This patient’s biopsy will likely show:

A. Mononuclear cells with abundant cytoplasm around superficial vessels

B. Eosinophils at the dermoepidermal junction
C. Leukocytoclasia around superficial vessels
D. Lymphocytes at the dermoepidermal junction
E. Neutrophils at the dermoepidermal junction

MCQ Dermatology D. In 1860, von Hebra first described erythema exudativum multiforme. The
original disease described by von Hebra is now called erythema multiforme minor or herpes
simplex associated erythema multiforme (HAEM). It is strongly associated with a preceding
herpetic infection. In contrast, Stevens–Johnson syndrome (SJS) and toxic epidermal necrolysis
(TEN) usually represent adverse reactions to medications . There is, however, overlap in this
spectrum of diseases, with herpes being causative in 6–10% of cases of SJS, and in some series
Mycoplasma causing up to 25%. Biopsy should show a lichenoid infiltrate of lymphocytes at the
dermoepidermal junction.
What is the most likely diagnosis?
A. Lichen planus
B. Scabies
C. Lichen sclerosus
D. Morphea
E. Psoriasis

E) Psoriasis is a common, chronic, and recurrent inflammatory disease of the skin characterized by
circumscribed, erythematous, dry, scaling plaques of various sizes. The lesions are usually covered by
silvery white lamellar scales. The lesions have a predilection for the scalp, nails, extensor surfaces of the
limbs, umbilical region, and sacrum. If scalp
The most likely diagnosis
A Pityriasis alba
B Impetigo
C Dermatomyositis
D Dermatitis herpetiformis
E Atopic dermatitis

D) The hallmark of Atopic Dermatitis (AD) is pruritus, which is often intense and relentless,disrupting
every aspect of the patient’s life. The course of AD tends to be chronic and relapsing. As an
inflammatory skin disease, AD will present with varying degrees of erythema, inflammatory papules,
which often coalesce to form eczematous plaques, as well as areas of weepy dermatitis. Often areas of
involvement will evolve into scaly, xerotic plaques, and as the disease becomes chronic, lichenified
changes are evident and indicative of extended periods of itching and scratching. Morphology and
distribution vary with age . Typically in infants and very young children, AD will affect the face and
extensor arms and legs . The diaper region, where moisture tends to be retained, is often spared. In
older children and adults, distribution favors flexural areas, including anterior neck, antecubital fossa,
and popliteal space, and can affect the breasts, nipples, and trunk . The scalp, face, and eyelids can also
be affected, and in general, the axillae and groin folds are spared at any age.

The most likely diagnosis:

A Irritant Contact Dermatitis
B Allergic contact dermatitis
C Phytophotodermatitis
D Asteatotic Eczema
E Acquired keratoderma

B)Allergic contact dermatitis is an inflammatory process induced by direct contact of the skin of a
sensitized individual to an allergen. Within hours, red macules or patches develop that usually evolve
rapidly, sometimes through an intermediate stage ofurticarial papules or plaques, into vesicles that may
become bullae. Because the lesions, i.e., macules, papules, vesicles, and bullae, are not in themselves
specific, diagnosis clinically is made by virtue of distinctive distribution that reflects the manner in which
a particular allergen was contacted. Topical corticosteroids are the mainstay of treatment, while a
variety of symptomatic treatments can provide short-term relief of pruritus. However, the definitive
treatment of allergic contact dermatitis is thedentification and removal of any potential causal agents
Pityriasis versicolor is common superficial fungal skin infection caused by Malassezia sp., most
commonly M. furfur and M. globosa. The yeast proliferates in moist and sebum-rich areas of the
body. It is most common in tropical climates (high heat and humidity) and young adults with
hyperhidrosis (eg, athletes).
-Clinical: Characterized by scaly, hyper or hypopigmented macules and patches, hence the name
“versicolor.” Commonly located on the upper chest, shoulders and back. Lesions may clear
during cold and dry winter months and reappear in the summer.
Hyperpigmented type: Fungus induces melanocytes to produce more melanin resulting in
patches of scaly, hyperpigmented skin surrounded by normal skin.
Hypopigmented type: Fungus produces azelaic acid that inhibits tyrosinase enzyme in the
melanin synthesis pathway. The affected skin does not
tan on sun exposure resulting in lighter spots surrounded by tanned skin.
-Diagnosis Clinical with KOH prep of infected skin showing short hyphae (“spaghetti”) and
yeast (“meatballs”). Wood’s lamp examination accentuates skin color variation and can aid in
diagnosis.
-Treatment topical antifungal creams or shampoos (eg, zinc pyrithione, selenium sulfide,
ketoconazole or ciclopirox). Oral azoles (eg, itraconazole, fluconazole) for recalcitrant or severe
disease.
This patient may need blood tests to check her:
A. Renal function
B. White blood cell count
C. Liver function
D. Thyroid
E. Glucose

