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DERM > MISCELLANEOUS SKIN CONDITIONS > Flashcards

MISCELLANEOUS SKIN CONDITIONS Flashcards

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Dermatology Board Prep flashcards
1
Q
  • benign SUBCUTANEOUS tumor

- soft, rounded and movable against overlying skin

A

LIPOMA

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2
Q

lipomas are composed of

A

fat cells that have the same morphology as normal fat cells

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3
Q

an autosomal dominant trait appearing in early adulthood where an individual may have hundreds of lipomas

A

Familial Lipoma Syndrome

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4
Q

very common, button-like dermal nodule

A

dermatofibroma

  • lesion may be tender
  • benign, but can be confused with dangerous lesions
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5
Q

epidermoid cyst can also be called

A

sebaceous cyst
infundibular cyst
epidermal cyst

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6
Q

most common cutaneous cyst

A

epidermoid cyst

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7
Q

how does an epidermoid cyst form

A
  • derived from epidermis or epithelium of a hair follicle
  • formed by cystic enclosure of epithelium; becomes filled with keratin & lipid-rich debris
  • rupture is common, and may result in painful inflammatory mass
  • may become secondarily infected, communicates with skin
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8
Q

usual onset of vitiligo

A

20s-30s

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9
Q

where do vitiligo lesions primarily occur

A

lesions primarily occur on the face, upper trunk, fingertips, hands, armpits, genitalia, bony prominences and perioral region

hair may appear white in those areas

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10
Q

PATHOPHYS OF VITILIGO

A

autoimmune - formation of antibodies to melanocytes

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11
Q

**Vitiligo often occurs in the context of other autoimmune conditions such as

A

⦁ Pernicious anemia

⦁ Hashimoto’s thyroiditis

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12
Q

VITILIGO TREATMENT

A

TREATMENT
- re-pigmentation can be achieved to variable degrees with
⦁ topical steroids
⦁ tacrolimus
⦁ Psoralens = light-sensitive drug that absorbs UV
⦁ UVA / UVB
⦁ surgical skin grafting

  • treatment = a long process that requires patient commitment
  • may need psychological support
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13
Q
  • rare, chronic, potentially fatal disease of the mucous membranes and skin
  • Intraepidermal blistering secondary to an autoimmune process
A

PEMPHIGUS

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14
Q

PEMPHIGUS = ____________ blistering secondary to an autoimmune process

A

INTRAEPIDERMAL

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15
Q

diagnosis of pemphigus

A

biopsy

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16
Q

pemphigus rash

A

starts out as FLACCID BULLAE in the oropharynx, then may spread to face, scalp, chest, axillae, groin

the bullae are tender and painful

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17
Q

Nikolsky sign (superficial detachment of skin under pressure - pulls off in sheets)

A

pemphigus vulgaris (but not bullous pemphigoid)

also with SJS / TEN

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18
Q

starts out as FLACCID BULLAE in the oropharynx, then may spread to face, scalp, chest, axillae, groin

the bullae are tender and painful

A

pemphigus vulgaris

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19
Q

treatment for pemphigus

A
  • recognize & refer!
  • may require hospital admission for severe dz
  • treat with systemic corticosteroids & immunosuppressives

⦁ 1st line = high-dose corticosteroids!
⦁ immunosuppressives: MTX**, azathioprine, cyclophosphamide, etc

  • local wound care (treat like burns), treat 2ndary infections with antibiotics
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20
Q

_________ is intraepidermal blistering

_________ is subepidermal blistering

A

pemphigus vulgaris = intraepidermal

bullous pemphigoid = subepidermal

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21
Q

________ occurs more in younger patients (30s-40s)

__________ occurs almost exclusively in older patients (>60)

A

pemphigus vulgaris

bullous pemphigoid

pemphigus vulgaris = younger (30s-40s) & is intraepidermal

bullous pemphigoid = older (>60) & is subepidermal (so no nikolsky sign)

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22
Q

most common presentation of bullous pemphigoid

A

widespread blistering eruption

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23
Q

bullous pemphigoid rash

A
  • *NO NIKOLSKY SIGN (unlike pemphigus vulgaris) - more urticarial plaques with tense bullae that don’t rupture easily
  • have associated urticarial plaques; blisters are tense and fluid filled

