Skin Disorders

Dr. Dharmesh B. Patel

Chief Medical Officer,
J.J.Bajaj Naturecure & Health Centre,
Gujarat Vidyapith, Randheja.
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 STRUCTURE OF THE SKIN

• OUTERMOST layer is the EPIDERMIS

• Consists of stratified or squamous epithelium
• Top layer of epidermis contains KERATIN – a
tough, fibrous protein that protects skin from
harmful substances
• Bottom layer of epidermis contains MELANIN
– dark pigment in skin that protects body from
harmful rays of the sun
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 STRUCTURE OF THE SKIN
• DERMIS – “True Skin”
lies below the epidermis
• Composed of connective
tissue
• Supports blood & lymph
vessels, elastic fibers,
nerves, hair follicle, sweat
glands & sebaceous (oil)
glands
• SUBCUTANEOUS –lies
under the dermis
• Connects the skin to
underlying structures (i.e.
muscle, fat)
• Contains adipose (fat
cells) tissue – helps
insulate body from cold &
heat
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 Structure Of Skin
બા વચા (Epidermis) ત ્ વચા (Dermis)

• બા વચા ુ પડ માણમાં • બા વચાની દરની બા ુ એ

ુ અને કઠણ હોય છે . આવેલી હોય છે .
• પગના ત ળયા તથા હથેળ ની • તેમાં કશવા હનીઓ,
ચામડ ડ હોય છે . રસવા હનીઓ, ાનતં ુ ઓ,
• વચા કોષોના અનેક થરની વેદિપડો, નેહિપડો, વાળના
બનેલી હોય છે . ૂ ળ તથા ના ુ ત ં ુ ઓ આવેલા
• ાનતં ુ ઓ અને હોય છે .
ર તવાહ નીઓ હોતી નથી. • આત ્ વચાની ઉપરની સપાટ
• સૌથી નીચેના થરમાં મેલેનીન વાંક ૂ ં ક હોય છે .
ના કણો આવેલા હોય છે .

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 વેદિપડ (Sweat Gland)

• ચામડ ના નીચેના ભાગમાં આવેલા હોય છે.

• ૂ મ ર તવાહ નીઓ ુ એક ૂ ં ચ છે .
• ચામડ પર દખાતા િછ ો તે ુ ુ ખ છે.
• ના ારા પરસેવો બહાર ફકાય છે .
• પરસેવામાં પાણી, ુ ર યા,મી ુ ં તથા ગારવા ુ હોય
છે .

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 વેદિપડના કાય

• શર રમાંથી નકામો કચરો બહાર ફકવો.

• શર ર ુ ઉ ણતામાન ળવ .ુ

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 નેહિપડ (Sebaceous Gland)

• નેહિપડો ત ્ વચામાં વાળના ૂળની પાસે

હોય છે .
• તેમાંથી તૈલી ય નીકળ ચામડ પર પથરાય છે .
• ચામડ તથા વાળ બ ે લીસાં, ુ ં વાળા અને ચમકતાં
રહ છે

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વાળ (Hair)

• વાળની ઉ પિ બા વચામાંથી થાય છે .

• િશગડા વા કઠણ પદાથનો બનેલો હોય છે .
• વાળ શર રના સ દયમાં વધારો કર છે
• શર રને ઠં ડ થી બચાવે છે .
• પશ ાન થવામાં મદદ પ થાય છે .
• મર,પાંપણ,નાક અને કાનમાંના વાળ ૂ ળના કણોથી
ર ણ કર છે .
• વાળમાં ાનતં ુ ઓ અને ર તવાહ નીઓ હોતી
નથી. થી વાળ કપાવતી વખતે ુ ખાવો થતો નથી.

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 નખ (Nail)

• િશગડા વા કઠણ પદાથના બનેલા હોય છે .

• નખની ઉ પિ બા વચામાંથી થાય છે .
• નખ ુ ૂ ળ ત ્ વચામાં સખત ર તે જડા
યે ુ
હોય છે .

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 FUNCTIONS OF THE SKIN
• The skin or the integument is a vital organ
• Regulates body temperature
• Senses pain / touch
• Protective wrap - harmful substances &
microorganisms from entering body
• Provides a shield from harmful effects of the sun
and helps in Vit-D production
• Largest organ of the human body
• Absorption
• Excretion 14
 FUNCTIONS OF THE SKIN

• Indicates malfunction within the body through

color changes
• Cyanosis (blue) is lack of O2-cardiovascular
problem
• Jaundice (yellow) – indicates liver disease
from accumulation of bilirubin in the blood
• Abnormal redness – due to polycythemia,
carbon monoxide poisoning, & fever
• Pallor (whitening) may indicate anemia
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CLASSIFICATIONS OF SKIN DISEASES

• Skin diseases are identified and classified

according to characteristic lesions (size,
shape, color & location) and other S & Sx’s
• PRURITIS – itching
• EDEMA – swelling
• ERYTHEMA – redness
• Inflammation –usually accompany lesions
and are helpful in making a diagnosis (DX)

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CLASSIFICATIONS OF SKIN DISEASES
• VESICLES – small blister-like eruptions or
larger fluid-filled lesions called bullae.
• PUSTULES – lesions that contain pus
• MACULAR – flat lesions
• PAPULAR – raised lesions
• ERYTHEMATOUS – reddened area due to
inflammation &/or injury
• Nodules & tumors – hard to the touch
• Pruritis – itching, which accompanies many
skin diseases, especially allergic & parasitic
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 INFECTIOUS SKIN DISEASES
BACTERIAL
• IMPETIGO – is acute, contagious & common
in children
• Caused by streptococcal & staphylococcal
organisms in the nose & passed to the skin
• Erythema, reddened area develops and oozing
vesicles and pustules form
• Area ruptures & yellow crust covers lesion
• Face & Hands most frequently affected
• Fever & enlarged lymph nodes may present
• Wash with soap & H20, dry, keep open to air
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Impetigo

Erysipelas 21
 INFECTIOUS SKIN DISEASE
BACTERIAL
• ERYSIPELAS – inflammatory skin infection
caused by streptococci
• Commonly appears on face, arm or leg
• Infection begins where skin is broken
• Shiny, swollen, red rash initially develops, often
with small blisters
• Red rash is hot & tender to touch
• Fever & chills present when infection severe
• Treatment with antibiotics (ABX) when severe22
 INFECTIOUS SKIN DISEASE
BACTERIAL

• CELLULITIS - spreading infection of the

skin most often caused by streptococcus
• Most common on the legs and begins with
skin damage
• Affected area is swollen, red, & tender
• Sx’s may include fever & chills
• Treatment (TX)– prompt TX prevents the
spread of infection to the blood & vital organs
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Cellulitis

Folliculitis

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 INFECTIOUS SKIN DISEASES
BACTERIAL
• FOLLICULITIS – inflammation of hair follicles by
staphylococci
– Small number of pustules develop in follicle
– Commonly occurs in young men and affects thighs, buttocks,
beard & scalp TX-severe cases require oral ABX
• CARBUNCLES- clusters of boils.
– Arise in cluster of hair follicles
– Develop & heal more slowly than furuncles
– Mostly appears in men and commonly found on back of neck
• FURUNCLES – “ boils ” are large, tender, swollen raised
lesions caused by staph Appears in hair follicles on face, neck,
breast, or buttocks
– The core of furuncle is necrotic & liquefies to form pus

• TX-moist heat, antiseptic skin cleansing, oral ABX, I & D25

 VIRAL SKIN INFECTIONS
Most common viruses cause cold sores or fever
blisters & warts
• HERPES SIMPLEX – causes cold sores &
fever blisters
• VERUCCA VULGARIS – causes WARTS
– Keratinocytes proliferate making the surface rough
– Most common in children & young adults
– Affects mostly the hands
– Multiple & CONTAGIOUS – spread by scratching
– Reoccurs if virus remains in body, not serious
– May disappear spontaneously, not painful
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Verucca Vulgaris Plantar Warts

