COMMON

DERMATOLOGICAL
PROBLEMS
PRESENTERS;
MRUMA E, ROBERT E, MWANGANIKANI E.

SUPERVISOR;
PROF. PALANGYO
 Outline
• Introduction
• Common dermatological conditions
• Skin infections
• Eczema⁄ Dermatitis
• Papulo-squamous eruptions
• Vesiculobullous eruptions
• Inherited skin disorders
• Pigmented lesions
• Malignancy
• references
Introduction
• Skin diseases have a high prevalence throughout the world. In
developing countries infectious diseases such as TB, leprosy
and onchocerciasis are common whereas in developed
countries inflammatory disorders such as acne and eczema are
common

• Skin disorders can be inherited, part of normal development

e.g. acne vulgaris or may present as part of systemic disorder

• Rarely skin diseases can be fatal i.e. malignant melanoma, toxic

epidermal necrolysis and pemphigus
• 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.
• Its important to identify if the lesion is
primary or secondary.
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:
• Macules are nonpalpable lesions ≤1 cm that vary in pigmentation
from the surrounding skin, Patches are nonpalpable lesions >1 cm.
• Papules are palpable, discrete lesions measuring ≤5 mm in diameter.
They may be isolated or grouped.
• Plaques are large (>5 mm) superficial slightly raised lesions, often
formed by a confluence of papules.
• Nodules are palpable, discrete lesions measuring ≥5 mm in diameter.
They may be isolated or grouped. Tumors are large nodules.
• Telangiectasia is a dilated superficial blood vessel.
• Purpura are red-purple lesions that do not blanch under pressure,
resulting from the extravasation of blood from cutaneous vessels into
the skin. Purpuric lesions can be macular or raised.

• Pustules are small, circumscribed skin papules containing purulent

material.
• Vesicles are small (<5 mm diameter), circumscribed skin papules
containing serous material. Bullae are large (≥5 mm) vesicles.
• Wheals are 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.
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
• Lichenification is increased skin markings and thickening with
induration secondary to chronic inflammation caused by scratching
or other irritation.
• Edema is swelling due to accumulation of water in tissue .
• Scale describes superficial epidermal cells that are dead and cast off
from the skin.
• Crust is dried exudate, a "scab".
• Fissure is a deep skin split extending into the dermis.
• Erosion is a superficial, focal loss of part of the epidermis
• Ulceration is focal loss of the epidermis extending into the dermis.
Lesions may heal with scarring
• Atrophy is decreased skin thickness due to skin thinning.
• Scar is abnormal fibrous tissue that replaces normal tissue after skin
injury.
• Hyperpigmentation is increased skin pigment; hypopigmentation is
decreased skin pigment; and depigmentation is total loss of skin
pigment.
 SKIN INFECTIONS

BACTERIAL INFECTIONS
 Infections of epidermis; Impetigo.
 Infections of the dermis; Erysipelas and cellulitis.
 Common hair follicle infections; Superficial folliculitis, furuncles(Boils) and
Carbuncles.

IMPETIGO
Clinical Presentation; acute purulent infection which appears vesicular;
progresses to golden yellow “honey-crusted” lesions surrounded by erythema.
Can present with bullae
Common sites: face, arms, legs, and buttocks
Etiology; GAS, S.aureus, or both
Epidemiology; preschool and young adults living in crowded conditions, poor
hygiene, neglected minor trauma
 Differential Diagnosis; infected eczema, HSV, VZV
Investigations; Gram stain and culture of lesion fluid or biopsy
Management;
 Remove crusts, use saline compresses, and topical antiseptic soaks
twice a day
 Oral antibiotics for 7-10 days: flucloxacillin 500mg 6 hrly or
erythromycin 250-500mg 6hrly, mupirocin cream 2% 12 hrly
 Isolation
Prevention:
Good personal hygiene particularly washing hands with soap
Cellulitis
Presents as tender erythema, edematous and warm area of the skin due to
infection in the deep subcutaneous layers of the skin.
Often affecting lower limbs causing an upward spreading. Occasionally with
blister especially if edema is persistent
It may also occur on the face affecting one side.
• Aetiology
GABHS, rarely staph, and sometimes community acquired MRSA.
In immunocompromised or diabetic patients gram negative organisms,
anaerobes should be suspected
• Diagnosis
Confirm infection serologically-ASOT.
Swabs are usually unhelpful
• Treatment
oral flucloxacillin or erythromycin 500mg 6 hrly 5-7 days.
If cellulitis is wide spread give iv antibiotics 5-7 days followed by oral therapy 2
weeks.
Treat any identifiable underlying cause
Erysipelas
• Erysipelas is a type of superficial cellulitis with dermal
lymphatic involvement
• It is characterized clinically by shiny, raised indurated and
tender plaque-like lesions with distinct margins
• Most common caused by group A beta hemolytic streptococci
most frequently on the legs and face.
• Erysipelas of the face must be differentiated form herpes zoster
and contact dermatitis
• Commonly accompanied by fever chills, and malaise
• It may be recurrent and may result in chronic lyphoedema.
• Erysipelas and cellulitis overlap so it is often impossible to
distinguish
Diagnosis
Characteristic appearance
Blood culture in toxic patients

Management
• Penicillin V or erythromycin 500mg oraly 6hourly for two weeks
or more
• Penicillin G 1.2 million units IV 6h which can be replaced by oral
therapy after 36 to 48h is indicated in severe cases
• In case of resistance to these antibiotics cloxacillin or
cephalexin can be used
• Cold packs and analgesics for relieving discomfort and pain
Folicullitis
• Folliculitis-inflammation of hair follicles presents as
itchy/tender, erythematous papules and pustules.
• Aetiology: staph aureus
• Extensive itchy folliculitis on the upper trunk and limbs- suspect
HIV
• Treatment
Topical antibiotic i.e mupirocin, oral antibiotics;
flucloxacillin/erythromycin 500mg 6 hrly 2-4 wks
prevention
Suspected irritants should be avoided e.g.. Shaving agaist
direction of hair growth, long term use of antibiotics for acne,
exposure to heated swiming pools
Boils(furuncles)

