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ZERA INTERNATIONAL COLLEGE OF HEALTH SCIENCES
INTERNAL MEDICINE
CLINICAL OFFICER (COG)
DR M KATASO MD
DERMATOLOGICAL CONDITIONS
THE SLIDE CONTAINS THE FOLLOWING TOPICS
1. Cutaneous Fungal Infections
2. DERMATITS
COMMON FUMGAL INFECTIONS
INTRODUCTION
1. Fungal infections are the most common type of infection worldwide
2. An estimated 20-25% of the world’s population has some form of fungal infection
3. Cutaneous infections are divided into superficial and deep mycoses
4. Most mycotic infections are superficial and limited to the stratum corneum, hair, and nails
5. Most deep mycoses are evidence of disseminated infection, typically with a primary pulmonary
focus
6. Few deep mycoses result from direct inoculation into the skin by a thorn or other foreign body
RISK FACTORS FOR MYCOTIC INFECTIONS
1. Local and systemic immunosuppression
2. There may be genetic susceptibility to certain forms of fungi due to the types of keratin
3. A hot, humid environment or occlusive footwear predisposes to dermatophyte infections
SUPERFICIAL MYCOSES
DERMATOPHYTOSIS
1. The major fungi that cause only stratum corneum, hair, and nail infection are the dermatophytes
2. They are classified in 3 genera: Microsporum, Trichophyton, and Epidermophyton
3. They are fungi that have developed the ability to live on keratin (epidermis, hair, nails, feathers, horns and
hooves)
TINEA CAPITIS
1. Also known as scalp ringworm
2. Mostly caused by trychophyton tonsurans
3. Pet exposure is associated with tinea capitis caused by M. Canis
4. It occurs mainly in children, although it may be seen at all ages
5. Incubation period lasts 2-4 days, although the period is highly variable and asymptomatic carriers are
common. Asymptomatic carriers are a source of infection for classmates and siblings.
CLINICAL MANIFESTATION
1. Scaly, erythematous, papular eruptions with loose and broken-off hairs.
2. Deep, tender, boggy plaques exuding pus are known as kerion celsii.
3. Kerion may be followed by scarring and permanent alopecia in the areas of inflammation and suppuration.
4. Favus: appears chiefly on the scalp but may affect glabrous skin and nails.
DIAGNOSIS
1. Wood’s light can be used for fluorescent-positive infections
2. Microscopy
3. Culture
4. Molecular sequencing
TINEA CAPITIS KERION FAVUS
TINEA CAPITIS
DIFFERENTIA DIAGNOSIS
1. Psoriasis
2. Seborrheic dermatitis
3. Secondary syphilis
4. Trichotillomania
5. Alopecia areata
6. Lupus erythematosus
7. Chronic staphyloccocal folliculitis
8. Pediculosis capitis
9. Lichen planus
TREATMENT
1. Griseofulvin remains the most commonly used antifungal agent in children due to its effectiveness and safety
profile.
2. Numerous clinical trials demonstrate the effectiveness of itraconazole, terbinafine, and fluconazole
3. Selenium sulfide and ketoconazole shampoos can be used as adjunctive therapy to oral antifungals.
PROGNOSIS
1. Recurrence usually does not occur when adequate amounts of antifungals have been taken
2. Exposure to infected persons, asymptomatic carriers, or contaminated fomites will increase the relapse rate
3. Without medication, there is spontaneous clearing at about the age of 15, except with T. tonsurans which
persists into adult life.
TINEA BARBAE
1. Ringworm of the beard, also known as tinea sycosis and barbers itch
2. Usually seen in those in contact with farm animals
3. Involvement is mostly on one side of the neck or face
4. Two clinical types are distinguished: 1) deep, nodular, suppurative lesions; and 2) superficial, crusted,
partially bald patches with folliculitis.
DIAGNOSIS
1. KOH mount of hair, scales, biopsy specimen
2. Fungal culture
TREATMENT
1. Oral antifungals: griseofulvin terbinafine, itraconazole
2. Topical agents are only helpful as adjunctive therapy
DIFFERENTIA DIAGNOSIS
1. Staphylococcal folliculitis (sycosis vulgaris)
2. Herpetic infections
TINEA CORPORIS
1. Tinea corporis includes all superficial dermatophyte infections of the skin other than those involving the
scalp, beard, face, hands, feet, and groin
2. This form of ringworm is characterized by circular, sharply circumscribed, slightly erythematous, dry, scaly,
usually hypopigmented patches. An advancing scaling edge is usually prominent
3. Widespread tinea corporis may be the presenting sign of AIDS, or may be related to the use of a topical
corticosteroid or calcineurin inhibitor
TINEA CORPORIS
DIAGNOSIS
1. Microscopy of skin scrapings
2. Culture of skin scrapings
TREATMENT
1. Localized disease without fungal folliculitis may be treated with topical therapy: (sulconazole, oxiconazole,
miconazole, clotrimazole, econazole, naftifine, ketoconazole, ciclopirox olamine, terbinafine, butenafine).
