Pharm-D Pharmacotherapeutics 3rd Year notes [Dermatology]

1. PHARMACOTHERAPEUTICS –II: CHAPTER –V DERMATOLOGY
PSORIASIS
INTRODUCTION:-
1. Psoriasis is a chronic autoimmune condition that causes the rapid buildup
of skin cells.
2. It is a common skin condition that speeds up the life cycle of skin cells.
3. Psoriasis is a long-lasting autoimmune disease characterized by patches of
abnormalskin.
4. These skin patches are typically red, dry, itchy, and scaly.
5. On people with darker skin the patches may be purple in colour
6. Psoriasis varies in severity fromsmall, localized patches to complete body
coverage
7. Injury to the skin can trigger psoriatic skin changes at that spot, which is
known as the Koebner phenomenon.
8. There is no cure for psoriasis, butyou can manage symptoms.
9. Lifestyle measures, such as moisturizing, quitting smoking and managing
stress, may help.
10.The main goal of treatment is to stop the skin cells fromgrowing so quickly.
TYPES OF PSORIASIS:-
There are five main types of psoriasis:-
1. Plaque psoriasis,
2. Guttate psoriasis,
3. Inversepsoriasis,
4. pustular psoriasis,
5. Erythrodermic psoriasis.
Other forms includes:-
1. Psoriatic arthritis,
2. Nail psoriasis.
Plaque psoriasis:-
Plaque psoriasis, also known as psoriasis vulgaris, makes up about90 percent of
cases. Ittypically presents as red patches with white scales on top.Areas of the

2. body most commonly affected are the back of the forearms, shins, navelarea,
and scalp.
Guttate psoriasis :-
Guttate psoriasis is common in childhood. This type of psoriasis causes smallpink
spots. The mostcommon sites for guttate psoriasis includethe torso, arms, and
legs. These spots arerarely thick or raised like plaque psoriasis.
Pustular psoriasis :-
Pustular psoriasis is morecommon in adults. It causes white, pus-filled blisters
and broad areas of red, inflamed skin. Pustular psoriasis is typically localized to
smaller areas of the body, such as the hands or feet, but it can be widespread.
Inverse psoriasis :-
Inversepsoriasiscauses brightareas of red, shiny, inflamed skin. Patches of
inversepsoriasis develop under armpits or breasts, in the groin, or around
skinfolds in the genitals.
Erythrodermic psoriasis:-
Erythrodermic psoriasis is a severe and very rare type of psoriasis. This formoften
covers large sections of the body at once. The skin almost appears sunburned.
Psoriatic arthritis:-
Psoriatic arthritis is a formof chronic inflammatory arthritis that has a highly
variable clinical presentation and frequently occurs in association with skin and
nail psoriasis. Ittypically involves painfulinflammation of the joints and
surrounding connectivetissueand can occur in any joint, but most commonly
affects 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, spine(spondylitis), and sacroiliac joint (sacroiliitis).
Nail psoriasis:-
Psoriasis can affect the nails and produces a variety of changes in the appearance
of finger and toe nails. Nail psoriasis occurs in 40–45% of people with psoriasis
affecting the skin and has a lifetime incidence of 80–90% in those with psoriatic
arthritis.
SYMPTOMS:-
The symptoms of psoriasis include:
 Scaly reddish patches of skin,
 Dry and cracked skin proneto bleeding
 Flaky skin
 Itching and burning in the affected area
 Soreness in the affected area

3.  Joint stiffness
 Discoloured, ridged and thickened nails
 Swollen and stiff joints
Medical signs:-
These may include,
 Auspitz's sign (pinpoint bleeding when scale is removed),
 Koebner phenomenon (psoriatic skin lesions induced by trauma to the
skin),
 Itching and pain localized to papules and plaques.
ETIOLOGY:-
 The aetiology of psoriasis is a combination of genetic and environmental
factors. In mostcases, there is a genetic pre- disposition and up to 70% of
patients report a family history of psoriasis.
 Recent advances in genome-wide association studies haveled to the
identification of at least nine chromo- somalpsoriasis susceptibility loci
 Multiple genes are likely to influence diseasesusceptibility, severity and
clinical subtype.
 The strongestassociation is with HLA-CW*06.
PATHOPHYSIOLOGY:-
STRESS,GENETIC,AUTOIMUNE REACTIONAND MEDICATIONS CAUSES
HYPER ACTIVATIONOF T-CELLS
EPIDERMIS INFILTRATIONAND KERATINOCYTES PROLIFERATION
DEGRANULATED INFLAMATORYPROCESS

