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BASIC Exam Study Guide > Group 2, Column 1 > Flashcards

Group 2, Column 1 Flashcards

1
Q

What other disorder does acute generalized exanthematous pustulosis mimic?

A

von Zumbusch pustular psoriasis

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2
Q

What is the typical onset after drug exposure for AGEP to occur?

A

It occurs rapidly - within four days.

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3
Q

Name the diagnosis.

  • What vital sign abnormality is this associated with?
  • What might this have that pustular psoriasis would not?
A

Acute Generalized Exanthematous Pustulosis (AGEP)

  • High fever with small non-follicular, sterile pustules arising on background of edematous skin
  • 50% of patients have purpuric or EM-like lesions, mucosal involvement, edema of hands/face, or bulla (pustular psoriasis WOULD NOT have these findings)
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4
Q

What lab derangements are classically seen in acute generalized exanthematous pustulosis (AGEP)?

  • What is a special test that can be used to identify the trigger?
A
  • Leukocytosis with neutrophilia +/- eosinophilia
  • Hypocalcemia
  • Renal insufficiency
  • Note patch test positive in majority of cases (50-60%)
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5
Q

What are the most common offending agents associated with acute generalized exanthematous pustulosis (AGEP)?

A
  • Beta-lactams
  • Macrolide antibiotics
  • Calcium channel blockers (diltiazem most common)
  • Antimalarials
  • Mercury exposure, radiocontrast and enterovirus are other known causes
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6
Q

What is the histopathology of AGEP?

  • What occurs in the epidermis? Dermis?
  • Where is the infiltrate and what is it composed of?
A
  • Subcorneal and intraepidermal spongiform pustules, prominent superficial dermal edema with eosinophils, and perivascular mixed inflammatory infiltrate with eosinophils
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7
Q

What is the treatment for acute generalized exanthematos pustulosis (AGEP)?

A
  • Stop offending drug
  • Supportive therapy with topical steroids and antipyretics
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8
Q

How would you discriminate between AGEP and pustular psoriasis?

  • On clinical exam?
  • On histology?
A
  • 50% of patients with AGEP have purpuric or EM-like lesions, mucosal involvement, edema of hands and face, and bullae (not usually seen in pustular psoriasis)
  • Presence of dermal edema and eosinophils and lack of significant acanthosis occurs in AGEP only
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9
Q

Name the lesion and association we worry about in childhood.

  • These lesions on the face can be associated with what TWO other diseases?
A

Angiofibromas

  • Multiple angiofibromas with onset of childhood associated with tuberous sclerosis
  • Lesions in this case are also called “adenoma sebaceum”
  • Also associated with MEN1 and Birt-Hogg-Dubé syndrome
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10
Q

Name the diagnosis.

A

Angiofibroma (specifically fibrous papule of the nose)

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11
Q

What is the classic histopathology of angiofibroma?

  • What cells are present in the dermis?
  • What happens to the vessels?
A
  • Stellate (dermal) stromal cells
  • Concentric perivascular fibrosis
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12
Q

Name the diagnosis.

A

Angiokeratoma of Mibelli

  • Rare
  • Several 1-5mm dark, red-grey papules over acral areas with verrucous surface
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13
Q

Name three diseases associated with multiple facial angiofibromas.

A
  1. Tuberous sclerosis
  2. MEN1
  3. Birt-Hogg-Dubé
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14
Q

What are the five types of angiokeratoma?

A
  1. Angiokeratoma of Mibelli
  2. Angiokeratoma of Fordyce
  3. Angiokeratoma corporis diffusum (associated with Fabry disease)
  4. Angiokeratoma circumscriptum
  5. Solitary and multiple angiokeratomas
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15
Q

What is the classic histology of angiokeratoma?

  • What occurs in the epidermis and to vessels?
A
  • Dilated superficial dermal vessels
  • Epidermal hyperplasia
  • Rete hug vessels
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16
Q

Name the diagnosis.

  • When is the typical onset?
A

Angiokeratoma circumscriptum

  • Large verrucous papules or plaques typically involving extremitiy/fingers/toes
  • Onset in early childhood/infancy
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17
Q

Name the diagnosis.

A

Angiokeratoma of Fordyce

  • Seen in older men (scrotum) and females (vulva)
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18
Q

Name the diagnosis.

