Derm Intro and Common Dermatoses I and II Flashcards

1
Q

Three main ways to describe/characterize skin lesions

A

(1) Morphology of the primary lesion
- elevated, flat, depressed
- size
- color
- secondary characteristics

(2) Configuration
- shape
- border

(3) Distribution

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2
Q

Differentiate primary and secondary lesions

A

Primary lesions = what came first

  • secondary lesions = a process that happens to the primary lesion
    ex: scabbing, inflammation, scale, crust, scar, erode, ulcer
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3
Q

Name the primary lesion:

Flat less than 1 cm

A

Macule = flat lesion

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4
Q

Name the primary lesion:

Flat > 1 cm

A

Patch = flat lesion > 1 cm

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5
Q

Name the primary lesion:

Raised less than 1 cm

A

Papule = raised

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6
Q

Name the primary lesion:

Raised > 1 cm

A

Plaque = raised > 1 cm

think plaques are raised off the wall

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7
Q

Name the primary lesion:

Blister less than 1 cm

A

Vesicles = blisters

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8
Q

Name the primary lesion:

Blister > 1 cm

A

Bullae = blisters > 1 cm

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9
Q

Define acral

A

= type of distribution on the hands and feet

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10
Q

Define koebnerizing

A

= skin lesions appearing on lines of trauma

-can be spread in linear patterns by self-scratching

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11
Q

Where is the lesion in a macule?

A

Macule = flat lesion less than 1 cm

-lesion is superficial: in the epidermis or superficial dermis

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12
Q

Where is the lesion in a patch?

A

Patch = flat lesion > 1 cm

  • non palpable
  • lesion is superficial: in the epidermis or superficial dermis
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13
Q

Mechanism of a papule and plaque lesions

A

Papule = palpable, elevated lesion less than 1 cm

-proliferation of cells in the epidermis or superficial dermis

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14
Q

Define pustule

(a) Location

A

Pustule = superficial elevated lesion w/ yellow or white fluid (pus)

pus = protein rich, contains neutrophils

(a) w/in or just beneath the epidermis
ex: acne, fungal infection

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15
Q

Differentiate vesicle and pustule

A

Vesicles contain clear fluid, while pustules contain pus (yellow or white fluid)

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16
Q

Define nodule

A

Nodule = palpable, firm

-proliferation of cells in the mid-deep dermis or subcutis

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17
Q

Differentiate nodules and plaques

A

Nodules are deeper than papules/plaques

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18
Q

Define scale

A

= masses of keratin
-due to rapid proliferation of epidermal cells => the pathology is in the epidermis (not the dermis or subcutaneous tissue)

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19
Q

Define verrucose

A

Covered in warts/warty

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20
Q

Differentiate scale and crust

A

Scale = when skin is proliferating quickly

vs

Crust = when something dries on top of something else

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21
Q

Define crust

A

= dried serum, pus, or blood

  • can be mixed w/ epithelial and/or bacterial debris
    ex: scab is a crust
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22
Q

‘Honey colored crusts’

A

Honey colored crusts = impetigo

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23
Q

What kind of process won’t scar?

A

Scar is CT replacing lost substance in the dermis or deeper => a process in the epidermis won’t scar

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24
Q

Will an erosion scar?

A

Erosion = loss of all or part of the epidermis

Will heal w/o scaring (b/c scaring is replacing lost substance in dermis or deeper- not epidermis)