4. LARGE PRODUCTIONOF VARIOUS CYTOKINES
VASODILATIONAND VASCULAR ENORGEMENT
EPIDERAL HYPERPLASIA AND IPROPERCELL MATURATION
FAILS TO RELEASE ADEQUATELIPIDS WHICH LEADS TO FLAKING AND SCALNG
SILVERSCALING OF SKIN
PSORIATICLESIONS FORMATIONONSKIN
PSORIASIS TRIGGERS :-
 Infections, such as strep throat or skin infections
 Injury to the skin, such as a cut or scrape, a bug bite, or a severesunburn
 Stress,
 Smoking
 Heavy alcohol consumption,
 Vitamin D deficiency,
 Certain medications — including lithium, which is prescribed for bipolar
disorder, high blood pressuremedications such as beta blockers,
antimalarial drugs, and iodides.
RISK FACTORS :-

5. Anyonecan develop psoriasis, butthese factors can increase your risk of
developing the disease:
FAMILY HISTORY:-
This is one of the most significantrisk factors. Having one parent with psoriasis
increases your risk of getting the disease, and having two parents with psoriasis
increases your risk even more.
VIRAL AND BACTERIAL INFECTIONS:-
People with HIV aremore likely to develop psoriasis than people with healthy
immune systems are. Children and young adults with recurring infections,
particularly strep throat, also may be at increased risk.
STRESS:-
Because stress can impact your immune system, high stress levels may increase
your risk of psoriasis.
OBESITY:-
Excess weight increases the risk of psoriasis. Lesions (plaques) associated with all
types of psoriasis often develop in skin creases and folds.
SMOKING:-
Smoking tobacco not only increases your risk of psoriasis butalso may increase
the severity of the disease. Smoking may also play a role in the initial
development of the disease.
Complications:-
If you have psoriasis, you'reatgreater risk of developing certain diseases. These
include:
Psoriatic arthritis,
Eye conditions,
Obesity,
Type 2 diabetes,
Cardiovascular disease.
DIAGNOSIS :-
In mostcases, diagnosis of psoriasis is fairly straightforward.
1. Physical examand medical history:-
Your doctor usually can diagnose psoriasis by taking your medical history
and examining your skin, scalp and nails.
2. Skin biopsy:-

6. Rarely, your doctor may take a small sample of skin (biopsy). Heor she will
likely first apply a local anesthetic. The sample is examined under a microscopeto
determine the exact type of psoriasis and to rule out other disorders.
TREATMENT:-
Psoriasis treatments reduce inflammation and clear the skin.
Treatments can be divided into three main types:
1. Topical treatments,
2. Light therapy and
3. Systemic medications.
Topical psoriasis treatments include:
1. Topical corticosteroids:-
 These drugs arethe most frequently prescribed medications for
treating mild to moderate psoriasis.
 They reduce inflammation and relieve itching and may be used with
other treatments.
 Mild corticosteroid ointments are usually recommended for sensitive
areas, such as your face or skin folds, and for treating widespread
patches of damaged skin.
2. VitaminD analogues:-
 These synthetic forms of vitamin D slow skin cell growth.
Calcipotriene (Dovonex) is a prescription cream or solution
containing a vitamin D analogue that treats mild to moderate
psoriasis along with other treatments.
 Calcipotriene might irritate your skin. Calcitriol (Vectical) is expensive
but may be equally effective and possibly less irritating than
calcipotriene.
3. Anthralin:-
 This medication helps slow skin cell growth. Anthralin (Dritho-Scalp)
can also remove scales and make skin smoother.
 But anthralin can irritate skin, and it stains almost anything it
touches. It's usually applied for a shorttime and then washed off
4. Topical retinoids:-
 These are vitamin A derivatives that may decrease inflammation.
 The most common side effect is skin irritation
5. Calcineurininhibitors:-

