Vitiligo, pityriasis rosea dermatological diseases

1. Discoid lupus erythemathodes

2. • DL is a chronic autoimmune disease affecting the skin.
• Discoid lupus should not be confused with systemic lupus.
Systemic lupus can also cause a mild rash, usually on the
face, but it also affects the internal organs. A person with
systemic lupus can also have discoid lesions. Discoid lupus
doesn’t affect internal organs, but the rash tends to be much
more severe.

3. • Epidemiology
• The prevalence is between 17 and 48 per 100,000 people.
• Women are much more often affected than men.
• DLE usually presents in people aged between 20 and 40 years of age.
• DLE is more common in smokers.[1]
• DLE can be present in a small proportion of patients with systemic
lupus erythematosis (SLE).[2

4. Presentation
•Red scaly patches develop which leave pigmentation, atrophy and
white scars.
•The lesions are usually asymptomatic but they may present with mild
pruritus or sometimes pain within the lesions.
•DLE mainly affects are
•as exposed to sunlight, such as the cheeks, nose, ears, auricle, upper
back, neck and the backs of hands. It may rarely occur on the palms or
soles.
•DLE lesions may become hypertrophic, causing wart-like lesions, most
often on the extensor aspects of the arms.
•The scalp may be affected and cause permanent scarring alopecia.
•DLE may affect the lips and inside the mouth, causing ulcers and
scaling.

5. Specific
• CDLE lesions start as bright red papules
evolving into plaques, sharply marginated,
with adherent scaling. Scales are difficult to
remove
• CDLE may be localised and generalized,
occuring predominantly on the face and scalp,
dorsa of forearms, hands, fingers, toes and
less frequently the trunk.

9. • Getting worse by exposing sunlight
• Stress
• Infection
• Some medication
• Mechanical trauma

10. Management
• One of the most important ways to manage
discoid lupus, and prevent the discoid rash
from getting worse, is to protect the body
from exposure to the sun's harmful UV rays:
• use UVA or UVB sunscreen with a high sun
protection factor (SPF) of 50 or above
• wear a wide-brimmed hat when out in the sun
• choose clothing that covers most of the body

11. Management
• glucocorticoids and calcineurin inhibitors-
usually not very effective, topical
fluorinated glucocortics, intralesional
triamcinolone acetonide, 3-5mg/ml
• Antimalarials: Hydroxychloroquine ≤
6.5
𝑚𝑔
𝑘𝑔
𝑏𝑜𝑑𝑦 𝑤𝑒𝑖𝑔ℎ𝑡 𝑝𝑒𝑟 𝑑𝑎𝑦. 𝐼𝑓 ℎ𝑦𝑑𝑟𝑜𝑥𝑦𝑐ℎ𝑙𝑜𝑟𝑜
• Retinoids: hyperkeratotic CDLE lesions
respond well to systemic acitretin

12. Erythema exsudativum multiforme

13. • Erythema multiforme (EM) is an acute, self-
limited, and sometimes recurring skin
condition that is considered to be a type IV
hypersensitivity reaction associated with
certain infections, medications, and other
various triggers

14. • Multiple slightly elevated, round, edematous and
erythematous lesions develop symmetrically on the dorsa
of the hands and the extensor surfaces of the joints.
• It frequently occurs in the young and middle aged women
• Tends to appear during the spring and summer
• Infectious symptoms, including high fever, and
pharyngodynia may precede the onset
• Infection by the herpes simplex virus or Mycoplasma
pneumoniae is the dominant etiological factor, but drug
sensitivity is also important.
• Some cases develop Stevens-Johnson syndrome

15. Conditions associated with erythema multiforme
Infection /e.g human simplex virus,
streptococcus, mycoplasma, non-tuberculous
mycobacteria/ , chlamydia, rickettsia
Drug reaction / antibiotics, NSAID,
antineoplastic agents/
Collagen disease, allergic disorder / insect
bite, disease especially SLE, sarcoidosis…
Other /physical stimulation e.g cold,
pregnancy…..

16. Classification
• Localized cutaneous
lesions
• Mucosal lesions with
systemic involvement ‘
Stevens-johnson’
syndrome

17. Clinical features
• The eruptions occur symmetrically on the extensor
aspects of the joints /elbows, knees, the dorsal hands
and feet/ as erythematous papules or edematous
erythema, and they spread centrifugally to form
sharply circumscribed, round or irregularly shaped
erythema with a diameter of 6-20mm.
• The center of the eruption typically has concave or
severe erythema, presenting as bull’s eye or iris like
lesion

19. Pathogenesis
• EM is caused by various factors such as viral or
bacterial infections, drugs, and malignancies.
Type 111 allergy to the herpes simplex antigen
is suspected as an etiology of erythema,
because immune complexes are found in the
blood or tissues of patients with erythema.