Most treatment times are between 2 and 4 weeks with twice a day use. Combination products with a potent
corticosteroid frequently produce widespread tinea and fungal folliculitis
2. Extensive disease or fungal folliculitis requires systemic antifungal treatment. Absorption of griseofulvin is
improved when given with whole milk or ice cream. Effective griseofulvin blood levels in children occur at
doses of 10-20 mg/kg/day, although higher doses may be needed. Terbinafine at 250mg/day for 1-2weeks;
itraconazole at 200mg/day for 1 week; and fluconazole at 150mg once a week for 4 weeks, have been
effective doses for adults.
TINEA CRURIS
1. Affects the upper and inner surfaces of the thighs, especially during the summer when the humidity is high
2. It begins as a small erythematous and scaling or vesicular and crusted patch that spreads peripherally and
partly clears in the center
3. The patch is characterized chiefly by its curved, well-defined border, particularly on its lower edge
4. The border may have vesicles, pustules, or papules
5. It may extend downward on the thighs and backward on the perineum or about the anus
6. The scrotum is rarely involved.
DIFFERENTIAL DIAGNOSIS.
1. Infection with C. albicans may closely mimic
tinea cruris, but is usually moister, more
inflammatory.
2. Seborrheic dermatitis: involves central chest
and axilla in addition to the groin
3. Intertriginous psoriasis.
TREATMENT
1. Reduction of perspiration and enhancement of
evaporation are important prophylactic
measures
2. Antifungal powders are helpful
3. Topical and oral treatment as in tinea corporis
TINEA PEDIS
1. Dermatophytosis of the feet is by far the most common fugal disease
2. Also known as athlete’s foot
3. There may be an autosomal-dominant predisposition to this form of infection
CLINICAL FEATURES
1. Characterized by a dull erythema and pronounced silvery scaling that may involve the entire sole and sides of
the foot
2. The eruption may also be limited to a patch between or under the toes
3. Some dermatophytes may produce acutely inflammatory multilocular bullae
4. The burning and itching that accompany formation of the vesicles may cause great discomfort, relieved by
opening the tense vesicles
5. Secondary bacterial infection may be present.
TINEA PEDIS
DIAGNOSIS
1. Microscopy
2. Culture
PROPHYLAXIS
Hyperhydrosis is a predisposing factor for tinea infections: Feet should be kept dry, and dried thoroughly after
bathing.
TREATMENT
1. Topical Antifungal drugs:Clotrimazole, miconazole, sulconazole, oxiconazole, ciclopirox, econazole,
ketoconazole, naftifine, terbinafine, and butefafine are effective topical antifungal agents. When there is
maceration between the toes, cotton inserts may be helpful.
2. Griseofulvin in doses of 500-1000mg/day can be effective. Period of therapy depends on the response of the
lesions. Shorter courses are possible with newer antifungal agents such as terbinafine 250mg/day for 1-2
weeks, itraconazole 200mg twice a day for 1 week, and fluconazole 150mg once a week for 4 weeks.
TINEA MANUM
1. Tinea infection of the hands.
2. Characterized by dry, scaly, and erythematous patches
3. Other areas are frequently affected at the same time, especially the feet.
DIAGNOSIS
1. As in tinea pedis
TREATMENT
1. As in tinea pedis
TINEA UNGUIUM (ONYCHOMYCOSIS)
1. Onychomycosis is infection of the nail plate by fungus
2. Many fungi may be causative
3. Fingernails and toenails present a similar appearance
4. Common features of onychomycosis include nail-plate thickening, opacification, and onycholysis.
DIAGNOSIS
1. Microscopy with KOH solution
2. Culture
3. Histology
4. PCR
TREATMENT
1. For disease involving fingernails, terbinafine is given in doses of 250mg/day for 6-8 weeks, toenails require
12-16 weeks of treatment
2. Itraconazole is given as pulsed dosing, 200mg bd for 1 week of each month, for 2 months when treating
fingernails and 3-4 months when treating toenails
3. Fluconazole at 150-300mg once a week for 6-12 months.
TINEA VERSICOLOR
1. A.K.A Pityriasis Versicolor
2. Not a dermatophyte infection
3. Caused by malassezia furfur and related fungi
CLINICAL FEATURES
1. Commonly presents as hypo- or hyperpigmented coalescing scaly macules on the trunk and upper arms.The
eruption is more common during summer months. Sites of predilection are the sternal region and the sides
of the chest, abdomen, back, pubis, neck, and intertriginous areas. The face and scalp may also be affected.