7.  Calcineurin inhibitors — tacrolimus (Prograf) and pimecrolimus
(Elidel) — reduce inflammation and plaque buildup.
 Calcineurin inhibitors are not recommended for long-termor
continuous use becauseof a potential increased risk of skin cancer
and lymphoma.
6. Salicylic acid:-
1. Available over-the-counter (nonprescription) and by prescription,
salicylic acid promotes sloughing of dead skin cells and reduces
scaling.
7. Coal tar:-
2. Derived from coal, coal tar reduces scaling, itching and inflammation.
Coal tar can irritate the skin.
 It's also messy, stains clothing and bedding, and has a strong odor..
Light therapy (phototherapy):-
 This treatment uses natural or artificial ultraviolet light.
 The simplest and easiest formof phototherapy involves exposing
your skin to controlled amounts of natural sunlight.
 Other forms of light therapy include the useof artificial ultraviolet A
(UVA) or ultraviolet B (UVB) light, either alone or in combination with
medications.
1. Sunlight.:-
 Exposureto ultraviolet (UV) rays in sunlightor artificial light slows
skin cell turnover and reduces scaling and inflammation.
 Brief, daily exposures to small amounts of sunlightmay improve
psoriasis, butintense sun exposurecan worsen symptoms and cause
skin damage
2. UVB phototherapy:-
 Controlled doses of UVB light froman artificial light sourcemay improve
mild to moderate psoriasis symptoms.
 UVB phototherapy, also called broadband UVB, can be used to treat
single patches, widespread psoriasis and psoriasis thatresists topical
treatments.
 Short-termside effects may include redness, itching and dry skin.
3. Narrowband UVB phototherapy:-
 A newer type of psoriasis treatment, narrow band UVBphototherapy
may be more effective than broadband UVB treatment.

8.  It's usually administered two or three times a week until the skin
improves, and then maintenance may requireonly weekly sessions.
 Narrow band UVB phototherapy may cause more- severe and longer
lasting burns, however.
4. Goeckermantherapy:-
 The combine UVBtreatment and coal tar treatment, which is known
as Goeckerman treatment.
 The two therapies together are more effective than either alone
because coal tar makes skin more receptive to UVB light.
5. Psoralenplus ultraviolet A (PUVA):-
 This formof photochemotherapy involves taking a light-sensitizing
medication (psoralen) beforeexposureto UVA light.
 UVA light penetrates deeper into the skin than does UVB light, and
psoralen makes the skin more responsiveto UVA exposure.
6. Excimer laser:-
 This formof light therapy, used for mild to moderate psoriasis,
treats only the involved skin withoutharming healthy skin.
 A controlled beam of UVB light is directed to the psoriasis
plaques to controlscaling and inflammation.
Oral or injectedmedications :-
1. Retinoids. Related to vitamin A, this group of drugs may help if you have
severepsoriasis that doesn'trespond to other therapies. Side effects may
include lip inflammation and hair loss. And because retinoids such as
acitretin (Soriatane) can causeseverebirth defects, women must avoid
pregnancy for at least three years after taking the medication.
2. Methotrexate. Taken orally, methotrexate (Rheumatrex) helps psoriasis by
decreasing the production of skin cells and suppressing inflammation. It
may also slow the progression of psoriatic arthritis in some people.
Methotrexate is generally well-tolerated in low doses but may causeupset
stomach, loss of appetite and fatigue. When used for long periods, it can
causea number of serious sideeffects, including severeliver damage and
decreased production of red and white blood cells and platelets.
3. Cyclosporine. Cyclosporine(Gengraf, Neoral) suppresses theimmune
systemand is similar to methotrexate in effectiveness, but can only be
taken short-term. Like other immunosuppressantdrugs, cyclosporine

