Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Dermatology > Autoimmune > Flashcards

Autoimmune Flashcards

You may prefer our related Brainscape-certified flashcards:
Dermatology Board Prep flashcards
1
Q

What is Cutaneous Lupus Erythematosus (CLE)?

A

Cutaneous Lupus Erythematosus (CLE) is a diverse group of autoimmune connective tissue disorders localized to the skin, which can be associated with systemic lupus erythematosus (SLE) to varying degrees.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How is Cutaneous Lupus Erythematosus (CLE) classified?

A

Acute (ACLE)
Subacute (SCLE)
Intermittent (Lupus Tumidus)
Chronic (CCLE), which includes discoid lupus (DLE), lupus profundus, and chilblain lupus erythematosus.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the features of localized Acute Cutaneous Lupus Erythematosus (ACLE)?

A

Localized ACLE presents as a malar ‘butterfly’ rash, characterized by redness and swelling over both cheeks, sparing the nasolabial folds, and lasting hours to days.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the features of generalized Acute Cutaneous Lupus Erythematosus (ACLE)?

A

Generalized ACLE presents as diffuse or papular erythema of the face, upper limbs (sparing the knuckles), and trunk, resembling a morbilliform drug eruption or viral exanthem.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is Toxic Epidermal Necrolysis-like Acute Cutaneous Lupus Erythematosus?

A

Toxic Epidermal Necrolysis-like ACLE is associated with lupus nephritis or cerebritis and must be distinguished from drug-induced toxic epidermal necrolysis in a patient with SLE.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Where do SCLE skin lesions typically occur, and what triggers them?

A

SCLE skin lesions typically occur on the trunk and upper limbs and are triggered or aggravated by sun exposure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the common presentations of SCLE skin lesions?

A

SCLE presents as a psoriasiform papulosquamous rash or annular, polycyclic plaques with central clearing.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is Intermittent Cutaneous Lupus Erythematosus?

A

Intermittent Cutaneous Lupus Erythematosus, better known as lupus tumidus, is a dermal form of lupus erythematosus.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Discoid Lupus Erythematosus (DLE): Prevalence in CCLE

A

DLE is the most common form of CCLE, accounting for 80% of cases, particularly prevalent and severe in patients with skin of color.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

DLE: Lesion Characteristics

A

Presents as destructive scaly plaques with follicular prominence (carpet tack sign) which can result in scarring alopecia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Dermatomyositis: Gottron’s Sign

A

Violaceous erythematous papules over knuckles, elbows, knees, and malleoli.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Dermatomyositis: Nailfold Signs

A

Telangiectasia and hemorrhage on the nailfold.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Dermatomyositis: Heliotrope Erythema

A

Violaceous erythema and swelling of the upper part of the face, with potential involvement of the whole face, neck, and upper chest.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Dermatomyositis: Organ Involvement

A

Involves the heart (~40%), smooth muscles, lungs, and rarely the kidneys and liver; calcinosis of fasciae may occur.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Dermatomyositis: Diagnostic Tests

A

Elevated creatine kinase, aldolase, MRI of affected muscles, and possibly muscle biopsy. Important to search for tumors, especially in adults (≈ 50% are paraneoplastic).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Dermatomyositis: Initial Therapy

A

Corticosteroids at 1-2 mg/kg body weight to start.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Dermatomyositis: Immunotherapy

A

Intravenous immunoglobulins (2 mg/kg body weight/month for up to a year), methotrexate (15-25 mg/week), and mycophenolate.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Dermatomyositis: General Management

A

Rest in the beginning, with careful and mild physiotherapy as tolerated.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Morphea: Lesion Characteristics

A

Asymmetric sclerotic plaques, usually 2–15 cm in diameter.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Morphea: Active Lesion Appearance

A

Active lesions may have a lilac border with central hypo- or dyspigmentation; older lesions often become hyperpigmented.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Morphea: Depth of Sclerosis

A

Sclerosis may extend deeply into fat or underlying structures such as fascia, muscle, and bone, potentially causing disability.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Pemphigus Vulgaris: Demographic Associations

A

More common in Europeans and Indians compared to Africans.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Pemphigus Foliaceus: Demographic Associations

A

More common in Africans compared to Europeans and Indians; associated with HLA B8 in South Africa.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Pemphigus Vulgaris: Affected Areas

A

Affects skin and mucous membranes. Always check the mouth

25
Q

Pemphigus Vulgaris: Etiology

A

Caused by circulating IgG autoantibodies (90%) that bind to Desmoglein-3 (PV), a molecule involved in intercellular adhesion.

26
Q

Desmoglein-1 vs. Desmoglein-3 in Pemphigus

A

Desmoglein-1 is more associated with Pemphigus Foliaceus, while Desmoglein-3 is linked to Pemphigus Vulgaris.

27
Q

Pemphigus Foliaceus: Blister Visibility

A

Rarely visible blisters; often presents with more superficial erosions.