2. Mild itching and inflammation about the patches may be present
3. In some instances, many follicular papules are present
TINEA VERSICOLOUR
DIAGNOSIS
1. Microscopy
2. Culture
3. Wood’s light examination accentuates pigment changes
4. Biopsy
TREATMENT
1. Topical antifungal creams
2. Selenium sulfide shampoo
3. Systemic antifungals (ketoconazole 400mg weekly for 2 weeks, oral itraconazole 200mg od for 7 days,
fluconazole 400mg po stat)
4. Terbinafine is effective topically (twice daily applications)
5. Relapses are common, but prophylaxis may be successful with monthly applications of selenium sulfide
TINEA FACIEI
1. Superficial fungal infection of the face
2. Frequently misdiagnosed
3. May lack the typical annular rings and the lesions are exquisitely photosensitive
CLINICAL FEATURES
TREATMENT
1. If fungal folliculitis is present, oral medication is required: Systemic anti fungal.
2. If no folliculitis is present, the infection responds well to topical therapy
3. Oral agents are appropriate for widespread infections.
CANDIDIASIS
1. Also known as candidosis
2. C. albicans is a common inhabitant of the human GI and GU tracts, and skin
3. Under the right conditions, it becomes a pathogen, causing lesions of the skin, nails, and mucous membranes
4. Intertriginous areas are frequently affected
5. Warmth, moisture, and maceration of the skin permit the organism to thrive
6. Areas most often involved are the perianal and inguinal folds, abdominal creases, inframammary creases,
interdigital areas, nailfolds, and axillae
7. C. albicans is an opportunistic organism, acting as a pathogen in the presence of impaired immune response, or
where local conditions favor growth
RISK FACTORS
1. Immunosupression
2. Warmth and moisture favor candidal growth
3. Reductions in competing flora during antibiotic therapy can also favor candidal growth
4. Higher skin pH also favors candidal growth.
DIAGNOSIS
1. Microscopy with KOH solution
2. Gram stain: dense gram positive ovoid bodies seen
3. Histology
4. Culture
FORMS OF CANDIDIASIS
1. OROPHARYNGEAL CANDIDIASIS
Oral candidiasis (thrush): involvement of the mucous membrane of the mouth. Saliva inhibits the growth of
candida, and a dry mouth predisposes to candidal growth.
CLINICAL FEATURES
1. Greyish-white membranous plaques are found on the surface of the mucous membrane.The base of these
plaques is moist, reddish, and macerated
2. Perlèche (angular cheilitis): characterized by maceration and transverse fissuring of the oral commissures.
Similar changes may occur in riboflavin deficiency or other nutritional deficiency.
2. CANDIDAL VULVOVAGINITIS
C. albicans is a common inhabitant of the vaginal tract
Risk factors include: pregnancy, diabetes mellitus, use of broad-spectrum antibiotics
Clinical features: severe pruritus, burning, and discharge: The vaginal discharge is not usually profuse and
varies from watery, to thick and white.
3. OTHER FORMS OF CANDIDIASIS INCLUDE: diaper dermatitis, candidal intertrigo etc.
TREATMENT
1. Oral thrash: Topical: nystatin wash. Systemic anti fungal: fluconazole, voriconazole.
2. Esophageal candidiasis: Fluconazole, caspofungin.
3. Vanginal candidiasis: Nystatin pessaries, systemic Fluconazole.
DERMATITIS
Under this section, we will cover the following conditions:
1. Atopic dermatitis
2. Exfoliative
3. Seborrheic dermatitis
4. Contact dermatitis
5. Psoriasis
WHAT IS DERMATITIS?
1. Dermatitis (eczema) refers to a heterogeneous group of disorders that share similarities in clinical
appearance and histopathologic findings, but may have very different etiologies.
2. Eczema is synonymous with the term dermatitis and the two words are interchangeable.
3. Eczema originates from a Greek word meaning “to boil”.
4. Pruritus is a common symptom of all types of dermatitis. The hall mark of eczema.
ATOPIC DERMATITIS
1. Atopic dermatitis (AD) is a chronic, inflammatory skin disease that is characterized by pruritus and a
chronic course of exacerbations and remissions.
2. It is associated with other allergic conditions, including asthma and allergic rhino conjunctivitis
3. “AD is not an allergic disease, but a skin disease with allergies
4. There is what is known as atopic triad.
ATOPIC TRIAD
CLINICAL MANIFESTATION
AD can be divided into three stages:
1. Infantile AD, occurring from 2 months to 2 years of age
2. Childhood AD, from 2 to 10 years; and
3. Adolescent/adult AD.
In all stages, pruritus is the hallmark
Itching often precedes the appearance of lesions; hence the concept that AD is “the itch that rashes”
INFANTILE AD CLINICAL PICTURE
1. 50% of AD cases present in the first year of life, but usually not until after 2 months of age.
2. AD in infancy usually begins as erythema and scaling of the cheeks.
3. The eruption may extend to the scalp, neck, forehead, wrists, and extensor extremities
4. Areas of involvement correlate with the capacity of the infant to scratch or rub the site, and activities such
as crawling.
INFANTILE AD CLINICAL PICTURE
5. There may be a significant amount of exudate and infection may result in crusts and pustules
6. Chronic scratching and rubbing may result in lichenification.
7. It can be aggravated by viral infections, dry air in winter, and wool
CHILDHOOD ATOPIC DERMATITIS
1. Lesions are less exudative in childhood
2. Classic locations are the antecubital and popliteal fossae, flexor wrists, eyelids, face, and around the neck.
3. Lesions are often lichenified, indurated plaques
4. Pruritus is a constant feature resulting in a vicious itch-scratch cycle.
AD IN ADOLESCENTS
1. In older patients, AD may occur as localized erythematous, scaly, papular, exudative, or lichenified plaques.
TREATMENT
GENERAL MANAGEMENT
1. Parent/patient education
2. Psychological support
3. Barrier repair: petrolatum-based emollients
4. Antimicrobial therapy: when infection is present
5. Address environmental factors: stress, heat, wool etc.
6. Antipruritics
SPECIFIC MANAGEMENT
1. Topical corticosteroid therapy
2. Topical calcineurin inhibitors
3. 1-5% crude coal tar
4. Phototherapy: if topical modalities fail. UVB
5. Systemic corticosteroids: to control acute
exacerbations
6. Cyclosporine: highly effective in treatment of
severe AD
7. Azathioprine, mycophenolate mofetil, and
methotrexate have also been used.
SEBORHEIC DERMATITIS
Seborrheic dermatitis is a chronic, superficial, inflammatory disease with a predilection for the scalp,
eyebrows, eyelids, nasolabial creases, lips, ears, sternal area, axillae, sub mammary folds, umbilicus, groins, and
gluteal crease.
ETIOLOGY
The yeast pityrosporum ovale has been associated with this disorder. The density of the yeast has been
correlated with the severity of the disease, and reduction of the yeast occurs with response to therapy.
RISK FACTORS
1. Hiv
2. Diabetes Mellitus
3. Obesity
CLINICAL FEATURES
1. It is characterized by scaling on an erythematous base
2. The scaling often has a yellow, greasy appearance.
3. It may be accompanied by severe itching
4. In extreme cases the entire scalp is covered by a greasy, dirty crust with an offensive odor
5. In infants, yellow or brown scaling lesions on the scalp, with accumulated adherent epithelial debris, are
called cradle cap
DIFFERENTIAL DIAGNOSIS
1. Psoriasis
2. Impetigo
3. Tinea capitis
SEBORHEIC DERMATITIS
SEBORHEIC DERMATITIS
TREATMENT
1. Topical corticosteroids
2. Topical calcineurin inhibitors
3. Topical antifungals (ketoconazole cream)
4. Oral itraconazole and oral terbinafine
PSORIASIS
INTRODUCTIION
1. Psoriasis is a chronic, autoimmune, non-infectious inflammatory dermatosis that can result in decreased
quality of life.
2. It affects 3% of the world-population.
3. well-demarcated itchy erythematous plaques with silvery scales.
4. It commonly affects extensor surface, the skin of elbows, knees, scalp, lumbosacral areas, inter-gluteal
clefts, scalp and glans penis. It can affect joints 30% of the time.
5. It tends to flare with systemic and environmental factors. Precipitating factors include: trauma (Koebner
phenomenon), Infection, drugs (e.g. beta blockers ,lithium, anti malarial and iodides), and psychological
stress. Cold obesity, alcohol and low humidity are also triggers.
6. Diets high in fish oils seem to be protective against the development of psoriasis
PSORIASIS: PRIMARY LESION
Chronic, well demarcated, erythematous plaques with silvery scaling. Lesions commonly seen on extensor
surfaces and scalp.
TYPES OF PSORIASIS
1. MORPHOLOGICAL VARIANTS
2. ANATOMICAL VARIANTS.
MORPHOLOGICAL VARIANTS
1. CHRONIC PLAQUE PSORIASIS
This is the most common (80%) type of psoriasis.
The plaques are topped with white silvery scales.
It also tends to present with itch and is found on the scalp, extensor surfaces of the knees, elbows, lower
back, and groin.
GUTTATE PSORIASIS
1. Affects 10% of individuals(usually children and young adults).
2. Presents as small, red individual spots on the trunk and limbs.
3. Starts in childhood and is sometimes triggered by an infection e.g. streptococcal throat infection.
4. This variant is more likely to itch sometimes severely.
PATULAR PSORIASIS
1. Presents on the palms and soles
2. It may be tender
3. Pustules are non-infectious
PASTULAR PSORIASIS
ERYTHRODERMIC PSORIASIS
1. Presents as fire red scales that can cover any large area of the skin (more than 90% of the body surface
area).
2. It is extremely itchy and painful.
3. Scales fall off in sheets.
4. Patient may develop chills, rigors (temperature balance dysregulation) and electrolyte disturbances because
the skin barrier is disturbed.
