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Question 1

120-kDa protein corresponds to the

Answer 1

linear immunoglobulin A dermatosis autoantigen.1

Question 2

autoantibodies to 290- and 145-kDa proteins of type VII collagen, a major component of anchoring fibrils

Answer 2

Bullous SLE

Question 3

Autoantibodies against either the 180- or 230-kDa located in the hemidesmosomal complex of the BMZ.1

Answer 3

are known as human bullous pemphigoid antigens (BP180 and BP230),

Question 4

major autoantigen in cicatricial pemphigoid.

Answer 4

E. Laminin 5

Question 5

What is the most appropriate medication to control Bullous SLE

Answer 5

lesions respond to treatment with dapsone in the first 48 hours.

Question 6

prognosis of this condition sarcoid?

Answer 6

Good response after treatment; vigilance is recommended for local and systemic relapses

Question 7

In >90% of cases, scleromyxedema is associated with

Answer 7

an underlying paraproteinemia.2 This is usually a monoclonal gammopathy of immunoglobulin G lambda light chains.

Question 8

Severe systemic involvement may be seen with long-standing scleromyxedema, including

Answer 8

progressive pulmonary and renal disease, as well as a life-threatening dermatoneurologic syndrome marked by encephalopathy.

Question 9

This form of sarcoidosis typically presents with fever, polyarthralgias, uveitis, bilateral hilar adenopathy, fatigue, and erythema nodosum.

Answer 9

Löfgren syndrome—

Question 10

familial juvenile systemic granulomatosis,

Answer 10

Blau syndrome—

Question 11

strong association with sarcoidosis of the respiratory system 75%and 50% will have sarcoidosis of the upper respiratory tract.

Answer 11

Lupus pernio

Question 12

uveoparotid fever, this form of sarcoidosis typically presents with parotid gland swelling, lacrimal gland enlargement, uveitis, fever, and facial nerve palsy.

Answer 12

Heerfordt syndrome—

Question 13

autosomal dominant syndrome caused by mutations in CARD15/NOD2

Answer 13

Blau syndrome

Question 14

presents early in life with granulomatous dermatitis, recurrent uveitis, symmetric arthritis, and rarely systemic involvement.

Answer 14

Blau syndrome

Question 15

form of sarcoidosis typically presents with bilateral involvement of the parotid, submandibular, sublingual, and lacrimal glands.

Answer 15

Mikulicz syndrome—

Question 16

monoclonal gammopathy of immunoglobulin G lambda light chains. Diagnosis is best made by

Answer 16

performing serum protein electrophoresis and immunofixation for screening. A urine protein electrophoresis is also useful to rule out the presence of Bence–Jones proteins

Question 17

Hypocalcemia— can occur in sarcoidosis.

Answer 17

F . Hypercalcemia, not hypocalcemia,

Question 18

increased angiotensin-converting enzyme level that may be used to follow the clinical course.

Answer 18

Sarcoidal granulomas produce angiotensin-converting enzymes, and 60% of patients

Question 19

Hypercalcemia occurs in ?% of patients with sarcoidosis.

Answer 19

11%

Question 20

Sarcoidal granulomas up-regulating calcium absorption from the bowel via?

Answer 20

contain the enzyme 1-alpha hydroxylase, converts vitamin D to its active form

Question 21

Necrotizing sialometaplasia NSM pathogenesis is considered to result from

Answer 21

ischemia.

Question 22

local trauma predisposing factors described are dental injection, denture, and anesthesia injection.1 Upper respiratory infection, cocaine use, smoking, allergy, and general factors related to autonomic neuropathy, such as diabetes, arteriosclerosis, and malnutrition

Answer 22

Necrotizing sialometaplasia NSM

Question 23

Five histologic stages are described: infarction, sequestration, ulceration, reparative stage, and healed stage.

Answer 23

NSM

Question 24

prognosis of NSM

Answer 24

excellent, and spontaneous resolution usually occurs within weeks.

