dermatologylecturenotes-200629034218.pdf

DERMA

1. Dermatology Lectures
Abdelmoiz Elsadig

2. Introduction to skin diseases
Objectives
•Review of the normal structure and physiology
of the skin
•Description of skin lesions

3. Normal structure of the skin

4. skin
•The skin is the heaviest single organ of the body,
accounting for about 16% of total body weight
•It is composed of the epidermis,which is the
outermost layer of the skin& has no blood vessels,
•and the dermis,a layer of connective tissue, which
contains blood vessels, nerves and sensory
receptors.
•Beneath the dermis lies the hypodermis, or
subcutaneous tissue,a loose connective tissue that
may contain a pad of adipose cells

5. Skin cont’d
Functions:
•Protection
•Sensation
•Thermoregulation
•Metabolic funtions

6. Approach to Dermatologic Dx
Introduction:
•Approximately 7 percent of all adult outpatients have a
primary skin complaint
•and 60 percent of outpatient visits for skin disease are
made to non dermatologists
•Patients with common, chronic medical conditions,
such as obesity and diabetes, have increased numbers
of skin conditions
.

7. Approach cont’d
•The initial approach to the patient presenting
with a skin problem requires a detailed history
of the current skin complaint and a complete
skin examination .
•In many cases the patient’s general medical
history may be relevant to the diagnosis of
skin disorders.

8. Approach cont’d
HISTORY —
The most important initial questions to ask patients with a
skin problem include the following:
•How long has the rash/lesion been present?
•How did it look when it first appeared, and how is it now
different?
•Where did it first appear, and where is it now?
•What treatments have been used, and what was the
response, this time and previously?

9. Appoach cont’d
•What associated symptoms, such as itching or pain, are associated
with the lesion?
•Are any other family members affected or have a similar history?
•Has the patient ever had this rash before? If so, what treatment was
used/response?
•What does the patient think caused the rash?
•Is anything new or different, ie, medications, personal care
products, occupational or recreational exposures?

10. Approach cont’d
Additional questions that may be helpful include:
•Does the patient have any chronic medical conditions?
•What medications does the patient take currently, what have they recently
taken, including over-the-counter and herbal therapies?
•Has there been any increase in stress in their life?
•What is the social history, including occupation, hobbies, travel?
•Does the patient have any underlying allergies?
•Will the patient's education, or financial status influence treatment
considerations, such as compliance?

11. Approach cont’d
PHYSICAL EXAMINATION —
•On physical examination, it is important to
include characteristics such as distribution
•lesion morphology (wheals, macules, papules),
and
•secondary characteristics of lesions (thick, silvery
scale, thickening, or lichenification).

12. Approach cont’d
The physical examination of skin complaints should
include the following:
•Type of lesion
•Shape of individual lesions
•Arrangement of multiple lesions (eg, scattered,
grouped, linear, etc.)
•Distribution of lesions
•Color
•Consistency and feel

13. Approach cont’d
Primary lesions -
Primary lesions are either the first visible lesion or involve the
initial skin changes. The terms used to describe primary
skin lesions include the following:
•Maculesare nonpalpable lesions that vary in pigmentation
from the surrounding skin , There are no elevations or
depressions.
•Papulesare palpable, discrete lesions measuring ≤5 mm
diameter .,They may be isolated or grouped.
•Plaquesare large (>5 mm) superficial flat lesions, often
formed by a confluence of papules .

14. Approach cont’d
•Nodules are palpable, discrete lesions
measuring ≥6 mm diameter . They may be
isolated or grouped. Tumorsare large nodules.
•Cystsare enclosed cavities with a lining that
can contain a liquid or semisolid material.
•Telangiectasiais a dilated superficial blood
vessel

15. Approach cont’d
•Pustules are small, circumscribed skin papules
containing purulent material
•Vesiclesare small (<5 mm diameter), circumscribed
skin papules containing serous material (). Bullaeare
large (≥6 mm) vesicles.
•Whealsare irregularly elevated edematous skin areas
that are often erythematous),The borders of a wheal
are sharp but not stable; they may move to adjacent
uninvolved areas over periods of hours.

16. Approach cont’d
Secondary lesions —
Secondary lesions of the skin represent evolved changes
from the skin disorder, due to secondary manipulation
or as a result of infection. Examples include:
•Excoriation describes superficial, often linear, skin
erosion caused by scratching
•Lichenificationis increased skin markings and
thickening with induration secondary to chronic
inflammation caused by scratching or other irritation

17. Approach cont’d
•Edema is swelling due to accumulation of
water in tissue
•Scaledescribes superficial epidermal cells that
are dead and cast off from the skin .
•Crust is dried exudate, a "scab" .

18. Approach cont’d
•Atrophyis decreased skin thickness due to
skin thinning
•Scaris abnormal fibrous tissue that replaces
normal tissue after skin injury
•Hypopigmentationis decreased skin pigment;
hyperpigmentationis increased skin pigment;
and depigmentationis total loss of skin
pigment.

19. Skin lesions
Raised
•Papule
•Plaque
•Nodule
•Cyst
•Wheal
•Scar
Depressed
Erosion
Ulcer
Atrophy
Burrow

20. Skin lesions con’d
Surface Change
Scale Fluid Filled
Crust Vesicle
Excoriation Bulla
Fissure Pustule
Lichenification Furuncle
Eschar Abscess

21. Skin lesions cont’d
Flat
•Macule
•Patch
•Erythema

22. Raised skin lesions ( papule, plaque,cyst,nodule,wheal
in order)

23. Fluid filled skin lesions(vesicle, bulla,pustule in order)

24. Surface change( scale, crust, lichenification)

25. Depressed lesions(erosion, ulcer)

26. Flat skin lesions( macule, patch)

27. Bacterial infections of the skin
Impetigo
Folliculitis, Furuncle, Carbuncle
Cellulitis and Erysipelas
Leprosy(assignment)

28. Impetigo
•Impetigo is a contagious superficial infection of
the skin.
•It is caused by Streptococci or Staphylococci or by
both organisms.
•Infection is acquired either from external sources
by direct contact or through objects or from
internal infection, e.g.nasopharyngeal sources

29. Impetigo cont’d
Two clinical patterns:
•Non bullous impetigo
•Bullous impetigo and

30. Impetigo cont’d
Non bullous Impetigo:
•Accounts for about 7o% of impetigo
•Occurs in children of all ages and adults
•usually spreads from nose to normal skin
•lesions are thick, adherent and recurrent dirty
yellow crusts(honey colored) with an
erythematous margin.