  • What is the typical distribution for this condition?
  • What disorder is this condition classically seen in?
A

Angiokeratoma corporis diffusum

  • Multiple lesions in childhood/adolescence
  • Bathing suit distribution
  • Seen in Fabry disease and other enzyme deficiencies
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19
Q

Name the diagnosis.

A

Solitary angiokeratoma

  • Single red to dark brown papule usually over lower extremity
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20
Q

Name the diagnosis.

A

Arthropod bites

(Notice grouped lesions in an exposed area)

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21
Q

Name the diagnosis.

A

Arthropod bite

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22
Q

Name the clinical finding.

A

Beau’s lines​

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23
Q

Name the diagnosis.

  • Onset?
  • What syndrome may this be associated with?
  • What is seen on histology? What other lesion is nearly identical on histology alone?
A

Becker’s nevus (aka Becker’s melanosis)

  • Hyperpigmented, irregular plaque of upper torso
  • Onset around puberty
  • May have ipsilateral breast hypoplasia (Poland syndrome)
  • Histology: increased basal melanocytes, acanthosis, elongated rete ridges, dermal smooth muscle hamartoma-like changes
    • Hard to distinguish from smooth muscle hamartoma
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24
Q

On histology alone, a Becker’s nevus is difficult to distinguish from what other lesion?

A

Smooth muscle hamartoma (see photo)

  • A Becker’s nevus has dermal smooth muscle hamartoma-like changes
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25
Q

What are associations with Beau’s lines?

  • What causes Beau’s lines?
A

Temporal stoppage of growth at proximal nail matrix

  • Chemotherapy
  • Systemic illness
  • Mechanical trauma or skin diseases of proximal nail fold
  • Stress on body (e.g. childbirth)
  • Major injury
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26
Q

What are associations with Becker’s melanosis (Becker’s nevus)?

  • Onset?
  • What syndrome may this be associated with?
A
  • Thought to be due to androgen-mediated hyperplasia
  • More common in teenage and young adult males
  • Onset around puberty
  • Look for ipsilateral breast hypoplasia (Poland syndrome)
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27
Q

What is the classic histopathology of Becker’s melanosis (Becker’s nevus)?

  • What happens in the epidermis? Dermis?
  • What other lesion is nearly identical on histology alone?
A
  • Increased basal melanocytes
  • Acanthosis
  • Elongation of rete ridges
  • Dermal smooth muscle hamartoma-like changes
    • ​Difficult to distinguish histologically from smooth muscle hamartoma
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28
Q

What activating mutations are seen in blue nevi?

  • What other lesion has the same mutation?
A
  • GNAQ and GNA II (seen in 83%), resulting in downstream MAPK pathway activation
  • Also seen in uveal melanoma
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29
Q

Name the diagnosis.

A

Blue nevus

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30
Q

What disease is associated with multiple blue nevi or epithelioid blue nevi?

A

Carney complex

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31
Q

Name the four variants of blue nevus.

A
  1. Common blue nevus
  2. Cellular blue nevus
  3. Epithelioid blue nevus
  4. Malignant blue nevus ( = melanoma)
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32
Q

Name the diagnosis.

A

Blue nevus

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33
Q

What is the target of autoantibodies in bullous pemphigoid?

  • What type of immunoglobulin (Ig) is involved?
A
  • IgG autoantibodies bind to hemidesmosomal proteins
  • BP180 (a.k.a. BPAG2, primary mediator of BP)
  • BP230 (a.k.a. BPAG1)
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34
Q

Name the diagnosis.

A

Bullous pemphigoid

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35
Q

What is the classic histopathology for urticarial phase bullous pemphigoid?

  • What occurs in the epidermis? DEJ?
  • What special histologic finding may be seen at any phase of BP?
A
  • Eosinophilic spongiosis with eosinophils lining up at DEJ and scattered in superficial dermis
  • Vacuoles at DEJ (early blister formation)
  • May see flame figures (eosinophil granules of MBP) at any phase
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36
Q

What is the classic histopathology for bullous phase bullous pemphigoid?

  • What occurs in the epidermis? What type of cells predominate the blister cavity?
  • What composes the inflammatory infiltrate?
  • What special histologic finding may be seen at any phase of BP?
A
  • Subepidermal split with numerous eosinophils in blister cavity
  • Dense dermal lymphoeosinophilic inflammation
  • May see flame figures (eosinophil granules of MBP) at any phase
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37
Q

Name the diagnosis.

A

Bullous pemphigoid

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38
Q

What is the most sensitive skin test for bullous pemphigoid?

  • What kind of pattern is seen and with what is it composed of?
A
  • DIF of perilesional skin
  • Look for linear C3 (n-serrated pattern) and IgG along DEJ
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39
Q

What are treatment options for bullous pemphigoid?

  • First line?
  • Second/third/last line?
  • What can be used for mucosal-predominant disease?
A
  • First line: systemic steroids and steroid-sparing agents (MMF, MTX, azathioprine, cyclophosphamide)
  • Other options:
    • Tetracyclines + nicotinamide (mild disease)
    • Dapsone (mucosal-predominant disease)
    • Rituximab
    • IVIG, plasma exchange
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40
Q

Where do antibodies localize on salt-split skin DIF of perilesional skin with BP and EBA?

  • Staining/pattern?
A
  • BP: “roof staining” ( = n-serrated pattern on standard DIF)
  • EBA: “floor staining” ( = u-serrated pattern on standard DIF)
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41
Q

Which IIF substrate is used in the following: PV, PF and PNP?

A
  • PV: monkey esophagus (“Monkeys are so vulgar.”)
  • PF: guinea pig esophagus (“Guinea pigs eat foliage.”)
  • PNP: rat bladder (“Rats, I have cancer!”)
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42
Q

What lab test correlates with BP disease activity, IIF or ELISA?

  • What does it test for?
A

ELISA levels (IgG and IgE to BP180 and BP230)

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43
Q

Name the diagnosis.

A

Calciphylaxis

  • Painful stellate or retiform purpuric plaques on legs
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44
Q

Name the diagnosis.

A

Calciphylaxis

  • Painful stellate or retiform purpuric plaques on legs
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45
Q

What are notable associations with calciphylaxis?

A
  • ESRD (increased calcium-phosphate product)
  • Diabetes
  • Hyperparathyroidism (i.e., partial parathyroidectomy may help treat calciphylaxis)
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46
Q

What is the treatment for calciphylaxis?

  • Including procedures and medicines
A
  • Treat underlying renal failure
  • Partial parathyroidectomy
  • Debridement
  • Sodium thiosulfate, pentoxifylline, apixaban (and stop taking warfarin)
  • Treat any infections
47
Q

Name the diagnosis.

A

Chondrodermatitis nodularis helicis

48
Q

What is the classic histopathology of chondrodermatitis nodularis helicis (CNH?)?

A
  • Central ulceration with adjacent acanthosis overlying zone of fibrin
  • Degenerating (eosinophilic) cartilage
49
Q

Name the diagnosis.

  • What is the source?
A

Cutaneous larva migrans

  • Erythematous, serpiginous “tract” that is very itchy
  • Typically occurs after walking barefoot in area contaminated by animal feces (eggs in animal feces –> passed to soil and larvae hatch) –> larvae unable to penetrate basement membrane of skin and die
50
Q

What is the treatment of cutaneous larva migrans?

A
  • Topical/oral thiabendazole
  • Oral albendazole
  • Oral ivermectin
  • LN2
51
Q

Name the diagnosis.

  • What may be the only finding on exam?
  • Classic distribution?
  • What may be present on hands?
A

Dermatitis herpetiformis

  • Extremely itchy herpetiform vesicles arising on urticarial plaques
  • Vesicles rupture easily, so excoriations usually only finding on clinical exam
  • Classically involves symmetric extensor extremities, buttocks, back/neck
  • Hemorrhagic palmoplantar lesions may be present (see photo)
52
Q

97% of those with dermatitis herpetiformis have which HLA II alleles?

A
  • HLA-DQ2 (90%)
  • HLA-DQ8 (7%)
53
Q

Dermatitis herpetiformis is strongly associated with which other autoimmune diseases (3)?

A
  • Hashimoto’s thyroiditis (most common, > 50%)
  • Pernicious anemia
  • Type 1 diabetes
54
Q

What are the autoantigens and antibodies involved in dermatitis herpetiformis?

  • In the gut?
  • In the skin? (2)
  • Immunoglobulin (Ig) type?
A

Autoantigens:

  • Epidermal transglutaminase
  • Tissue transglutaminase (endomysial; a.k.a. TTG)
    • TTG2: responsible for gut involvement
    • TTG3: responsible for skin involvement

Antibody:

  • IgA
55
Q

Name the diagnosis.

  • Most common cause in children? Adults?
A

Erythema nodosum

  • Erythematous subcutaneous nodules commonly over pretibial areas
  • Progress to bruise-like color, +/- fever, arthralgias, malaise
  • Most common cause in children: streptococcal infection
  • Most common causes in adults: sarcoidosis, IBD and medications (especially OCPs)
56
Q

Name the diagnosis.

  • Most common cause in children? Adults?
A

Erythema nodosum

  • Erythematous subcutaneous nodules commonly over pretibial areas
  • Progress to bruise-like color, +/- fever, arthralgias, malaise
  • Most common cause in children: streptococcal infection
  • Most common causes in adults: sarcoidosis, IBD and medications (especially OCPs)
57
Q

What is the histopathology for dermatitis herpetiformis?

  • In the epidermis? The dermal papillae?
  • What other condition does this look like under the microscope?
A
  • Subepidermal bullae
  • Neutrophilic papillitis (neutrophils “stuffing” dermal papillae)
  • Looks like linear IgA bullous dermatosis under the microscope
58
Q

What do you see on DIF for dermatitis herpetiformis?

  • What is the pattern, and what composes it?
A

Granular IgA deposits +/- C3 in dermis

59
Q

What is the treatment for dermatitis herpetiformis?

  • What can help with just skin disease? Both skin and GI disease?
  • What compound can trigger a flare?
A
  • Dapsone (check for G6PD deficiency before starting)
    • No effect on GI disease/lymphoma risk
  • Sulfapyridine can be used if dapsone cannot
  • Gluten-free diet (controls both skin and GI disease, decreases risk of GI lymphoma)
  • Avoid iodide, which may trigger flare
60
Q

What is the most common panniculitis, and what is its type of immune response?

A

Erythema nodosum

  • Delayed hypersensitivity response (Th1 cytokine pattern) to various antigens
61
Q

What are the most common causes of erythema nodosum?

Think about:

  • Infections
  • Drugs
  • Other conditions
A
  • Idiopathic (most common)
  • Streptococcal infections (#1 identifiable cause)
  • Other infections (bacterial GI infections, viral URIs, TB, histoplasmosis, coccidioidomycosis)
  • OCPs, sulfonamides, NSAIDs
  • Sarcoidosis, IBD
62
Q

What is Löfgren’s Syndrome?

  • What is its general prognosis?
A

Type of sarcoidosis that presents with:

  • Erythema nodosum
  • Hilar lymphadenopathy
  • Fever
  • Polyarthritis
  • Uveitis

Associated with a good prognosis

63
Q

What is the classic histopathology of erythema nodosum?

  • What is found it the fat septae?
  • What cells are present in early lesions?
A
  • Septal panniculitis with thickening/fibrosis of septae
  • Neutrophils seen in early lesions
  • Miescher’s microgranulomas (small histiocytic aggregates in subcutaneous fat septae)
  • +/- thrombophlebitis
64
Q

What are treatment options for erythema nodosum?

  • What if it’s Behcet’s associated? IBD associated?
A
  • Treat underlying medical issue (if present)
  • Bed rest/elevation
  • NSAIDs
  • SSKI (potassium iodide)
  • Colchicine (if Behcet’s associated)
  • Dapsone
  • TNF-alpha inhibitors (if IBD associated)
65
Q

Name the diagnosis.

  • What should you look for to make the diagnosis?
A

Factitial dermatitis (dermatitis artefacta)

  • Geographic excoriations/erosions/ulcers
  • Look for acute angles
66
Q

Name the diagnosis.

  • What should you look for to make the diagnosis?
A

Factitial dermatitis (dermatitis artefacta)

  • Geographic excoriations/erosions/ulcers
  • Look for acute angles
67
Q

What are the most common medications causing a fixed drug eruption (FDE)?

  • Most common cause? Most common cause on genitalia?
  • Classic cause of non-pigmented FDE?
A
  • Sulfonamides (75% of cases; #1 cause on genitalia)
  • NSAIDs (especially naproxen; predilection for lips)
  • Tetracyclines
  • Phenolphthalein (previously in laxatives)
  • Pseudoephedrine (Sudafed; classic cause of non-pigmented FDE)
68
Q

Name the diagnosis.