G) Pemphigoid gestationis is skin blistering disorder that occurs in women of childbearing age. It usually
presents in mid to late pregnancy (13 to 40 weeks gestation, known as the second and third trimesters)
with an itchy rash that develops into blisters. Itching is common and often starts around the umbilicus. It
starts with urticarial wheals and large raised red patches (plaques) commonly occurring on the trunk,
back, buttocks and limbs. Large tense blisters then occur on the red patches within 1-2 weeks,and may
also occur on palms and soles. heal without scarring. The primary aim of treatment is to relieve itching,
prevent blister formation and treat secondary infections. Topical corticosteroids are used in mild disease
whilst oral corticosteroids are necessary in more extensive cases. Minimum effective doses should be
used to reduce the risk of side effects to both mother and fetus. Oral antihistamines may be used to
relieve itching. Herpes gestationis is associated with an increased incidence of Graves’ disease.
The most likely diagnosis
A. Noonan syndrome
B. Bloom syndrome
C. Turner syndrome
D. Down syndrome
E. Griscelli syndrome

D) Down syndrome is a condition in which a person has an extra chromosome. Chromosomes are
small “packages” of genes in the body. They determine how a baby’s body forms during
pregnancy and how the baby’s body functions as it grows in the womb and after birth. Typically,
a baby is born with 46 chromosomes. Babies with Down syndrome have an extra copy of one of
these chromosomes, chromosome 21. A medical term for having an extra copy of a chromosome
is ‘trisomy.’ Down syndrome is also referred to as Trisomy 21.
DOWN SYND
Waardenburg syndrome is a genetic disorder that may be evident at birth (congenital). The range
and severity of associated symptoms and findings may vary greatly from case to case. However,
primary features often include distinctive facial abnormalities; unusually diminished coloration
(pigmentation) of the hair, the skin, and/or the iris of both eyes (irides); and/or congenital
deafness. More specifically, some affected individuals may have an unusually wide nasal bridge
due to sideways (lateral) displacement of the inner angles (canthi) of the eyes (dystopia
canthorum). In addition, pigmentary abnormalities may include a white lock of hair growing
above the forehead (white forelock); premature graying or whitening of the hair; differences in
the coloration of the two irides or in different regions of the same iris (heterochromia irides);
and/or patchy, abnormally light (depigmented) regions of skin (leukoderma). Some affected
individuals may also have hearing impairment due to abnormalities of the inner ear
(sensorineural deafness). Researchers have described different types of Waardenburg syndrome
(WS), based upon associated symptoms and specific genetic findings. For example,
Waardenburg syndrome type I (WS1) is characteristically associated with sideways displacement
of the inner angles of the eyes (i.e., dystopia canthorum), yet type II (WS2) is not associated with
this feature. In addition, WS1 and WS2 are known to be caused by alterations (mutations) of
different genes. Another form, known as type III (WS3), has been described in which
characteristic facial, eye (ocular), and hearing (auditory) abnormalities may be associated with
distinctive malformations of the arms and hands (upper limbs). A fourth form, known as WS4 or
Waardenburg-Hirschsprung disease, may be characterized by primary features of WS in
association with Hirschsprung disease. The latter is a digestive (gastrointestinal) disorder in
which there is absence of groups of specialized nerve cell bodies within a region of the smooth
(involuntary) muscle wall of the large intestine. In most cases, Waardenburg syndrome is
transmitted as an autosomal dominant trait. A number of different disease genes have been
identified that may cause Waardenburg syndrome in certain individuals or families (kindreds).
Four genotypic variants of Waardenburg syndrome exist, with overlapping phenotypic features;
all are autosomal-dominant. Types 1 and 3 are caused by mutations in the PAX3 gene, encoding
a transcription factor. Type 2 is caused by mutations in the MITF gene, also encoding a
transcription factor, and type 4 is due to either a heterozygous mutation in the SOX10 gene
(encoding a transcription factor), or homozygous mutations in the endothelin-3 (EDN3) or the
endothelin B receptor (EDNR3) gene. These mutations impair the ability of melanoblasts to
reach their final target sites (inner ear, eye, skin) during embryogenesis.
The most likely diagnosis
A. Porphyria cutanea tarda
B. Discoid lupus
C. Tinea capitis
D. Alopecia areata
E. Telogen effluvium