31. Non bullous impetigo

32. Non bullous impetigo

33. Impetigo cont’d
Bullous Impetigo:
•Occurs more commonly in the newborn and in older infants
•characterised by superficially thin walled bullous lesions
that rupture and develop thin, transparent, varnish like
crust.
•Bullae usually arise on areas of grossly normal skin, initially
contain clear yellow fluid that subsequently becomes dark
yellow and turbid
•The bullaeare superficial, and within a day or two, they
rupture and collapse,at times forming thin, light-brown
golden-yellow crusts

37. Impetigo cont’d
Treatment
•good hygiene removal of crusts.
•Antibiotics
-topical if mild -mupirocin, fusidic acid,
-Systemic if severe, multiple lesions:
cloxacillin, erythromycin, cephalexin

38. Folliculitis
•a pyoderma that begins within the hair follicle
•a small, fragile, dome-shaped pustule occurs at the
opening of a hair follicle
•Children –scalp
•Adults -beard area, axillae, extremities, and buttocks
•Can complicate to Furuncles if untreated

40. folliculitis
Treatment:
•For Localized: Topical antibiotics like Mupirocin,
2% ointment, or Fusidic acid cream applied twice
daily to the affected area for 7-10 days.
•For generalized :Cloxacilline,cephalexine,
Erythromycyin

41. Furuncle
•Furuncle is a deep seated infectious folliculitis
and perifolliculitis with a purulent core
•caused by Staphylococcus aureus, It affects
mainly young men who are healthy
•patients must be evaluated for predisposing
factors: alcoholism,medicine abuse, diabetes
mellitus, leukemias and other malignancies, AIDS
and chronic liver disease.

42. Furuncle cont’d
•Fever, Pain, swelling and erythema of the
involved area.
•Occur mostly in areas subjected to
maceration or friction, poor personal hygiene,
acne or dermatitis; e.g.face, neck, axillae

44. Furuncle
Treatment
•a systemic antibiotic as impetigo for mild
cases
•severe infections or infections in a dangerous
areas -maximal antibiotic dosage by the
parenteral route
•drain if abscess

45. Carbuncle
more extensive, deeper, communicating,
lesion that develops when multiple, closely
set furuncles coalesce.
more serious inflammation
red and indurated, and multiple pustules soon
appear on the surface, draining externally
around multiple hair follicles scar
fever and malaise -ill

46. carbuncle

47. Carbuncle
Treatment:
•Incision and drainage usually necessary
•Systemic antibiotic usage as furuncle

48. Erysipelas
•caused by group A β-hemolytic streptococcus
•acute infection of skin-level of part of dermis
•superficial cellulitis with marked dermal lymphatic
vessel involvement
•face or a lower extremity
•superficial erythema, edema with a sharply defined
margin to normal tissue

49. Erysipelas
•there may be portal of entry
•Recurrent erysipelas –tineapedis,lymphedema
surgery
•Can cause lymphedema

52. Erysipelas
Treatment:
•Bed rest, limb elevation ,Immobilization and
warm compresses
•Antibiotics: procaine pencilline(IM),
Erythromycine,cephalexine, Cloxacilline
•Severe cases require intravenous therapy with
crystalline penicillin in hospital until the fever
subsides, at which time treatment is continued
with procaine penicillin

53. Cellulitis
infection extends deeper into the dermis and
subcutaneous tissue
S. aureus and GAS –common causes
looks erysipelas but lack of distinct margins, deeper
edema, surface bulla/necrosis
can go deep if untreated –fasciitis
portal of entry evident if half of cases

55. Cellulitis
Treatment:
•Supportive
-rest, immobilization, elevation, moist heat,
analgesia.
•Dressings
-cool sterile saline dressings for removal of
purulent exudates and necrotic tissue
•Surgical -Drain abscess

56. cellulitis
Antimicrobial Therapy:
•against staph in cellulitis + /-against strept
Cloxacillin
Cephalexin

58. Leprosy
Introduction:
•Leprosy is a chronic infectious disease mainly affecting
the skin and peripheral nerves, although other tissues,
such as the eye, mucosa of the upper respiratory tract,
joints and testis can also be involved.
•Leprosy is considered to be transmitted from person to
person through the nasal discharge from droplet
infection from untreated leprosy patient to individuals
living in the same household and/or infrequent
contact with the index case.

59. Leprosy
•The disease has a long incubation
period,averaging 3 to 5 years, occurring usually in
people in the age group between 15 and45 years.
•If not properly treated, leprosy can cause severe
disability, mainly as a result of peripheral nerve
damage.
•leading cause of permanent physical disability. It
is caused by Mycobaterium leprae

60. Leprosy
Clinical presentation:
Hx:
•Pale or reddish patches on the skin with loss of,
or decreased sensation on the skin
•Painless swelling or lumps on the face and
earlobes
•Numbness or tingling of the hands and/or the
feet
•Weakness of eyelids, hands or feet
•Difficulty closing the eyes

61. Leprosy
•Burning sensation in the skin
•Dry palms
•Skin cracks on palms and soles with sensation
loss
•Painless wounds or burns on the hands or
feet
•Decreased vision
•History of close contact with a leprosy patient

62. Leprosy
PE:
•Hypo-pigmented or erythematous skin lesions
•Loss of, or decreased sensation on the skin
patches when touched with a wisp of cotton
•Enlarged/ thickned peripheral nerves
•Painful and/or tender nerves on palpation

63. Leprosy
•Loss of muscle strength or paralysis of
muscles of the eyes, hands and feet
•Sensory loss on the soles of he feet and/or
palm of the hands when examined with ball
point pain
•Cracks on palms and soles with sensation loss
•Wounds, ulcer on palms and soles with
sensation loss

64. Leprosy cont’d

65. Leprosy cont’d

66. Leprosy cont’d
Diagnosis:
•Skin slit smear microscopy
•Leprosy cases can be diagnosed on clinical
grounds. Laboratory investigation is indicated
for confirmation in doubtful cases

67. Leprosy cont’d
•Diagnosis of leprosy is confirmed when one of
the cardinal signs of leprosy are present
The cardinal signs of leprosy are:
1. Definite loss of sensation in a pale (hypo-
pigmented) or reddish skin lesion.
2. Thickened or enlarged peripheral nerve/s with or
without tenderness
3. Presence of the acid-fast bacilli Mycobacterium
leprae in slit skin smears from skin lesions.

68. Leprosy cont’d
Treatment:
•Objectives
-Cure leprosy by rapidly eliminating the bacilli
-Prevent the emergence of medicine resistance
-Prevent relapse
-Prevent disability

69. Leprosy cont’d
•Leprosy is managed with multi drug
therapy(MDT)
•With a combination of Rifampicine,
Clofazamine and Dapsone

70. Superficial Fungal Infections
Dermatophytosis
Candidiasis
Onychomycosis

71. Superficial fungal infections
Introduction:
•Cutaneous fungal infections are broadly divided into
those that are limited to the stratum corneum, hair and
nails, and those that involve the dermis and
subcutaneous tissues
•The superficial mycoses are due to fungi that only invade
fully keratinized tissues, i.e. stratum corneum, hair and
nails.
•Superficial fungal infections of the skin are due primarily
to dermatophytes and Candida species.

72. Superficial cont’d
superficial fungal infections (Dermatophytoses) usually affect
all parts of the skin from head to toes. These include:
•Infection of the scalp -tinea capitis
•Infection of the skin of the trunk and extremities-tinea
corporis
•Infection of the axillae or groin-tinea cruris
•Infection of the nails-tinea unguium (onychomycosis)
•Infection of the palms and soles-tinea palmo-plantaris
•Infection of the cleft of the fingers and toes-tinea
interdigitalis
•Infection of hands-Tinea Mannum

73. Superficial cont’d

74. Tinea Capitis
•Tinea capitis describes dermatophyte infection
of hair and scalp
•Tinea capitis is most commonly observed in
children between 3 and 14 years of age.
•The fungistatic effect of fatty acids in sebum
may help to explain the sharp decrease in
incidence after puberty.

75. Tinea capitis
Clinical findings:
•The clinical appearance of tinea capitis depends on
the causative species as well as other factors such as
the host immune response
•In general, dermatophyte infection of the scalp
results in hair loss, scaling and varying degrees of an
inflammatory response.

76. Tinea capitis
Types:
•Seborrheic like scaling.
•Inflammatory kerion.
•Favus.

77. Tinea Capitis…scaling

78. Tinea capitis… Kerion

79. Tinea capitis…Favus

80. Tinea capitis
Diagnosis:
•From a highly inflammatory plaque two or three
loose hairs are carefully removed with epilating
forceps
•Hairs are placed on a slide covered with a drop of
10% to 20% KOH solution.
•Culture with Sabouraud dextrose agar with
chloramphenicol
•Diagnosis is made by the gross appearance of the
culture growth, together with the microscopic
appearance

81. Tinea capitis
Treatment:
•Griseofulvin tablets; griseofulvin V oral suspension is
less readily absorbed
•Fluconazole, 6mg/kg/day for 2-3 weeks
•Terbinafine
•Itraconazole, 5mg/kg/day for 2-3 weeks
•Without medication there is spontaneous clearing at
about the age of 15

82. Tinea Corporis
•Refers to all superficial dermatophyt infections
of the skin other than those involving the
scalp, beard, face, hands, feet and groin
•The classic presentation is that of an annular
“ring-worm” like with scale across the entire
active erythematous border.

83. Tinea corporis

84. Tinea corporis

85. Tinea Corporis
Diagnosis:
•Skin scraping and then Potassium hydroxide
(KOH) mount or Culture

86. Tinea Corporis
Treatment:
•Topical therapy
Clotrimazole,Miconazole,ketoconazole, ,Terbinafine
between 2-4 wks, usually B.I.D.
•Systemic antifungal treatment
for extensive disease or fungal folliculitis
Griseofulvin, Adult 500-1000 mg/day for 4-6 weeks
Children 10-20 mg/kg/day
Terbinafine, 250mg/day; 1-2 weeks
Itraconazole ; 200mg/day for one week
Fluconazole; 150 mg once a week for 4 weeks

87. Tinea Cruris
•Tinea cruris is a dermatophytosis of the groin,
genitalia,pubic area, and perineal and perianal
skin.
•The designation is a misnomer, because in
Latin “cruris”means of the leg

88. Tinea Cruris
•Tinea cruris presents classically as
a well mariginated annular plaque
with scaly raised border
which extends from inguinal fold on the inner
thigh often , bilaterally.

89. Tinea Cruris

90. Tinea Cruris

91. Tinea barbae
•Tinea barbae, as its name would imply, occurs
predominantly in males
•Tinea barbae affects the face unilaterally and
involves the beard area more often than the
moustache or upper lip
•Two types: superficial and inflammatory types

92. Tinea barbae

93. Tinea faciei
•Typical annular rings are usually lacking
•For fungal folliculitis→oral medication
•If no folliculitis→topical therapy

94. Tinea faciei

95. Tinea Pedis and Tinea mannum
•Tinea pedis denotes dermatophytosis of the
feet,whereas tinea manuum involves the
palmar and interdigital areas of the hands
•Infection of the dorsal aspects of feet and
hands is considered to be tinea corporis.
•Tinea pedis is also called “Athlets’ foot

96. Tinea pedis

97. Tinea pedis

98. Tinea palmaris

99. Tinea Pedis
Treatment:
•Clotrimazole,miconazole,ketoconazole,
terbinafine
•Toes separated by foam or cotton inserts, when
maceration between toes
•Fungal infections of the hands and feet with
systemic griseofulvin, terbinafine, itraconazole
and fluconazole with a similar regimen to tinea
corporis

100. Tinea Pedis
Some advises to prevent Tinea pedis:
•hyperhidrosisis a predisposition factor for
tinea infections, toes should be thorougly
dried after bathing.
•Antiseptic powders after bathing, e.g.. plain
talc, corn starch, rice powder dusted into
socks and shoes to keep the feet dry.

