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HemeDermMSK 2 > Derm Intro and Common Dermatoses I and II > Flashcards

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
Q

Will an ulcer scar?

A

Ulcer = complete loss of epidermis and part of dermis

-usually heals w/ scarring (b/c is deeper than the epidermis)

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26
Q

Differentiate a fissure from

(a) an erosion
(b) an ulcer

A

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

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27
Q

Define atrophy of skin

(a) Appearance

(b) Texture

A

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

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28
Q

What are excoriations?

A

= Superficial abrasions in the skin produced by mechanical means, usually by scratching

-usually only involves the epidermis, but can sometimes involve the upper dermis

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29
Q

Define lichenification

A

= thickening of skin associated w/ increased lines and skin markings
-chronic rubbing/scratching => hyperkeratosis

-due to chronic scratching, associated w/ eczema

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30
Q

What are some words to describe the configuration of skin findings?

A
  • targetoid
  • annular (ring like)
  • serpigenous (snake like)
  • polycyclic
  • geographic
  • linear
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31
Q

What would be the next step in a workup for someone w/ a ton of warts?

A

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

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32
Q

Why do you have to keep an eye on warts?

A

B/c certain HPV serotypes can be associated w/ squamous cell carcinoma

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33
Q

Define condyloma

(a) Causes

A

Condyloma = infection of the genitals, 2 subtypes

(i) Condylma acuminata = genital warts, caused by HPV
(ii) Condyloma lata = white lesions caused by secondary syphilis

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34
Q

What might be a visual indication that a wart is active?

(a) And what does it mean that it’s active…?

A

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
Q

Mechanism of wart infection

A

HPV virus infects the basal epithelial cells and induces hyperproliferation

36
Q

How are warts spread?

A

Skin to skin contact

-or genital contact (gross)

37
Q

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

A

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
Q

Describe the characteristic psoriatic lesion

A

Psoriasis- bright red plaque w/ a sharply defined border and silvery white scale

39
Q

What are the characteristic sites for psoriasis?

A

Elbows, knees, scalp, lumbosacral region

40
Q

What physical exam finding in psoriasis is correlated w/ increased risk of psoriatic arthritis

A

Nail involvement

  • nail involvement in up to 40% o psoriasis cases
    ex: pitting, oil droplet discoloration, onycholysis
41
Q

Besides arthritis, what does psoriasis increased risk for?

A

Cardiac disease

ex: arrhythmias

42
Q

Distinguish the classic locations for psoriasis vs. eczema

A

Psoriasis typically on extensor surfaces (like back of the elbow), while eczema is typically on flexor surfaces

43
Q

Give some examples of intertrigenous areas

A

Intertrigenous areas = where two skin areas touch or rub

ex: under boob, armpit, groin

44
Q

Treating psoriasis

(a) Topical
(b) Light therapy
(c) Systemic options
(d) Immunotherapy

A

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
Q

Describe the diseases mechanism of psoriasis

A

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
Q

What is a critical proinflammatory cytokine in psoriasis

A

TNF-alpha

hence why Remicade is so beneficial in treatment

47
Q

Describe the disease mechanism of tinea versicolor

A

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
Q

What does a KOH prep test for?

A

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
Q

What is the most common cause of dandruff?

A

= Seborrheic dermatitis = irritated, oily scalp due to inflammatory desquamative reaction in oil rich areas

50
Q

Disease mechanism of seborrheic dermatitis

(a) describe the scale

A

=inflammatory desequamative rxn in oil rich areas (face, scalp, ears)
-increased sebum production

(a) scale often yellow and greasy

51
Q

What disease is found most commonly in the glabella and nasolabial folds?

A

Seborrheic dermatitis

-glabella = skin btwn eyebrows above nose

52
Q

Seborrheic dermatitis treatment

(a) Scalp
(b) Face

A

Treating seborrheic dermatitis

(a) scalp = azole shampoo or cream
- OTC anti-dandruff shampoos

(b) Face = combo of topical antifungal and hydrocortisone

53
Q

Distinguish blackheads and whiteheads

A

Comedones = plug of sebum and keratin in the sebaceous gland

blackheads = open comedones

whiteheads = closed comedones

54
Q

Acne treatment

(a) Topical
(b) Systemic

A

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
Q

What does seborrheic refer to?