D) Alopecia areata is a chronic inflammatory skin disorder of the hair follicles with a lifetime incidence of
1–2 %. It affects both women and men equally. The disease most often starts in young adults with
children frequently affected. The disease has a sudden onset of patchy areas of hair loss that can occur
on the scalp or elsewhere on the body. The individual extent of psychological distress in patients with
the disease is often underestimated and frequently leads to severe psychological distress and social
impairment. Traditionally, alopecia areata is distinguished into limited disease, i.e. unifocal or multifocal
alopecia areata and extensive disease, i.e. complete loss of the scalp hair ( alopecia totalis ) or complete
loss of hairs of the total body ( alopecia universalis ). Ophiasis describes a band-like pattern of hair loss
on the occipital scalp. Alopecia areata is considered a CD8+T-cellmediated, organ-specific autoimmune
disease with several genetic factors contributing to the disease origin (about 20 % of affected patients
have a positive family history for the disease). about 10–20 % of the patients with alopecia areata have
structural nail abnormalities including pits and other forms of nail dystrophy (e.g. “sand paper nails”).
Treatment: topical/intralesional corticosteroid, other topicals (squaric acid, anthralin, minoxidil),
excimer laser, systemic corticosteroid or cyclosporine.

The most likely diagnosis

A Dyshidrotic Eczema
B Contact Dermatitis, Allergic
C Erythrasma
D Pityriasis Rubra Pilaris
E Tinea Pedis

E) Tinea pedis is a dermatophyte infection of the feet, which is commonly known as athlete’s foot. It
tends to occur almost exclusively in adults. Three dermatophytes may cause tinea pedis: Trichophyton
sp.,Epidermophyton sp., or Microsporum sp., with T. rubrum as the most common pathogen. Infection is
spread by humans, animals, or soil. Moist environments,such as wet socks, public showers, and pools,
tend to spread infection. Patients who are elderly, obese, and diabetic are at increased risk for infection.
If the infection is found between the toes, it is called the interdigital tinea pedis, the most common type.
It typically is found in the digit interspaces of the fourth and fifth toes. Patients complain of itching,
burning, scaling, and malodor. The moccasin type of infection is located on the lateral aspects and
bottom of the foot. It is often found bilaterally, and the patients tend to have scaly, erythematous, and
hyperkeratotic areas. Vesiculobullous type is a less common variant that presents with vesicles and
bullae on the plantar surfaces of the feet. Patients should keep their feet dry with foot powder and
should wear nonocclusive footwear. Four weeks of topical antifungal creams such as butenafine,
ketoconazole, econazole, and ciclopirox are normally effective, but oral griseofulvin, itraconazole,
fluconazole, or terbinafine may be needed for more resistant.
Most likely implicated
A Topical calcineurin inhibitor
B Topical corticosteroid
C Topical doxepin
D Topical pramoxine
E Topical acyclovir
B) Short courses of topical steroids (fewer than four weeks) are usually safe and usually cause no
problems. Problems may develop if topical steroids are used for long periods, or if short courses of
stronger steroids are repeated often. With long-term use of topical steroid the skin may develop
permanent stretch marks (striae), bruising, discolouration, or thin spidery blood vessels (telangiectasias
The most likely diagnosis
A Anhidrotic ectodermal dysplasia
B Neurofibromatosis
C Epidermolysis bullosa
D Tuberous sclerosis
E Darier’s disease

D) Tuberous sclerosis (TS) is an autosomal dominant genetic disorder described by Desiree-Magloire