101. Onychomycosis
•Onychomycosis describes fungal infection of the nail
caused by dermatophytes,non dermatophyte
molds,or yeasts.
•Tinea unguiumrefers strictly to dermatophyte
infection of the nail

102. Types of Onychmycosis
•Distal subungal onychomycosis
•White superficial onychomycosis:
An invasion of the toenail plate in the surface of
the nail.
•Proximal subungal onychomycosis: may be an
indicaton of HIV
•Candida onychomycosis: It produces
destruction of the nail and massive nail bed
hyperkeratosis and is seen in patients with
chronic mucocutaneous candidiasis

103. Distal subungal onychomycosis

104. Proximal subungal Onychomycosis

105. White superficial Onychomycosis

106. Onychomycosis
Diagnosis:
•Microscopic examination
•Culture
•Histopathologic examination with a periodic
acid –Schiff stain(PAS)

107. Onychomycosis
Treatment:
•Griseofulvin
•Terbinafine, for finger nails 250mg/day for 6-8
weeks, for toe nails 12-16 week
•Itraconazole, pulse therapy of 200 mg twice a
day for 1 week of each month, for 2-3 months
when treating finger nails, and for 3-4 months
when treating toe nails
•Fluconazole, 150-300mg/once a week for 6-12
months

108. Candidiasis
•Candidiasis refers to a diverse group of acute and chronic
integumentary or disseminated yeast infections, most
commonly caused by Candida albicans.
•Candida species are the most common cause of fungal
infection in immunocompromised persons.
•Potassium hydroxide preparation of skin scrapings
demonstrates the characteristic fungal elements that
identify Candida

109. Oral Candidiasis(Oral thrush)
•In the newborn may be acquired from contact
with the vaginal tract of the mother
•In older children and adults , following antibiotic
therapy it may also be a sign of
immunosuppression
•Grayish-white membranous plaques with
moist,reddish,and macerated base
•Saliva inhibits the growth of Candida, and a dry
mouth predisposes to candidial growth.

110. Oral candidiasis

111. Oral Candidiasis
Treatment:
•Infants : oral nystatin suspension
•Adults: A single dose of 150 mg. fluconazole
•Itraconazole,200mg./day for 5-10 days
•Terbinafine,250 mg./day

112. Vulvo vaginal candidiasis
•C.albicans is a common inhabitant of vaginal
tract.
•Overgrowth can cause severe pruritis,burning
and discharge.
•Discharge varies from watery to thick and white
or curd like.
•Predisposing factors:
pregnancy, diabetes, secondary to
therapy with broad-spectrum antibiotics

113. Vulvo vaginal Candidiasis
•Oral fluconazole, 150 mg given once.
•In some patients with predisposing factor
longer courses of 150-200 mg/day or
itraconazole, 200 mg/day for 5-10 days.
•Topical options:
miconazole,nystatin,clotrimazole

114. Candida intertrigo
•Between the folds of the genitals; in groins
or armpits; between the buttocks; under large
pendulous breasts; under overhanging
abdominal folds; or in the umbilicus
•Often ,tiny, superficial, white pustules closely
adjacent to the patches

115. Candidia intertrigo

116. Candida intertrigo

117. Tinea Versicolor
•Tinea versicolor (ie, pityriasis versicolor) is a
common superficial fungal infection
•Patients with this disorder often present with
hypopigmented, hyperpigmented, or
erythematous macules on the trunk and
proximal upper extremities
•unlike other disorders utilizing the term tinea
(eg, tinea pedis, tinea capitis), tinea versicolor
is not a dermatophyte infection

118. Tinea versicolor cont’d
•The causative organisms are saprophytic, lipid-
dependent yeasts in the genus Malassezia
•Tinea versicolor most commonly affects
adolescents and young adults, but can also
occur in children
•Tinea versicolor occurs worldwide, but the
highest incidence is found in tropical climates
•The disorder is not contagious

119. T.versicolor

120. T.versicolor

121. T.vesicolor

122. T. vesicolor
Diagnosis:
•The variable clinical features of tinea
versicolor and the existence of other skin
disorders with similar findings make it
preferable to confirm the diagnosis with a
potassium hydroxide (KOH) preparation
•Both hyphae and yeast cells are evident in a
pattern that is often described as "spaghetti
and meatballs"

123. T.versicolor

124. Tinea versiclolor cont’d
Treatment:
•Topical anti fungals:Selenium
sulfide,ketoconazole cream,
•Systemic therapy:
are used when either the topical tx fails or there
is extensive involvement.
fluconazole
Itraconazole

125. Cutaneous Viral Infections
Warts
Molluscum Contagiosum
Herpes simplex infection and Herpes zoster
Genital herpes

126. Warts
•Warts occure as a result of Human Papilloma
virus infection(HPV)
•Warts are often classified by their anatomic
location or morphology
•Can be classified into common warts,flat warts
and plantar&palmar warts

127. Common warts( Verruca vulgaris)
•Verruca Vulgaris is a benign epidermal
overgrowths caused by human papilloma virus
(HPV).
•It is transmitted by contact, often at small skin
breaks, abrasions, or other trauma
•In children, approximately two-thirds of warts
spontaneously regress within 2 years.
•Warts in immunocompromised persons can be
widespread and chronic.
•Common sites are the hands, periungual skin,
elbows, knees and planter surfaces.