Herpes Simplex

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 VIRAL SKIN INFECTIONS
WARTS
• PLANTAR WARTS – found on the SOLES OF
THE FOOT
– GROWS INWARD, unlike other warts on the
body which grow outward (elevated)
– Painful, due to pressure on the soles of the foot
when walking or standing
– Difficult to remove permanently
• GENITAL (VENEREAL) WARTS – very
serious & difficult to remove
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 FUNGAL INFECTIONS

• DERMATOPHYTES (FUNGI) – live on the

dead, top layer of the skin
• Symptoms may or may not appear
• Serious infections – itching, swelling,
blisters & severe scales
• Minor infections – mild irritation &
swelling

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 FUNGAL INFECTIONS
• RINGWORM (TINEA) –
caused by many different
fungi. Classified by its
location on the body
• Found on warm, moist areas of
the body and hairy skin on
head, groin, arms, & legs
• SX’s – mild scales, cracking
skin, to painful raw rashes
• TX- keep area clean & dry,
apply antifungal meds.
• TINEA CORPORIS –
Body ringworm, smooth
areas, arms, legs, body
• TINEA PEDIS –
”ATHLETES FOOT”
soles, btwn toes, toenail
• TINEA CRURIS –
“JOCK ITCH” groin &
upper thighs
• TINEA CAPITIS –
“SCALP” ringworm.
HIGHLY CONTAGIOUS
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 Tinea Pedis
Tinea Corporis

Tinea Cruris
Tinea Capitis 31
 PARASITIC INFESTATIONS

• PEDICULOSIS – Louse (lice) infestations

• HEAD LICE – common among children
– Spread from head to head (direct)
– Indirect – combs, scarves, hats, bed linen,etc
– Itching – caused by saliva of lice penetrating skin &
engorging on human blood
– Scratching – can open up skin to other invading organisms
– Adult head lice – hard to see, lay white eggs “NITS” along
hair shaft
– TX – Medicated shampoo followed by fine tooth comb to
remove nits

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 PARASITIC INFESTATIONS

• PUBIC LICE – infest pubic hair and

generally spread by sexual contact.
– Lice does not spread other STD’s
• BODY LICE – most common among
underprivileged, transient people.
– Lice CAN SPREAD DISEASE – such as typhus
epidemics among soldiers during war
– Prevention – good grooming & hygiene

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 PARASITIC INFESTATIONS

• SCABIES “THE ITCH” – caused by a parasitic MITE

– HIGHLY CONTAGIOUS
– Female mite – burrows into skin folds of groin, under
breasts, between fingers & toes. Lays eggs in tunnels of
folds, eggs hatch, cycle begins again
– Spread via close contact & linked to other VD’s
– Blisters & pustules appear
– Itching – caused by hypersensitivity to mite & opens up skin
to other bacterial infections
– Epidemics common in camps & barracks (poor living)
– TX & Recovery – Hot baths & scrubbing & meds.
Underwear & bedding changed & washed frequently.

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 IMMUNE DISEASES OF THE SKIN

• HYPERSENSITIVITY

• INSECT BITES

• URTICARIA

• ECZEMA

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• HYPERSENSITIVITY – ALLERGIC
reactions of the skin. Emotional stress may
trigger or exacerbate an allergy-caused skin
disease.
• INSECT BITES – Bites & stings can
produce local inflammatory reactions.
– Acute reactions – hives
– Chronic reactions – papules (solid elevations)
– Bullous - blisters