Bourneville in 1880, is also called epiloia (epi = epilepsy, loi = low intelligence, a = adenoma sebaceum).
This classic triad of adenoma sebaceum , mental deficiency, and epilepsy, however, is present in only a
minority of patients. Other associated features include periungual fibromas, shagreen plaques
(collagenoma), oral papillomatosis , gingival hyperplasia, ash-leaf hypomelanotic macules , skin
fibromas,and café-au-lait spots. Adenoma sebaceum (angiofibromas) are 1–3 mm,
yellowishred,translucent, discrete, waxy papules that are distributed symmetrically, principally over the
cheeks, nose, and forehead. TS is caused by a mutation in one of two genes: TSC1, which encodes
hamartin, and TSC2, which encodes tuberin. Adenoma sebaceum can be treated by shaving,
dermabrasion, or laser therapy. Lesions are likely to recur, requiring repeat treatment. Cranial
irradiation of astrocytomas should be avoided because this may result in the subsequent development
of glioblastomas. Topical and systemic rapamycin shows some promise for prevention of tumor growth,
and is effective in models of the disease. If TS is suspected, refer to a dermatologist, neurologist, or
genetic counselor. Care is multidisciplinary; referral to a specialty center is recommended once diagnosis
is made.
The most likely diagnosis :
A Molluscum contagiosum
B Smallpox
C Milker’s nodules
D Chancroid
E Wart
 A) Molluscum contagiosum is a viral infection of the skin produced by a poxvirus that is more
closely related to the virus that produces smallpox. they are more common in children and
immunocompromised individuals, and can be sexually acquired. They may occur anywhere on
the skin surface and present as firm, skin-colored umbilicated papules with a central core of
keratin . Some lesions may demonstrate an intense host response. Usually self-limited
Treatment: catharidin, cryosurgery, curettage and imiquimod

What is the most likely diagnosis?

A. Lichen planus
B. Scabies
C. Lichen sclerosus
D. Morphea
E. Psoriasis

D) En coup de sabre is a type of linear scleroderma characterized by a linear band of atrophy and a
furrow in the skin that occurs in the frontal or frontoparietal scalp. Multiple lesions of en coup de sabre
may coexist in a single patient. Unlike skin in localized morphea, skin in linear scleroderma may be fixed
to underlying tissue. Calcinosis may rarely occur. Cutaneous changes accompanying the facial
hemiatrophy associated with the Parry-Romberg syndrome may be similar to those found in en coup de
sabre . Serologic abnormalities may include anti-nuclear antibodies, anti-single-stranded DNA
antibodies, and rheumatoid factor. Eosinophilia may be present and may correlate with disease activity.
modalities used in the management of en coup de sabre have included topical, intralesional, or systemic
glucocorticoids; vitamin E; vitamin D3; phenytoin; retinoids; penicillin; griseofulvin; interferon-(x), D-
penicillamine; antimalarials; ultraviolet A phototherapy with or without psoralens; and surgery .

The most likely diagnosis:

A Henoch-Schonlein purpura
B Dermatographism
C Meningism
D Acute hemorrhagic edema of infancy
E Still disease
D) Acute hemorrhagic edema of childhood affects children and infants < 2 years of age. It
presents with painful, edematous petechiae and ecchymoses on the head and distal extremities.
Facial edema may be the initial sign. Triggering factors include infection, drugs, and
immunization. It lacks the systemic features of HSP, and resolves in 1-3 weeks without sequelae.

The name of procedure

A Radioallergosorbent test
B Cryosurgery
C Electrosurgery
D Skin patch test
E Skin prick test

B) Cryosurgery is the controlled application of cold to cause tissue damage. most cryosurgeons
use liquid nitrogen. It is readily available, inexpensive, easy to store, easy to use, and it works
quickly. with cryosurgery, the degree of tissue damage is controlled in order to destroy the
target lesion with minimal damage to normal surrounding tissue. freezing causes intracellular
and extracellular ice crystals to form, and the subsequent vascular stasis causes tissue anoxia
and necrosis. The most efficient technique employs a rapid freeze and slow thawing. multiple
short freezes produce more damage than a long freeze Different. more damage than a long
freeze. different cell types have variable susceptibility to the effects of freezing, with
melanocytes being damaged at a much higher temperature than keratinocytes (25° C versus
250° C). This differential freezing has implications for the treatment of melanocytic lesions, as
well as the use of cryosurgery in patients with darkly pigmented skin. both benign and malignant
lesions can be treated by cryosurgery. The most common lesions are warts, actinic keratoses,
seborrheic keratoses, and molluscum contagiosum.