128. Common warts(VV)
Clinical Presentation:
•Flesh-colored papules that evolve into dome-
shaped, gray-brown surface black dots and are
usually few

129. Common warts

130. Common warts
Treatment:
•Saliclyic acid
•Cryotherapy
•Curettage & surgical excision

131. warts
Flat warts:
•are 1–4 mm, slightly elevated, flat top Papules
that have minimal scale
•These are most frequent on the face, hands,
and lower legs
Plantar and palmar warts:
•are thick, endophytic, and hyperkeratotic
papules, which may be painful with pressure

132. Plantar warts

133. Flat warts

134. Molluscum Contagiosum
•Molluscum Contagiosum is a common childhood
disease caused by Pox virus.
•Its second peak in incidence occurs in young
adults because of sexual transmission.
•The typical lesion is a pearly, skin colored papule
with central umblication.
•Diagnosis is clinical

135. MC

136. MC

137. Molluscum Contagiosum
Treatment:
•KOH 5-10% solution
•Iodine
•Retinoic acid
•Curettage&
•cryotherapy

138. Herpes simplex and Herpes zoster
•Herpes simplex viruses (HSV-1, HSV-2; ) produce
a variety of infections involving mucocutaneous
surfaces, the central nervous system (CNS), and—
on occasion—visceral organs
•Transmission can result from contact with
persons who have active ulcerative lesions or
with persons who have no clinical manifestations
of infection but who are shedding HSV from
mucocutaneous surfaces

139. HSV infection

140. HSV infection
Clinical features:
•Herpes simplex skin lesion is characterised by
painful grouped micro vesicles which soon
rupture to form yellow crust
•The site of predilection is the adjacent areas of
mucous membranes and skin.
•It has a tendency to recur

141. HSV infection

142. Oro-facial infections
•Gingivostomatitis and pharyngitis are the most
common clinical manifestations of first-episode HSV-
1 infection
•Clinical symptoms and signs, which include fever,
malaise, myalgias, inability to eat, irritability, and
cervical adenopathy, may last 3–14 days
•Lesions may involve the hard and soft palate, gingiva,
tongue, lip, and facial area

143. HSV infection

145. HSV( oro-facial)
Treatment:
•Acyclovir, 200mg P.O., 5 times daily OR 400mg P.O.,
three time daily for 7 days.
•Children <2 years; half adult dose.
•Children >2 years; adult dose.
plus
Paracetamol for pain
•Secondary bacterial infection can be treated by
systemic antibiotics

146. Genital Herpes
•Majority of infections are asymptomatic
•Caused by both HSV-1&HSV-2,but HSV-2 in the
majority of the cases.
•Symptoms include painful vesicles in the vagina and
penis.
•Systemic symptoms include fever, malaise and myalgia.
•Latency occures in sacral nerve ganglia

147. Genital Herpes

148. Genital Herpes

149. Genital Herpes
Treatment:
•Acyclovir, 200 mg P.O 5 times daily for 10
days OR 400 mg P.O. TID for 10 days

150. Varicella Zoster
•Varicella-zoster virus (VZV) infection causes two
clinically distinct forms of disease.
•Primary infection with VZV results in varicella
(chickenpox), characterized by vesicular lesions in
different stages of development on the face, trunk,
and extremities

151. Varicellal Zoster
•Herpes zoster, also known as shingles, results
from reactivation of endogenous latent VZV
infection within the sensory ganglia
•This clinical form of the disease is
characterized by a painful, unilateral vesicular
eruption, which usually occurs in a restricted
dermatomal distribution.

152. VZV

153. VZV

154. VZV

155. Describe the lesion and and tell the Dx

156. VZV
Complications:
Chicken Pox
•are more often seen in patients who acquire the infection as
adults, and particularly in pregnant women.
•Complications may include pneumonia,encephalitis, hepatitis
or haemorrhagic syndromes.

157. VZV
Complications
Chicken pox
•Varicella in pregnancy carries a high risk of
complications.
•If acquired before 28 weeks’ gestation, it will
cause congenital abnormalities in the child (also
called congenital varicella syndrome).
•If acquired around the time of birth, it can cause
neonatal varicella, which carries a high rate of
pneumonia and other complications.

158. VSV
Treatment:
Chicken Pox:
In adults including pregnant women:
•Oral acyclovir, 800mg 5 times daily for 7 days.
•In immunocompromised adults or those with
disseminated disease:
IV aciclovir 10mg/kg 3 times daily for 7 days;
OR high-dose oral aciclovir, if no IV available.

159. VZV
Complications:
Herpes Zoster
•Herpes Zoster Ophthalmicus:Blindness due to
corneal involvement.
•Post-herpetic neuralgia: chronic pain in the
area where the lesions occurred that can last
for months to years after the acute episode.

160. VZV
Treatment:
•Aciclovir 800mg 5 times daily for 7 days can be considered for all
adults, and is recommended for all HIV-positive adults.
•Start aciclovir within 72 hours from the onset of symptoms.
Paracetamol for fever
Antihistamines or calamine lotion may be used to reduce itching
Amitriptyline 25–50mg before bed for neuropathic pain and post-
herpetic neuralgia.
•Secondary bacterial infections may require antibiotics.
N.B. For ophthalmic involvement, topical acyclovir, 3% eye ointment
applied into the eye every 4 hours should be given.

161. Topics to be covered
Acne vulgaries
Eczemas
Psoriasis
Scabies
Common skin manifestation of HIV /AIDS

162. Acne vulgaries
•Acne vulgaris is a self-limited disorder primarily
of teenagers and young adults, although perhaps
10–20% of adults may continue to experience
some form of the disorder.
•The permissive factor for the expression of the
disease in adolescence is the increase in sebum
production by sebaceous glands after puberty.

163. Cont’d
•Small cysts, called comedones, form in hair
follicles due to blockage of the follicular orifice by
retention of keratinous material and sebum.
•The activity of bacteria (Propionibacterium
acnes) within the comedones releases free fatty
acids from sebum, causes inflammation within
the cyst, and results in rupture of the cyst wall.
•An inflammatory foreign-body reaction develops
as result of extrusion of oily and keratinous debris
from the cyst.