  • may occur from vesicles or bullae
  • may form crusts
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25
Will an ulcer scar?
Ulcer = complete loss of epidermis and part of dermis -usually heals w/ scarring (b/c is deeper than the epidermis)
26
Differentiate a fissure from (a) an erosion (b) an ulcer
Fissure = linear or wedge shape tear in the epidermis (like in winter and the edges of your mouth crack) (a) Erosions are wider than fissures, but both erosions and fissures are of the epidermis - differ by shape and size, not depth (b) Ulcers are deeper than fissures- ulcers involve the dermis
27
# Define atrophy of skin (a) Appearance | (b) Texture
Atrophy = thinning or depression of skin due to reduction in underlying tissue -clinical chance due to a decrease in the dermal CT and/or epidermis (a) Skin appears thin, smooth, finely wrinked, possible telangiectasias. (b) Feels soft and dry
28
What are excoriations?
= Superficial abrasions in the skin produced by mechanical means, usually by scratching -usually only involves the epidermis, but can sometimes involve the upper dermis
29
Define lichenification
= thickening of skin associated w/ increased lines and skin markings -chronic rubbing/scratching => hyperkeratosis -due to chronic scratching, associated w/ eczema
30
What are some words to describe the configuration of skin findings?
- targetoid - annular (ring like) - serpigenous (snake like) - polycyclic - geographic - linear
31
What would be the next step in a workup for someone w/ a ton of warts?
Warts = HPV infections -increased infection in immunocompromised pts => if someone has a ton of warts test for HIV -would be abnormal to have someone w/ a healthy immune system who has a ton of warts
32
Why do you have to keep an eye on warts?
B/c certain HPV serotypes can be associated w/ squamous cell carcinoma
33
# Define condyloma (a) Causes
Condyloma = infection of the genitals, 2 subtypes (i) Condylma acuminata = genital warts, caused by HPV (ii) Condyloma lata = white lesions caused by secondary syphilis
34
What might be a visual indication that a wart is active? (a) And what does it mean that it's active...?
Little black dots on the wart are blood vessels, indicate that the wart is active (a) An active wart can be frozen but will just come back
35
Mechanism of wart infection
HPV virus infects the basal epithelial cells and induces hyperproliferation
36
How are warts spread?
Skin to skin contact | -or genital contact (gross)
37
Describe the 2 approaches to treating warts (a) Caustic agents or surgical/chemical destruction (b) Immunotherapy, ex: candida antigen (c) 2 ways to prevent genital warts
Treating warts (a) Caustic agents to destroy the epidermis where the wart in living ex: salicyclic acid, cryo (freezing), laser, blister beetle, topical 5-FU (b) Trick the immune system into attacking the wart ex: inject candida antigen into the base of the wart- immune system recognizes the candida and attacks the wart (c) Prevent genital warts w/ condoms and Guardisil vaccine
38
Describe the characteristic psoriatic lesion
Psoriasis- bright red plaque w/ a sharply defined border and silvery white scale
39
What are the characteristic sites for psoriasis?
Elbows, knees, scalp, lumbosacral region
40
What physical exam finding in psoriasis is correlated w/ increased risk of psoriatic arthritis
Nail involvement - nail involvement in up to 40% o psoriasis cases ex: pitting, oil droplet discoloration, onycholysis
41
Besides arthritis, what does psoriasis increased risk for?
Cardiac disease | ex: arrhythmias
42
Distinguish the classic locations for psoriasis vs. eczema
Psoriasis typically on extensor surfaces (like back of the elbow), while eczema is typically on flexor surfaces
43
Give some examples of intertrigenous areas
Intertrigenous areas = where two skin areas touch or rub ex: under boob, armpit, groin
44
Treating psoriasis (a) Topical (b) Light therapy (c) Systemic options (d) Immunotherapy
Treating psoriasis (a) Topical = corticosteroids, vitamin D analoges (b) Light therapy: UVB light, unclear mechanism (c) Systemic: methotrexate and retinoids (d) Anti-TNFalpha monoclonal antibody = Remicade
45
Describe the diseases mechanism of psoriasis
Immunologic factors (both polygenetic and environmental) induce epidermal hyperproliferation (by shortening the cell cycle) - systemic immunologic disease => increased cardiac and arthritis risk - presence of activated T cells and excess neutrophils in lesions
46
What is a critical proinflammatory cytokine in psoriasis
TNF-alpha | hence why Remicade is so beneficial in treatment
47
Describe the disease mechanism of tinea versicolor
Tinea versicolor = chronic, asymptomatic, superficial fungal infection caused by the yeast malassezia furfur -yeast is in the outermost layer of the skin = stratum corneum
48
What does a KOH prep test for?
The yeast malassezia furfur = causes tinea versicolor -see 'spaghetti and meatball' appearance of the both hyphae and spores of the years in the stratum corneum or scale of lesion
49
What is the most common cause of dandruff?
= Seborrheic dermatitis = irritated, oily scalp due to inflammatory desquamative reaction in oil rich areas
50
Disease mechanism of seborrheic dermatitis (a) describe the scale
=inflammatory desequamative rxn in oil rich areas (face, scalp, ears) -increased sebum production (a) scale often yellow and greasy
51
What disease is found most commonly in the glabella and nasolabial folds?
Seborrheic dermatitis -glabella = skin btwn eyebrows above nose
52
Seborrheic dermatitis treatment (a) Scalp (b) Face
Treating seborrheic dermatitis (a) scalp = azole shampoo or cream - OTC anti-dandruff shampoos (b) Face = combo of topical antifungal and hydrocortisone
53
Distinguish blackheads and whiteheads