28
Q

Pemphigus Foliaceus: Localization

A

Often localized rather than widespread.

29
Q

Pemphigus Foliaceus: Oral Involvement

A

Oral involvement is very rare in Pemphigus Foliaceus

30
Q

Bullous Pemphigoid: Age Group

A

Primarily affects the elderly.

31
Q

Bullous Pemphigoid: Pathogenesis

A

Caused by IgG autoantibodies against BP230 and BP180 antigens, which are associated with hemidesmosomes.

32
Q

Bullous Pemphigoid: Blister Formation

A

Inflammation leads to the formation of subepidermal bullae.

33
Q

Bullous Pemphigoid: Initial Treatment

A

Managed with low-dose steroids, tapered within one week.

34
Q

Chronic Bullous Disease of Childhood: Age of Onset

A

Usually occurs before the age of 5 years

35
Q

Chronic Bullous Disease of Childhood: Affected Areas

A

Commonly affects the face and genital area.

36
Q

Chronic Bullous Disease of Childhood: Blister Pattern

A

New blisters form around healing old blisters, creating a “string of pearls” appearance.

37
Q

Chronic Bullous Disease of Childhood: Treatment Options

A

Treated with Dapsone or sulfapyridine; erythromycin or clarithromycin may also be used.

38
Q

Dermatitis Herpetiformis: Primary Symptom

A

Characterized by itchy blisters on extensor surfaces.

39
Q

Dermatitis Herpetiformis: Antibody Formation

A

Formation of IgA antibodies to gluten-tissue transglutaminase (t-TG) in the gut.

40
Q

Dermatitis Herpetiformis: Genetic Predisposition

A

Linked to a genetic predisposition for gluten sensitivity

41
Q

Dermatitis Herpetiformis: Cross-Reactivity

A

IgA antibodies cross-react with epidermal transglutaminase (e-TG), which is homologous to t-TG.

42
Q

Dermatitis Herpetiformis: Pathogenesis

A

Deposition of IgA and epidermal TG complexes in the papillary dermis causes the lesions of dermatitis.

43
Q

Epidermolysis Bullosa: Common Feature

A

Development of blisters following minor trauma or skin traction.

44
Q

Epidermolysis Bullosa Simplex (EBS)

A

Blisters form within the basal layer of the epidermis due to defects in keratin filaments, typically following minor trauma.(keratin 5 & 14)

45
Q

Junctional Epidermolysis Bullosa (JEB)

A

Blisters occur at the level of the lamina lucida within the basement membrane, often leading to severe and widespread blistering.

46
Q

Dystrophic Epidermolysis Bullosa (DEB)

A

Blisters form below the basement membrane in the upper dermis due to mutations in the collagen VII gene, leading to scarring

47
Q

EBS Weber-Cockayne: Affected Areas

A

Involvement of palms and soles; heat can exacerbate blistering and may lead to scarring.

48
Q

EBS Dowling-Meara (Herpetiformis): Onset and Mortality

A

Onset just after birth; slight mortality rate associated

49
Q

EBS Dowling-Meara: Blister Characteristics

A

Presents with herpetiform, hemorrhagic blisters on the trunk & Palmoplantar keratoderma, nail dystrophy, and mucosal erosions are common.

50
Q

Junctional EB (Herlitz): Severity and Onset

A

Most severe subtype, often lethal; onset at birth.

51
Q

Junctional EB (Herlitz): Clinical Features

A

Ulceration around the mouth, face, axilla, groin; oral blisters, dental anomalies, growth retardation.

52
Q

Junctional EB (Herlitz): Complications

A

Esophageal ulceration leading to malnutrition, anemia, pain, and respiratory difficulties.

53
Q

Junctional EB (Non-Herlitz): Clinical Features

A

Nail loss, scarring alopecia, modest mucosal involvement, and association with pyloric atresia.

54
Q

Dominant Dystrophic EB: Onset and Presentation

A

Onset at birth; widespread blisters that heal with scars and milia, leading to mutilation of fingers and toes.

55
Q

Dominant Dystrophic EB: Collagen Alteration

A

Caused by altered type VII collagen.

56
Q

Recessive Dystrophic EB (Hallopeau-Siemens): Collagen Absence

A

Caused by the absence of type VII collagen.

57
Q

Recessive Dystrophic EB (Hallopeau-Siemens): Onset and Severity

A

Onset at birth; similar to severe dominant dystrophic EB but with additional mucosal involvement, dental anomalies, scarring alopecia, anemia, and growth retardation.

58
Q

Dystrophic EB: Complications

A

Pseudosyndactyly of the hands and feet, also known as “mittens and socks” deformity.
SCC

59
Q

Epidermolysis Bullosa: General Treatment Approach

A

No cure for inherited EB; treatment focuses on managing clinical manifestations.

Dermatology (41 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions