Brainscape's Knowledge GenomeTM

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


See full index

Dermatology and Musculoskeletal > Dermatology Week 1 > Flashcards

Dermatology Week 1 Flashcards

1
Q

What is psoriasis?

A

Chronic papulosquamous skin disease of unknown etiology

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

How does psoriasis present?

A

Psoriasis presents as well defined red plaques with silvery scale

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

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

What form of psoriasis is the most common in children?

A

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

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

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

What are the triggers of psoriasis?

A

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

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

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

A

Psoriasis

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

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

What are the symptoms of Psoriasis?

A

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

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

What is atopy?

A

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

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

What’s the atopic march and what are the steps

A

atopic dermatitis –> asthma –> allergic rhinitis

“DAR” - Dermatitis-Asthma -allergic Rhinitis

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

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

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

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

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

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

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

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

A

Temperature, wool, stress, soap

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

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

A

Spongiosis (intra-epidermal edema) and acanthosis

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

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

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

What is the standard treatment of atopic dermatitis?

A

Address sleep issues

Nutritional advice

topical steroid

topical or oral antibiotics

Oral antihistamines

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

What type of a reaction is allergic contact dermatitis?

A

Type 4 hypersensitivity reaction

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

What are the two phases of allergic contact dermatitis?

A

1) Sensitization phase
2) Elicitation phase

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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

How do you treat contact dermatitis?

A

identify irritant or allergen

topical/oral corticosteroids

antihistamines

antipruritic lotion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

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

A

Wheals and dermographism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is the histopathology of urticaria/angioedema

A

Edema of dermis and subcutanous tissue

Mixed inflammatory cell infiltrate around dermal blood vessels

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Urticaria treatment

A

Antipruritic lotions
Antihistamines

Epinephrine if there is anaphylaxis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is the site of disease for acne vulgaris?

A

The pilosebaceous unit (hair follicle and attached sebaceous gland)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is the clinical findings distribution of acne vulgaris?

A

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

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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
Q
A
86
Q
A
87
Q
A
88
Q
A

Dermatology and Musculoskeletal (10 decks)

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