20. Pathology
Lymphocytic infiltration at the dermal-
epidermal junction and vascular degeneration
of the basal cells occur in the early stage.
When the symptoms progress, lymphocytic
infiltration reaches the epidermis and
dyskeratosis and subepidermal blister occur

21. Diagnose
• It is easy to diagnose by its characteristic
clinical features and by the distribution of the
eruptions
• A history of previous diseases such as recent
infection supports the diagnose

22. Treatment
• To find the cause is important not only for
treatment but also for the prevention of
recurrence.
• For treating the eruptions, topical steroids and
oral antihistamines are used

23. Vitiligo

25. Epidemiology
Equal in both genders
Typically starts onset in 10-30
year olds
1% of world population
Affects all races
Genetic background, 30%< in
parent or sibling
More in patients with DM,
thyroid disease

26. Pathogenesis
Autoimmune theory:
selected melanocytes are
destroyed by certain
activated lymphocytes
1
Neurogenic hypothesis:
based on interaction of
melanocytes and nerve
cells
2
Self destruct hypothesis:
melanocytes are destroyed
by toxic substances formed
as part of normal melanin
biosynthesis
3

27. Cause
Physical trauma
(Koebner phenomenon)
Emotional stress
Illness
Sunburn

28. Clinical features
• Macules 5 mm-5cm
• Sharp margins
• Pale white
• Gradual enlargement of old macules
• Coalesces
• Trichrome vitiligo (white, light/dark brown)
represent different stages
• Asymptomatic
• Areas of white hair (poliosis)

29. Trichrome
Vitiligo

31. Clinical course
• Generalized
• Segmental

32. Generalized
• Low back, elbows, knees, digits,
genitals, around eyes and lips
• Lip-tip pattern
• Very symmetrical
• Vitiligo universalis
• Hair can depigment too
• Associated with immune disease
• Hair follicles may repigment

35. Segmental
• Develops in one unilateral
region
• Doesn’t extend
• Very stable
• More repigmentation
• Responds poorly to treatment
• Less likely associated with
immune disease
• Occurs earlier in age

37. Differential
Diagnosis
Contact with
depigmenting chemicals
Pityriasis versicolor
Post-inflammatory
depigmentation
Piebaldism

38. Prognosis
• Highly variable
• Rapid onset, slow progression
• Rapidly progressive - everywhere
except eyes
• Treatment of vitiligo associated disease
has no impact

39. Diagnosis
Wood’s lamp
Medical history and
exam
Biopsy
Blood test for
autoimmune conditions

40. Management
Sunscreen
Cosmetic cover up
Segmental – topical glucocorticoids,
topical calcineurin inhibitors
(tacrolimus), UVB, excimer laser, topical
photochemotherapy, psoralen
Generalized – systemic
photochemotherapy for 1 year, narrow
band UVB for <6 year olds

41. Narrowband UVB

45. Management
• Minigrafting – stable segmental
• Depigmentation – bleaching with
hydroquinone 20% cream.

46. Pityriasis Rosea

47. Epidemiology
and Etiology
• 10-43 year olds
• Spring and fall
• Reactivation of HHV-6 or HHV-7

48. Clinical
Manifestation
Skin lesions. Herald patch
80%. Oval, slightly raised
plaque 2-5 cm, salmon-red,
peripheral scaling, may be
multiple. At the trunk.
Exanthem. One or two
weeks later. Fine scaling
papules and patches, 1-2 cm
dull pink, oval, scattered, x-
mas tree pattern, itching.
Trunk, limbs.

51. Course
Lasts 6-12 weeks
Spontaneous remission
Sometimes leaves
hyperpigmented
patches that heal slowly

52. Pathology
• Thickening of
epidermis
• Spongiosis
• Parakeratosis
• Intraepidermal
filtration of
mononuclear cells

53. Differential
Diagnosis
Tinea corporis
Guttate psoriasis
Secondary syphilis
Captopril, barbiturate
Vaccine

54. Management
• Symptomatic. Oral antihistamines and topical
antipruritic lotions. Topical glucocorticoids.
May be improved by UVB phototherapy. Short
course of systemic glucocorticoids.

55. Test
>:)

56. 1. Which of the following terms is used
to describe the initial lesion of
pityriasis rosea?
A. Christmas tree
B. Guttate plaque
C. Herald patch
D. Nummular patch

57. 2. Vitiligo can be caused by?
A. Hereditary conditions
B. Immune system disorders
C. Injury to specific area
D. All of the above

58. 3. Herald patch lasts for 24 hours and
disappears
A. True
B. False

59. 4. Vitiligo is caused by the
malfunctioning or death of _____.
A. Melanocytes
B. Keratinocytes
C. Leukocytes
D. Golgi apparatus

60. 5. Pityriasis rosea recurs often
A. True
B. False

61. • 6.bull-eye буюу Iris syndrome гэж юу вэ?
Ямар өвчний үед илрэх вэ?

62. 7.Өсгийтэй гутлын шинж гэж юу вэ?
Ямар өвчний үед илрэх вэ?

63. • 8.Бенье Мешерскийн шинж гэж юу вэ

64. • 9. Butterfly rash ямар өвчний үед илрэх вэ
Тууралтын онцлог

65. • 10. халдвар харшлын шалтгаант буюу
herpes simplex virus-аар сэдээгддэг өвчин
юу вэ?