Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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
What are the key facts about clinical history of allergic contact dermatitis?
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
26
What are the histopathologic features of: acute contact dermatitis? subacute dermatitis? chronic dermatitis?
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
27
How do you treat contact dermatitis?
identify irritant or allergen topical/oral corticosteroids antihistamines antipruritic lotion
28
What are the findings on a physical exam of an individual with Urticaria?
Wheals and dermographism
29
What is the histopathology of urticaria/angioedema
Edema of dermis and subcutanous tissue Mixed inflammatory cell infiltrate around dermal blood vessels
30
What is the pathophysiology of urticaria/angioedema?
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
31
Urticaria treatment
Antipruritic lotions Antihistamines Epinephrine if there is anaphylaxis
32
What is the site of disease for acne vulgaris?
The pilosebaceous unit (hair follicle and attached sebaceous gland)
33
What is the clinical findings distribution of acne vulgaris?
face, neck, ears, upper chest, back and arms
34
What is the "beard distribution" about and what causes it?
This is acne that appears around the jaw line. It is found in women who are in a hyperandrogenic state
35
What are the four types of rosacea and describe them?
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
36
What causes warts?
Warts are caused by HPV (Human Papilloma Virus)
37
What type of a virus is HPV? And describe its class
HPV is a papovirus - slow growing, double stranded, naked (lack envelop) DNA virus
38
Where do warts occur?
Warts occur anywhere on skin or on mucous membranes. Genital HPV is associated with sexual activity
39
How does HPV cause damage to the skin or lead to warts?
It infects the epidermis or dermis layer only. It infects cells in the upper epidermal layers - causing proliferation and hyperkeratosis (accumulation of keratin)
40
What are the three presentation levels in HPV infection?
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
List the types of warts?
Verruca valguris - common warts Verruca plana - flat warts Verruca plantaris - plantar warts Condyloma accuminata - genital warts
42
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?
Flat warts Often found in kids and yound adults Described as small flat topped papules Commonly seen on the face, legs and arms
43
What is a plantar wart?
This is a wart seen on the feet. It often appears at pressure points
44
What is a mosaic wart?
This is a coalesced group of warts
45
What is a myrmecia?
This is a deep, dome shaped, often inflammed wart
46
Which HPV subtypes are associated with Genital warts?
HPV 16 and 18
47
The HPV high risk subtypes are associated with genital warts and also...............?
dysplasia that may progress to malignancy --\>Example - cervical cancer Periungual squamous cell carcinoma
48
Describe the wart pathology?
Hyperkeratosis and parakeratosis Increased stratum granulosum layer Increased capillaries in the papillary dermis
49
What's the treatment for warts?
Some spontaneouly regress Topical tx - cryotherapy (freezing), cantharadin (blistering), imiquimod - Aldara (topical immune modulator Surgery Laser Oral cimetidine, ranitidine Duct tape
50
What causes molluscum contagiosum?
It is caused by molluscum contagiousum virus - a poxvirus
51
How is molluscum contagiosum trasmitted?
Molluscum contagiosum is transmitted by skin to skin contact
52
Who is most commonly affected by molluscum contagiosum?
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
What is the clinical appearence of molluscum contagiosum?
Dome-shaped, flesh colored papules Central umbilication Crusting and erythema if irritated Molluscum dermatitis - surrounding erythema like reaction
54
What is the pathology of molluscum contagiosum?
Epidermal thickening - Acanthosis Cup shaped Molluscum bodies present in spinous layer of epidermis - cytoplasmic inclusions in the spinous cells
55
What is the function of melanocytes and where do they originate?
Melanocytes produce pigment and they originate from the neural crest and migrate to epidermis, dermis, retina, inner ear, leptomeninges
56
What is a junctional nevi and what are its characteristics?
A type of benign nevi These are flat and brown characterized by melanocytic nests present to the dermo-epidermal junction
57
What is an intradermal nevi and what are its characteristics?
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
What is a compound nevi and what are its characteristics?
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
What type of congenital melanocytic nevi has the higherst melanoma risk?
The large or giant type (\>20cm) especially if it is a midline lesion
60
Why is a blue nevi blue and where on the body is it commonly found?
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
What kind of nevi has a "fried egg" appearence - raised center with macular border
Dysplastic nevi - irregular border and color, greater than 6mm
62
What is Familial atypical mole-melanoma syndrome?
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
What genes are associated with Familial Atypical Mole-Melanoma Syndrome?
CDKN2a - a tumor suppresor. Mutation causes abnormal proliferation of melanocytes. Certain mutations are also associted with PANCREATIC CANCER CDK4
64
Two relatives with melanoma, dysplastic nevi, Fhx of pancreatic cancer. What are you most likely worried about?
This person possible inheritedthe CDKN2A mutation --\> Familial Atypical Mole-Melanoma syndrome
65
What is the most commonly found somatic mutation in melanoma? What is the treatment for melanomas positive for this mutation
BRAF Verumafinib
66
What are the subtypes of melanoma?
Superficial spreading Nodular Lentigo maligna Acral lentiginous Amelanotic
67
What are the characteristics of superficial spreading melanoma
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
Nodular melanoma
Usually only a papulle - friable, fungating or ulcerated. Bleeding seen later in course Common in men Seen in sun-exposed areas
69
What subtype of melanoma is most common in dark or Asian patients? And common site on the body Metastasis?
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
What is a subungual melanoma
This is a melanoma of the nail bed Can mimick wart, traumatic hematoma, KS(?) Hutchinson's sign
71
What is Hutchinson's sign?
This is pigmentation of proximal nail bed fold at the end of a pigmented band, suggestive of melanoma
72
What are the characteristics of Lentigo maligna What is the common site
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
What is Lentigo maligma melanoma
Lentigo maligna that has developed an invasive component
74
Amelanotic melanoma
Doesnt really look like a melanoma - can mimick PG(?) and BCC(?) Differs in its lack of color Seen in patients with albinism
75
What are the factors considered in staging and prognosis of melanoma?
Lymph node status (most important prognostic factor) Organ metastases Mitoses in the lesion on histology Thickness of the tumor
76
What is Breslow's depth?
It says how deeply tumor cells are going in the skin (thickness of the tumor). Used as part of prognosis
77
In melanoma, what indicates an increased risk of metastasis?
Lymph nodes are enlarged and felt by touch Tuumor is thicker than 1mm Advanced tumor or patient has indicating symptoms
78
What is a sentinel lymph node?
This is the first lymph node that is draining a cancer. Highest probability of finding metastases
79
What is the most important prognostic factor in melanoma?
Lymph node status
80
Describe the pathogenesis of acne? Include the 4 main factors that are involved in the development of acne
1) Epidermal proliferation 2) Increased sebum production 3) Proprionibacterium acnes bacteria (P. acnes) 4) Inflammation
81
What stimulates sebum production?
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
What are the histologic features of a dysplastic nevi?
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
Describe the shoulder phenomenon and in what type of lesions is it found?
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
Which subtype of melanoma has no radial growth phase?
Nodular melanoma Other melanomas have a radial in situ growth phase before they develop into an invasive tumor
85
86
87
88

Dermatology and Musculoskeletal (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions