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Dermatology and Musculoskeletal > Dermatology Week 1 > Flashcards

Dermatology Week 1 Flashcards

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1
Q

What is psoriasis?

A

Chronic papulosquamous skin disease of unknown etiology

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2
Q

How does psoriasis present?

A

Psoriasis presents as well defined red plaques with silvery scale

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3
Q

At what age is psoriasis most likely to be seen? Sex predominance?

A

20s and 50s. Although it can be found in individuals of any age. M=F

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4
Q

What form of psoriasis is the most common in children?

A

Guttate psoriasis - appears as little dots as like a paint brush

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5
Q

Describe the pathogenesis of Psoriasis

A

T cells are the driving force (mostly Th1 more than Th2) and significant amount of T cells are present in the dermis and epidermis. Also immune dysregulation leads to increase in inflammatory mediators leading to epidermal proliferation, differentiation and angiogenesis

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6
Q

What are the triggers of psoriasis?

A

external trauma (Koebner phenomenon), infections (esp strep pharyngitis), HIV disease, hypocalcemia, stress, drugs, alcohol, smoking

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7
Q

Sharply demarcated thick skin + silvery scale are characteristics of what dermatological lesion?

A

Psoriasis

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8
Q

What is Auspitz sign?

A

This is when bleeding is present after you scrap a psoriasis lesion. It shows that presence of angiogenesis in the disease

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9
Q

What are the symptoms of Psoriasis?

A

Frequent itch, occasionally painful. Improved in the summer and worse during the winter.

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10
Q

What is atopy?

A

Tendancy towards allergic diseases like allergic rhinits, asthma, atopic dermatitis

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11
Q

What’s the atopic march and what are the steps

A

atopic dermatitis –> asthma –> allergic rhinitis

“DAR” - Dermatitis-Asthma -allergic Rhinitis

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12
Q

What is involved in the pathogenesis of atopic dermatitis? Key players

A

1) T cells activation leading to increased IgE
2) Hyperresponsive dendritic cells aka langerhan cells (these are antigen presenting cells) – they meet the allergen and present it to the T cells leading to increased IgE
3) Defective epidermal barrier

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13
Q

What type of T cells are produced in acute vs chronic atopic dermatitis

A

In acute dermatitis there is increaed Th2 cells –> increased IL-4 which triggers B cells to make IgE –> increased IgE (seen during disease flares)

In chronic atopic dermatitis there is increased Th1 cells

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14
Q

What are the characteristic features of the defective barrier seen in Atopic dermatitis?

A

The epidermis has decreased CERAMIDES - affecting barrier function and inflammatory response

Dry skin

Increased transepidermal water loss

Increased penetration of irritants, allergens and microbes

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15
Q

What are some of the triggers of Acute Dermatitis?

A

Food allergens, aeroallergens

Infection (Staph aureus, cutaneous viruses)

Animal dender

Pollen

Dust mites

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16
Q

Why is there increased cutaneous infections in patients with Atopic dermatitis?

A

Loss of the epidermal barrier

There is also lack of innate antimicrobial peptides in skin like beta defensins and cathelicidines that are produced by keratinocytes

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17
Q

What is the the classic clinical history or presentation characteristics of a patient with atopic dermatitis

A

Pruritis

Usually in the first two years of life

Dry skin

Personal or family hx of atopy

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18
Q

Give examples of things that can worsen the itch in acute dermatitis?

A

Temperature, wool, stress, soap

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19
Q

In a histopathologic section of atopic dermatitis, what are the key characteristics of atopic dermatitis?

A

Spongiosis (intra-epidermal edema) and acanthosis

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20
Q

What’s the prognosis of atopic dermatitis?

A

It exacerbates and remitts. Improves by 3-4 years. An infant unlikely to have AD as an adult

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21
Q

What are the general skin care principals for Acute Dermatitis

A

Hydration is very important

Avoid long hot showers

Avoid soap, especially fragranced

Apply think emollients to help with barrier - some of these replace absent ceramides

Bleach baths reduce staph infection and help with atopic dermatitis

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22
Q

What is the standard treatment of atopic dermatitis?

A

Address sleep issues

Nutritional advice

topical steroid

topical or oral antibiotics

Oral antihistamines

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23
Q

What type of a reaction is allergic contact dermatitis?

A

Type 4 hypersensitivity reaction

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24
Q

What are the two phases of allergic contact dermatitis?

A

1) Sensitization phase
2) Elicitation phase

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25
Q

What are the key facts about clinical history of allergic contact dermatitis?

A

Presence of pruritis or burning

Acutely lasts days to weeks, and chronically lasts months to years

First exposure - takes 7-10 days to react

Second exposure - takes 12 horus or more to react

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26
Q

What are the histopathologic features of:

acute contact dermatitis?

subacute dermatitis?

chronic dermatitis?

A

Acute - Spongiosis and vesicles in the epidermis, and lymphocytes in the dermis

Subacute - spongiosis but no vescicles, acanthosis, scale/crust

Chronic - psoriasiform, epidermal hyperplasia, parakeratosis, fibrosis

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27
Q

How do you treat contact dermatitis?

A

identify irritant or allergen

topical/oral corticosteroids

antihistamines

antipruritic lotion

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28
Q

What are the findings on a physical exam of an individual with Urticaria?

A

Wheals and dermographism

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29
Q

What is the histopathology of urticaria/angioedema

A

Edema of dermis and subcutanous tissue

Mixed inflammatory cell infiltrate around dermal blood vessels

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30
Q

What is the pathophysiology of urticaria/angioedema?

A

It is a type 1 immediate hypersensitivity reaction

Antigen binds to IgE on the surface of mast cells and basophils

This leads to activation, degranulation, release of vasoactive amines like histamine, leukotrienes and prostaglandins

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31
Q

Urticaria treatment

A

Antipruritic lotions
Antihistamines

Epinephrine if there is anaphylaxis

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32
Q

What is the site of disease for acne vulgaris?

A

The pilosebaceous unit (hair follicle and attached sebaceous gland)

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33
Q

What is the clinical findings distribution of acne vulgaris?

A

face, neck, ears, upper chest, back and arms

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34
Q

What is the “beard distribution” about and what causes it?

A

This is acne that appears around the jaw line. It is found in women who are in a hyperandrogenic state

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35
Q

What are the four types of rosacea and describe them?

A

1) Erythematotelangiectasis - redness, telangiectasias (dilated blood vessels)
2) Papulopustular - pimples, pustules, redness
3) Occular - eye irritation, conjuctival injection / bloodshot look
4) Rhinophymatous - thickening of the skin of the nose. Can also affect chin

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36
Q

What causes warts?

A

Warts are caused by HPV (Human Papilloma Virus)

37
Q

What type of a virus is HPV? And describe its class

A

HPV is a papovirus - slow growing, double stranded, naked (lack envelop) DNA virus

38
Q

Where do warts occur?

A

Warts occur anywhere on skin or on mucous membranes. Genital HPV is associated with sexual activity

39
Q

How does HPV cause damage to the skin or lead to warts?

A

It infects the epidermis or dermis layer only.

It infects cells in the upper epidermal layers - causing proliferation and hyperkeratosis (accumulation of keratin)

40
Q

What are the three presentation levels in HPV infection?

A

Clinical - infection is visible to the naked eye

Subclinical - infection is visible with the aid of diagnostics tools like acetic acid which causes whitening

Latent - virus present in apparently normal skin

41
Q

List the types of warts?

A

Verruca valguris - common warts

Verruca plana - flat warts

Verruca plantaris - plantar warts

Condyloma accuminata - genital warts

42
Q

Verruca plana

In what age group is it mostly seen?

Described the kind of lesion and what places of the body it is commonly found?

A

Flat warts

Often found in kids and yound adults

Described as small flat topped papules

Commonly seen on the face, legs and arms

43
Q

What is a plantar wart?

A

This is a wart seen on the feet. It often appears at pressure points

44
Q

What is a mosaic wart?

A

This is a coalesced group of warts

45
Q

What is a myrmecia?

A

This is a deep, dome shaped, often inflammed wart

46
Q

Which HPV subtypes are associated with Genital warts?

A

HPV 16 and 18

47
Q

The HPV high risk subtypes are associated with genital warts and also……………?

A

dysplasia that may progress to malignancy –>Example - cervical cancer

Periungual squamous cell carcinoma

48
Q

Describe the wart pathology?

A

Hyperkeratosis and parakeratosis

Increased stratum granulosum layer

Increased capillaries in the papillary dermis

49
Q

What’s the treatment for warts?

A

Some spontaneouly regress

Topical tx - cryotherapy (freezing), cantharadin (blistering), imiquimod - Aldara (topical immune modulator

Surgery

Laser

Oral cimetidine, ranitidine

Duct tape

50
Q

What causes molluscum contagiosum?

A

It is caused by molluscum contagiousum virus - a poxvirus

51
Q

How is molluscum contagiosum trasmitted?

A

Molluscum contagiosum is transmitted by skin to skin contact

52
Q

Who is most commonly affected by molluscum contagiosum?

A

Children - face, trunk extremeties

Sexually active young adults - genital lower abdomen, upper thighs

Immunocompromised CD4<100 - face, eyelids, genitals –> “giant mollusca”

4th group less likely than the groups above is eczema compromised skin

53
Q

What is the clinical appearence of molluscum contagiosum?

A

Dome-shaped, flesh colored papules

Central umbilication

Crusting and erythema if irritated

Molluscum dermatitis - surrounding erythema like reaction

54
Q

What is the pathology of molluscum contagiosum?

A

Epidermal thickening - Acanthosis

Cup shaped

Molluscum bodies present in spinous layer of epidermis - cytoplasmic inclusions in the spinous cells

55
Q

What is the function of melanocytes and where do they originate?

A

Melanocytes produce pigment and they originate from the neural crest and migrate to epidermis, dermis, retina, inner ear, leptomeninges

56
Q

What is a junctional nevi and what are its characteristics?

A

A type of benign nevi

These are flat and brown characterized by melanocytic nests present to the dermo-epidermal junction

57
Q

What is an intradermal nevi and what are its characteristics?

A

This is a raise, tan colored lesion

Made up of nests of melanocytes ONLY in the dermis.

Nests become smaller as you go down deeper into the dermis

58
Q

What is a compound nevi and what are its characteristics?

A

This is a raised lesion (papule or plaque), light to medium brown

Nests of melanocytes are at the junction of the epidermis and dermis, and also in the dermis

59
Q

What type of congenital melanocytic nevi has the higherst melanoma risk?

A

The large or giant type (>20cm) especially if it is a midline lesion

60
Q

Why is a blue nevi blue and where on the body is it commonly found?

A

It is blue because of the Tyndall effect (the transmission through the skin causes that color)

Most often found on the dorsal hands, feet, scalp, face

61
Q

What kind of nevi has a “fried egg” appearence - raised center with macular border

A

Dysplastic nevi - irregular border and color, greater than 6mm

62
Q

What is Familial atypical mole-melanoma syndrome?

A

This is a syndrome associated wth increased risk of dysplastic nevi and melanoma - it has numerous nevi (>50), melanoma in 1 or more relatives, nevi’s are histologically dysplastic

High risk for developing melanoma - 100% by 80 years

63
Q

What genes are associated with Familial Atypical Mole-Melanoma Syndrome?

A

CDKN2a - a tumor suppresor. Mutation causes abnormal proliferation of melanocytes. Certain mutations are also associted with PANCREATIC CANCER

CDK4

64
Q

Two relatives with melanoma, dysplastic nevi, Fhx of pancreatic cancer. What are you most likely worried about?

A

This person possible inheritedthe CDKN2A mutation –> Familial Atypical Mole-Melanoma syndrome

65
Q

What is the most commonly found somatic mutation in melanoma?

What is the treatment for melanomas positive for this mutation

A

BRAF

Verumafinib

66
Q

What are the subtypes of melanoma?

A

Superficial spreading

Nodular

Lentigo maligna

Acral lentiginous

Amelanotic

67
Q

What are the characteristics of superficial spreading melanoma

A

most common type

median age 50

upper back in both sexes, but women additionally found on legs

Radial (Horizontal) growth phase then veritcal growth phase with appearence of a nodule

Can show regression

68
Q

Nodular melanoma

A

Usually only a papulle - friable, fungating or ulcerated. Bleeding seen later in course

Common in men

Seen in sun-exposed areas

69
Q

What subtype of melanoma is most common in dark or Asian patients?

And common site on the body

Metastasis?

A

Acral lentiginous melanoma - its incidence is the same as whites with other melanomas

Median 50 yes, M=W

Growth is junctional, later vertical growth

In blacks, #1 site is the foot. Thumb and hallux are most often affected digits

Can metastasize to axillary and epitrochlear nodes - due to delayed diagnosis

70
Q

What is a subungual melanoma

A

This is a melanoma of the nail bed

Can mimick wart, traumatic hematoma, KS(?)

Hutchinson’s sign

71
Q

What is Hutchinson’s sign?

A

This is pigmentation of proximal nail bed fold at the end of a pigmented band, suggestive of melanoma

72
Q

What are the characteristics of Lentigo maligna

What is the common site

A

This is a IN SITU melanoma - resultof lentiginous proliferation of atypical melanocytes extending over at least 3 rete ridges in chronic sun damaged skin

Most commonly found in old patients with chronic sun exposure

Head is the common site

Slow growing with radial phase that can last 5-20 years

Proliferation is at the dermo-epidermal junction and the lesion can have indistinct borders (often larger than appears)

73
Q

What is Lentigo maligma melanoma

A

Lentigo maligna that has developed an invasive component

74
Q

Amelanotic melanoma

A

Doesnt really look like a melanoma - can mimick PG(?) and BCC(?)

Differs in its lack of color

Seen in patients with albinism

75
Q

What are the factors considered in staging and prognosis of melanoma?

A

Lymph node status (most important prognostic factor)

Organ metastases

Mitoses in the lesion on histology

Thickness of the tumor

76
Q

What is Breslow’s depth?

A

It says how deeply tumor cells are going in the skin (thickness of the tumor). Used as part of prognosis

77
Q

In melanoma, what indicates an increased risk of metastasis?

A

Lymph nodes are enlarged and felt by touch

Tuumor is thicker than 1mm

Advanced tumor or patient has indicating symptoms

78
Q

What is a sentinel lymph node?

A

This is the first lymph node that is draining a cancer. Highest probability of finding metastases

79
Q

What is the most important prognostic factor in melanoma?

A

Lymph node status

80
Q

Describe the pathogenesis of acne? Include the 4 main factors that are involved in the development of acne

A

1) Epidermal proliferation
2) Increased sebum production
3) Proprionibacterium acnes bacteria (P. acnes)
4) Inflammation

81
Q

What stimulates sebum production?

A

Androgens stimulate sebum production

Androgens are highest during first 6 months of life and during puberty

High androgens are found in infants, adrenarche (9-10 years), women with hyperandrogenic states “beard area”

82
Q

What are the histologic features of a dysplastic nevi?

A

Assymetric and broad

“Shoulder” phenomenon

Lentiginous melanocytic hyperplasia

Irregular shape and distribution of epidermal nests

Bridging of rete

Dermal fibrosis

Inflammatory infiltrate

Cytologic atypia of melanocytes

83
Q

Describe the shoulder phenomenon and in what type of lesions is it found?

A

The bridging phenomenon is found in compound dysplastic lesions

Epidermal component extends beyond the lateral border of the dermal nevus cells in compound lesions

84
Q

Which subtype of melanoma has no radial growth phase?

A

Nodular melanoma

Other melanomas have a radial in situ growth phase before they develop into an invasive tumor

85
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Dermatology and Musculoskeletal (10 decks)

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