5. If this type of psoriasis is not treated early it may become an emergency requiring admission
ANATOMIC VARIANTS
NAIL CHANGES IN PSORIASIS
1. Nail pitting
2. Discoloration
3. Onycholysis (oil spots)
4. Subungual hyperkeratosis
5. Nail deformity.
PSORIASIS
TREATMENT
TOPICAL TREATMENT
1. Topical steroids
2. Topical Vitamin D analogues
3. Coal Tar Ointment
4. Topical retinoids
SYTEMIC TREATMENT
1. Methotrexate
2. Ciclosporin
3. Acitretin (Pustular Psoriasis)
4. Biologics

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DERMATOLOGY COG LECTURE 1.pdcghkgfhfgyyf

  • 1. ZERA INTERNATIONAL COLLEGE OF HEALTH SCIENCES INTERNAL MEDICINE CLINICAL OFFICER (COG) DR M KATASO MD DERMATOLOGICAL CONDITIONS THE SLIDE CONTAINS THE FOLLOWING TOPICS 1. Cutaneous Fungal Infections 2. DERMATITS
  • 2. COMMON FUMGAL INFECTIONS INTRODUCTION 1. Fungal infections are the most common type of infection worldwide 2. An estimated 20-25% of the world’s population has some form of fungal infection 3. Cutaneous infections are divided into superficial and deep mycoses 4. Most mycotic infections are superficial and limited to the stratum corneum, hair, and nails 5. Most deep mycoses are evidence of disseminated infection, typically with a primary pulmonary focus 6. Few deep mycoses result from direct inoculation into the skin by a thorn or other foreign body RISK FACTORS FOR MYCOTIC INFECTIONS 1. Local and systemic immunosuppression 2. There may be genetic susceptibility to certain forms of fungi due to the types of keratin 3. A hot, humid environment or occlusive footwear predisposes to dermatophyte infections
  • 3. SUPERFICIAL MYCOSES DERMATOPHYTOSIS 1. The major fungi that cause only stratum corneum, hair, and nail infection are the dermatophytes 2. They are classified in 3 genera: Microsporum, Trichophyton, and Epidermophyton 3. They are fungi that have developed the ability to live on keratin (epidermis, hair, nails, feathers, horns and hooves) TINEA CAPITIS 1. Also known as scalp ringworm 2. Mostly caused by trychophyton tonsurans 3. Pet exposure is associated with tinea capitis caused by M. Canis 4. It occurs mainly in children, although it may be seen at all ages 5. Incubation period lasts 2-4 days, although the period is highly variable and asymptomatic carriers are common. Asymptomatic carriers are a source of infection for classmates and siblings. CLINICAL MANIFESTATION 1. Scaly, erythematous, papular eruptions with loose and broken-off hairs. 2. Deep, tender, boggy plaques exuding pus are known as kerion celsii. 3. Kerion may be followed by scarring and permanent alopecia in the areas of inflammation and suppuration. 4. Favus: appears chiefly on the scalp but may affect glabrous skin and nails. DIAGNOSIS 1. Wood’s light can be used for fluorescent-positive infections 2. Microscopy 3. Culture 4. Molecular sequencing
  • 5. TINEA CAPITIS DIFFERENTIA DIAGNOSIS 1. Psoriasis 2. Seborrheic dermatitis 3. Secondary syphilis 4. Trichotillomania 5. Alopecia areata 6. Lupus erythematosus 7. Chronic staphyloccocal folliculitis 8. Pediculosis capitis 9. Lichen planus TREATMENT 1. Griseofulvin remains the most commonly used antifungal agent in children due to its effectiveness and safety profile. 2. Numerous clinical trials demonstrate the effectiveness of itraconazole, terbinafine, and fluconazole 3. Selenium sulfide and ketoconazole shampoos can be used as adjunctive therapy to oral antifungals. PROGNOSIS 1. Recurrence usually does not occur when adequate amounts of antifungals have been taken 2. Exposure to infected persons, asymptomatic carriers, or contaminated fomites will increase the relapse rate 3. Without medication, there is spontaneous clearing at about the age of 15, except with T. tonsurans which persists into adult life.
  • 6. TINEA BARBAE 1. Ringworm of the beard, also known as tinea sycosis and barbers itch 2. Usually seen in those in contact with farm animals 3. Involvement is mostly on one side of the neck or face 4. Two clinical types are distinguished: 1) deep, nodular, suppurative lesions; and 2) superficial, crusted, partially bald patches with folliculitis. DIAGNOSIS 1. KOH mount of hair, scales, biopsy specimen 2. Fungal culture TREATMENT 1. Oral antifungals: griseofulvin terbinafine, itraconazole 2. Topical agents are only helpful as adjunctive therapy DIFFERENTIA DIAGNOSIS 1. Staphylococcal folliculitis (sycosis vulgaris) 2. Herpetic infections
  • 7. TINEA CORPORIS 1. Tinea corporis includes all superficial dermatophyte infections of the skin other than those involving the scalp, beard, face, hands, feet, and groin 2. This form of ringworm is characterized by circular, sharply circumscribed, slightly erythematous, dry, scaly, usually hypopigmented patches. An advancing scaling edge is usually prominent 3. Widespread tinea corporis may be the presenting sign of AIDS, or may be related to the use of a topical corticosteroid or calcineurin inhibitor
  • 8. TINEA CORPORIS DIAGNOSIS 1. Microscopy of skin scrapings 2. Culture of skin scrapings TREATMENT 1. Localized disease without fungal folliculitis may be treated with topical therapy: (sulconazole, oxiconazole, miconazole, clotrimazole, econazole, naftifine, ketoconazole, ciclopirox olamine, terbinafine, butenafine). Most treatment times are between 2 and 4 weeks with twice a day use. Combination products with a potent corticosteroid frequently produce widespread tinea and fungal folliculitis 2. Extensive disease or fungal folliculitis requires systemic antifungal treatment. Absorption of griseofulvin is improved when given with whole milk or ice cream. Effective griseofulvin blood levels in children occur at doses of 10-20 mg/kg/day, although higher doses may be needed. Terbinafine at 250mg/day for 1-2weeks; itraconazole at 200mg/day for 1 week; and fluconazole at 150mg once a week for 4 weeks, have been effective doses for adults.