Etiology: staph aureus

Presentation: Red hot, tender, inflammatory nodules
with central yellowish point.
Large boils= carbuncles i.e. Deep seated abscess formed
by multiple coalescing furuncles.
Swabs should be taken to check sensitivity as MRSA is
increasingly common
• Treatment
Oral antibiotics erythromycin 500mg 6 hrly 10-14 days
Incision and drainage ocassionally
VIRAL SKIN INFECTIONS

• Herpes simplex
• Herpes zoster
• Human papilloma virus
Herpes simplex
• Two genomic subtypes exist; HSV type 1 and HSV type2. the
hall mark of all herpes infection is the ability of the virus to
establish latent infection that persist for life in an individual.
• HSV 1 major cause of herpetic stomatitis ~ 70% of the
population is infected whereas HSV 2 is responsible for genital
and systemic infections. This division is however not rigid.
Clinical presentation:
• Primary infection may be subclinical or produce severe
inflammatory reaction with cluster of vesicles formation on the
face or gingival stomatitis, genital skin surface which coalesce
and form painful shallow ulcers
• Systemic symptoms vary, may include fever, myalgia, inguinal
lymphadenopathy and headache
• Clinical manifestations in immunosuppressed patients may be
more severe.
Reactivation of the virus is facilitated by several stress stimuli
such as
• Febrile illness
• Uv radiation
• Surgical trauma to the neurones
Diagnosis
• High suspicious index of the disease from history and physical
examination and a firm dx is made by detection of the virus
from within the skin lesions through HSV DNA PCR
Treatment
• Primary infection: Drug of choice is acyclovir 400mg 8 hrly for
7-10 days. Is useful when the vesicles are still forming. If the
lesions are crusting antiviral therapy will do a little to change
the clinical course
Treatment

• Recurrence: Acyclovir 400mg 8 hourly for 7-10 days plus long

term suppressive therapy 200mg 8 hourly for 1 month
• For immunosuppressed patients 1st lesions 400mg 6hrly for 7-
10 days. Similar for recurrences
Other managements
Treatment of sec bacterial infection appropriately
• Prevention
-Health education
-Avoidance of sexual intercourse during the prodromal
phase
-Notify and examine sexual partners
 HERPES ZOSTER (SHINGLES)
Clinical Presentation
• unilateral dermatomal eruption occurring 3-5 days after pain and
paraesthesia of that dermatome
• vesicles, bullae, and pustules on an erythematous, oedematous base
• lesions may become eroded/ulcerated and last days to weeks
• pain can be pre-herpetic, synchronous with rash, or post-herpetic
• severe post-herpetic neuralgia(burning pain due to nerve involvement)
often occurs in elderly
• Hutchinson’s sign: shingles on the tip of the nose which signifies ocular
involvement. Shingles in this area involves the nasociliary branch of the
ophthalmic branch of the trigeminal nerve (V1)
Distribution: thoracic (50%), trigeminal (10-20%), cervical (10-20%);
disseminated in HIV
Aetiology
• caused by reactivation of VZV
• risk factors: immunosuppression, old age, occasionally associated with
hematologic malignancy
 Differential Diagnosis
• before thoracic skin lesions occur, must consider other
causes of chest pain
• contact dermatitis, localized bacterial infection, HSV
infection.
Investigations
• Tzanck test, direct fluorescence antibody test, or viral culture
to rule out HSV
Management
• compress with normal saline,or povidone solution
• analgesics (NSAIDs, amitriptyline)
• acyclovir PO 800mg 5x a day for 7-10 days
• Gabapentin 300-900 mg PO once or in two divided for post-
herpetic neuralgia
• Mupirocin cream or gentamycin1% ointment for secondary
bacterial infection
Human papilloma virus

Anogenital warts are among the most common sexually

acquired infections. Causative agent is HPV 6 & 11. acquires
through direct sexual contact

Clinical presentation
• Warts which develop around the external genitalia and
perianal area, vagina and cervix may also be involved in
women.
• In males penile shaft and sub preputial space are commonly
affected.
Diagnosis
• Is essentially clinical. Its crucial to differentiate it from
condylomata-lata of secondary syphilis. Unusual lesions should
be biopsied if the dx is in doubt.
Treatment
Medical therapy
• Podophyllum resins 25% soln or Podophyllotoxin 0.5% soln are
cytodestructive therapies that can be applied topically to kill
the wart cells
• Trichloroacetic acid-destroys cell via chemical coagulation of
tissue proteins
surgical therapy( ablation and excisional procedures)
• Cryoablation (with liquid nitrogen destroys warts tissue via cell
lysis)
• Laser ablation ( lasers produces light that leads to thermal
damage and resultant ablation)
Prevention
• Vaccination- two vaccines exist against hpv one is effective
against hpv typ 16 & 18. the second against type 6,11,16 &
18.
• Regular cervical screening for women with male partners
with warts
• Practice of protected sex. use of condoms up to 8 months
after treatment
FUNGAL SKIN INFECTIONS

• Dermatophytes – Tinea corporis,T.capitis, T.pedis,T.cruris.

• Candida albicans
• pityrosporum
DERMATOPHYTES;
Fungi that live within the epidermal keratin or hair follicle and do
not penetrate into deeper structures.
 Causes infection of skin, hair and nails
Pathophysiology; digestion of keratin by dermatophytes results in
scaly skin, broken hairs, crumbling nails/onycholysis
Etiology; Trichophyton, Microsporum, Epidermophyton species
 Spread by direct contact
Clinical presentation
Depends in part on the organism involved.
• Tinea corporis – its is ring worm of the body. Presents as
asymmetrical scaly patches which show central clearing and
advancing scaly raised edge.
• Tinea cruris – it’s a ring worm of groin. Appears well demarcated
red plaques with an arc like border extending down to the upper
thigh.
• Tinea pedis – athlete's foot may be confined to the toe cleft
where the skin looks white, macerated and fissured.
• Tinea capitis – more common in black African children. Clinical
appearance is variable from mild diffuse scaling with no hair
loss similar to dandruff to the more typical appearance of
circular scaly patches in the scalp associated with alopecia and
broken hairs
Treatment
• Localized infection – Topical antifungal (eg clotrimazole,
miconazole or terbinafine applied 3 times daily for 1-2 weeks
• More widespred infection – oral antifungal therapy (eg
itraconazole 100 mg daily, terbinafine 250 mg daily for 1-2
months.
• High dose griseofluvin can be used with scalp ringworm (15-20
mg /kg per day for 8 weeks)
CANDIDA ALBICANS
• Is a yeast that sometimes found as a part of normal flora ( esp
in GI). It acts as opportunist when there suitable warm moist
environment ( eg nappy rash)
• Flexural areas affected are red with rather ragged peeling edge
that may contain few small pustules.
• Satellite lesions may also be seen
• It can affect the moist interdigital clefts of the toes, finger web
spaces or the damaged skin around the nail folds
• It can also affect mucosal surface of the mouth or genital tract.
Clinically superficial white or creamy pseudomembranous
plaques appear which can be scraped of leaving raw areas
underneath.
Treatment
• Remove any underlying
predisposing factors
• Topical antifungal creams
( clotrimazole, miconazole)
• Candida nail infection requires
systemic antifungal therapy with
imidazole (itraconazole 100 mg
daily for 3-6 months)
 PITYRIASIS (TINEA) VERSICOLOR
Clinical Presentation; asymptomatic superficial fungal infection
with brown/white scaling macules. Affected skin is darker than
surrounding skin in winter, lighter in summer (does not tan).
Common sites: upper chest and back
Pathophysiology; microbe produces azelaic acid → inflammatory
reaction inhibiting melanin synthesis yielding variable
pigmentation. Affinity for sebaceous glands; require fatty acids to
survive
Etiology; Pityrosporum ovale (Malassezia furfur) also associated
with folliculitis and seborrheic dermatitis.
 Predisposing factors: summer, tropical climates, excessive
sweating, Cushing’s syndrome, prolonged corticosteroid use.
Investigations; clinical diagnosis
but can perform microscopic
examination, KOH prep of scales
for hyphae and spores
Management; ketoconazole
shampoo or cream daily. Topical
terbinafine. Systemic fluconazole
or itraconazole for 7 d if
extensive
Parasitic Infections
SCABIES;
Clinical Presentation; it highly contagious,characterized by intense
pruritic rashes (especially nocturnal), and secondary infection
which is due to severe itching.
 Common sites: axillae, groin, buttocks, hands/feet (especially web
spaces), sparing of head and neck (except in infants).
Pathophysiology; scabies mite remains alive 2-3 d on
clothing/sheets, incubation of 1 mo, then pruritus begins
Etiology; Sarcoptes scabiei (a mite), risk factors: sexual promiscuity,
crowding, poverty, nosocomial and immunocompromised.
Investigations; microscopic examination of root and content of
burrow and mineral oil mount for mite, eggs, feces.
Management; bathe, then apply permethrin 5% cream from neck
down to soles of feet (must be left on for 8-14 h and requires
second treatment 7 d after first treatment)
onchocerciasis

• Onchocerciasis, commonly known as “river blindness”, is caused by

the parasitic worm Onchocerca volvulus.
• It is transmitted to humans through exposure to repeated bites of
infected blackflies of the genus Simulium.
• Symptoms include severe itching, disfiguring skin conditions, and
visual impairment, including permanent blindness.
• Symptoms are caused by the microfilariae, which move around the
human body in the subcutaneous tissue and induce intense
inflammatory responses when they die.
• More than 99% of infected people live in 31 African countries. The
disease also exists in some foci in Latin America and Yemen.
• Onchocerciasis is an eye and skin disease.
• Infected people may show symptoms such as severe itching and
various skin changes.
• Some infected people develop eye lesions which can lead to visual
impairment and permanent blindness. In most cases, nodules under
the skin form around the adult worms
• Community-directed treatment with ivermectin is the core strategy
to eliminate onchocerciasis in Africa. In the Americas the strategy is
biannual large-scale treatment with ivermectin
Skin manifestation of onchocerciasis
PAPULO-SQUAMOUS LESIONS

• Psoriasis
• Lichen planus
Psoriasis
• Psoriasis is an immunologically mediated chronic inflammatory
skin disease.
• Characterized by well-defined salmon-pink plaques bearing
large adherent silvery centrally attached scales.
• Affects 1-3% of most populations, and it is most prevalent in
European and north American whites.(Light skinned people)
• People between 15-40years of age are affected more, rare
under 10yrs.
• There are two peaks of onset of psoriasis.
• Type I has onset in the second and third decade and a more
common family history of psoriasis.
• Type II has onset in late adulthood in patients without obvious
family history.
• Its course is unpredictable but is usually chronic with
exacerbations and remissions.
Etiology

• Primary cause is unknown. (but genetic has been

suspected)
• There are two key abnormalities in a psoriatic plaque:
• Hyper proliferation of keratinocytes
• Inflammatory cell infiltrate in which neutrophils,
TNF and T lymphocytes predominate.

• Each abnormalities can induce the other, and perhaps the

genetic abnormality leads first to keratinocyte
hyperproliferation.
• And this, in turn, produces a defective skin barrier
allowing the penetration by, or unmasking of, hidden
antigens to which an immune response is mounted.
• Alternatively, the psoriatic plaque might reflect a
genetically determined reaction to different types of
trauma (e.g. physical wounds, environmental irritants and
drugs) in which the healing response is exaggerated and
uncontrolled.
• A child with one affected parent has a 14% chance of
developing the disease, and 41% if both are affected.
• The disorder is concordant in around 70% of monozygotic
(identical) twins but in only 20% of dizygotic ones.
Precipitant factors
• Trauma- skin damaged by scratches or surgical wounds (the
Köbner phenomenon)
• Infection – tonsillitis caused by β- haemolytic streptococci,
Staphylococcus aureus and certain streptococci.
• Hormonal – psoriasis frequently improves in pregnancy
only to relapse postpartum. Rarely hypo parathyroidism
• Sunlight – improves most psoriatic but 10% become worse.
• Drugs – antimalarial, β-blockers, IFN-α and lithium.
• Cigarette smoking and alcohol –more common in smokers
and ex-smokers.
• Emotion – emotional upsets seem to cause some
exacerbations
Patterns of psoriasis
• A: Plaque pattern
• Most common type. (85-90%)
• well demarcated and range from a few mm to many cm
in diameter.
• Pink or red with large centrally adherent silvery-white
built-up polygonal scales.
• Symmetrical sites on the elbows, knees, lower back
and scalp are sites of predilection
• B: Guttate pattern
• Numerous small, scaly, red or pink, droplet-like lesions
(papules) over large areas of the body, primarily the
trunk, but also the limbs and scalp.
• Often triggered by a streptococcal infection, typically
streptococcal pharyngitis often in children and
adolescent.
• The rash often clears in a few months but plaque
psoriasis may develop later
C: Pustular psoriasis
• Raised bumps filled with non-infectious pus (pustules)
• The skin under and surrounding the pustules is red and
tender.
• Can be localized, commonly to the hands and feet
(palmoplantar pustulosis)
• or generalized with widespread patches.
D:Flexural psoriasis
• Smooth, inflamed patches of skin.
• Frequently affects skin folds, around the genitals (between
the thigh and groin), the armpits, in the skin folds of an
obese, inter gluteal cleft, and the inframammary fold.
• Heat, trauma, and infection are thought to play a role.
E: Erythrodermic psoriasis
• widespread inflammation and exfoliation of the skin.
• may be accompanied by severe itching, swelling, and pain.
• exacerbation of unstable plaque psoriasis, particularly
following the abrupt withdrawal of systemic glucocorticoids
Investigations

• Usually the diagnosis of common plaque psoriasis is obvious

from clinical appearance. Therefore biopsy is seldom needed.
• Throat swabbing for β-haemolytic streptococci (guttate
psoriasis)
• Skin scrapings and nail clippings may be required to exclude
tinea.(there is epidermal thickening-psoriasis).

Differential diagnoses
• Discoid eczema, Seborrheic eczema, Pytiriasis rosea
• Secondary syphilis, Cutaneous T-cell lymphoma,Tinea unguium
 Management & treatment

• Psoriasis not contagious and at present there is no cure for it.

• All treatments are suppressive and aimed at either inducing a remission or
making the condition more tolerable.
• Spontaneous remissions will occur in 50% of patients
• Main types of treatment are divided into four main categories:
• Topical, ultraviolet radiation (UV rays), systemic and biological
• Topical: corticosteroids, vit. D analogues (Calcipotriol/ calcipotriene ),
calcitriol and tacalcitol - mild to moderate psoriasis (40% of the skin),
corticosteroids (betamethasone),retinoids (tazarotene), coal- tar preparation,
Salicylic acid (creams), Calcineurin inhibitors (topical immunomodulators:
tacrolimus and pimecrolimus)

• UV radiations: Improve with natural sunlight and should be encouraged to sunbathe.

Artificial ultraviolet radiation (UVB)
• Systemic: Photochemotherapy with psoralen and ultraviolet A (PUVA)
treatment, retinoids, methotrexate, ciclosporin, fumaric acid (fumarate),
hydroxyurea (hydroxycarbamide) and an array of biological agent
Lichen planus
• The cause is unknown, but it is not contagious.
• Thought to be T cell mediated autoimmune reaction which triggers
apoptosis of the epithelial cells.
• Cytokines are involved (TNF-α, interferon ᵞ, IL-1, IL-6, and IL- 8)
• Where a triggering agent is identified, this is termed a lichenoid reaction
rather than lichen planus. These may include:

• Drug reactions: (gold salts, beta blockers, traditional antimalarial (e.g.

quinine), thiazide diuretics, spironolactone, metformin etc.
• Reactions to amalgam (metal alloys) fillings.
• Graft-versus-host disease lesions
• Hepatitis, specifically hepatitis B and hepatitis C infection, and primary
biliary cirrhosis.
• Lichen planus is also associated with autoimmune disorders, such as
alopecia areata, vitiligo and ulcerative colitis
Presentation

• Violaceous or lilac-colored, intensely itchy, flat-topped

papules that usually arise on the extremities, particularly on
the volar aspects of the wrists
• White streaky pattern on the surface of these papules
(Wickham’s striae).
• White asymptomatic lacy lines, dots, and occasionally small
white plaques, are also found in the mouth, particularly
inside the cheeks, in about 50% of patient oral lesions may
be the sole manifestation of the disease.
• The genital skin may be similarly affected.
• Skin plaques are usually
itchy, and patients rub
rather than scratch, so that
excoriations are uncommon.
Köbner phenomenon may
occur.
• about 10% of patients show
nail changes ranging from
fine longitudinal grooves to
destruction of the entire
nail fold and bed
• Scalp lesions can cause a
patchy scarring alopecia
Investigations
• The diagnosis is usually obvious clinically. The histology is
characteristic, so a biopsy will confirm the diagnosis if
necessary.
Differential diagnoses
• Lichen planus should be differentiated from the other papulosquamous
diseases
• Lichenoid drug reactions can mimic lichen planus closely.
• Wickham’s striae or oral lesions favor the diagnosis of lichen planus. Oral
candidiasis can also cause confusion.