Comedones = plug of sebum and keratin in the sebaceous gland blackheads = open comedones whiteheads = closed comedones
54
Acne treatment (a) Topical (b) Systemic
Treating acne (a) Topical - often a combo of topical antibacterial, abx, and retinoids - topical antibacterial = benzoyl peroxide - retinoids help against the hyperkeratinosis process that clogs pores (b) Systemic = Accutane (= Isotretinoin, for scaring acne), OCPs or spironolactone (testosterone inhibitor) for hormonal acne - no longer use oral abx b/c chronic usage => microbiome effects, resistance etc
55
What does seborrheic refer to?
Greasy appearance and distribution in greasy rich areas (ex: face)
56
Treatment for seborrheic keratosis
Removal- curretage (scoop up ew), liquid nitrogen, electrodessication
57
Differentiate tinae versicolor and pityriasis rosea (a) Staining (b) Color (c) Distribution (d) Other
Tinae versicolor vs. Pityriasis rosea (a) Tinae versicolor can be diagnosed w/ KOH prep (b) Tinae versicolor hypo or hyper-pigemented skin color, while pityriasis rosea is red (c) TV: scattered distribution vs. PR: Christmas tree distribution (d) PR has a Herald parch
58
Treatment for pityriasis rosea
No treatment usually needed, just reassurance to the pt that they're ok - spontaneously resolves (on its own) in 4-6 weeks - unknown cause => nothing really to treat it faster, can possibly use topical corticosteroids, narrow band UVB
59
What is a Herald Patch?
= initial lesion of Pityriasis Rosea | -2-6cm annular erythematous patch, then many smaller oval macules come several days later
60
Disease mechanism of impetigo
Erethematous macules (flat) that develop into fragile vesicles that rupture into an oozing erosion w/ honey colored crusts - caused by staphylococcus or group A streptococcus - can be a primary lesion or secondary such as impetigenized acne etc
61
Differentiate herpes and impetigo
Both have vacuoles but herpes vacuoles are much more regular appearing and impetigo have honey colored crusts
62
How to treat impetigo
Caused by bacterial infxn (staph or GAS) => bacteriostatic soask, topical abx, or if very severe oral abx
63
What is the most common cancer in humans?
Basal cell carcinoma | -25% of all cancers diagnosed in the US
64
Cell of origin of basal cell carcinoma (a) Environmental risk factor (b) Risk of metastasis
Malignant neoplasm from nonkeratinizing cells from the basal cell layer of the epidermis (a) UVB light exposure (sunburn) associated w/ mutation of tsgs (b) Won't really metastasize, just locally invasive (but still can be very destructive to surrounding tissue
65
What is the most common clinical type of basal cell carcinoma
Nodular-Ulcterative type = translucent papule (raised
66
Treatment for basal cell carcinoma
Removal (curettage, electrodessication, surgical) with clear borders
67
Differentiate the clinical picture of HSV-1 and HSV-2
HSV-1 = non-genital, 'cold sores' HSV-2 = genital warts
68
Where does the herpes virus lay dormant?
Neuronal cells in ganglia -then reactivated by stress, systemic infection etc.
69
What is a tzank smear?
Bedside smear of an opened herpetic (or other) vesicle, plate for cytologic exam Herpes findings = intranuclear occlusion and giant cells
70
How to confirm a diagnosis of herpes?
Tzank smear (bedside cytologic test), viral culture, viral PCR
71
Treatment for herpes
Avoid triggers and contact with active infection If treated w/ antivirals early in the flare up (ex: acyclovir, valacyclovir) it can shorten the course of the infection
72
What is atopic dermatitis? (a) Associated secondary lesions (b) Disease mechanism (c) Associated family history
= Eczema - chronic eruption of pruritic, erythematous, oozing papules often w/ (a) secondary lichenification (diffuse epidermial thickining) and excoriation (superficial skin abrasions) (b) Many have defect in flaggrin protein which interferes w/ the skin barrier fxn => increased transepidermial water loss => activation of inflammatory cascade and Th2 response => mast cell and eosinophil activation (c) Often FHx of allergic rhinitis or astham
73
Differentiate the distribution of atopic dermatitis in children and adults
Atopic dermatitis (eczema) Younger children: usually face, extensor surfaces (elbows, knees) Older children and adults: fossas (anticubital and popliteal), neck, hands, feet
74
Treatment for atopic dermatitis
1st line: topical steroids, possibly antihistamines to stop the itching (responsible for secondary excoriations) If very severe => immunosuppression
75
Define uticaria
Clinical term (many etiologies) of eruption of transient (
76
Mechanism of uticaria
Hives = release of histamine and other vasopermeable molecules from mast cells
77
Treatment for uticaria
Antihistamines -if severe (associated w/ anaphylaxis) => epinephrine
78
Two types of contact dermatitis
80% primary irritant type = contact w/ irritating substance (ex: watch allergy, waist band) 20% allergic type- delayed type IV (cell mediated) hypersensitivity to external allergen (ex: poison ivy, poison oak)
79
Describe the reaction of contact dermatitis
= inflammation of the skin induced by contact w/ specific allergen which causes edema and erythema usually w/ superimposed vesicles or bullae
80
What is key to the diagnosis of contact dermatitis
Distribution -can often be confused w/ other processes, but the unique and specific distribution (ex: of a sandal, watch, waist band etc) is a give away
81
Treatment for contact dermatitis
Soaks, topical steroids, antihistamines
82
What is the most common type of nevi? (a) Mechanism
Common mole = melanocytic nevus = benign nevus (a) benign proliferation/accumulation of melanocytes in clusters or nests w/in the epidermis and/or dermis
83
How to distinguish benign nevus from malignant melanoma
ABCDE Benign nevus - symmetric shape - regular border - uniform color - small diameter - no change