSIS CAPITIS
 Pediculosis capitis is an infestation of
the scalp by the head louse. it can
spread to axilla and pubic area.
 Clinical manifestation:
 Pruritis
 Scartching
 PEDICULOSIS CORPORIS AND PUBIS
 Pediculosis corporis is an infestation of
the body by the body louse. This is a
disease of unwashed people or those
who live in close quarters and do not
change their clothing. Pediculosis pubis
is extremely common. The infestation is
generally localized in the genital region
and is transmitted chiefly by sexual
contact.
 Clinical Manifestations
 Chiefly involved are those areas of
the skin that come in closest
contact with the underclothing (ie,
neck, trunk, and thighs).
 intense itching and scratching,
especially on the trunk and neck.
 Among the secondary lesions
produced are slight degree of
eczema.
 In long-standing cases, the skin
may become thick, dry and scaly,
with dark pigmented areas.
 Itching is the most common
symptom of pediculosis pubis,
particularly at night.
 Infestation by pubic lice may
coexist with sexually transmitted
diseases such as gonorrhea,
herpes, or syphilis.
 Gray-blue macules may
sometimes be seen on the trunk,
thighs, and axilla
MANAGEMENT:
 The patient is instructed to bathe with
soap and water, after which lindane
(Kwell) or 5% permethrin (Elimite) is
applied to affected areas of the skin and
to hairy areas.
SCABIES:
 Scabies is an infestation of the skin by the itch
mite Sarcoptes scabiei. It is parasitic
infestation cause extreme skin itching.
Etiology:
 Scarpotes scabiei
 Constant contact with infected cloth, bedding
and animals
PATHOPHYSOLOGY:
Pregnant mite burrow into skin

Produce 2-3 eggs for about month

Egg hatching occur in 3-5 days and larvae

came to surface of skin but burrow into
skin for food

Become adult mites in 10 days

clinical manifestation
 Spread by skin to skin contact with
infected person
 Itching, severe at night
 Burrow which is thin, grey, red, irregular
on the skin
 Rashes, small blister
 Nodules on the skin
 Vesicles, papules and crust formation
Diagnostic evaluation:
 History collection
 Physical examination

Management:
 Scabicide lotion: lindane, crotimiton or
permethrin application over skin.
 Antihistamin drugs
 Calamine lotion to reduce itching and
pain
 Apply cold water cloth
ALOPECIA
 Alopecia is defined as loss of hair from
body.

 There are mainly two types.

 Alopecia areata : it occur when the
body’s immune system attack hair
follicle and hair fall may cause.
 Androgenetic alopecia: it is inherited
hair loss. It is permanent hair loss.
ETIOLOGY
 Genetic prediposition
 Systemic disease- SLE, thyroid, pituitary
insufficiency
 Previous trauma, radiation, skin
infection
 Certain medication: chemotheraputic
agent
 Androgen also cause post menopause in
women.
 Autoimmune disoder
CLINICAL MANIFESTATION
 Gradual thining of hair
 Complete hair loss at hair top line and
top of head.
 Men can go for complete bald
Diagnostic evaluation:
 History collection(medication, family
or trauma)
 Biopsy of hair
 Blood test (andogen)
MANAGEMENT:
 Minoxidil: topical minoxidil 1 ml for bd.
Hair growth take place in 8 to 12 month.
 Finasteride: 1 mg oral once/day. It is not
indicated for female.
 Corticosteroids:
 Hair massage
 Aroma therapy
Surgical management:

 hair transplantation small hair is taken

from back or side of scalp is replaced in
area of alopecia.
 Flaps: flap is taken is taken from hair
bearing area of scalp and transplanted
on the bald area of scalp.
PSORIASIS
 It is a chronic, non infectious, recurrent
erythamatous inflammation characterized
by redness, scale or plaques formation.
Causes:
 Idiopathic
 Family history
 Genetic predispotion
 Environmental factor- seasonal changes,
sunburn
 Hormonal imbalance
 Medication like corticosteroids, lithium
PATHOPHYSIOLOGY
Keratocyte epidermis cell travel to basal cell
to the stratum corneum within 4-7 days (ie,
skin surface) and be cast off in 3 to 4 days,
called hyperkeratosis

increased number of basal cells and rapid cell

passage

the normal events of cell maturation and

growth cannot take place which lead to
erythema

does not allow the normal protective layers of

the skin to form(inflammation and plaque
formation)
CLINICAL MANIFESATION:
 Lesion occur on scalp, elbows, knees,
genitalia,
 Well defined erythematous plaque with
silver white scales
 Red or pink thicken area
 Severe itching and pain
 Skin crack or bleed
 Sleep derivation
 Low self esteem
 Depression
 Sadness, embarrassment
 DIAGNOSTIC EVALUATION
 history collection
 skin biopsy or scraping
MANAGEMENT:
 MEDICAL MANAGEMENT:
 Topical therapy: corticosteroids hydrocortisone ,
betamethasone
 keratolytics- it breakdown the outer layer of skin
n decrease the thickness of psoriatic plaque eg
salicylic acid to loosen or removal of scar
 Vitamin D analogues: calcipotrience (duvonex)
cream or lotion it slow the skin growth
 Anthralin: it remove the scale and sooth the skin
 Topical retinoids: decrease inflammation vitamin
A derivatives. Tazarotene don’t go to sunlight
and containdicated in pregnant women.
 Mosturizers, mineral oil or petroleum
jelly sooth effect and reduce dryness.
 Oils (eg, olive oil, mineral oil, Oatmeal
Bath) or coal tar preparations (eg,
Balnetar) can be added to the bath
water and a soft brush used to scrub the
psoriatic plaques gently
 2. phototherapy: it may be helpful for
inhibiting the abnormally rapid
production of psoriatic cell.
ACNE VALGARIS
 it is common and chronic skin disorder
of pilosebaceous that affect the face,
chest and back.
 Onset occur in puberty because
increase level of androgens. Sometimes
it will persist through life time.
ETIOLOGY
 Excessive sebum production
 Bacterial infection
 Abnormal keratinization
 Increased androgen production
 Change in hormone during puberty and
menstrual cycle
 Genetic
 Family history
 Inflammation by immune reaction
 industrial exposure
 Hair gel or oil based cosmetics
 Sports equipment eg helmet
 Medication lithium, corticosteroids, oral
contraceptive pills
 Type of acne

1. Non inflammatory acne

2. Inflammatory acne
3. Cystic acne
PATHOPHYSIOLOGY
Due to etiology

Excessive production of sebum

Pilosebaceous gland get plugged

Cutaneous flora microorganism will

multiplies in anaerobic environment

Inflammation occur acne

develop(comodones)
CLINICAL MANIFESTATION
 Lesion on face, neck, back, chest and
shoulder
 Painful, tenderness
 Comodones: whiteheads(close) and
blackheads(open comodones)
 Papules and pustules
 Nodules
 Cyst, abscess and scar formation
DIAGNOSTIC EVALUATION:
 History collection
 Physical examination
Management:
 Medical management:
1. Acne over counter medication: salicylic
acid, sulfur, benzoyle peroxide
containing lotion. It will dry up the oil
and kill the bacteria
2. Topical treatment: tazarotene, tretinoin,
adapalene. These drugs derived from
vitamin A. it will kill the bacteria and
prevented plugging of hairfollicles.
3. Antibiotics:
4. Laser therapy and light therapy: laser
therapy damage the sebaceous gland so
less oil production occur and light
therapy kills the bacteria.
5. Cosmetic procedure: chemical peeling
and microdermabrasion it will help in
sunburn and removing of fine lines and
lighting the facial scar.
PRESSURE ULCER
 A Pressure ulcer is localized injury to the
skin and underlying tissue, usually over a
bony prominence as a result of pressure or
pressure in combination with friction.
 It is also called as bedsore, decubitus ulcer.

Etiology:
 Immobility and inactivity
 Injury
 Bedridden patients
 Lack of sensory perception
 Diabetes or other vascular disease
PATHOPHYSIOLOGY
Pressure on soft tissue between bony
prominent and occlusion of blood flow

Blister formation

Ruputre of the blister and colonization of

bacteria in open wound

Proliferation of bacteria is form

bioflim(slough in the wound)
Increase pressure may cause ischemia
and necrosis

Necrotic tissue develop scar

CLINICAL MANIFESTATION
 Stage 1
 Intact skin with redness in localized area
 Dark skin pigmentation
 pain

Stage 2
 Partial thickness of loss of dermis
 Open ulcer with reddish or pink wound
 Open(rupture) or intact(serum filled )
blister ulcer
 Wound is shiny or dry, pus like draining
 Swallon, warm and red area
 Stage 3
 Full thickness tissue loss
 Subcutanous fat is visible but bone,
tendon, muscles are not visible
 Foul smell, oozing of pus andfluid
 Stage 4
 thickness tissue loss with bone, tendon,
muscles.
 Slought or eschar formation in some
area
Unstageable
Suspected deep tissue injury
MANAGEMENT:
Medical management:
 NSAIDs: ibrupen and napoxen sodium to
relieve pain
 antibiotic
 Cleaning and Wound dressing
 Debridement
 Flap reconstruction
 Pressure reduction: using support device
and repostioning
 Air or water bed
 Improve nutrition
 Monitor the complication : septicemia,
osteomyelitis, bacteremia, cellulitis
BENIGN SKIN LESIONS
 CYST:
 CYST IS SAC LIKE GROwth with well
defined wall that may contain liquid,
semi fluid or solid material.
 A cyst is firm, gobular, movable and
nontender cyst with 1-5 cm in range.
 Develop at result of infection, clogging
of sebaceous gland or around foreign
bodies.
 It seen in face, neck or upper body
TREATMENT:
 Surgical excision
 Intralesion steroids therapy.
 Law dose of radiation therapy.
KELOIDS
 Keloids are smooth overgrowth of
fibroblastic tissue arise in the area of
injury.
 Wound or poor alienment of skin are the
risk factors.
 They appear in upper trunk, upper back
and mid chest.
 Keloids are shinny, smooth and slightly
pink or hyperpigmented
TREATMENT
 Corticosteroids: triamcinolone acetonide
 Surgical or laser excision
KERATOSIS
KERATOSES
 A benign skin lesion that is pigmented
light tan to dark brown patches.
 The cause is unknown. It occur in middle
age older patient.
 It occur on trunk, scalp, face and
extremitie.
 They may be oval or round and flesh
colour, brown and black.
 It can removed by cryotherapy.
LIPOMAS
 Soft, movable, subcutaneous nodule of
adipose tissue. It is single or multiple
 It appear on trunk and extremities.
 It is asymptomatic but sometimes
tender or painful.
 Treatment: excision or liposuction.
MALIGNANT MELANOMA
 It is a cancer of melanocyte, which produce
melanin.
 The most dangerious skin cancer. These
cancerous growth occur when unrepaired
DNA to damage skin cell.
 Etiology
 Unknown
 Sun exposure
 Chronic UV exposure without sun protection
 Family history
 Fair skin and blue eye people
 Immunosupressant
 Atypical mole syndrome
PATHOPHYSICAL
Due to etiology