165. Cont’d
•The clinical hallmark of acne vulgaris is the comedone,
which may be closed (whitehead) or open (blackhead).
•Closed comedones
appear as 1-to 2-mm pebbly white papules,
accentuated when the skin is stretched.
They are the precursors of inflammatory lesions of acne
vulgaris.
The contents of closed comedones are not easily
expressed.

166. Cont’d
Open comedones
have a large dilated follicular orifice
are filled with easily expressible oxidized,
darkened, oily debris.

167. Cont’d
•Comedones are usually accompanied by
inflammatory lesions: papules, pustules, or
nodules.

168. Classification
Mild Comedonal
Moderate papulo-pustular
Severe Nodular

174. Con’td

175. Cont’d
•The earliest lesions seen in adolescence are
generally mildly inflamed or noninflammatory
comedones on the forehead.
•Subsequently, more typical inflammatory lesions
develop on the cheeks, nose, and chin
•The most common location for acne is the face,
but involvement of the chest and back is
common.
•Most disease remains mild and does not lead to
scarring.

176. Cont’d
•A small number of patients develop large
inflammatory cysts and nodules, which may drain
and result in significant scarring.
•Regardless of the severity, acne may affect a
patient's quality of life.
•If adequately treated, this may be a transient
effect.
•In the case of severe, scarring acne, the effects
can be permanent and profound.
•Early therapeutic intervention in severe acne is
essential.

177. Cont’d
•Exogenous and endogenous factors can alter
the expression of acne vulgaris.
•Friction and trauma (from headbands or chin
straps of athletic helmets), application of
comedogenic topical agents (cosmetics or hair
preparations), or chronic topical exposure to
certain industrial compounds may elicit or
aggravate acne.

178. Cont’d
•Glucocorticoids, topical or systemic, may also
elicit acne.
•Other systemic medications such as oral
contraceptive pills, lithium, isoniazid, androgenic
steroids, halogens, phenytoin, and phenobarbital
may produce acneiform eruptions or aggravate
preexisting acne.
•Genetic factors and polycystic ovary disease may
also play a role.

179. Treatment
Objectives
•Improve cosmetic appearance
•Prevent complications particularly scarring.

180. Non pharmacologic
•Cleansing the face with oil-free cleansers twice
daily
•Avoiding oil containing moisturizers and vaseline.
•Use oil free moisturizers and alcohol containing
toners instead.
•Avoiding squeezing

181. pharmacologic
1. Mild Acne:
First line
•Retinoic acid (Tretinoin) –start with 0.025% cream or
0.01% gel and gradually
•increase the concentration to 0.05% cream or 0.025%
gel, then to 0.1% cream, then to 0.05% lotion.
•Start with every other day regimen and make twice
daily based on tolerance of the skin for irritating effect
of retinoids.
•Improvement is seen after 2–5 months.

182. Pharmacologic Tx cont’d
Alternatives
•Clindamycin, 1% gel or lotion;
•Erythromycin 2-4% gel, lotion or cream,
•Azelaic Acid 20% applied twice daily.

183. Cont’d
Moderate Acne
First line
•The above topical medications plus
•Doxycycline, 100mg P.O., QD for
a minimum of 6 months depending on clinical response
OR
•Tetracycline, 250-500mg two to four times daily for a
minimum of six months.
OR
•Azithromycin, 250-500mg three times weekly 12 weeks

184. Cont’d
Severe Acne
First line
•Isotretinoin,0.5-2mg per kilogram of body weight in
two divided doses with food for 15 to 20 weeks.
N.B. Contraception should be secured in females for
treatment time and for 4 months after treatment and
serum lipid monitoring in all patients is mandatory.
•Dosage form: Capsule, 10mg, 20mg

185. Cont’d
Alternatives
•Dapsone, 50-100 mg P.O, daily
OR
•Spironolactone, 50–100 mg daily for up to six months
OR
•Combined oral contraceptive pill for women for up to six
months.
OR
•Intralesional Triamcinolone acetonide 40mg per ml diluted
with equal amount of Normal saline or local anesthesia
repeated every four weeks is effective for few nodules or
hypertrophied acne scars.

186. Eczema
Atopic dermatitis
Contact dermatitis
Irritant contact dermatitis
Allergic contact dermatitis
Lichen simplex chronicus
Seborrheic dermatitis

187. •Eczema is a type of dermatitis and these terms
are often used synonymously (atopic eczema or
atopic dermatitis).
•Eczema is a reaction pattern that presents with
variable clinical findings and the common
histologic finding of spongiosis (intercellular
edema of the epidermis).
•lesions may include erythematous macules,
papules, and vesicles, which can coalesce to form
patches and plaques.
Eczema

188. Cont’d
•In severe eczema, secondary lesions from
infection or excoriation, marked by weeping
and crusting, may predominate.
•In chronic eczematous conditions,
lichenification (cutaneous hypertrophy and
accentuation of normal skin markings) may
alter the characteristic appearance of eczema.

189. Atopic Dermatitis
•Atopic dermatitis (AD) is the cutaneous
expression of the atopic state, characterized
by a family history of asthma, allergic rhinitis,
or eczema.

190. AD….
•The etiology of AD is only partially defined, but
there is a clear genetic predisposition.
•When both parents are affected by AD, >80% of
their children manifest the disease.
•When only one parent is affected, the prevalence
drops to slightly over 50%.
•Patients with AD may display a variety of
immunoregulatory abnormalities including
increased IgE synthesis; increased serum IgE; and
impaired, delayed-type hypersensitivity reactions.