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Urticaria

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Examples of Urticaria

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 Causes
Auto-reactivity
20%

Intolerance
Infection 38%
26%

Other
2%

No known cause
30%
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 Common Causes of Acute Urticaria
 Idiopathic
 Infection
• Upper respiratory, streptococcal infections,
helminthes
 Food reactions
• Shellfish, nuts, fruit, etc.
 Drug reactions
 IV administration
• Blood products, contrast agents
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 Etiology of Chronic Urticaria
 Idiopathic: over 50% of chronic urticaria
 Physical urticarias: many patients with chronic urticaria have
physical factors that contribute to their urticaria
• These factors include pressure, cold, heat, water (aquagenic),
sunlight (solar), vibration, and exercise
• Cholinergic urticaria is triggered by heat and emotion
• The diagnosis of pure physical urticaria is made when the sole cause
of a patient’s urticaria is a physical factor
 Chronic autoimmune: possibly a third or more of patients with
chronic urticaria
 Other: infections, ingestions, medications
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 Summary
• Urticaria is often incredibly annoying and often
disfiguring
• The most common form is chronic spontaneous
urticaria
• Possible causes are infections, food intolerances
or autoimmune processes
• The treatment of choice is:
1. Antihistamines
2. More antihistamines
3. Mast cell inhibition 42
 ECZEMA –CONTACT DERMATITIS
(non-contagious inflammatory skin disorder)

• Cause – sensitization that develops from

skin contact with various agents, plants,
chemical, & metals. Poison ivy and poison
oak, dyes used for hair & clothes, metals,
particularly nickel used in jewelry.
• S & Sx’s – Vesicles & bullae appear with
itching. Scaly crusts form on ruptured
lesions.
• Scratching – causes the lesions to burst &
ooze which spreads the eczema.

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 Dermatitis
Subacute Dermatitis

Commonly misdiagnosed as tinea 44

 Dermatitis
Chronic Dermatitis

Commonly misdiagnosed as psoriasis 45

 Allergic Contact Dermatitis
• Type 4 Hypersensitivity Response
• Classically well demarcated/patterned
• Exposure can be infrequent (once a month)
• Patch testing is gold standard for diagnosis
• Severe reactions need systemic steroids

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• POISON IVY – causes
extreme itching with blisters
and hive-like swelling typical of
a contact dermatitis
– Develops in few hours or
few days
• Severity – depends on amount
of plant resin on skin &
sensitivity of ind.
• TX- Topical cortisone-type
cream, gel or spray.
• Table 18-2 Common rashes
caused by Drugs p. 407.
• DRUG ERUPTIONS –
Adverse drug reactions
manifest more often on the skin
than any other organ system.
• Topical drugs – mild pimples
over sm. Area to peeling of the
skin
• Serious reactions may lead to
anaphylaxis shock or death.
• Most common offending drugs
are penicillin, sulfa, morphine,
codeine, etc.
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 Allergic Contact Dermatitis
• Poison Ivy/Oak/Sumac
linearity

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 Allergic Contact Dermatitis

• Potassium Dichromate
in Leather

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 Allergic Contact Dermatitis
• Latex
• Cleaning products
• Cosmetics
• Occupational
exposures
Check the feet
and nails!!!
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Allergic Contact Dermatitis

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40 y/o female homemaker with dry,
itchy hands

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 Irritant Contact Dermatitis
• Most contact dermatitis is irritant in nature
• Occupational
morbity
• Irritant vs allergic
• Prevention is key!

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 Treatment
• Antihistamines
– Mechanism of action: soporific

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 BENIGN TUMORS
• NEVUS (MOLE) – small, dark skin growth that
develops from pigment-producing cells or
melanocytes.
• Appear flat or raised & vary in size
• Most people have about 10 moles
• Usually harmless, but can become malignant
• Sudden changes in moles such as enlargement,
irregular border, darkening, inflammation &
bleeding are warning signs of malignancy

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 SKIN CANCER
• BASAL CELL CARCINOMA – most common skin
cancer. Slow growing, generally non-metastasizing
(spreading) tumor.
• Develops on face of light skinned people exposed to sun
• Lesions begin as a pearly nodule with rolled edges that may
bleed and form a crust
• Ulceration occurs and size increases if neglected
• TX- surgical removal, cauterize, or radiation.

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 SKIN CANCER
• SQUAMOUS CELL CARCINOMA – more serious than
basal cell carcinoma because it grows more rapidly,
infiltrates underlying tissue, and metastasizes in lymph
system.
• Malignancy of the keratinocytes in the epidermis of people
who are excessively exposed to sun.
• Lesion is crusted nodule that ulcerates & bleeds.
• May develop in any squamous epithelium of the body
including the skin or mucous membranes lining a natural
body opening (mouth, nose, ear, etc.)
• TX – complete surgical removal or radiation therapy.

