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FPP MSS > Skin Disorders > Flashcards

Skin Disorders Flashcards

1
Q

What is Pemphigus Vulgaris?

A

An acquired autoimmune bullous disease that attacks desmosomal proteins (Desmoglein 1 and 3)

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2
Q

What are the clinical features of Pemphigus Vulgaris?

A

It causes intra-epidermal blisters that are fragile and easily ruptured. There are oral and mucosal lesions as well as a positive Nikolsky’s sign.

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3
Q

What is the treatment for Pemphigus Vulgaris?

A

Prednisone, Azathioprine, Mycophenolate Mofetil, Rituximab (Immune suppression)

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4
Q

What is Ichthyosis Vulgaris?

A

Autosomal dominant genetic condition caused by mutation in Profilaggrin gene. Results in defective filaggrin protein that is part of keratohyalin granules.

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5
Q

What are the clinical features of Ichthyosis Vulgaris?

A

Fish scales - especially on shins
Dry skin
Hyperlinear palms

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6
Q

What other conditions are associated with Ichthyosis Vulgaris?

A

Allergic Rhinitis
Atopic dermatitis
Food Allergies
Asthma

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7
Q

What is Marfan Syndrome caused by?

A

Autosomal dominant mutation in Fibrillin

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8
Q

What are clinical features of Marfan’s?

A

There is variable expression including octopi lentis, myopia, long digits, flexible joints, aortic dilation, mitral valve prolapse and striae

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9
Q

What causes Ehlers-Danlos syndrome?

A

It is a group of inherited tissue disorders caused by abnormalities of collagen structure, production, processing and assembly.

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10
Q

Etiology of Morphea?

A

Acquired autoimmune disease that causes sclerosis (thickening of collagen).

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11
Q

What are the clinical features of Morphea?

A

There is localized sclerodoma. It starts as violaceous plaques and later on develops sclerotic plaques. There can be limb/joint complications or neurologic involvement.

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12
Q

Who is affected most by Morphea?

A

Women

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13
Q

What is Systemic Sclerosis?

A

Autoimmune disease that causes widespread sclerosis

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14
Q

What are the clinical features of Systemic Sclerosis?

A 
Sclerosis of skin
Sclerodactyly
Microstomia
Raynaud's phenomenon
Telangiectasia
Arthritis
Internal organ involvement
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15
Q

What is Erythema Nodosum?

A

Reactive Panniculitis caused by primary Streptococcal pharyngitis, Oral contraceptives, IBD or malignancy

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16
Q

What are clinical features of Erythema Nodosum?

A

Tender red nodules on the shins of women.

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17
Q

Histologically what is seen in Erythema Nodosum?

A

Increased numbers of inflammatory cells in the fat.

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18
Q

What is Bullous Pemphigoid?

A

The most common autoimmune bullous dermatosis. Caused by autoantibodies to BP antigen 1 (230) and BP antigen 2 (180)

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19
Q

Who normally gets Bullous Pemphigoid?

A

Elderly

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20
Q

What are clinical features of Bullous Pemphigoid?

A

Starts with pruritic urticaria without blistering –> becomes tense blisters with serous or rarely hemorrhagic content that appear in phases (STABLE blisters because consists of entire epidermis)

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21
Q

What does DIF testing for Bullous Pemphigoid show?

A

Linear deposits of IgG and C3 along BMZ.

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22
Q

What does Indirect IF show for Bullous Pemphigoid?

A

Linear staining on epidermal side of salt-split skin.

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23
Q

How does ELISA relate to severity of BP?

A

Number of BP 180/230 on ELISA correlates positively with disease activity.

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24
Q

Between bullous pemphigoid and pemphigus vulgaris, which has a better prognosis?

A

Bullous Pemphigoid

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25
Q

How is Bullous Pemphigoid treated?

A

Oral steroids and other immunosuppressants for severe disease. Less severe cases are treated with high potency steroids.

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26
Q

What do you see histologically for Bullous Pemphigoid?

A

Clear separation of epidermis and dermis.

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27
Q

What is Generalized Atrophic Benign Epidermolysis Bullosa?

A

Caused by mutated protein BP 180 (antigen 2) as known as Collagen type 17. It causes loss of hair, teeth and skin lesions.

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28
Q

What is Mucous Membrane Pemphigoid?

A

It is caused by an autoantibody against bullous pemphigoid antigen 180. (Subsets have autoantibodies against BP 230, integrin B4 and laminin 332).

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29
Q

What are clinical features of Mucous Membrane Pemphigoid?

A

Recurrent blistering of mucous membranes and skin. Patients develop scars, strictures, synechiae and blindness.

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30
Q

What is associated with MMP anti-laminin 332?