Treatment
• If drugs are suspected as the cause, they should be stopped.
• Potent topical steroids will sometimes relieve symptoms and flatten the
plaques.
• Systemic steroid are recommended only in special situations (e.g. unusually
extensive involvement, nail destruction or painful and erosive oral lichen
planus).
• Photochemotherapy with psoralen and ultraviolet A
(PUVA) or with narrowband UVB may reduce pruritus and
help to clear up the skin lesions.
• Oral ciclosporin or acitretin have also helped some
patients with stubborn lichen planus.
• Antihistamines may blunt the itch.
Complications
• Nail and hair loss can be permanent.
• The ulcerative form in the mouth may lead to squamous
cell carcinoma.
• Ulceration, usually over bony prominences, may be
disabling, especially if it is on the soles
ECZEMAS/DERMATITIS

Definition
inflammation of the skin
Clinical Presentation
• poorly demarcated erythematous patches or plaques
• symptoms include pruritus and pain
acute dermatitis: papules, vesicles
subacute dermatitis: scaling, crusting, excoriations
chronic dermatitis: lichenification, xerosis, fissuring
Atopic eczema
Atopic eczema is the most common type - usually develops by
early childhood and resolves during teenage years (but may
recur)
Epidemiology; frequently affects infants, children, and young
adults, almost 15% of children in developed countries under the
age of 5 are affected
Causes; Not fully understood, but a positive family history of
atopy (i.e. eczema, asthma, allergic rhinitis) is often present
• Exacerbating factors such as infections, allergens (e.g.
chemicals, food, dust, pet fur), sweating, heat and severe stress
 Presentation; Commonly present as itchy, erythematous dry scaly
patches
• More common on the face and extensor aspects of limbs in
infants, and the flexor aspects in children and adults
• Acute lesions are erythematous, vesicular and weepy (exudative)
• Chronic scratching/rubbing can lead to excoriations and
lichenification
Management; General measures - avoid known exacerbating
agents, frequent skin moisturizers +/- bandages and bath oil/soap
substitute
• Topical steroids eg. 1% hydrocortisone
• Oral therapies - antihistamines eg cetirizine for symptomatic relief,
antibiotics (e.g. flucloxacillin) for secondary bacterial infections,
and antivirals (e.g. aciclovir) for secondary herpes infection
• Phototherapy and
immunosuppressants (e.g.
oral prednisolone,
azathioprine, ciclosporin) for
severe non- responsive cases
Complications; Secondary
bacterial infection (crusted
weepy lesions)
• Secondary viral infection -
molluscum contagiosum
(pearly papules with central
umbilication), viral warts and
eczema herpeticum
 Contact Dermatitis

Clinical Presentation; cutaneous inflammation caused by an external agent(s)

Irritant Contact Dermatitis Allergic Contact Dermatitis

Mechanism of Toxic injury to skin; non- Cell-mediated delayed (Type

Reaction immune mechanism IV) hypersensitivity reaction
Type of Reaction Acute: quick reaction, sharp Erythema with a
margins (e.g. from papulovesicular eruption,
acid/alkali exposure) swelling,
Cumulative insult: slow to pruritus
appear, poorly defined
margins (e.g. from soap),
more common

Frequency Majority; will occur in Minority; patient acquires

anyone given sufficient susceptibility to allergen that
concentration of irritants persists indefinitely
 Irritant Contact Dermatitis Allergic Contact Dermatitis

Distribution Hands are the most common Areas exposed to allergen

site

Examples Soaps, weak alkali, Many allergens are irritants,

detergents, organic so may coincide with irritant
solvents, alcohol, oils dermatitis

Management Avoidance of irritants Avoid allergen and its cross-

Wet compresses with reactants
Burow’s solution(Aluminium Steroid cream (e.g.
acetate solution) hydrocortisone 1%,
Barrier moisturizers betamethasone
Topical/oral steroids valerate 0.05% or 0.1%
cream; bid)
Systemic steroids
(prednisone 1 mg/kg, taper
over 2 week)
VESICULOBULLOUS DISEASES

• Pemphigus vulgaris
• Bullous pemphigoid
• Dermatitis Herpetiformis
• Steven-johnson syndrome (sjs) and toxic epidermal
necrolysis (ten)
 Pemphigus Vulgaris
Clinical Presentation; autoimmune blistering disease characterized by
flaccid, non-pruritic intraepidermal bullae/vesicles on an
erythematous or normal skin base
• may present with erosions and secondary bacterial infection
• sites: mouth (90%), scalp, face, chest, axillae, groin, umbilicus
• Nikolsky’s sign: epidermal detachment with shear stress
• Asboe-Hansen sign: pressure applied to bulla causes it to extend
laterally
Pathophysiology; IgG against epidermal desmoglein-1 and -3 lead to
loss of intercellular adhesion in the epidermis
Epidemiology; 40-60 yr old, M=F, higher prevalence in Jewish,
Mediterranean, Asian populations
Investigations
• immunofluorescence: shows IgG and C3 deposition intraepidermally
• circulating serum anti-desmoglein IgG antibodies
 Prognosis; lesions heal with hyperpigmentation but do not scar
• may be fatal unless treated with immunosuppressive agents
Management
• prednisone 1-2 mg/kg until no new blisters, then 1-1.5 mg/kg until
clear, then taper ± steroid-sparing agents (e.g. azathioprine,
methotrexate, cyclophosphamide and cyclosporine
Bullous Pemphigoid