9. increases your risk of infection and other health problems, including
cancer. Cyclosporinealso makes you more susceptibleto kidney problems
and high blood pressure—the risk increases with higher dosages and
long- term therapy.
4. Drugs that alter the immune system(biologics):- Severalof these drugs
are approved for the treatment of moderate to severe psoriasis. They
include etanercept (Enbrel), infliximab (Remicade), adalimumab (Humira),
ustekinumab (Stelara), golimumab (Simponi), apremilast(Otezla),
secukinumab (Cosentyx) and ixekizumab (Taltz).
Most of these drugs aregiven by injection (apremilastis oral) and are usually
used for people who havefailed to respond to traditional therapy or who have
associated psoriatic arthritis. Biologics mustbe used with caution becausethey
have strong effects on the immune systemand may permit life-threatening
infections. In particular, people taking these treatments mustbe screened for
tuberculosis. Other medications. Thioguanine (Tabloid) and hydroxyurea (Droxia,
Hydrea) are medications that can be used when other drugs can't be given.
Alternativemedicine:-
These treatments would be most appropriatefor those with milder, plaque
diseaseand not for thosewith pustules, erythroderma or arthritis.
1. Aloe vera. Taken fromthe leaves of the aloe vera plant, aloe extract cream
may reduceredness, scaling, itching and inflammation.
2. Fishoil. Omega-3 fatty acids found in fish oil supplements may reduce
inflammation associated with psoriasis, although results fromstudies are
mixed.
3. Oregongrape. Also known as barberry, topical applications of Oregon
grape may reduce inflammation and ease psoriasis symptoms.
SCABIES
INTRODUCTION:-
1. Scabies is a skin infestation caused by a mite known as the Sarcoptes
scabiei.
2. Scabies is also known as seven-year itch.
3. Tiny ites called sarcoptes scabieisetup shop in the outer layer of huan skin
4. Untreated, these microscopic mites can live on your skin for months.

10. 5. They reproduceon the surfaceof your skin and then burrow into it and lay
eggs.
6. This causes an itchy, red rash to formon the skin.
7. The urge to scratch ay be especially strong at night
SCABIES MITES:-
Scabies is an infestation of the skin caused by the scabies mite Sarcoptesscabiei.
The mite is very tiny, 0.2 mm to 0.4 mm long, and cannot easily be seen without
magnification.
They feed using their mouths and frontlegs to burrow into the outer layer of skin
(epidermis), wherethey lay eggs.
After 3 to 4 days, the baby mites (larvae) hatch and moveto the surfaceof the
skin, wherethey mature into adults.
The mite can survivefor about 3 to 4 days without being on a human.
Scabies mites can live anywhereon the body, but some of their favoritespots
include:
 Between the fingers
 The folds of the wrist, elbow, or knee
 Around the waistline and navel
 On the breasts or genitals
 The head, neck, face, palms, and soles in very young children
MODEOF TRANSMISSION:-
The mite can travel fromthe infected person to another person.
Most people get scabies fromdirect, skin-to-skin contact.
Less often, people pick up mites frominfested items such as bedding, clothes, and
furniture.
Worldwide, there are millions of cases of scabies each year.
Scabies is not an indication of poor hygiene.
INCUBATION PERIOD:-
(time between becoming infected and developing symptoms)Itching begins 2 to 6
weeks after infestation in individuals not previously exposed to scabies and within
1 to 5 days in individuals previously exposed.
INFECTIOUS PERIOD:-
(time during which an infested person can transmit the infestation to others)Until
the mites and eggs are destroyed by treatment. People can be infectious even
before the itching begins.
SCABIES SYMPTOMS:-

11. When a person is infested with scabies for the first time, it can take four to six
weeks for the skin to react.
The most common symptoms are:
 Intenseitching, especially at night
 A pimple-like rash
 Scales or blisters
 Sores caused by scratching
PATHOPHYSIOLOGY:-
1. The symptoms arecaused by an allergic reaction of the host's body to mite
proteins, though exactly which proteins remains a topic of study.
2. The mite proteins are also present fromthe gut, in mite feces, which are
deposited under the skin.
3. The allergic reaction is both of the delayed (cell-mediated) and immediate
(antibody-mediated) type, and involves IgE(antibodies are presumed to
mediate the very rapid symptoms on reinfection).
4. The allergy-type symptoms (itching) continue for some days, and even
severalweeks, after all mites are killed.
5. New lesions may appear for a few days after mites are eradicated. Nodular
lesions from scabies may continue to be symptomatic for weeks after the
mites have been killed.
6. Rates of scabies are negatively related to temperature and positivelyrelated
to humidity.
DIAGNOSIS:-
A definitive diagnosis is made by finding either the scabies mites or their eggs and
fecal pellets. Searches for these signs involveeither scraping a suspected area,
mounting the sample in potassiumhydroxideand examining it under a
microscope, or using dermoscopy to examine the skin directly.
DIFFERENTIAL DIAGNOSIS:-
Symptoms of early scabies infestation mirror other skin diseases,
including dermatitis, syphilis, erythema multiforme, various urticaria-related
syndromes, allergic reactions, ringworm-related diseases, and
other ectoparasites such as lice and fleas.
PREVENTION:-
Mass-treatmentprograms thatuse topical permethrin or oral ivermectin have
been effective in reducing the prevalence of scabies in a number of populations.
No vaccine is available for scabies.
TREATMENT:-