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 SKIN CANCER

• KAPOSI’S SARCOMA – Purplish neoplasm

of the lower extremities.
• Lesions – red to purple lesions varying from
macules (flat) to nodules (hard nodes)
• This skin cancer is epidemic in AIDS patients
• Cause of 11% of AIDS-related deaths

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 SKIN CANCER

• MALIGNANT MELANOMA – the MOST SERIOUS

skin cancer. Arises from the melanocytes of the epidermis.
• HIGHLY MALIGNANT and metastasis is early
• Sometimes develops as a mole that changes in size, color
& becomes itchy & sore.
• TX-surgical removal with the surrounding lymph nodes to
reduce metastasis
• Prognosis-depends on depth of infiltration, previous
metastasis, & how completely the tumor is removed.
• Fig. 18-21 Malignant melanoma spread to brain.

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 SEBACEOUS GLAND DISORDERS

• Hyperactivity of the sebaceous glands causes acne and

chronic dandruff. Raised, horny lesions result from an
excessive production of keratinocytes.
• ACNE (VULGARIS) – blackheads, pimples and pustules.
• Affects many adolescents, about 80% between the ages of 12
– 15.
• Mild form – non-inflammatory acne with few white & black
heads.
• Inflammatory acne – severe breakout of pus-filled pimples &
cysts that cause deep pitting & scarring

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 SEBACEOUS GLAND DISORDERS
ACNE
 Result of hormonal changes that
occur at puberty
 Increased level of estrogen &
testosterone stimulates not only
growth at this time but also
glandular activity
 SEBACEOUS GLANDS increase
secretion of SEBUM, the oily fluid
that is released through the hair
follicles.
 If duct becomes clogged by dirt or
make-up, the sebaceous secretion
accumulates, causing a little bump
or whitehead
• Sebaceous accumulation at the
surface becomes oxidized and turns
black, causing a blackhead
• Blackheads should not be squeezed
or picked because the broken skin
offers entry of bacteria that’s
always present on the skin
• Once pyogenic (pus producing)
bacteria enters the skin, pus forms
and a pimple or pustule
“whitehead” results.
• Squeezing the pimple spreads the
infection
• TX- daily frequent & thorough
washing to remove excess oil &
bacteria. Dermatologist may
prescribe topical or oral ABX.
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 SEBACEOUS GLAND DISORDERS
SEBORRHEIC DERMATITIS

• Known as “CHRONIC DANDRUFF”

• CAUSE-same as acne, an excessive secretion of
sebum from the sebaceous gland
• SX’s- Oily scalp, with scales that form from
excess sebum
• Can spread to face, ears & eyebrows
• TX – frequent shampooing with medicated
shampoo and thorough brushing of hair loosens
dandruff scales & washes out easily
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DIAGNOSTIC TESTS FOR SKIN DISEASES

• Skin conditions are normally identified by its

characteristics such as size, shape, color, location &
presence or absence of systemic S&SX’s
• Culturing the purulent lesion usually identifies the
bacterial, fungal, and viral infections.
• Culture grows & specimen is identified under a
microscope
• Biopsies (tissue sample) are usual for neoplastic (abnormal
new growth) lesions, chronic eruptions, and nodular
lesions
• Excised tissue is about 1/8 inch in diameter and is
examined under a microscope.
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METABOLIC SKIN DISORDER

PSORIASIS

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• Psoriasis is a disease which affects the skin and
joints.
• It commonly causes red scaly patches to appear
on the skin.
• The scaly patches caused by psoriasis, called
psoriatic plaques, are areas of inflammation and
excessive skin production.
• Skin rapidly accumulates at these sites and takes
a silvery-white appearance.
• Plaques frequently occur on the skin of the
elbows and knees, but can affect any area
including the scalp and genitals.
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• Psoriasis is an inflammatory skin disease in which skin cells
replicate at an extremely rapid rate. New skin cells are
produced about eight times faster than normal--over several
days instead of a month--but the rate at which old cells slough
off is unchanged. This causes cells to build up on the skin's
surface, forming thick patches, or plaques, of red sores
(lesions) covered with flaky, silvery-white dead skin cells
(scales).

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 Prevalence

• Psoriasis occurs in 2% of the world’s

population
• Prevalence in the U.S may be as high as 4.6%
• In Africans, African Americans and Asians
between 0.4% and 0.7%

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 Prevalence

• Equal frequency in males and females

• May occur at any age from infancy to the
10th decade of life
• First signs of psoriasis
– Females mean age of 27 years
– Males mean age of 29 years

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 Prevalence
• Two Peaks of Occurrence
– One at 20-30 years
– One at 50-60 years
• Psoriasis in children
– Low – between 0.5 and 1.1% in children 16
years old and younger
– Mean age of onset - between 8 and 12.5 years

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 Prevalence
• Two-thirds of patients have mild disease
• One-third have moderate to severe disease
• Early onset (prior to age 15)
– Associated with more severe disease
– More likely to have a positive family history
• Life-long disease
– Remitting and relapsing unpredictably
– Spontaneous remissions of up to 5 years have been
reported in approximately 5% of patients

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• The cause of psoriasis is not known, but it is believed
to have a genetic component.
• Several factors are thought to aggravate psoriasis.
These include stress, excessive alcohol consumption,
and smoking.
• Individuals with psoriasis may suffer from
depression and loss of self-esteem.
• As such, quality of life is an important factor in
evaluating the severity of the disease.
• Certain medicines, including lithium salt and beta
blockers, have been reported to trigger or aggravate
the disease.
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• There are two main hypotheses about the process that occurs
in the development of the disease.
• The first considers psoriasis as primarily a disorder of
excessive growth and reproduction of skin cells. The problem
is simply seen as a fault of the epidermis and its keratinocytes.
• The second hypothesis sees the disease as being an immune-
mediated disorder in which the excessive reproduction of skin
cells is secondary to factors produced by the immune system.
T cells (which normally help protect the body against
infection) become active, migrate to the dermis and trigger the
release of cytokines (tumor necrosis factor-alpha TNFα, in
particular) which cause inflammation and the rapid production
of skin cells. It is not known what initiates the activation of the
T cells.
• The immune-mediated model of psoriasis has been supported
by the observation that immunosuppressant medications can
clear psoriasis plaques.
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 Genetics and Pathogenesis
• Psoriasis and the Immune System
– The major histocompatibility complex (MHC)
• Short arm of chromosome 6
– Histocompatibility Antigens (HLA)
• HLA-Cw6
• HLA-B13, -B17, -B37, -Bw16
– T-lymphocyte-mediated mechanism

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 Psoriasis as a Systemic Disease

• Koebner Phenomenon
• Elevated ESR
• Increased uric acid levels → gout
• Mild anemia
• Elevated α2-macroglobulin
• Elevated IgA levels
• Increased quantities of Immune Complexes

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 Psoriasis as a Systemic Disease

• Psoriatic arthropathy
• Aggravation of psoriasis by systemic factors
– Medication
– Focal infections
– Stress
• Life-threatening forms of psoriasis

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 Types of Psoriasis
• Plaque psoriasis (psoriasis vulgaris) is the
most common form of psoriasis. It affects 80
to 90% of people with psoriasis. Plaque
psoriasis typically appears as raised areas of
inflamed skin covered with silvery white scaly
skin. These areas are called plaques.

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• Flexural psoriasis (inverse
psoriasis) appears as smooth
inflamed patches of skin. It occurs
in skin folds, particularly around
the genitals (between the thigh
and groin), the armpits, under an
overweight stomach (pannus), and
under the breasts (inframammary
fold). It is aggravated by friction
and sweat, and is vulnerable to
fungal infections.