  • Where is commonly affected?
  • When is its onset?
A

Fixed drug eruption

  • Most commonly affects oral and genital mucosa
  • Well-demarcated, edematous plaques with erythematous/violaceous hue
  • Commonly get central dusky hue, bulla or erosion
  • Prominent post-inflammatory hyperpigmentation
  • Onset is 1-2 weeks after initiating offending drug
69
Q

Name the diagnosis.

  • Where is commonly affected?
  • When is its onset?
A

Fixed drug eruption

  • Most commonly affects oral and genital mucosa
  • Well-demarcated, edematous plaques with erythematous/violaceous hue
  • Commonly get central dusky hue, bulla or erosion
  • Prominent post-inflammatory hyperpigmentation
  • Onset is 1-2 weeks after initiating offending drug
70
Q

How long does a fixed drug eruption take to develop?

  • Initial episode?
  • Subsequent episodes?
A
  • Initial episode: develops 1-2 weeks after administration of causative drug
  • Subsequent episodes: eruption recurs at same site very rapidly after reexposure (30 min to 8 hrs)
71
Q

What is the classic histopathology of fixed drug eruption (FDE)?

  • What is the inflammatory pattern?
  • What kind of infiltrate is present?
  • How is the corneum affected?
  • What may be present if it is not the first occurrence?
A
  • Vacuolar interface dermatitis
  • Polymorphous infiltrate (including eosinophils and neutrophils)
  • Acute (normal) stratum corneum
  • Chronic dermal changes may be present if not first occurrence
    • Papillary dermal fibrosis
    • Melanin pigment incontinence in perivascular location
72
Q

What skin testing can be performed to help identify the culprit medication causing a fixed drug eruption?

A

Patch testing within a site of prior involvement

73
Q

Name the diagnosis.

  • What is this associated with?
  • What other condition does this look like histologically?
A

Geographic tongue

  • Well-demarcated patches of atrophy with surrounding erythema surrounded by white/yellow scalloped border on dorsal tongue
  • Associated with psoriasis and atopic dermatitis
  • Histologically looks like psoriasis
74
Q

What is important to know about the virus Coxsackie A6?

  • What is it associated with?
A
  • Causes more widespread and severe vesiculobullous eruptions
  • Associated with atypical HFMD presentations, including eczema coxsackium (in atopics; see photo), Gianotti-Crosti-like eruptions and onychomadesis (nail matrix arrest at time of acute infection)
75
Q

Name the diagnosis.

  • Areas typically affected?
  • Most common causes? (3)
A

Hand-foot-and-mouth disease

  • Vesicular eruption most commonly involving palms/soles/buttocks/oral cavity
  • Erythematous macules and oval, deep-seated erythematous vesicles and bulla with gray center
  • Caused by Coxsackie A16 virus (> Coxsackie A6 and Enterovirus)
76
Q

Name the diagnosis.

  • Areas typically affected?
  • Most common causes?
A

Hand-foot-and-mouth disease

  • Vesicular eruption most commonly involving palms/soles/buttocks/oral cavity
  • Erythematous macules and oval, deep-seated erythematous vesicles and bulla with gray center
  • Caused by Coxsackie A16 virus (> Coxsackie A6 and Enterovirus)
77
Q

What virus causes hand-foot-and-mouth disease? (3)

  • Which is most common?
A

Coxsackie A16 virus (most common) > Coxsackie A6 and Enterovirus

78
Q

Name the diagnosis.

  • Areas typically affected?
  • Cause?
A

Hand-foot-and-mouth disease

  • Vesicular eruption most commonly involving palsm/soles/buttocks/oral cavity
  • Erythematous macules and oval, deep-seated erythematous vesicles and bulla with gray center
  • Caused by Coxsackie A16 virus (> Coxsackie A6 and Enterovirus)
79
Q

Name the diagnosis.

  • What glands are thought to be affected?
  • How might sinus tracts present?
A

Hidradenitis suppurativa

  • Affects apocrine gland-bearing areas (axilla, inguinal, anogenital, inframammary)
  • Inflammatory nodules, sterile abscesses
  • Can develop sinus tracts, hypertrophic scars, contractures
  • Superficial sinus tracts present as double-ended comedones
80
Q

What viral exanthem is this finding classically associated with?

A

Hand-Foot-Mouth (HFM) disease (caused by Coxsackie A16 and A6) is associated with onychomadesis

81
Q

Name the diagnosis.

  • What glands are thought to be affected?
  • How might sinus tracts present?
A

Hidradenitis suppurativa

  • Affected apocrine gland-bearing areas (axilla, inguinal, anogenital, inframammary)
  • Inflammatory nodules, sterile abscesses
  • Can develop sinus tracts, hypertrophic scars, contractors
  • Superficial sinus tracts present as double-ended comedones
82
Q

What comprises the follicular occlusion tetrad?

A
  1. Hidradenitis suppurativa
  2. Acne congoblata
  3. Dissecting cellulitis of the scalp
  4. Pilonidal cyst
83
Q

What are the associations seen in hidradenitis suppurativa patients?

A
  • Obesity
  • Smoking
  • Metabolic syndrome
  • Depression
84
Q

What is the classic histopathology of hidradenitis suppurativa?

  • What glands may be involved?
A
  • Suppurative folliculitis with abscess formation
  • Follicular plugging
  • Granulation tissue
  • Inflammation “spills over” to apocrine glands
85
Q

Name the diagnosis.

  • Onset?
  • What is present on palms and soles?
  • What areas are spared?
A

Icthyosis vulgaris

  • Fine white scales on extensor surfaces
  • Flexures spared
  • Hyperlinearity palms/soles, atopic diathesis
  • Presents few months after birth to early childhood
86
Q

Name the diagnosis.

  • Onset?
  • What is present on palms and soles?
  • What areas are spared?
A

Ichthyosis vulgaris

  • Fine white scales on extensor surfaces
  • Flexures spared
  • Hyperlinear palms/soles, atopic diathesis
  • Presents few months after birth to early childhood
87
Q

What is the inheritance pattern pattern of ichthyosis vulgaris?

A

Autosomal dominant

88
Q

What gene and gene product is involved in ichthyosis vulgaris?

A

FLG, which encodes profillagrin

89
Q

What are the histopathologic features of ichthyosis vulgaris?

  • How is the epidermis and corneum affected?
A
  • Attenuated/absent granular layer
  • Orthohyperkeratosis
90
Q

Name the diagnosis.

A

Kaposi sarcoma

91
Q

What are the four clinical variants of Kaposi sarcoma (KS)?

  • Who is classically affected with each type?
A
  1. Classic KS: Mediterranean or Ashkenazi Jewish descent; elderly men; initially on distal extremities
  2. African endemic: Young African males; fatal
  3. Iatrogenically immunocompromised: transplant/cancer/autoimmune patients
  4. AIDS-associated: gay men; initially on midface and trunk
92
Q

Name the diagnosis.

A

Kaposi sarcoma

93
Q

Name the diagnosis.

A

Kaposi sarcoma

94
Q

What virus is associated with Kaposi sarcoma?

  • What immunohistochemistry can be done to diagnose this on histology?
A

HHV-8

  • Do immunohistochemistry for LANA-1 of HHV-8 (latency-associated nuclear antigen); 100% sensitive and specific
95
Q

What is the classic histopathology of Kaposi sarcoma?

  • What immune cells are involved?
  • What special sign may be seen?
A
  • Infiltrative small vessels with bland endothelium associated with plasma cells
  • RBC extravasation and hemosiderin
  • Look for promontory sign (newly formed vessel projects into existing space)
96
Q

Name the disorder.

A

Lichen sclerosis

  • Sclerotic, ivory-white, atrophic and flat-topped papules and plaques
97
Q

Name the disorder.

A

Lichen sclerosis

  • Sclerotic, ivory-white, atrophic and flat-topped papules and plaques
98
Q

Name the disorder.

A

Lichen sclerosis

  • Sclerotic, ivory-white, atrophic and flat-topped papules and plaques
99
Q

What is lichen sclerosus called when it involves the penis?

A

Balanitis xerotica obliterans (BXO)

  • A common cause of phimosis
100
Q

80% of patients with lichen sclerosis have which autoantibodies?

  • What immunoglobulin (Ig) is involved?
A

IgG autoantibodies against ECM-1 (a BMZ glycoprotein)

101
Q

What is the most common autoimmune disease seen in association with lichen sclerosis?

  • What are other less common disease associations?
A

Autoimmune thyroid disease (15%)

Can also see pernicious anemia, localized scleroderma/morphea, psoriasis and vitiligo but much less common

102
Q

What is the classic histopathology of lichen sclerosus?