A

Greasy appearance and distribution in greasy rich areas (ex: face)

56
Q

Treatment for seborrheic keratosis

A

Removal- curretage (scoop up ew), liquid nitrogen, electrodessication

57
Q

Differentiate tinae versicolor and pityriasis rosea

(a) Staining
(b) Color
(c) Distribution
(d) Other

A

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
Q

Treatment for pityriasis rosea

A

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
Q

What is a Herald Patch?

A

= initial lesion of Pityriasis Rosea

-2-6cm annular erythematous patch, then many smaller oval macules come several days later

60
Q

Disease mechanism of impetigo

A

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
Q

Differentiate herpes and impetigo

A

Both have vacuoles but herpes vacuoles are much more regular appearing and impetigo have honey colored crusts

62
Q

How to treat impetigo

A

Caused by bacterial infxn (staph or GAS) => bacteriostatic soask, topical abx, or if very severe oral abx

63
Q

What is the most common cancer in humans?

A

Basal cell carcinoma

-25% of all cancers diagnosed in the US

64
Q

Cell of origin of basal cell carcinoma

(a) Environmental risk factor
(b) Risk of metastasis

A

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
Q

What is the most common clinical type of basal cell carcinoma

A

Nodular-Ulcterative type = translucent papule (raised

66
Q

Treatment for basal cell carcinoma

A

Removal (curettage, electrodessication, surgical) with clear borders

67
Q

Differentiate the clinical picture of HSV-1 and HSV-2

A

HSV-1 = non-genital, ‘cold sores’

HSV-2 = genital warts

68
Q

Where does the herpes virus lay dormant?

A

Neuronal cells in ganglia

-then reactivated by stress, systemic infection etc.

69
Q

What is a tzank smear?

A

Bedside smear of an opened herpetic (or other) vesicle, plate for cytologic exam

Herpes findings = intranuclear occlusion and giant cells

70
Q

How to confirm a diagnosis of herpes?

A

Tzank smear (bedside cytologic test), viral culture, viral PCR

71
Q

Treatment for herpes

A

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
Q

What is atopic dermatitis?

(a) Associated secondary lesions
(b) Disease mechanism
(c) Associated family history

A

= 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
Q

Differentiate the distribution of atopic dermatitis in children and adults

A

Atopic dermatitis (eczema)

Younger children: usually face, extensor surfaces (elbows, knees)

Older children and adults: fossas (anticubital and popliteal), neck, hands, feet

74
Q

Treatment for atopic dermatitis

A

1st line: topical steroids, possibly antihistamines to stop the itching (responsible for secondary excoriations)

If very severe => immunosuppression

75
Q

Define uticaria

A

Clinical term (many etiologies) of eruption of transient (

76
Q

Mechanism of uticaria

A

Hives = release of histamine and other vasopermeable molecules from mast cells

77
Q

Treatment for uticaria

A

Antihistamines

-if severe (associated w/ anaphylaxis) => epinephrine

78
Q

Two types of contact dermatitis

A

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
Q

Describe the reaction of contact dermatitis

A

= inflammation of the skin induced by contact w/ specific allergen which causes edema and erythema usually w/ superimposed vesicles or bullae

80
Q

What is key to the diagnosis of contact dermatitis

A

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
Q

Treatment for contact dermatitis

A

Soaks, topical steroids, antihistamines

82
Q

What is the most common type of nevi?

(a) Mechanism

A

Common mole = melanocytic nevus = benign nevus

(a) benign proliferation/accumulation of melanocytes in clusters or nests w/in the epidermis and/or dermis

83
Q

How to distinguish benign nevus from malignant melanoma

A

ABCDE

Benign nevus

  • symmetric shape
  • regular border
  • uniform color
  • small diameter
  • no change

HemeDermMSK 2 (11 decks)

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