• Guttate psoriasis is
characterized by numerous small
oval (teardrop-shaped) spots.
These numerous spots of psoriasis
appear over large areas of the
body, such as the trunk, limbs,
and scalp. Guttate psoriasis is
associated with streptococcal
throat infection 77
• Pustular psoriasis appears as raised bumps
that are filled with non-infectious pus
(pustules). The skin under and surrounding
pustules is red and tender. Pustular psoriasis
can be localised, commonly to the hands and
feet , or generalised with widespread patches
occurring randomly on any part of the body.

78
• Nail psoriasis produces a variety of changes in
the appearance of finger and toe nails. These
changes include discolouring under the nail
plate, pitting of the nails, lines going across the
nails, thickening of the skin under the nail, and
the loosening (onycholysis) and crumbling of
the nail.

79
• Psoriatic arthritis involves
joint and connective tissue
inflammation.
• Psoriatic arthritis can affect
any joint but is most
common in the joints of the
fingers and toes. This can
result in a sausage-shaped
swelling of the fingers and
toes known as dactylitis.
Psoriatic arthritis can also
affect the hips, knees and
spine (spondylitis). About
10-15% of people who have
psoriasis also have psoriatic
arthritis. 80
• Erythrodermic psoriasis
involves the widespread
inflammation and exfoliation
of the skin over most of the
body surface. It may be
accompanied by severe
itching, swelling and pain.
• It is often the result of an
exacerbation of unstable
plaque psoriasis, particularly
following the abrupt
withdrawal of systemic
treatment. This form of
psoriasis can be fatal, as the
extreme inflammation and
exfoliation disrupt the body's
ability to regulate
temperature and for the skin
to perform barrier functions.
81
82
• A diagnosis of psoriasis is usually based on the
appearance of the skin. There are no special
blood tests or diagnostic procedures for
psoriasis. Sometimes a skin biopsy, or
scraping, may be needed to rule out other
disorders and to confirm the diagnosis. Skin
from a biopsy will show clubbed pegs if
positive for psoriasis.
• Another sign of psoriasis is that when the
plaques are scraped, one can see pinpoint
bleeding from the skin below (Auspitz's sign).
83
 Treatment options
• There can be substantial variation between individuals
in the effectiveness of specific psoriasis treatments.
Because of this, dermatologists often use a trial-and-
error approach to finding the most appropriate
treatment for their patient.
• The decision to employ a particular treatment is based
on the type of psoriasis, its location, extent and
severity. The patient’s age, gender, quality of life,
comorbidities, and attitude toward risks associated
with the treatment are also taken into consideration.
84
• Medications with the least potential for adverse
reactions are preferentially employed.
• As a first step, medicated ointments or creams are
applied to the skin. If topical treatment fails to
achieve the desired goal then the next step would be
to expose the skin to ultraviolet (UV) radiation. This
type of treatment is called phototherapy.
• The third step involves the use of medications which
are taken internally by pill or injection : systemic
treatment.
• Over time, psoriasis can become resistant to a specific
therapy. Treatments may be periodically changed to
prevent resistance developing (tachyphylaxis) and to
reduce the chance of adverse reactions occurring:
treatment rotation.
85
86
 Topical treatment
• Salicylic acid
• Coal Tar
• Dithranol
• Topical CS
• Phototherapy
• Systemic Therapy

87
 Systemic Therapy
• Immunomodulators
- Cyclosporin, methotrexate commonly used

- Antibiotics in case of secondary bacterial

infections

88
 Systemic Therapies
• Oral
– Methotrexate
– Neoral (cyclosporine)
– Soriatane (acitretin)
• Parenteral
– Amevive (alefacept)
– Raptiva (efalizimab)
– Enbrel (etanercept)

89
 Psychological Impact of
Moderate/Severe Disease
• Patients with extensive • Aggressive treatment of
Skin involvement often the patient’s disease is
afraid to be in public or often warranted in these
wear revealing clothing. cases as the severity of the
• Some patients shed scale disease justifies the
constantly onto clothing, risks/side effects inherent
furniture, floors, etc. in the treatments.
• Many patients eventually • Patients often motivated to
become depressed if try anything that might be
disease poorly controlled. effective.