Diagnosis = biopsy required

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24
Q

diagnosis of bullous pemphigoid

A

biopsy

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25
Q

treatment of bullous pemphigoid

A
  • recognize & refer!
  • 1st line = topical high dose steroids (preferred) or oral steroids
  • may require immunosuppressants
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26
Q

urticaria is _________ mediated

A

IgE

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27
Q
  • hives

- immune-mediated skin eruption of well-circumscribed wheals on an erythematous base

A

urticaria

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28
Q
  • hypersensitivity reaction involving the deep layers of the skin
  • swelling of the lips, eyelids, palms, soles and genitalia
A

ANGIOEDEMA

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29
Q

if pt has urticaria, be on the lookout for

A

angioedema…and vice/versa

⦁ 50% urticaria + angioedema
⦁ 40% urticaria alone
⦁ 10% angioedema alone

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30
Q

PATHOPHYS OF URTICARIA & ANGIOEDEMA

A

PATHOPHYS: allergen exposure –> IgE antibody attaches to mast cell –> sudden release of histamine –> inflammation

⦁ principle mediator released by mast cells = HISTAMINE**

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31
Q

Idiopathic chronic urticaria thought to be caused by ___________ process

A

autoimmune

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32
Q

edematous, erythematous, well-circumscribed blanching wheals

A

hives / urticaria

  • can range from a few mm to several cm in diameter
  • has serpiginous borders
  • lesions may persist for 12-24 hours, but most resolve sooner than this
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33
Q
  • has serpiginous borders
A

hives / urticaria

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34
Q

URTICARIA DUE TO FOOD OR DRUGS

A

⦁ attacks tend to be brief
⦁ usually do NOT cause chronic urticaria
⦁ may be accompanied by angioedema

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35
Q

PHYSICAL URTICARIAS (different types)

A

⦁ Dermatographism - gentle stroking of skin produces immediate wheal & flare response

⦁ Pressure Urticaria = pressure to skin @ right angle –> red swelling after latent period of up to 4 hours

⦁ Cold Urticaria = eruptions within minutes following application of cold

⦁ Cholinergic Urticaria = punctate hives triggered by exercise or hot shower

⦁ Aquagenic Urticaria = hives after contact with water

⦁ Solar Urticaria = hives after exposure to UV light

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36
Q

theory to describe the idiopathic cases of chronic urticaria that occur

A

AUTOIMMUNE disease potentially…

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37
Q

ASSOCIATION OF URTICARIA & INFECTIOUS DISEASE

A
  • hep B
  • h. pylori

urticarial symptoms occur during prodromal phase of Hepatitis B**

There are reports that some patients with chronic “idiopathic” urticaria had resolution of symptoms following treatment for Helicobacter pylori infection

38
Q

goal of urticaria / angioedema

A

Goal = identify a specific cause or precipitant

39
Q

Key to the evaluation of urticaria / angioedema is a

A

thorough history (much more important than the physical)

40
Q

substances that may aggravate urticaria / angioedema

A

ASA, NSAIDS, ETOH, ACEI

41
Q

management of urticaria / angioedema

A

MANAGEMENT = avoid the etiologic agent(s) if identified, and avoid substances that may aggravate the condition (ASA, NSAIDS, ETOH, ACEI)

42
Q

empiric measures for symptomatic relief of urticaria / angioedema

A

o Antihistamines
⦁ sedating and/or non-sedating H1-blockers (Diphenhydramine, fexofenadine)
⦁ refractory (stubborn) cases = H2-blockers (Ranitidine)
⦁ Doxepin (Sinequan) = TCA with some H1 & H2 blocking activity

o Steroids = systemic or local: generally reserved after a trial of max antihistamine doses

o SubQ Epi = for severe attacks (anaphylaxis rxn)

43
Q

h. pylori association with urticaria

A

⦁ It is thought that infection with H. pylori increases the permeability of the stomach lining and thus increases the exposure to allergens in the GI tract

44
Q

If the mass (usually a cyst) is epidermal, it is going to feel more ______. If subcutaneous, generally _______

A

fixed = epidermal

mobile = subcutaneous

45
Q

often occurs in the context of other autoimmune conditions such as pernicious anemia and hashimoto’s thyroiditis.

A

vitiligo

46
Q

if urticaria = consider checking for

A

thyroid dz
h. pylori
hep B

47
Q

the principle mediator of the inflammation with urticaria and angioedema is

A

HISTAMINE

which is why one of the staple treatments = antihistamines

48
Q

psoriasis is more prevalent the further away from the

A

equator

49
Q

biggest risk factor for psoriasis

A

family hx!

psoriasis is HEREDITARY

40% of patients have a 1st degree relative with psoriasis or psoriatic arthritis

50
Q

PATHOPHYS OF PSORIASIS

A
  • patients have increased cell turnover (usual cell turnover = 27 days, but in psoriasis = 4 days)
  • have a massive increase in number of cells produced & normal cell keratinization does not take place
  • Subdermal blood vessel dilation also seen –> contributes to the erythema

autoimmune component = buildup of T cells in psoriatic lesions. Have excess of T cells & dendritic cells in psoriatic lesions, so treatment = T-lymphocyte suppressants

51
Q

can trigger guttate psoriasis

A

strep infxn

52
Q

which medications are risk factors for psoriasis

A

beta blockers
lithium
anti-malarial medications

53
Q

risk factors for psoriasis

A

⦁ family hx
⦁ strep infection - can trigger guttate psoriasis
⦁ medications - beta blockers, lithium, anti-malarial meds
⦁ smoking
⦁ obesity
⦁ alcohol
⦁ vitamin D deficiency?

54
Q

hx of improvement of psoriasis with

A

sun exposure

55
Q

presentation of psoriasis

A
  • bimodal age distribution
    ⦁ early = 30-39
    ⦁ late = 50-60
  • can also occur in children, but less common than in adults
  • may be gradual in onset or sudden
  • pruritus = common
  • hx of improvement with sun exposure
    `
56
Q

CONDITIONS THAT ARE OFTEN ASSOCIATED WITH PSORIASIS

A 
⦁	psoriatic arthritis
⦁	CV disease
⦁	malignancy
⦁	DM
⦁	metabolic syndrome
⦁	HTN
⦁	IBD
⦁	serious infections
⦁	ocular involvement = swollen lids, conjunctivitis, xerosis, uveitis
57
Q

TYPES OF PSORIASIS

A 
Plaque
Inverse
Guttate
Erythrodermic
Pustular
Nails
58
Q

most common type of psoriasis

A

plaque

59
Q

AUSPITZ SIGN

A

psoriasis

removing scales results in small blood droplets

pinpoint bleeding under the scale

60
Q

KOEBNER’S PHENOMENON

A

Plaques develop at sites of former skin injury

this isn’t specific to plaque psoriasis, can occur with eczema, etc.). Up to 50% of patients may experience this; get plaques at sites of injury 1-2 weeks after injury

- may occur from
⦁	bug bites
⦁	bruises / scrapes
⦁	poison ivy / poison oak
⦁	burns (chemical or sunburn)
⦁	constant pressure / rubbing, medical processes such as injections or vaccinations, skin blemishes from acne, herpes or chickenpox, or from acupuncture / tattoo needles
61
Q

PSORIATIC LESION DISTRIBUTION

A
  • often symmetrical
  • favors elbows / knees / intertriginous areas
  • uncommon on the face
  • can be single lesions, lesions localizied to one area, or over entire body
62
Q

INVERSE PSORIASIS

A
  • sharply demarcated plaques - found in axilla, groin, naval, sub-mammary region, palms, scalp, soles
  • no scales, like plaque psoriasis
  • more common in overweight persons
  • difficult to distinguish from candidiasis without biopsy (even in same areas as candidiasis)
63
Q

psoriasis that occurs in young adults / children

A

guttate psoriasis

is abrupt in onset
also called eruptive psoriasis

64
Q

strong association with recent strep infection

A

guttate psoriasis

65
Q

have multiple small tear-drop shaped erythematous papules

A

guttate psoriasis

66
Q

guttate psoriasis locations

A

proximal arms & trunk

not classically on elbows / knees / scalp

67
Q

psoriasis with no scales

A

inverse psoriasis

68
Q

guttate psoriasis

A
  • also known as eruptive psoriasis = abrupt onset
  • characteristically occurs in young adults & children
    ⦁ ***strongly associated with recent STREP INFECTION (usually strep pharyngitis) in the preceding 2-3 weeks
  • have multiple small tear-drop shaped erythematous papules
  • scattered diffusely on proximal extremities and trunk (not classically on elbows/knees/scalp)
  • usually self-limited in a few weeks to months
69
Q
  • psoriasis that is most generalized - often affects most or all of the body’s surface
A

erythrodermic psoriasis

70
Q

least common psoriasis

A

ERYTHRODERMIC PSORIASIS

71
Q

2 forms of psoriasis that are emergent

A

erythrodermic psoriasis

pustular psoriasis

72
Q
  • HIGH RISK OF SYSTEMIC INFECTION & ELECTROLYTE IMBALANCES
A

erythrodermic psoriasis

73
Q

most common precipitating factor for erythrodermic & pustular psoriasis

A

ACUTE WITHDRAWAL OF SYSTEMIC CORTICOSTEROIDS

⦁ can occur with or without prior hx of psoriasis; can have another form of psoriasis and then get one of these, or may never have had psoriasis before and get one of these