Malignant melanoma develop

Tumor develop lesion are flat and benign

Lesion penetrate to dermis layer mix with

blood and lymph.

Metastasis
STAGE:
 Stage I and II/: localised primary
melanoma
 Stage III: metastasis to regional lymph
node
 Stage IV: distance organ metastasis
CLINICAL
MANIFESTATION:
 Skin lesion
 Grow fast and double in size
 Irregular raised surface
 Lesion have brown colour with black,
red, pink or white
 Ozzing, bleeding or nodule
DIAGNOSTIC EVALUATION
 History collection
 Physical examination
 Biopsy
 Chest x ray
 Ct
 MRI
 Surgical removal of lymph nodes
 Chemotherapy:
 Radiation therapy
 Target therapy: debrafenib, trametinib
 Biological therapy: boost immune
system to fight against cancer
interlukin-2, nivolunab
VITILIGO
 vitiligo is a disease that causes loss of skin
color in patches. The discolored areas
usually get bigger with time. The condition
can affect the skin on any part of the body. It
can also affect hair and the inside of the
mouth.
 Etiology
 pigment-producing cells (melanocytes) die
or stop producing melanin — the pigment
that gives skin, hair and eyes color. The
involved patches of skin become lighter or
white. It's unclear exactly what causes these
pigment cells to fail or die.
 It may be related to:
 A disorder of the immune system
(autoimmune condition)
 Family history (heredity)
 A trigger event, such as stress, severe
sunburn or skin trauma, such as contact
with a chemical
CLINICAL MANIFESTATION
 Patchy loss of skin color, which usually
first appears on the hands, face, and
areas around body openings and the
genitals
 Premature whitening or graying of the
hair on your scalp, eyelashes, eyebrows
or beard
 Loss of color in the tissues that line the
inside of the mouth and nose (mucous
membranes)
MANAGEMENT
 Corticosteroid cream
 calcineurin inhibitors. tacrolimus (Protopic) or
pimecrolimus (Elidel) might be effective for people
with small areas of depigmentation, especially on
the face and neck. The U.S(FDA) has warned about
a possible link between these drugs and lymphoma
and skin cancer
 Light therapy. Phototherapy with narrow band
ultraviolet B (UVB) has been shown to stop or slow
the progression of active vitiligo. It might be more
effective when used with corticosteroids or
calcineurin inhibitors. You'll need therapy two to
three times a week. It could take 1 to 3 months
before you notice any change, and it could take 6
months or longer to get the full effect.
 Laser therapy: to remove small stable
area of vitiligo. Vitiligo are treated twice
weekly.
 Surgical management
 Tissue or cellular grafting
PEMPHIGUS
 It is a group of rare disease caused by
autoimmune disorder that form blister
on the skin.
TYPES:
 There is different types,
 Pemphigus valgaris: this is most
common type blister doesn’t itch & first
appear in mouth slowly they spread to
skin& genitals can be painful.
 Pemphigus faliaceus: in this condition
the blister first appear on the face &
scalp but doesn’t occur in mouth. Blister
appears on chest and neck and usually
are itchy.
 Pemphigus vegetans: blister appear on
groin, under arms & on the feet.
PARANEOPLASTIC
PEMPHIGUS
 This is very uncommon condition some
cancer cell present.
 Risk factor
 People who live in rainforest in brazil
 Older adults
 Side effect of ACE inhibitor, penecilin
PATHOPHYSIOLOGY
Due to etiology
Antibody breakdown the bond between
the cell
Fluid collection between the layer ofskin
Blister formation
 Clinical manifestation
 Blister in mouth
 Painful blister
 Oozing, crusting and peeling of the
blister
 Dysphagia
DIAGNOSTIC EVALUATION
 History collection
 PE
 Skin biopsy
 Endoscopy
 Management
 Corticosteroid- prednisone
 Supplimentation of calcium, VIT D, law
salt diet.
 Immunosupressant- cyclophosphamide
methotrexate
 Plasmapheresis- the procedure include
the removal and change of blood
plasma & its compartments.