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Fifth Stage Dermatology Dr. Hadaf – Lecture 7

1

Papulosquamous disorders

Lichen planus
• A common pruritic inflammatory disease of the skin &
/mucosa, nail & hair follicles that resemble lich en.

Pathogenesis

• Thought to be an auto immune process with unknown
trigger
If the trigger is known then it is called lichenoid reaction
• Exposure to medicines, dyes, other chemicals as gold, antimalarials, antibiotics,
diuretics.
• Diseases such as hepatitis C

Epidemiology

• Race: no racial predisposition
• Sex: Female to male ratio 3:2
• Age: more than 2/3 are 30 -60 years age, although
can occur at any age

Clinical presentation

• 3 types of lesions
• 1- skin lesions
• 2- mouth lesions
• 3- other manifestations hair & nail lesions

Skin lesions

• Characteristic; almost pathognomonic primary lesions:
small, violaceous, flat -topped, polygonal papules.
• Described as the 5 Ps disease:
• Pruritic, polygonal, purplish, plane, papules

• The surface is dry, shiny with whitish streaks

or puncta called Wickham’s striae
• Sites: flexor wrists, med. thighs,
• trunk, shins, dorsal hands &
glans penis
• Pos itive Koebner phenomenon
• prominent itching

2

M ucosa

Mucous membrane involvement: 50% of patients,
asymptomatic
White lacy lines & dots, or small plaques
Usually inside cheeks, lips
Sometimes may be the sole manifestation (oral LP)
Genital mucosa may show same picture

Hair
70 -80% are females leading
to scarring alopecia

Nail
In 5 -10% of patients
May be the only manifestation esp. children
Longitudinal ridging, splitting , onychlysis, red lunula
Pterygium formation is characteristic of LP

3

Actinic lichen planus

mostly middle east, sun exposed skin, in spring or
su mmer.
Adolescents & young adults
Face is target organ; forehead, cheeks, & lips
Annular, hyperpigmented plaques with hypopigmented
margin, & minimal itching

Diagnosis

• 1- Clinical
• 2- histopathology

Prognosis

Individual lesions may las t months
The disease itself may last for 1 year
Hyperpigmentation usually follow resolution
Recurrence rate is 1 in 6

Treatment

May be difficult
1)Limited lesions by superpotent topical or intralesional steroids
2)Indications of systemic steroids:
Extensive lesions
nail destruction
painful erosive oral lesions.
3)phototherpy: PUVA+ narrow -band UVB
4)Retinoids: in hypertrophic types
5) Antihistamines to relieve itching

Pityriasis rosea

Mild inflammatory exanthem characterized by pinkish, macular & papular lesions;
begin as discrete, then
become confluent.

Epidemiology

Mainly children & young adults.
More in spring & autumn
W omen more than men
Herpes virus 6 & 7 implicated in etiology
Not contagious, 2% recurrence rate

4

Begin with herald patch

which is larger, redder, more
scaly than remaining rash ;
Which consist of oval or
circinate patches covered with dry, crinkled, su rface,
desquamates leaving a collarette scale
Mainly trunk, extremities, neck
Inverted Christmas tree pattern
Mild pruritus & constitutional symptoms

Prognosis

• Last 6 -8 weeks & r esolve spontaneously
• Sometimes they leave post inflammatory hyperpigmentation

Treatment

Most cases no treatment is required
To shorten the course or decrease itching:
1- UVB in erythema doses
2-Corticosteroids are the standard therapy
3-Oral antihistamines
4-Emollients to relieve dryness & irritation
5-Erythromycine 250mg q.d.s for 2 weeks

5

REACTIVE ERYTHEMA

ERYTHEMA MULTIFORMI
A reaction pattern of multiform erythematous lesions.

ETIOLOGY

1-Viral: preceding oral herpes 1 -2 weeks previously, also
orf, mycoplasma, hepatitis A,B,C.
2-bacterial, fungal, & parasit ic infection.
3-Drugs: sulfa, NSAID, anticonvulsants, & others
4-Pregnancy
5-Malignancy or its treatment with radiotherapy

Start as sharply marginated, erythematous macule.

Become raised edematous papules over 24 -48 hours.
A ring of erythema forms around the periphery, with flatter, purpuric dusky center,
giving” target lesions” of 3 zones

Bilateral, symmetrical, & acral distribution

Mostly starting on dorsa of hand s
Sites of predilection are extensor limbs, face, elbows, knees, palms & soles

Steven johnson syndrome

a severe variant with bullous lesions, fever & extensive mucosal involvement.
May be complicated by:
asphyxia, blindness

6

Treatm ent

Most cases are self -limited with symptomatic treatment.
Remove precipitating factors.
Recurrent HHV infection may be prevented by oral acyclovir 200mg 3 -5 times/day.
Steven -Johnson may require aggressive treatment: I.V. gamma globuline, good nu trition,
fluid & electrolyte balance, prevent secondary infection,+ high dose short course
systemic steroids & good nursing care for eyes & mouth.

Erythema nodosum

Inflammation of subcutaneous fat (panniculitis), elicited by many factors:
1) Bacterial infection: as T.B, strept., bruce lla, leprosy, yersinia.
2) viral, mycoplasma, rickettsia,& chlamydia
3)Fungal as coccidiomycosis
4)malignancy, sarcoidosis, ulcerative colitis, Behcet disease
5)drugs: sulfa & oral contraceptives.

7

Clinical features

Characteristic lesion is a tender red nodule , alone or
grouped on shins or forearms.
Other a reas as thighs, face, breast.
Bilateral, symmetrical lesions.
Mostly in young adult women

Acute onset, frequently with constitutional symptoms

Resolve within few days leaving bruise like
The whole course last 6 -8 weeks

D iagnosis

Thorough history
physical examination
Chest x -ray
Throat culture
ASO titre

Treatment

Simple consisting of bed rest, NSAID as aspirin, indomethacin, ibuprofen
Systemic steroids not used
Potassium iodide in a dose of 400 -900 mg/day but not for more than 6 months

Thank you,,,


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