  • 9. TINEA CRURIS 1. Affects the upper and inner surfaces of the thighs, especially during the summer when the humidity is high 2. It begins as a small erythematous and scaling or vesicular and crusted patch that spreads peripherally and partly clears in the center 3. The patch is characterized chiefly by its curved, well-defined border, particularly on its lower edge 4. The border may have vesicles, pustules, or papules 5. It may extend downward on the thighs and backward on the perineum or about the anus 6. The scrotum is rarely involved. DIFFERENTIAL DIAGNOSIS. 1. Infection with C. albicans may closely mimic tinea cruris, but is usually moister, more inflammatory. 2. Seborrheic dermatitis: involves central chest and axilla in addition to the groin 3. Intertriginous psoriasis. TREATMENT 1. Reduction of perspiration and enhancement of evaporation are important prophylactic measures 2. Antifungal powders are helpful 3. Topical and oral treatment as in tinea corporis
  • 10. TINEA PEDIS 1. Dermatophytosis of the feet is by far the most common fugal disease 2. Also known as athlete’s foot 3. There may be an autosomal-dominant predisposition to this form of infection CLINICAL FEATURES 1. Characterized by a dull erythema and pronounced silvery scaling that may involve the entire sole and sides of the foot 2. The eruption may also be limited to a patch between or under the toes 3. Some dermatophytes may produce acutely inflammatory multilocular bullae 4. The burning and itching that accompany formation of the vesicles may cause great discomfort, relieved by opening the tense vesicles 5. Secondary bacterial infection may be present.
  • 11. TINEA PEDIS DIAGNOSIS 1. Microscopy 2. Culture PROPHYLAXIS Hyperhydrosis is a predisposing factor for tinea infections: Feet should be kept dry, and dried thoroughly after bathing. TREATMENT 1. Topical Antifungal drugs:Clotrimazole, miconazole, sulconazole, oxiconazole, ciclopirox, econazole, ketoconazole, naftifine, terbinafine, and butefafine are effective topical antifungal agents. When there is maceration between the toes, cotton inserts may be helpful. 2. Griseofulvin in doses of 500-1000mg/day can be effective. Period of therapy depends on the response of the lesions. Shorter courses are possible with newer antifungal agents such as terbinafine 250mg/day for 1-2 weeks, itraconazole 200mg twice a day for 1 week, and fluconazole 150mg once a week for 4 weeks.
  • 12. TINEA MANUM 1. Tinea infection of the hands. 2. Characterized by dry, scaly, and erythematous patches 3. Other areas are frequently affected at the same time, especially the feet. DIAGNOSIS 1. As in tinea pedis TREATMENT 1. As in tinea pedis
  • 13. TINEA UNGUIUM (ONYCHOMYCOSIS) 1. Onychomycosis is infection of the nail plate by fungus 2. Many fungi may be causative 3. Fingernails and toenails present a similar appearance 4. Common features of onychomycosis include nail-plate thickening, opacification, and onycholysis. DIAGNOSIS 1. Microscopy with KOH solution 2. Culture 3. Histology 4. PCR TREATMENT 1. For disease involving fingernails, terbinafine is given in doses of 250mg/day for 6-8 weeks, toenails require 12-16 weeks of treatment 2. Itraconazole is given as pulsed dosing, 200mg bd for 1 week of each month, for 2 months when treating fingernails and 3-4 months when treating toenails 3. Fluconazole at 150-300mg once a week for 6-12 months.
  • 14. TINEA VERSICOLOR 1. A.K.A Pityriasis Versicolor 2. Not a dermatophyte infection 3. Caused by malassezia furfur and related fungi CLINICAL FEATURES 1. Commonly presents as hypo- or hyperpigmented coalescing scaly macules on the trunk and upper arms.The eruption is more common during summer months. Sites of predilection are the sternal region and the sides of the chest, abdomen, back, pubis, neck, and intertriginous areas. The face and scalp may also be affected. 2. Mild itching and inflammation about the patches may be present 3. In some instances, many follicular papules are present
  • 15. TINEA VERSICOLOUR DIAGNOSIS 1. Microscopy 2. Culture 3. Wood’s light examination accentuates pigment changes 4. Biopsy TREATMENT 1. Topical antifungal creams 2. Selenium sulfide shampoo 3. Systemic antifungals (ketoconazole 400mg weekly for 2 weeks, oral itraconazole 200mg od for 7 days, fluconazole 400mg po stat) 4. Terbinafine is effective topically (twice daily applications) 5. Relapses are common, but prophylaxis may be successful with monthly applications of selenium sulfide
  • 16. TINEA FACIEI 1. Superficial fungal infection of the face 2. Frequently misdiagnosed 3. May lack the typical annular rings and the lesions are exquisitely photosensitive CLINICAL FEATURES TREATMENT 1. If fungal folliculitis is present, oral medication is required: Systemic anti fungal. 2. If no folliculitis is present, the infection responds well to topical therapy 3. Oral agents are appropriate for widespread infections.