Clinical Presentation; chronic autoimmune bullous eruption

characterized by pruritis, pruritic, tense, subepidermal bullae on an
erythematous or normal skin base
• Can present as urticarial plaques without bullae
• Common sites: flexor aspect of forearms, axillae, medial thighs, groin,
abdomen, mouth in 33%
Pathophysiology; IgG produced against dermal-epidermal basement
membrane proteins (hemidesmosomes) leads to subepidermal bullae
Epidemiology; mean age of onset: 60-80 yr old, F=M
Investigations; immunofluorescence shows linear deposition of IgG
and C3 along the basement membrane
• Anti-basement membrane antibody (IgG) (pemphigoid antibody
detectable in serum)
 Prognosis
• heals without scarring, usually chronic
• rarely fatal
Management
• prednisone 0.5-1 mg/kg/day until clear, then taper ± steroid-sparing
agents (e.g. azathioprine, methotrexate)
• topical potent steroids (clobetasol) may be as effective as systemic
steroids in limited disease
• tetracycline ± nicotinamide is effective for some cases
• immunosuppressants such as azathioprine, mycophenolate mofetil,
cyclosporine and plasmapheresis for refractory cases
Dermatitis Herpetiformis

Clinical Presentation; grouped papules or vesicles on an

erythematous base, associated with intense pruritus, burning,
stinging and excoriations or erosions
• lesions grouped, bilaterally symmetrical
• common sites: extensor surfaces of elbows/knees, buttocks and back
Pathophysiology; transglutaminase IgA deposits in the skin alone or
in immune complexes leading to eosinophil and neutrophil infiltration
• 90-100% associated with an often subclinical gluten-sensitive
enteropathy (i.e. celiac disease)
• iron/folate deficiency is common
 Epidemiology
20-60 yr old, M:F = 2:1
Investigations
• biopsy
• immunofluorescence shows IgA deposits in
perilesional skin
Management
• dapsone (sulfapyridine or tetracycline if dapsone is contraindicated
or poorly tolerated)
• gluten-free diet for life – this can reduce risk of lymphoma
STEVENS- JONSON SYNDROME
(SJS)/TOXIC EPIDERMAL NECROLYSIS
(TEN)

• Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN)

are severe mucocutaneous reactions, most commonly triggered by
medications, characterized by extensive necrosis and detachment of
the epidermis .
• According to a widely accepted classification, SJS and TEN are
considered a disease continuum and are distinguished chiefly by
severity, based upon the percentage of body surface involved with
blisters and erosions
 .

• SJS is the less severe condition, in which skin detachment is <10

percent of the body surface. Mucous membranes are affected in over
90 percent of patients, usually at two or more distinct sites (ocular,
oral, and genital)
• TEN involves detachment of >30 percent of the body surface area
(BSA). Mucous membranes are also involved in over 90 percent of
patients.
• SJS/TEN overlap describes patients with skin detachment of 10 to 30
percent of BSA.
• the term "SJS/TEN" to refer collectively to SJS, TEN,
and SJS/TEN overlap syndrome
 Clinical Presentation; targetoid lesions ± purpura, or diffuse
erythema), confluence of flaccid blisters, positive Nikolsky sign
(epidermal detachment with shear stress), full thickness epidermal
loss; darkish tender skin, bullae, desquamation/skin sloughing

• classification: BSA with epidermal detachment: <10% in SJS, 10-

30% in SJS/TEN overlap, and >30% in TEN
Spread: face and extremities; may generalize; scalp, palms, soles
relatively spared; erosion of mucous membranes (lips, oral mucosa,
conjunctiva, GU mucosa)
• Systemic features: fever (higher in TEN), cytopenias, renal tubular
necrosis/AKI, tracheal erosion, infection, contractures, corneal
scarring, phimosis, vaginal synechiae

• time course: appears 1-3 wk after drug initiation; progression <4 d;

epidermal regrowth in 3 wks
Epidemiology; SJS: 1.2-6/million; TEN: 0.4-1.2/million
Common causative agents: drugs (allopurinol, anti-epileptics,
sulfonamides, NSAIDs, cephalosporins) responsible in 50% of SJS and
80% of TEN; viral or mycoplasma infections;Nevirepine
 SCORTEN Score for TEN Prognosis
• One point for each of: age ≥40, malignancy, body surface area
detached ≥10%, tachycardia ≥120 bpm, serum urea >10 mmol/L,
serum glucose >14 mmol/L, serum bicarbonate <20 mmol/L
• Used to determine appropriate clinical setting:
• score 0-1 can be treated in non-specialized wards
• score ≥2 should be transferred to intensive care or burn unit
Management; discontinue offending drug
• admit to intermediate/intensive care/burn unit
Supportive care: IV fluids, electrolyte replacement, nutritional
support, pain control, wound care, sterile handling, monitor for and
treat infection.
Inherited skin abnormalities
Xeroderma pigmentosum
• Xeroderma pigmentosum is a rare disorder transmitted in
an autosomal recessive manner. It is characterized by
photosensitivity, pigmentary changes, premature skin
aging, and malignant tumor development.
• These manifestations are due to a cellular hypersensitivity
to ultraviolet (UV) radiation resulting from a defect in DNA
repair.
• Cases of xeroderma pigmentosum are reported in persons
of all races.
• An equal prevalence has been reported in males and
females.
• The disease is usually detected at age 1-2 years.
Pathophysiology
The basic defect in xeroderma pigmentosum is in nucleotide
excision repair (NER), leading to deficient repair of DNA damaged
by UV radiation.
Clinical presentation
• Hx of severe persistent sunburn can be found in many patients
• The disease typically passes through 3 stages
• The first stage appears after age 6 months. This stage is characterized by
diffuse erythema, scaling, and frecklelike areas of increased pigmentation
• The second stage is characterized by poikiloderma. Poikiloderma consists of
skin atrophy, telangiectasias, and mottled hyperpigmentation and
hypopigmentation, giving rise to an appearance similar to that of chronic
radiodermatitis
• the third stage is heralded by the appearance of numerous malignancies,
including squamous cell carcinomas, malignant melanoma, basal cell
carcinoma, and fibrosarcoma. These malignancies may occur as early as age
4-5 years and are more prevalent in sun-exposed areas.
Treatment
• Use of sunsceen to protect against UV light
• Malignant skin lesions should be exised
• Medication – aim at preventing some neoplasms in XP.
Disorders of pigmentation
• Hypopimentation
• Vitiligo