Question 25

mild to moderate sensorineural hearing loss is also often associated with typical Vohwinkel syndrome

Answer 25

T. Ichthyosis is not observed.

Question 26

periodontitis is observed in early infancy

Answer 26

Papillon–Lefèvre syndrome

Question 27

PPK is observed, but sparse scalp hair and dysplastic nails

Answer 27

Clouston syndrome

Question 28

PPK with constricting bands encircling all fingers to varying degrees along with ichthyosis but without hearing loss is a unique clinical feature

Answer 28

loricrin keratoderma

Question 29

variant form of Vohwinkel syndrome.

Answer 29

Loricrin keratoderma

Question 30

Constricting bands (pseudoainhum) are ringlike constrictions around the digits, limbs, or trunk, occurring both congenitally and in association with a wide variety of hereditary and nonhereditary disorders. Collodion baby is sometimes reported in the disease.3 The disease is an autosomal dominant genodermatosis.

Answer 30

Loricrin keratoderma

Question 31

causative gene of PLS

Answer 31

CTSC—

Question 32

causative gene of autosomal recessive congenital ichthyoses, including harlequin ichthyosis, lamellar ichthyosis, and congenital ichthyosiform erythroderma.

Answer 32

ABCA12

Question 33

causative gene of loricrin keratoderma (the variant form of Vohwinkel syndrome).

Answer 33

LOR.

Question 34

GJB2

Answer 34

causative gene of typical Vohwinkel syndrome and KID syndrome.

Question 35

GJB6

Answer 35

causative gene of Clouston syndrome.

Question 36

Granular nuclear positivity to LNA antigen

Answer 36

highly sensitive and specific for HHV-8 infection and KS

Question 37

distinguish KS from its histologic mimickers: kaposiform hemangioendothelioma, spindle cell hemangioma, pyogenic granuloma, and bacillary angiomatosis.

Answer 37

IHC instead of polymerase chain reaction (PCR) against HHV-8 because PCR can result in false positive reactions related to nonspecific amplification.

Question 38

allergen responsible for contact dermatitis from poison ivy

Answer 38

Urushiol—

Question 39

Antimalarials, minocycline, amiodarone, and chlorpromazine

Answer 39

pigmentation of the skin

Question 40

treatment of argyria

Answer 40

Q-switched laser | sun avoidance and sunscreens

Question 41

best therapeutic option Eccrine nevus

Answer 41

intracutaneous injections of botulinum toxin type A

Question 42

Eosinophilic pustular folliculitis Screen

Answer 42

for HIV infection

Question 43

Classic EPF must be differentiated from HIV-associated EPF

Answer 43

antiretroviral treatment is crucial for the latter.

Question 44

HIV-associated EPF tends to appear when the level of CD4+ lymphocytes is

Answer 44

<300 cells/mm3.

Question 45

Elephantiasis nostras verrucosa occurs in the setting of

Answer 45

1) chronic obstruction of lymphatic drainage, leading to chronic lymphedema, enlargement of the affected tissue, and repeated lymphangitis. 2) Obesity is believed to be an important factor, facilitating increased interstitial and intravascular pressure. 3) Cutaneous and connective tissue changes subsequently occur, resulting in hypertrophy, verrucous plaques, and fibrosis. These changes can also worsen lymphatic obstruction.

Question 46

Elephantiasis nostras verrucosa treatment

Answer 46

- Compression wraps reducing or decreasing progression of the lymphedema - antibiotics if there is a concern for bacterial lymphangitis or cellulitis - pneumatic compression devices, and keratolytics. - Oral retinoids and surgical intervention

Question 47

. Perivascular basophilic rods in the papillary dermis—Incorrect.

Answer 47

invasive Gram-negative bacilli. One example is Pseudomonas aeruginosa, which is the most common causative agent of ecthyma gangrenosum.1

Question 48

Multinucleated keratinocytes with nuclear molding

Answer 48

herpes simplex virus,

Question 49

Bipolar-staining inclusion bodies in histiocytessafety pin–shaped inclusion bodies, known as Donovan bodies,

Answer 49

granuloma inguinale

Question 50

Psoriasiform hyperplasia with a plasma cell infiltrate

Answer 50

syphilis skin lesions