74
Q

may appear before the onset of cutaneous psoriasis

A

nail psoriasis

75
Q

nail psoriasis is more closely associated with

A

psoriatic arthritis

76
Q

nail psoriasis signs

A

pitting nails
oil drop signs & onycholysis
subungual hyperkeratosis

77
Q

drugs that may exacerbate psoriasis

A 
⦁	beta blockers
⦁	NSAIDS
⦁	lithium
⦁	ACEI
⦁	digoxin

tx = consider switching med if possible

  • combination therapy for treatment is the trend to minimize side effects
78
Q

topical therapy for psoriasis

A
  • Emollients
  • Steroids
  • Vitamin D analogues (calcipotriol)
  • Topical retinoids (tazorac)
  • Calcineurin inhibitors
  • Coal tar preparations
  • Phototherapy: UVA / UVB
79
Q

EMOLLIENTS ( therapy for psoriasis)

A

useful in ALL cases as an adjunct; hydrates the stratum corneum and decreases water evaporation. Softens the scales of the plaues. Apply lubricating creams BID after bathing, while skin is still damp

⦁ eucerin
⦁ lubriderm
⦁ moisturel

80
Q

1st line treatment for psoriasis

A

topical steroid therapy

betamethasone or clobetasol

81
Q

vitamin D analogue drug

A

Calcipotriol (Dovonex)

82
Q

SE of calcipotriol (dovonex)

A

hypercalcemia

hypercalcuria

83
Q

CALCIPOTRIOL (DOVONEX)

A

causes immune modulation;

used in mild to moderate plaque psoriasis

⦁ SE = Hypercalcemia & Hypercalcuria when topical doses > 100g/wk

  • too irritating on face or groin
  • can be used as monotherapy with steroids for breakthrough, or just a few days a week
84
Q

vitamin A analog for psoriasis

A

Tazarotene (Tazorac) = retinoid

85
Q

TAZORAC FOR PSORIASIS

A
  • modulates differentiation & proliferation of epithelial tissue, and exerts some degree of anti-inflammatory and immunological activity
  • may cause skin irritation
  • effective with little systemic absorption
86
Q

good for use in intertriginous areas & the face where steroid use should be limited

A

calcineurin inhibitors

  • Tacrolimus (Protopic)
  • Pimecrolimus (Elidel)
87
Q

MOA of Calcineurin Inhibitors (for psoriasis tx)

A

= inhibits T-lymphocyte activation by binding to an intracellular protein, FKBP-12 and complexes with calcineurin dependent proteins to inhibit calcineurin phosphatase activity

Calcineurin inhibitors inhibit the action of calcineurin. Calcineurin is an enzyme that activates T-cells of the immune system (so it is an immunosuppressant)

88
Q

tends to enhance the effects of UVB therapy

A

COAL TAR THERAPY

89
Q

COAL TAR THERAPY FOR PSORIASIS

A
  • when used alone = only as effective as mild to mid-potency topical steroids
  • primarily used as add-on therapy
  • also tends to enhance the effects of UVB therapy
  • tar shampoos = beneficial for scalp lesions in combo with topical steroid solutions
  • OTC
  • use is limited by staining of clothes & odor
90
Q

PHOTOTHERAPY FOR PSORIASIS

A
  • has anti-proliferative effects by slowing keratinization
  • has anti-inflammatory effects by inducing apoptosis of pathogenic T cells
  • UV radiation accelerates photodamage & the risk of skin cancer
  • UVB
  • PUVA = UVA radiation administered with Psoralen bath or oral dose (photosensitizing drug)
91
Q

SYSTEMIC THERAPY FOR PSORIASIS

A
  • for severe cases that are resistant to topical treatment
    ⦁ MTX
    ⦁ Acetretin (Psoriatane) = systemic retinoid
    ⦁ Cyclosporine = systemic calcineurin inhibitor
    ⦁ Infliximab (Remicade) = Biologic agents
    ⦁ Hydroxyurea, Azathioprine = other immunosuppressants

DERM (12 decks)

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