• Hyperpigmentation
• Lentigos
• freckles
Vitiligo
• Acquired progressive disorder in which some or all of the
melanocytes in the interfollicular epidermis, and occasionally
those in the hair follicles, are selectively destroyed.
• Focal loss of melanocytes results in the development of
patches of hypopigmentation.
• Incidence: 1% - 30% of cases have family history
• onset is most commonly observed in persons aged 10-30
years.
• The pathogenesis is unclear and, but it is thought that
melanocytes may be the target of a cell-mediated
autoimmune attack
• A positive family history of vitiligo is relatively common in
those with extensive disease, and this type is also associated
with other autoimmune diseases
• Can be clinically
• Localized
• Focal - One or more macules in 1 area.
• Segmental - One or more macules in a dermatomal pattern
• Mucosal - Mucus membrane alone
• Generalized (more symmetrical)
• Acrofacial - Distal extremities and face
• Vulgaris - Scattered macules
• Mixed - Acrofacial and vulgaris involvement, or segmental and
acrofacial and/or vulgaris involvement
• Universal - Complete or nearly complete depigmentation
Vitiligo
Treatment modalities

Topical therapies
• Topical corticosteroids-Mid- to super-high-potency topical
corticosteroids are commonly used as a first-line therapy for the
treatment of limited vitiligo. Their efficacy is attributed to
modulation of the immune response
• Topical calcineurin inhibitors — Tacrolimus and pimecrolimus are
topical immunomodulatory agents that affect the T-cell and mast-
cell function and inhibit the synthesis and release of multiple
proinflammatory cytokines.
• Systemic corticosteroids — Low-dose oral corticosteroids are
generally utilized for the stabilization of rapidly progressive vitiligo,
often in combination with NB-UVB phototherapy.
Phototherapy
• Narrowband ultraviolet B phototherapy — NB-UVB involves the use
of UV lamps with a peak emission of approximately 311 nm.
• These shorter wavelengths provide higher-energy fluences and
induce less cutaneous erythema.
• NB-UVB induces local immunosuppression and apoptosis; and
increases melanocyte proliferation and melanogenesis.
• PUVA photochemotherapy — Historically, photochemotherapy with
topical or systemic PUVA radiation was the "gold standard" treatment
for the repigmentation of vitiligo but has been largely replaced by
NB-UVB phototherapy dueto its phototoxicity.
• Surgical therapies — Surgical therapies have been used for vitiligo for
the past 25 years and remain viable options for patients with
localized depigmented areas that have been unresponsive to medical
intervention.
• It includes skin grafting which transfers a reservoir of healthy
melanocytes to vitiliginous skin for proliferation and migration into
areas of depigmentation.
Increased pigmentation

• Focal hypermelanosis: seen in lesions such as freckles and lentigines,

characterised by focal areas of increased pigmentation.
• Diffuse hyperpigmentation: most commonly due to hypermelanosis
but other pigments may be deposited in the skin, e.g. orange
discoloration with carotenaemia and bronze with haemochromatosis
• Endocrine pigmentation: may occur in several conditions. Addison’s
disease, Cushing’s syndrome, Nelson’s syndrome and chronic renal
failure due to increased levels of pituitary melanotrophic peptides,
including adrenocorticotrophic hormone (ACTH).
• Drug-induced pigmentation: may be diffuse or localised. It is not
always due to hypermelanosis but sometimes is caused by deposition
of the drug or a metabolite eg Amiodarone, Arsenic, Phenothiazines
Ephelides (freckles)
• Small light brown macules
appearing in sun-exposed skin
of fair-skinned individuals, often
with red or blond hair
• Normal number melanocytes
but increase melanin in the
basal epidermal layer.
• Freckles will increase in number
and darkness with sunlight
exposure
• Pronounced during spring and
summer
Lentigos

• These are more permanent

macule of pigmentation
similar to freckles, but
• A lentigo has an
increased number of
melanocytes.
• lentigines will stay stable in
their color regardless of
sunlight exposure.
• Solar lentigos occur in older
people on exposed skin due
to actinic damage.
• Establishing the cause is important. Photoprotection
may minimise the risk of increasing pigmentation.
• Topical hydroquinone preparations can be used for
skin lightening in some types of hyperpigmentation,
although caution is required, particularly in darker
skin types.
Congenital abnormalities

• Albinism
• neurofibromatosis
OCULOCUTANEOUS ALBINISM

• These are congenital

hypopigmentary diseases that
result from a defect in the
production of melanin due to
dysfunction of melanocytes in
the skin, eyes, and in the ears.
Oculocutaneous albinism (OCA)

• Is a group of rare genetic disorders of melanin biosynthesis inherited

in an autosomal recessive pattern.
• Seven nonsyndromic types of albinism, numbered as Oculocutaneous
albinism type 1 (OCA1) to Oculocutaneous albinism type 7 (OCA7),
have been recognized
• And Oculocutaneous albinism type 2 (OCA2) is the most common
type of albinism worldwide
• All types share reduced to absent pigmentation of skin, hair, and
eyes, but the clinical phenotypes vary along a broad spectrum of
disease severity
Pathogenesis

• Albinism results from a range of genetic abnormalities that lead to

reduced melanin biosynthesis in the skin and eyes; but the number
of melanocytes is normal (in contrast to vitiligo).
• Albinism is usually inherited as an autosomal recessive trait and there
are several different types and presentations.
• Type 1 albinism is due to a defect in the tyrosinase gene, whose
product is rate-limiting in the production of melanin.
• Affected individuals have an almost complete absence of pigment in
the skin and hair at birth, with consequent pale skin and white hair,
and failure of melanin production in the iris and retina.
Pathogenesis

• A second form of albinism is due to a defect in the P gene, which

encodes an ion channel protein in the melanosome.
• Patients may have gross reduction of melanin in the skin and in the
eyes, but may be more mildly affected than type 1 albinos.
• People with OCA2 generally have more pigment and better vision
than those with OCA1.
• People with OCA2 usually have fair skin compared to OCA1
CLINICAL MANIFESTATIONS

• Individuals with albinism type 1A (OCA1A) has almost complete

absence of skin, hair, and eye melanin pigmentation.
• albinism type 1B (OCA1B), albinism type 2 (OCA2), and
Oculocutaneous albinism type 4 (OCA4); have a variable amount of
brown pigmentation.
• And there is a reddish-brown pigmentation in Oculocutaneous
albinism type 3 (OCA3).
• The ocular manifestations, including congenital nystagmus,
photophobia, iris translucency, reduced pigmentation of the retinal
epithelium, foveal hypoplasia, and reduced visual acuity, are common
to all types of OCA.
OCA1A
• In OCA1A, or the classic tyrosinase-
negative OCA, there is a complete inability
to synthesize melanin in skin, hair, and
eyes, which results in the characteristic
"albino" phenotype.
• Born with white hair and skin, and there
are no changes as they mature
• The irides are translucent, appear pink.
OCA 2
• Hair and skin are light brown and
the irides are gray to tan at birth
• The iris has punctate and radial
translucency, and moderate
retinal pigment is present
MANAGEMENT

• The management of patients with OCA involves strict sun protection

beginning from infancy and treatment of high refractive errors with
glasses or contact lenses.
• Early diagnosis and treatment of skin tumours is essential.
Neurofibromatosis

• Neurofibromatosis encompasses two clinically and genetically

separate conditions, with an autosomal dominant pattern of
inheritance.
• The more common neurofibromatosis type 1 (NF1) is caused by
mutations in the NF1 gene on chromosome 17, half of which are new
mutations.
• NF1 is characterised by neurofibromas (benign peripheral nerve
sheath tumours) and skin involvement, and may affect numerous
systems
• The typical order of appearance of clinical manifestations is café-au-
lait macules of, axillary and/or inguinal freckling, Lisch nodules (iris
hamartomas), and neurofibromas
Axillary freckling in a patient with A café au lait spot andsubcutaneous
neurofibromatosis 1 nodules on the forearm of a patient
with neurofibromatosis type 1.
DiAgnosis of NF1
• Clinical diagnosis requires the presence of at least 2 of 7 criteria to
confirm the presence of neurofibromatosis, type 1. The 7 clinical
criteria used to diagnose NF1 are as follows:
• Six or more café-au-lait spots or hyperpigmented macules greater
than or equal to 5 mm in diameter in prepubertal children and 15
mm postpubertal
• Axillary or inguinal freckles (>2)
• Two or more typical neurofibromas or one plexiform neurofibroma
• Optic nerve glioma
• Two or more iris hamartomas (Lisch nodules), often identified only
through slit-lamp examination by an ophthalmologist
• Sphenoid dysplasia or typical long-bone abnormalities such as
pseudarthrosis
• First-degree relative (eg, mother, father, sister, brother) with NF1
NF2
• Neurofibromatosis type 2 (NF2) is caused by mutations of the NF2
gene on chromosome 22, and is characterised by schwannomas
(benign peripheral nerve sheath tumours comprising Schwann cells
only), with little skin involvement;
• the clinical manifestations are more restricted to the eye and
nervous system.
• The skin is Much less commonly affected than NF1 causing cutaneous
and Subcutaneous tumor and Skin plaques.
• The most frequent clinical features are Neurologic lesions like
bilateral vestibular schwannomas, Intracranial meningiomas, Spinal
tumors (both intramedullary and extramedullary) Peripheral
neuropathy
• Eye lesions like Cataracts, epiretinal and Retinal hamartomas
Management

• There is no one overall treatment for NF1 nor are there any
therapeutic agents specifically approved for patients with NF1.
Rather, the individual manifestations are treated as they arise.
• For example :The approach to treatment of the various tumors
associated with NF1 depends upon the type of tumor, its effect on
adjacent tissues, and related complications.
• The management of patients with NF2 is complex, and involves
multiple disciplines to prevent or treat the various complications that
may develop. including Tumor surveillance and follow-up, Treatment
of vestibular schwannomas and meningiomas and spinal tumors.
 References
• Kumar & Clark's clinical medicine 8 th edition
• Davidson’s principles & practice of medicine 23 rd edition
• Toronto notes 2017
• Dermatology Handbook for medical students 2nd edition
2014
• Old lecture notes
• Medscape
• Roderick J. Hay et al. The Global Burden of Skin Disease in
2010: An Analysis of the Prevalence and Impact of Skin
Conditions- journal of investigative dermatology.
published on Nov, 2013