90
 Summary
• Psoriasis is a lifelong condition.
• There is currently no cure but various treatments can
help to control the symptoms. Many of the most
effective agents used to treat severe psoriasis carry an
increased risk of significant morbidity including skin
cancers, lymphoma and liver disease.
• Psoriasis does get worse over time but it is not
possible to predict who will go on to develop
extensive psoriasis or those in whom the disease may
appear to vanish.
• Individuals will often experience flares and
remissions throughout their lives. Controlling the
signs and symptoms typically requires lifelong
therapy. 91
Natural Treatments

92
 Goals of Naturopathic Treatment

• Nourish the body

– Intake, digestion, and absorption of nutrients
• Remove the obstacles to cure
– Physical, mental, emotional, or spiritual blocks
• Optimize elimination by Detox treatment
– Lungs, colon, skin, kidney
• Stimulate the body’s healing force
– Acupressure, Meditation, Yoga, Natural herbs etc.

93
 Treatment

• ય તગત વા ય (Personal Heigene)

• શ તેટલા વ ુ ઉપવાસ તથા જ ર આરામ
• આહાર – ાર ય આહાર
• ડ ટો – વમન, એનીમા, કટ નાન, મડપેક ( ખ અને પેટ પર)
• વાત કોપ ઘટાડવા માટ - મસાજ, ટ મ બાથ, મડબાથ(લીમડો)
• લોકલ ટમે ટ – સાંધાની લપેટ, લોકલ ટ મ, ને ક ન શેક, લટબ બાથ,
ભીની ચાદર લપેટ.
• ચાલવા તથા તરવાની કસરત – ૂ મ યાઓ

94
• યોગા: શ આતમાં ૂ મ યાયામ,પછ ધીરધીર વધારતાં જઈને િ કોણાસન,
પાદહ તાસન, તાડાસન, વ ાસન, ુ તવ ાસન, પિ મો ાનાસન, શશાંકાસન,
ૂ જ ં ગાસન
, ગો ુ ખાસન, મકરાસન, અધમ ય ાસન વા આસનો કરવા તથા
કર શકાય તેમ હોય તો ૂ યનમ કાર કરવા.
• ાણાયામ: અ ુ લોમ-િવલોમ, ભ ીકા, એ ડોમીનલ ીધ ગ
• શવાસન- યોગિન ા
• પોઝીટ વ એફમશન - ાથના
• યાન (Meditation)

95
 આહાર (Diet)

સવાર ૂ ંફા ં પાણી પલાળે લી મેથી/ઉકાળો લીમડા રસ

6:30 થી
ગરમાળાનો ઉકાળો આમળા + હળદર રસ
7:00

સવાર ૂ ધ ઉકાળો(ગોળ/ગોળ વગર) ના ળયેર પાણી ખાખરા/મમરા/પ આ

8:00 થી
પલાળે લા ર/ ા /ખ ૂ ર શાકભા રસ ફળનો રસ ફળ
9:00

બપોર રોટલી/ભાખર /રોટલો સલાડ બાફ ુ ં શાક ચટણી ૂપ

12:00 થી
ફણગાવેલા કઠોળ ુ લી/દલીયો ઋ ુ ુ જબના ફળ મગ/મગપાણી
1:00

96
 બપોર ૂ ધ ઉકાળો(ગોળ/ગોળ વગર) પલાળે લા ર/ ા /ખ ૂ ર
3:30 થી
4:30 ફળ ૂ ધી/પાલક/કાકડ /કોબીજ રસ સરગવાનો ુપ

સાં રોટલી/ભાખર /રોટલો ુ લી/દલીયો ખીચડ /ભાત દાળ

6:30 થી
7:30 બાફલો સરગવો સલાડ બાફ ુ ં શાક ચટણી

ૂપ મગ/મગપાણી ઋ ુ ુ જબના ફળ

રા ે
9:30 પછ ગરમાળાનો ઉકાળો 2 થી 3 લાસ પાણી

97
98