191. AD……
•The clinical presentation often varies with age.
•Half of patients with AD present within the first
year of life, and 80% present by 5 years of age.
•80% ultimately co express allergic rhinitis or
asthma.
•The infantile patternis characterized by weeping
inflammatory patches and crusted plaques on the
face, neck, and extensor surfaces.
•The childhood and adolescent patternis marked
by dermatitis of flexural skin, particularly in the
antecubital and popliteal fossae

192. AD…….
•AD may resolve spontaneously, but
approximately 40% of all individuals affected
as children will have dermatitis in adult life.
•The distribution of lesions may be similar to
those seen in childhood; however, adults
frequently have localized disease, manifesting
as lichen simplex chronicus or hand eczema

193. AD…..
•In patients with localized disease, AD may be suspected
because of a typical personal history, family history, or the
presence of cutaneous stigmata of AD such as perioral pallor,
an extra fold of skin beneath the lower eyelid , increased
palmar skin markings, and an increased incidence of
cutaneous infections, particularly with Staphylococcus aureus.
•Regardless of other manifestations, pruritus is a prominent
characteristic of AD in all age groups and is exacerbated by dry
skin.
•Many of the cutaneous findings in affected patients, such as
lichenification, are secondary to rubbing and scratching

200. Clinical features of AD
1. Pruritus and scratching
2. Course marked by exacerbations and remissions
3. Lesions typical of eczematous dermatitis
4. Personal or family history of atopy (asthma, allergic rhinitis, food
allergies, or eczema)
5. Clinical course lasting longer than 6 weeks
6. Lichenification of skin

201. Tx of AD
Tx objectives
•Alleviate the pruritus, and prevent scratching.
•Decrease triggering factors
•Suppress inflammation
•Lubricate the skin
•Manage complications

202. Non pharmacologic
•Atopic patients should bathe with cold or luke
warm water once daily using mild soaps.
•Patient should dry quickly and immediately
(with in 3 minutes) and lubricate the skin.
Emollients:
•Vaseline cream OR Liquid paraffin applied
liberally all over the body

203. Pharmacologic mgt
First line
•Topical corticosteroids are the standard of care
compared with other treatments:
•Eczematous lesions should be treated by mid-high
strength topical steroids for up to 2 weeks except on
the face, neck, breast, axillary, groin and perianal areas.
•For the face, neck, axillae and other soft areas of the
body low-to-mild strength medications are preferred.
•Patients should apply the ointment after bathing.
•The use of long-term intermittent application of
corticosteroids appears helpful and safe.

204. PLUS
•Cloxacillin if a superimposed bacterial
infection is suspected.
•Antihistamins
•Diphenhydramine, 25-50mg P.O., QD
Pharmacologic mgt con’d

205. Contact Dermatitis
•Contact dermatitis is an inflammatory process in skin caused by an
exogenous agent or agents that directly or indirectly injure the skin.
•This injury may be caused by an inherent characteristic of a
compound—irritant contact dermatitis (ICD). An example of ICD
would be dermatitis induced by a concentrated acid or base.
•Agents that cause ACD induce an antigen-specific immune
response (poison ivy dermatitis).
•The clinical lesions of contact dermatitis may be acute (wet and
edematous) or chronic (dry, thickened, and scaly), depending on the
persistence of the insult

206. Allergic contact dermatitis(ACD)
•Allergic Contact Dermatitis is an inflammatory response of
the skin to an antigen that can cause discomfort or
embarrassment.
•Allergic contact Dermatitis can be classified as acute,
subacute and chronic
Clinical features
•Acute contact dermatitis manifests by fluid filled vesicles or
bullae on an edematous skin
•Subacute contact dermatits is characterised by less edema
and formation of papules, excorations and scaling
•Chronic eczema is characterised by scaling, skin fissuring
and lichenfication

207. ACD cont’d

208. ACD cont’d

210. Allergic contact dermatitis, acute phase, with
sharply demarcated, weeping, eczematous
plaques in a perioral distribution

211. Irritant Contact Dermatitis (ICD)
•ICD is inflammation of the skin which manifests with
edema and scaling and is non specific response to the
skin by irritants and direct chemical damage (e.g.
corrosive agents which cause chemical burn).
•The hands are the most important sites of ICD.
Clinical features
•Macular erythema, hyperkeratosis or fissuring
•Glazed, parched or scalded appearance of the
epidermis
•Healing process on withdrawal

212. Tx of Contact Dermatitis
Objectives
•Improve the quality of life by reducing symptoms.
Non pharmacologic
•Removal of the offending agent
•Lukewarm water baths (antipruritic)
Emollients:
•Vaseline cream OR Liquid paraffin applied liberally to
affected area
For acute lesions
•Topical soaks with cool tap water plus saline (TSP/Pint)

213. ICD cont’d

214. TX Cont’d
Topical steroids:
First line
Triamcinolone acetonide,thin films applied BID initially,
reduce to once daily as lesions remit.
Alternative
Hydrocortisone, thin films applied on face, axillae,
breasts, groins and perianal area
•twice daily initially, reduce as the lesions remits.
•Dosage forms: Cream, ointment, 1%
•OR
•Mometasone, thin films applied QD

215. Pharmacologic mgt con’d
Systemic steroids(for severe, recalcitrant and
generalized cases)
•Prednisone, 0.5mg/kg P.O. QD for 1-2 weeks.
Antihistamines: (adjuncts)
First line
•Diphenylhydramine, 25-50mg cap P.O., QD
Alternative
•Chlorpheniramine, 4-6mg P.O., QD

216. Lichen simplex chronicus
•Lichen simplex chronicus may represent the end
stage of a variety of pruritic and eczematous
disorders, including atopic dermatitis.
•It consists of a circumscribed plaque or plaques
of lichenified skin due to chronic scratching or
rubbing.
•Common areas involved include the posterior
nuchal region, dorsum of the feet, and ankles.

217. Tx of LSC
•Treatment of lichen simplex chronicus centers
on breaking the cycle of chronic itching and
scratching.
•High-potency topical glucocorticoids are
helpful in most cases, but in recalcitrant cases,
application of topical glucocorticoids under
occlusion, or intralesional injection of
glucocorticoids may be required

219. Seborrheic dermatitis
•Seborrheic dermatitis is a common, chronic
disorder, characterized by greasy scales overlying
erythematous patches or plaques.
•Induration and scale are generally less prominent
than in psoriasis, but clinical overlap exists
between these diseases—"sebopsoriasis.“
•The most common location is in the scalp, where
it may be recognized as severe dandruff.
•On the face, seborrheic dermatitis affects the
eyebrows, eyelids, glabella, and nasolabial folds .

220. SD Con’d
•Scaling of the external auditory canal is
common in seborrheic dermatitis.
•In addition, the postauricular areas often
become macerated and tender.
•Seborrheic dermatitis may also develop in the
central chest, axilla, groin, submammary folds,
and gluteal cleft.
•Rarely, it may cause a widespread generalized
dermatitis. Pruritus is variable.

223. SD cont’d

224. SD cont’d

225. SD cont’d

226. SD cont’d

227. Tx of SD
•Treatment with low-potency topical glucocorticoids in
conjunction with a topical antifungal agent, such as
ketoconazole cream is often effective.
•The scalp and beard areas may benefit from
antidandruff shampoos, which should be left in place
3–5 min before rinsing.
•High-potency topical glucocorticoid solutions
(betamethasone or clobetasol) are effective for control
of severe scalp involvement.
•High-potency glucocorticoids should not be used on
the face because this is often associated with steroid-
induced rosacea or atrophy.

228. Psoriasis
•Psoriasis is one of the most common
dermatologic diseases, affecting up to 1% of
the world's population.
•It is a chronic inflammatory skin disorder
clinically characterized by erythematous,
sharply demarcated papules and rounded
plaques, covered by silvery scale.

229. Psoriasis cont’d
•The skin lesions of psoriasis are variably pruritic.
•Traumatized areas often develop lesions of
psoriasis (Koebner's or isomorphic phenomenon).
•In addition, other external factors may
exacerbate psoriasis including infections, stress,
and medications (lithium, beta blockers, and
antimalarials).

239. Plaque psoriasis
•It is the most common variety of psoriasis.
•Patients with plaque-type psoriasis will have stable, slowly enlarging
plaques, which remain basically unchanged for long periods of time.
•The most commonly involved areas are the elbows, knees, gluteal cleft,
and the scalp.
•Involvement tends to be symmetric.
•Plaque psoriasis generally develops slowly and runs an indolent course.
•It rarely remits spontaneously.

241. Gutate Psoriasis
•Guttate psoriasis(eruptive psoriasis) is most
common in children and young adults.
•It develops acutely in individuals without
psoriasis or in those with chronic plaque
psoriasis.
•Patients present with many small erythematous,
scaling papules, frequently after upper
respiratory tract infection with B-hemolytic
streptococci.
•The differential diagnosis should include pityriasis
rosea and secondary syphilis.

242. Pustular Psoriasis
•Patients may have disease localized to the palms
and soles, or the disease may be generalized.
•Regardless of the extent of disease, the skin is
erythematous with pustules and variable scale.
•Localized to the palms and soles, it is easily
confused with eczema.
•Episodes of fever and pustules are recurrent.

244. Pustular cont’d
•Local irritants, pregnancy, medications, infections, and
systemic glucocorticoid withdrawal can precipitate this
form of psoriasis.
•Oral retinoidsare the treatment of choice in
nonpregnant patients.
•Fingernail involvement, appearing as punctate pitting,
onycholysis, nail thickening, or subungual
hyperkeratosis may be a clue to the diagnosis of
psoriasis when the clinical presentation is not classic.

246. Tx of psoriasis
Non pharmacologic
•Explain regarding precipitating factors and
chronicity.
•Counselling the patient never to rub or scratch
lesions (to minimize Koebner’s phenomenon).
•Advise frequent exposure to sunlight

247. Cont’d
Pharmacologic
For Local plaques
General Measures
•Liberal use of moisturizers like urea, 10 –20%
or liquid paraffin between treatments
•Removal of excessive scale by soaking in
water or by using salicylic acid,5–10% in
vaseline base applied twice daily

248. Cont’d
Topical
•First line
•Betamethasone dipropionate, thin film
applied twice daily for short period of time
are effective.
•For lesions of the face, neck, flexural areas
and genitalia mild potency steroids are
preferred.
•Dosage forms: Cream, 0.025%, 0.05%

249. Scabies
•Scabies is a persistent and intensely itchy skin
eruption due to the mite Sarcoptes scabiei.
•The disease is commonly seen in people with low
socio-economic status and poor personal hygiene.
Clinical features
•Red papules and burrow in the axillae, groin and
digital web spaces associated with complaints of
nocturnal pruritus.
•In infants, the face, palms and soles are often
involved and blisters may develop.

254. Tx of scabies
objectives
•Eradicate the mite
•Prevent transmission to family members and close contacts
Non pharmacologic
•Washing clothes in hot water or ironing clothes after
normal washing.

255. Tx cont’d
•Treat all family members and close contacts,
even if they are unaffected or asymptomatic,
simultaneously Asymptomatic mite carriers
in the household are very common and are
the reason for recurrence

256. Pharmacologic
Topical:
First line
Permethrin 5%, Thin films of cream applied to all areas of body from the neck
•down for 8-14 hrs. then washed off. Repeat the same dose after a week
Alternative
•Benzyl benzoate, applied to the entire body, neck to toe for 3 to consecutive
evenings. Bath should be taken before the first and after the last application.
•Dosage form: Lotion, 25%

257. Cont’d
•Sulphur ointment, Children 5%, Adult 10%: thinly
applied to the entire body for 3consecutive nights.
•The patient should wash thoroughly before each new
application and 24 hours after the last treatment
•Dosage forms: Ointment, 5%, 10%.
Systemic:
•Ivermectin, 200µg/kg as a single dose, for Norwegian
(crusted scabies) and resistant forms of scabies and
ideal for institutional outbreaks

258. references
•Fitzpatrick’s Dermatology in general Medicine
•Standard Treatment Guideline for General
Hospital 2014
•USMLE materials

259. THANK YOU!!!