  • Corneum?
  • Dermis?
  • What is the inflammatory pattern, and what composes it?
A

“Red, white and blue sign”

  • Orthohyperkeratotic stratum corneum
  • Hyalinized/edematous papillary dermis
  • Band-like (lichenoid) lymphocytic infiltrate
103
Q

Name the diagnosis.

A

Lichen simplex chronicus

  • Well-defined plaques with lichenification, hyperpigmentation and varying erythema
104
Q

What is the classic histopathology of lichen simplex chronicus?

  • What happens in the epidermis? Corneum?
  • What happens in the dermis?
  • How does its histology compare with prurigo nodularis?
A
  • Orthohyperkeratosis
  • Hypergranulosis
  • Irregular acanthosis
  • Papillary dermal fibrosis (vertical collagen)
  • Not as “dome-shaped” as prurigo nodularis
105
Q

Name the diagnosis.

  • What kind of distribution classically occurs?
A

Lichen striatus

  • Asymptomatic 2-4mm pink or hypopigmented scaly papules, linear/Blaschkoid distribution
  • Post-inflammatory hypopigmentation may persist for months to years
  • Nail dystrophy may occur
106
Q

Name the diagnosis.

  • What kind of distribution classically occurs?
A

Lichen striatus

  • Asymptomatic 2-4mm pink or hypopigmented scaly papules, linear/Blaschkoid distribution
  • Post-inflammatory hypopigmentation may persist for months to years
  • Nail dystrophy may occur
107
Q

Name the diagnosis.

  • What kind of distribution classically occurs?
A

Lichen striatus

  • Asymptomatic 2-4mm pink or hypopigmented scaly papules, linear/Blaschkoid distribution
  • Post-inflammatory hypopigmentation may persist for months to years
  • Nail dystrophy may occur
108
Q

Name the clinical finding.

  • Where is the classic site for this condition?
  • Buzzword?
A

Lipodermatosclerosis

  • Acute: rubor, dolor, calor
  • Chronic: well-defined induration, hyperpigmentation; “inverted champagne bottle” from sclerosis
  • Common site: medial lower leg, superior to malleolus
109
Q

Name the clinical finding.

  • Where is the classic site for this condition?
  • Clinical exam buzzword?
A

Lipodermatosclerosis

  • Acute: rubor, dolor, calor
  • Chronic: well-defined induration, hyperpigmentation; “inverted champagne bottle” from sclerosis
  • Common site: medial lower leg, superior to malleolus
110
Q

What is the classic histopathology of lipodermatosclerosis?

  • What happens in the septae?
  • What kind of change occurs to the fat?
A
  • Septal thickening and fibrosis
  • Cystic fat necrosis
  • Lipomembranous change (cystic cavities lined by hyaline membranes in fat)
111
Q

What is the treatment of lipodermatosclerosis?

A
  • Leg compression and elevation
  • Danazole, pentoxifylline
112
Q

What are the common medication culprits of lichenoid drug?

  • Name at least the first five most common.
A
  1. HCTZ
  2. B-blockers
  3. ACE inhibitors
  4. Antimalarials
  5. Gold salts
  6. TNF-alpha inhibitors
  7. NSAIDs
  8. Penicillamine
  9. Quinidine
113
Q

Name the diagnosis in this patient who took HCTZ (or a beta-blocker, or ACE inhibitor, or antimalarial, or gold…).

  • What is the average latency period before this classically occurs?
A

Lichenoid drug eruption (drug-induced LP)

  • Symmetric, flat-topped erythematous or violaceous papules, often grouped and confluent
  • Favors trunk and extremities
  • More eczematous or psoriasiform than classic LP
  • Wickham’s striae absent
  • Spares mucous membranes
  • Average latency period of 1 year
114
Q

Name the diagnosis in this patient who took HCTZ (or a beta-blocker, or ACE inhibitor, or antimalarial, or gold…).

  • What is the average latency period before this classically occurs?
A

Lichenoid drug eruption (drug-induced LP)

  • Symmetric, flat-topped erythematous or violaceous papules, often grouped and confluent
  • Favors trunk and extremities
  • More eczematous or psoriasiform than classic LP
  • Wickham’s striae absent
  • Spares mucous membranes
  • Average latency period of 1 year

BASIC Exam Study Guide (11 decks)

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