A

In 30% of case there is an association with malignancy.

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31
Q

What is Herlitz Junctional Epidermolysis Bullosa (EB)?

A

Inherited mutation of laminin 332 that causes terrible disease and high mortality.

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32
Q

What is Epidermolysis Bullosa Acquisita?

A

Acquired autoimmune disease with autoantibodies against type VII collagen.

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33
Q

What are clinical features of Epidermolysis Bullosa Acquisita?

A

Blisters, scarring, mutilation of fingers from slight trauma (Mechanically stressed areas). Healing of lesions leaves atrophy, milia, scars, pigmentation disorders. Often oral mucosa is involved.

34
Q

What is Inherited Epidermolysis Bullosa?

A

A skin fragility disease caused by mutations in genes encoding BMZ proteins. Targeted proteins include Keratin 5, Laminin 332, Collagen 7 and 17, a6B4, and plectin.

35
Q

What does TSC2 mutation cause?

A

Tuberous Sclerosis - TSC2 is Tuberin. (TSC1 is Hamartin)

36
Q

What is Tuberous Sclerosis?

A

Autosomal dominant disorder caused by mutation in TSC1 (Hamartin) or TSC2 (Tuberin) that causes non malignant tumors of the brain, eyes, heart, kidney, skin and lungs

37
Q

What are clinical features of Tuberous Sclerosis?

A

Hypopigmented macules (3 or more)
Angiofibromas and Fibrous plaque
Shagreen patch (flesh colored elevation)
Periungal fibromas

38
Q

What is Telogen Effluvium?

A

A stressor causes more hairs to enter Telogen phase –> excessive hair loss. Common after birth of baby or during febrile virus of children.

39
Q

What is Alopecia areata?

A

It is an autoimmune condition characterized by smooth patches of alopecia and nail pitting.

40
Q

How is Alopecia areata treated?

A

Topical corticosteroids

41
Q

What is Tinea Versicolor?

A

This is skin reaction caused by Malassezia yeast. It is characterized by round scaly patches of hyper pigmented or hypo pigmented skin.

42
Q

What is Vitiligo?

A

T cell mediated autoimmune disorder that destroys melanocytes and causes depigmented patches. It is acquired (not present at birth) and progressive. (Different from Piebaldism)

43
Q

What is Oculocutaneous Albinism?

A

Genetic disorder caused by TYR defect (Tyrosinase) that impairs Melanin production. Light skin and hair, lens defect.

44
Q

What are Ephelides?

A

Freckles - sun damage

45
Q

What are cafe au lait spots?

A

These are brown spots seen in Neurofibromatosis 1.

46
Q

What is Neurofibromatosis 1?

A

Autosomal dominant mutation in Neurofibromin that causes cafe au lait spots, neurofibromas and axillary/inguinal freckling.

47
Q

What is Solar Lentigo?

A

Age spots caused by sun exposure - bigger than elphides.

48
Q

What is Dermal Melanocytosis?

A

Mongolian spots - commonly in the lumbosacral location that fade over time.

49
Q

What are Melanocytic Nevi?

A

Moles - either junctional, compound or intradermal. Junctional tend to be flat and intradermal tend to be raised.

50
Q

What is Piebaldism?

A

Autosomal dominant disorder caused by mutation in KIT oncogene (Tyrosine Kinase signaling receptor) –> Causes impaired melanocyte migration. It is present at birth and NOT progressive (in contrast with Vitiligo)

51
Q

What is Waardenburg Syndrome?

A

Autosomal dominant rare disease caused by Pax3 mutation –> results in abnormal development of melanocytes –> causes achromia, deafness, heterochromia irides and dystopia canthorum

52
Q

What is Port-Wine Stain?

A

Capillary malformation in dermis that results in ecstatic, dilated vessels. It is present at birth and darkens over time. There is V1 distribution that may involve ocular conjunctiva, V2 distribution that doesn’t have complications normally, and V3 distribution that involves oral mucosa.

53
Q

What is Sturge-Weber Syndrome?

A

It is most commonly associated with the V1 dermatome and results in neurological deficits like seizures, migraines, developmental delay and tram track calcifications. It also has ocular defects like glaucoma and increased choroidal vascularity which causes ketchup tomato spots.

54
Q

What is Infantile Hemangioma?

A

It is the most common vascular tumor. It is composed of proliferating endothelial like cells that become visible within first months of life. They first appear as white patch and then begin to grow and slowly involute.

55
Q

What is PHACE syndrome?

A

When babies have big facial hemangiomas it is often associated with other problems. Posterior fossa abnormalities, Hemangiomas, Arterial anomalies, Cardiac anomalies, Eye anomalies and Sternal clefting/Supraumbilical raphe

56
Q

What is hypohidrotic Ectodermal Dysplasia?

A

X linked recessive condition. Most common form of Ectoermal Dysplasia - frontal bossing, low ears, flattened nasal bridge, sparse hair, decreased ability to sweat,

57
Q

What is treatment for Hypohidrotic Ectodermal Dysplasia?

A

Avoid overheating and consult dentistry

58
Q

What is the use of topical steroids in Psoriasis and what are the S/E?

A

Anti-inflammatory

S/E: Skin atrophy, hypopigmentation, striae

59
Q

What is the use of Calcipotriene in Psoriasis? What are it’s S/E?

A

Immunomodulator that inhibits keratinocyte proliferation.

S/E include skin irritation and photosensitivity

60
Q

What is the use of Tazarotene in Psoriasis? What are it’s S/E?

A

It is a topical retinoid that inhibits keratinocyte proliferation. S/E include skin irritation and photosensitivity.

61
Q

What is the use of Salicylic or Lactic acid in Psoriasis? What are S/E?

A

It is keratolytic (not used that much anymore). S/E include possibility of systemic absorption.

62
Q

What is the use of Calcineurin inhibitors in Psoriasis? What are the S/E?

A

It has anti-inflammatory effects and S/E include skin burning and itching.

63
Q

What are Systemic therapies for Psoriasis?

A

Phototherapy (Narrowband UVB or Psoralen +UVA), Methotrexate, Cyclosporine, Acitretin, TNF alpha blockers

64
Q

What is Lichen Planus?

A

Inflammatory disease of skin, hair, nails, mucous membranes that is Planar, Polygonal, Pruritic, Purple Papules or Plaques.

65
Q

What are Wichman’s Striae?

A

Found in Lichen Planus - network of grayish streaks over surface of papules

66
Q

What kinds of things are associated with Lichen Planus?

A

Hepatitis C virus, Hepatitis B vaccine and drugs like ACE inhibitors, beta blockers, thiazide diuretics, antimalarials

67
Q

Besides skin, in which areas do you find Lichen Planus?

A

Nail Lichen Planus, Mucosal Lichen Planus (oral)

68
Q

What are the types of Mucosal Lichen Planus?

A

Reticulated is a linear lace-like pattern of tiny white papules in buccal area that is typically asymptomatic. Erosive is on gingiva or tongue and is typically painful.

69
Q

What are the treatments for Lichen Planus?

A

Topical corticosteroids, Topical calcineurin inhibitors, NBUVB phototherapy or systemic drugs.

70
Q

What characterizes Infant Atopic Dermatitis?

A 
Facial involvement predominates early
Spares midface
Oozing, crusting common
Exacerbated by saliva, foods
Extensor involvement in late infancy
SPARING of diaper area
71
Q

What characterizes Childhood Atopic Dermatitis?

A

Flexural involvement (wrists, ankles, popliteal/antecubital fossa)
Neck
Hands
Less crusting than Infant form

72
Q

What characterizes Adult Atopic Dermatitis?

A

75% outgrow atopic dermatitis
Adult AD is usually chronic and severe
Limited to hands or more generalized

73
Q

What are Dennie-Morgan folds?

A

Folds under eyes seen in Atopic Dermatitis

74
Q

What is a possible complication of Atopic Dermatitis?

A

Secondary infection with Staph or strep

Infection with Herpes Simplex Virus that becomes widespread (Eczema Herpeticum)

75
Q

How do you manage atopic dermatitis topically?

A

Corticosteroid ointment

Immunomodulators like Tacrolimus (Calcineurin inhibitors)

76
Q

How do you treat the flare of atopic dermatitis?

A

Topicals, Antihistamines and Treat secondary infections (bleach baths)

77
Q

What are factors you need to consider when choosing topicals to treat atopic dermatitis?

A

Location and Duration (New lesions respond to weaker agents, thin skin has higher risk for side effects)

78
Q

What is Seborrheic dermatitis?

A

Cradle cap - inflammatory condition that affects scalp, face and torso.

79
Q

What is the infant form of Seborrheic Dermatitis?

A

Presents as yellow, greasy adherent scale on scalp.
Evolves to moist erythematous intertriginous patches in some.
Dissemination with scaly papules, patches and plaques resembling atopic dermatitis may occur.

80
Q

What is the adult form of seborrheic dermatitis?

A

Yellow-red papules
Erythema and scaling
Located on scalp primarily, sometimes face and trunk.

81
Q

How do you treat Seborrheic Dermatitis?

A

Infants - low potency topical steroid, sometimes just gentle skin care
Adults - relapse is common, treat with azole shampoo, low potency topical steroid or shampoo.

FPP MSS (6 decks)

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