  • 17. CANDIDIASIS 1. Also known as candidosis 2. C. albicans is a common inhabitant of the human GI and GU tracts, and skin 3. Under the right conditions, it becomes a pathogen, causing lesions of the skin, nails, and mucous membranes 4. Intertriginous areas are frequently affected 5. Warmth, moisture, and maceration of the skin permit the organism to thrive 6. Areas most often involved are the perianal and inguinal folds, abdominal creases, inframammary creases, interdigital areas, nailfolds, and axillae 7. C. albicans is an opportunistic organism, acting as a pathogen in the presence of impaired immune response, or where local conditions favor growth RISK FACTORS 1. Immunosupression 2. Warmth and moisture favor candidal growth 3. Reductions in competing flora during antibiotic therapy can also favor candidal growth 4. Higher skin pH also favors candidal growth. DIAGNOSIS 1. Microscopy with KOH solution 2. Gram stain: dense gram positive ovoid bodies seen 3. Histology 4. Culture
  • 18. FORMS OF CANDIDIASIS 1. OROPHARYNGEAL CANDIDIASIS Oral candidiasis (thrush): involvement of the mucous membrane of the mouth. Saliva inhibits the growth of candida, and a dry mouth predisposes to candidal growth. CLINICAL FEATURES 1. Greyish-white membranous plaques are found on the surface of the mucous membrane.The base of these plaques is moist, reddish, and macerated 2. Perlèche (angular cheilitis): characterized by maceration and transverse fissuring of the oral commissures. Similar changes may occur in riboflavin deficiency or other nutritional deficiency.
  • 19. 2. CANDIDAL VULVOVAGINITIS C. albicans is a common inhabitant of the vaginal tract Risk factors include: pregnancy, diabetes mellitus, use of broad-spectrum antibiotics Clinical features: severe pruritus, burning, and discharge: The vaginal discharge is not usually profuse and varies from watery, to thick and white. 3. OTHER FORMS OF CANDIDIASIS INCLUDE: diaper dermatitis, candidal intertrigo etc. TREATMENT 1. Oral thrash: Topical: nystatin wash. Systemic anti fungal: fluconazole, voriconazole. 2. Esophageal candidiasis: Fluconazole, caspofungin. 3. Vanginal candidiasis: Nystatin pessaries, systemic Fluconazole.
  • 20. DERMATITIS Under this section, we will cover the following conditions: 1. Atopic dermatitis 2. Exfoliative 3. Seborrheic dermatitis 4. Contact dermatitis 5. Psoriasis WHAT IS DERMATITIS? 1. Dermatitis (eczema) refers to a heterogeneous group of disorders that share similarities in clinical appearance and histopathologic findings, but may have very different etiologies. 2. Eczema is synonymous with the term dermatitis and the two words are interchangeable. 3. Eczema originates from a Greek word meaning “to boil”. 4. Pruritus is a common symptom of all types of dermatitis. The hall mark of eczema. ATOPIC DERMATITIS 1. Atopic dermatitis (AD) is a chronic, inflammatory skin disease that is characterized by pruritus and a chronic course of exacerbations and remissions. 2. It is associated with other allergic conditions, including asthma and allergic rhino conjunctivitis 3. “AD is not an allergic disease, but a skin disease with allergies 4. There is what is known as atopic triad.
  • 21. ATOPIC TRIAD CLINICAL MANIFESTATION AD can be divided into three stages: 1. Infantile AD, occurring from 2 months to 2 years of age 2. Childhood AD, from 2 to 10 years; and 3. Adolescent/adult AD. In all stages, pruritus is the hallmark Itching often precedes the appearance of lesions; hence the concept that AD is “the itch that rashes” INFANTILE AD CLINICAL PICTURE 1. 50% of AD cases present in the first year of life, but usually not until after 2 months of age. 2. AD in infancy usually begins as erythema and scaling of the cheeks. 3. The eruption may extend to the scalp, neck, forehead, wrists, and extensor extremities 4. Areas of involvement correlate with the capacity of the infant to scratch or rub the site, and activities such as crawling.
  • 22. INFANTILE AD CLINICAL PICTURE 5. There may be a significant amount of exudate and infection may result in crusts and pustules 6. Chronic scratching and rubbing may result in lichenification. 7. It can be aggravated by viral infections, dry air in winter, and wool CHILDHOOD ATOPIC DERMATITIS 1. Lesions are less exudative in childhood 2. Classic locations are the antecubital and popliteal fossae, flexor wrists, eyelids, face, and around the neck. 3. Lesions are often lichenified, indurated plaques 4. Pruritus is a constant feature resulting in a vicious itch-scratch cycle.
  • 23. AD IN ADOLESCENTS 1. In older patients, AD may occur as localized erythematous, scaly, papular, exudative, or lichenified plaques. TREATMENT GENERAL MANAGEMENT 1. Parent/patient education 2. Psychological support 3. Barrier repair: petrolatum-based emollients 4. Antimicrobial therapy: when infection is present 5. Address environmental factors: stress, heat, wool etc. 6. Antipruritics SPECIFIC MANAGEMENT 1. Topical corticosteroid therapy 2. Topical calcineurin inhibitors 3. 1-5% crude coal tar 4. Phototherapy: if topical modalities fail. UVB 5. Systemic corticosteroids: to control acute exacerbations 6. Cyclosporine: highly effective in treatment of severe AD 7. Azathioprine, mycophenolate mofetil, and methotrexate have also been used.
  • 24. SEBORHEIC DERMATITIS Seborrheic dermatitis is a chronic, superficial, inflammatory disease with a predilection for the scalp, eyebrows, eyelids, nasolabial creases, lips, ears, sternal area, axillae, sub mammary folds, umbilicus, groins, and gluteal crease. ETIOLOGY The yeast pityrosporum ovale has been associated with this disorder. The density of the yeast has been correlated with the severity of the disease, and reduction of the yeast occurs with response to therapy. RISK FACTORS 1. Hiv 2. Diabetes Mellitus 3. Obesity CLINICAL FEATURES 1. It is characterized by scaling on an erythematous base 2. The scaling often has a yellow, greasy appearance. 3. It may be accompanied by severe itching 4. In extreme cases the entire scalp is covered by a greasy, dirty crust with an offensive odor 5. In infants, yellow or brown scaling lesions on the scalp, with accumulated adherent epithelial debris, are called cradle cap DIFFERENTIAL DIAGNOSIS 1. Psoriasis 2. Impetigo 3. Tinea capitis
  • 26. SEBORHEIC DERMATITIS TREATMENT 1. Topical corticosteroids 2. Topical calcineurin inhibitors 3. Topical antifungals (ketoconazole cream) 4. Oral itraconazole and oral terbinafine PSORIASIS INTRODUCTIION 1. Psoriasis is a chronic, autoimmune, non-infectious inflammatory dermatosis that can result in decreased quality of life. 2. It affects 3% of the world-population. 3. well-demarcated itchy erythematous plaques with silvery scales. 4. It commonly affects extensor surface, the skin of elbows, knees, scalp, lumbosacral areas, inter-gluteal clefts, scalp and glans penis. It can affect joints 30% of the time. 5. It tends to flare with systemic and environmental factors. Precipitating factors include: trauma (Koebner phenomenon), Infection, drugs (e.g. beta blockers ,lithium, anti malarial and iodides), and psychological stress. Cold obesity, alcohol and low humidity are also triggers. 6. Diets high in fish oils seem to be protective against the development of psoriasis
  • 27. PSORIASIS: PRIMARY LESION Chronic, well demarcated, erythematous plaques with silvery scaling. Lesions commonly seen on extensor surfaces and scalp. TYPES OF PSORIASIS 1. MORPHOLOGICAL VARIANTS 2. ANATOMICAL VARIANTS. MORPHOLOGICAL VARIANTS 1. CHRONIC PLAQUE PSORIASIS This is the most common (80%) type of psoriasis. The plaques are topped with white silvery scales. It also tends to present with itch and is found on the scalp, extensor surfaces of the knees, elbows, lower back, and groin.
  • 28. GUTTATE PSORIASIS 1. Affects 10% of individuals(usually children and young adults). 2. Presents as small, red individual spots on the trunk and limbs. 3. Starts in childhood and is sometimes triggered by an infection e.g. streptococcal throat infection. 4. This variant is more likely to itch sometimes severely. PATULAR PSORIASIS 1. Presents on the palms and soles 2. It may be tender 3. Pustules are non-infectious PASTULAR PSORIASIS
  • 29. ERYTHRODERMIC PSORIASIS 1. Presents as fire red scales that can cover any large area of the skin (more than 90% of the body surface area). 2. It is extremely itchy and painful. 3. Scales fall off in sheets. 4. Patient may develop chills, rigors (temperature balance dysregulation) and electrolyte disturbances because the skin barrier is disturbed. 5. If this type of psoriasis is not treated early it may become an emergency requiring admission
  • 30. ANATOMIC VARIANTS NAIL CHANGES IN PSORIASIS 1. Nail pitting 2. Discoloration 3. Onycholysis (oil spots) 4. Subungual hyperkeratosis 5. Nail deformity.
  • 31. PSORIASIS TREATMENT TOPICAL TREATMENT 1. Topical steroids 2. Topical Vitamin D analogues 3. Coal Tar Ointment 4. Topical retinoids SYTEMIC TREATMENT 1. Methotrexate 2. Ciclosporin 3. Acitretin (Pustular Psoriasis) 4. Biologics