12. According to the American Academy of Dermatologists (AAD), somecommon
medicines used to treat scabies include:
1. 5 percent permethrin cream
2. 25 percent benzyl benzoatelotion
3. 10 percent sulfur ointment
4. 10 percent crotamiton cream
5. 1 percent lindane lotion
6. Oralivermectin
Other signs and symptoms: Somepatients need other treatment, too.
1. Antihistamine: To control the itch and help you sleep.
2. Pramoxine lotion: To control the itch.
3. Antibiotic: To wipe out an infection.
4. Steroid cream: To ease the redness, swelling, and itch.
ECZEMA (DERMATITIS)
INTRODUCTION:-
1. The terms ‘eczema’ and ‘dermatitis’ may be used interchange- ably
and describethe sameclinical and histological entity.
2. Eczema is an itchy erythematous (red) eruption consisting of ill-
defined erythematous patches or papules.
3. The skin surfaceis usually scaly and as time progresses, constant
scratching leads to thickened, ‘lichenified’ skin.
4. Eczema, also known as Dermatitis, is a group of diseases that results
in inflammation of the skin.
5. These diseases are characterized by itchiness, red skin and a rash.
6. In cases of shortduration, there may be small blisters, while in long-
term cases the skin may become thickened.
7. The area of skin involved can vary fromsmallto the entire body.
AETIOLOGY:-
The cause of dermatitis is unknown but is presumed to be a combination of
genetic and environmental factors.
ENVIRONMENTAL:-

13. 1. The hygiene hypothesis postulates that the cause of asthma, eczema, and
other allergic diseases is an unusually clean environment.
2. It is supported by epidemiologic studies for asthma.
3. The hypothesis states that exposure to bacteria and other immune system
modulators is important during development, and missing out on this
exposure increases risk for asthma and allergy.
4. While it has been suggested that eczema may sometimes be an allergic
reaction to the excrement from house dust mites,with up to 5% of people
showing antibodies to the mites, the overall role this plays awaits further
corroboration.
GENETIC :-
1. A number of genes have been associated with eczema, one of which is
filaggrin.
2. Genome-wide studies found three new genetic variants associated with
eczema: OVOL1, ACTL9 and IL4-KIF3A.
3. Eczema occurs aboutthree times more frequently in individuals with celiac
disease and about two times more frequently in relatives of those with celiac
disease, potentially indicating a genetic link between the conditions.
CLINICAL TYPES:-
ATOPIC ECZEMA :-
1 .Atopic eczema is the commonestskin disorder of childhood,
affecting between 10% and 20% of schoolage children in the
UK.
2 .The aetiology is a combination of genetic, environmental
and immunological factors.
3 . The term ‘atopy’ describes an exaggerated propensity to
formIgEto common allergens.
4 .In later life, approximately half of eczema patients will develop
associated a topic disorders such as asthma and allergic rhinitis.
5 .The molecular pathology in atopic eczema is complex.
6 . The epidermal Langerhans cells have high-affinity IgEreceptors
through which the T-helper cells (Th2 and Th1) release cytokines and
mediate skin inflammation.
EXACERBATING FACTORS:-
A number of factors can aggravateatopic eczema:

14. • Extremes of temperature
• Irritants: soap, detergents, shower gels, bubblebaths and
water
• Stress
• Infection, either bacterial or viral
• Contact allergens
• Food allergens
• Inhaled allergens
• Airborneallergens
CONTACTDERMATITIS:-
Contact dermatitis is classified as either allergic contact dermatitis
(ACD) or irritant contact dermatitis (ICD).
ALLERGIC CONTACTDERMATITIS:-
1. ACD is a delayed type IV hypersensitivity reaction that developsin
responseto an antigen to which the host immune systemhas been
previously sensitised.
2. As a consequence,symptomsrarely develop on first exposureto the
stimulus and may only manifest months or years later following
repeated re-exposure.
3. Many common compounds can lead to ACD. The mostcommon
compounds implicated are:
• Metals, for example nickel and cobalt
• Neomycin, a topical antibiotic found in over-the-counter
preparations sold in some countries
• Fragrance ingredients, for example Balsam of Peru
• Rubber compounds
• Hair dyes, for example p-phenylediamine
• Plants, for example poison ivy.
IRRITANTCONTACTDERMATITIS:-
1. This is the most common form of occupational dermatitis
and the commonest cause of hand eczema (Fig. 57.5).
2. Unlike ACD, ICD is not immunologically mediated.
3. The mechanism involves disruption of the epidermal permeability barrier

15. and a direct cytotoxic effect depending on the irritant.
4.Patients with pre-existing epidermal barrier dysfunction such
as atopic eczema are at higher risk
SEBORRHOEIC DERMATITIS:-
1. This common disorder is usually confined to areas with high
sebum production.
2. The likely aetiological mechanism is overgrowth of the commensal yeast
Malassezia furfur (Pityosporumovale).
3. The clinical features are pink-yellow greasy patches with‘bran-like’ scale
which occur in the sebaceous-rich scalp, nasal folds, medial eyebrow, pre-
sternal region and flexural sites.
DISCOID ECZEMA:-
1. Discoid eczema is also known as ‘nummular dermatitis’ and is a type of
chronic eczema presenting with disseminated coinshapedeczematous
lesions of the extremities.
2. Middle-aged males are most commonly affected.
STASIS ECZEMA:-
1. Stasis eczema is also called stasis dermatitis, gravitational dermatitis or
varicose eczema.
2. It is a clinical component of chronic venous insufficiency seen in addition to
other features which include varicose veins, skin discolouration, peripheral
oedema, leg discomfortand non-healing ulcers.
3. Clinical features include scaly eczematous plaques confined to the lower
legs
ASTEATOTIC ECZEMA:-
1. Asteatotic eczema, also called eczema craquele, usually affects the lower
legs and appears as dry, cracked skin likened to ‘cracked paving’.
2. This is associated with increasing age, low humidity and frequent bathing.
3. Treatment consists of emollients and mildly potent topical steroids.
SIGNS AND SYMPTOMS:-
1. Eczema is usually itchy. For many people, the itch is usually only mild,
or moderate.
2. But in some cases it can become much worse and you might develop
extremely inflamed skin.

16. 3. Sometimes the itch gets so bad that people scratch it until it bleeds,
which can make your eczema worse.
4. This is called the “itch-scratch cycle.”
SYMPTOMS:-
Atopic dermatitis (eczema) signs and symptoms vary widely from person to
person and include:
 Dry skin
 Itching, which may be severe, especially at night
 Red to brownish-gray patches, especially on the hands, feet, ankles, wrists,
neck, upper chest, eyelids, inside the bend of the elbows and knees, and in
infants, the face and scalp
 Small, raised bumps, which may leak fluid and crust over when scratched
 Thickened, cracked, scaly skin
 Raw, sensitive, swollen skin from scratching
PATHOPHYSIOLOGY:-
DIAGNOSIS:-
1. Diagnosis of eczema is based mostly on the history and physical
examination.

17. 2. In uncertain cases, skin biopsy may be useful.
3. Those with eczema may be especially prone to misdiagnosis of food
allergies.
4. Patch tests are used in the diagnosis of allergic contact dermatitis.
MANAGEMENT :-
1. There is no known cure for some types of dermatitis, with treatment
aiming to control symptoms by reducing inflammation and relieving
itching.
2. Contact dermatitis is treated by avoiding what is causing it.
MEDICATIONS:-
 Topical corticosteroid creams and ointments:
These are a type of anti-inflammatory medication and should relieve the
main symptoms of eczema, such as skin inflammation and itchiness.
 Systemic corticosteroids:
If topical treatments are not effective, systemic corticosteroids can be
prescribed.
These are either injected or taken by mouth, and they are only used for
short periods of time.
 Antibiotics:
These are prescribed if eczema occurs alongside a bacterial skin infection.
 Antiviral and antifungal medications:
These can treat fungal and viral infections that occur.
 Antihistamines:
These reduce the risk of nighttime scratching as they can cause drowsiness.
 Topical calcineurin inhibitors:
This is a type of drug that suppresses the activities of the immune system.
It decreases inflammation and helps prevent flare-ups.
 Barrier repair moisturizers:
These reduce water loss and work to repair the skin.
THERAPIES
 Wet dressings.:-
An effective, intensive treatment for severe atopic dermatitis involves
wrapping the affected area with topical corticosteroids and wet bandages..
 Light therapy:-

18. 1. This treatment is used for people who either don't get better with
topical treatments or who rapidly flare again after treatment.
2. The simplest form of light therapy (phototherapy) involves exposing
the skin to controlled amounts of natural sunlight.
3. Other forms use artificial ultraviolet A (UVA) and narrow band
ultraviolet B (UVB) either alone or with medications.
4. Though effective, long-term light therapy has harmful effects,
including premature skin aging and an increased risk of skin cancer..
 Counseling.:-
Talking with a therapist or other counselor may help people who are
embarrassed or frustrated by their skin condition.
 Relaxation, behavior modification and biofeedback:-
These approaches may help people who scratch habitually.
IMPETIGO
INTRODUCTION:-
1. A highly contagious skin infection that causes red sores on the face.
2. Impetigo is a bacterial infection that involves the superficial skin.
3. It is typically due to either Staphylococcus aureus or Streptococcus
pyogenes
4. The most common presentation is yellowish crusts on the face, arms, or
legs.
5. Less commonly there may be large blisters which affect the groin or
armpits.
6. The lesions may be painful or itchy.
7. Fever is uncommon.
8. It can occur at any age, but is most common in young children.
9. In some places the condition is also known as "school sores".
AETIOLOGY:-
1. Impetigo is primarily caused by Staphylococcus aureus, and
sometimes by Streptococcus pyogenes.
2. Both bullous and nonbullous are primarily caused by S. aureus, with
Streptococcus also commonly being involved in the nonbullous form.
CLINICAL TYPES:-
 Contagious impetigo

19.  Bullous impetigo
 Ecthyma
SIGNS AND SYMPTOMS:-
 Red sore near the nose or mouth which soon breaks, leaking pus or fluid,
and forms a honey-colored scab, followed by a red mark which heals
without leaving a scar.
 Sores are not painful, but they may be itchy
 Touching or scratching the sores may easily spread the infection to other
parts of the body,
 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 formyellow scabs.
PREDISPOSING FACTORS:-
 Impetigo is more likely to infect children ages 2–5, especially those
that attend school or day care.
 70% of cases are the nonbullous form and 30% are the bullous form.
 Other factors can increase the risk of contracting impetigo such as
diabetes mellitus, dermatitis, immunodeficiency disorders, and
other irritable skin disorders.
 Impetigo occurs more frequently among people who live in warm
climates.
TRANSMISSION :-
 The infection is spread by direct contact with lesions or with nasal
carriers.
 The incubation period is 1–3 days after exposure to Streptococcus
and 4–10 days for Staphylococcus.[15]
 Dried streptococci in the air are not infectious to intact skin.
Scratching may spread the lesions.
DIAGNOSIS:-
 Impetigo is usually diagnosed based on its appearance. It generally
appears as honey-colored scabs formed from dried serum, and is
often found on the arms, legs, or face.
 If a visual diagnosis is unclear a culture may be done to test for
resistant bacteria.
DIFFERENTIAL DIAGNOSIS :-

20.  Other conditions that can result in symptoms similar to the common
form include contact dermatitis, herpes simplex virus, discoid lupus,
and scabies.
 Other conditions that can result in symptoms similar to the blistering
form include other bullous skin diseases, burns, and necrotizing
fasciitis.
COMPLICATIONS
 Complications may include cellulitis or poststreptococcal
glomerulonephritis.
 Rheumatic fever does not appear to be relate
PREVENTION:-
 Hand washing,
 avoiding infected people,
 cleaning injuries.
TREATMENT:-
 Antibiotics, either as a cream or by mouth, are usually prescribed.
 Mild cases may be treated mupirocin ointments.
 In 95% of cases, a single 7-day antibiotic course results in resolution in
children.
 It has been advocated that topical antiseptics are not nearly as efficient as
topical antibiotics, and therefore should not be used as a replacement.[3]
 More severe cases require oral antibiotics, such as dicloxacillin,
flucloxacillin, or erythromycin.
 Alternatively, amoxicillin combined with clavulanate potassium,
cephalosporins (first-generation) and many others may also be used as an
antibiotic treatment.
 Alternatives for people who are seriously allergic to penicillin or infections
with methicillin-resistant Staphococcus aureus include doxycycline,
clindamycin, and trimethoprim-sulphamethoxazole.
ALTERNATIVE MEDICINE:-
 There is not enough evidence to recommend alternative medicine such as
tea tree oil or honey.