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

Group 2, Column 2 Flashcards

1
Q

Name the clinical finding/diagnosis.

  • What is the typical symptom?
  • How does this heal?
A

Atrophie blanche seen in livedoid vasculopathy.

  • Burning pain along ankle prior to ulceration
  • Painful ulcerations on lower legs +/- surrounding livedo reticularis
  • Heal with atrophic hypopigmented scars
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2
Q

What systemic disorders are classically associated with livedoid vasculopathy?

A
  • Hypercoagulable disorders (e.g., Factor V Leiden, protein C deficiency, prothrombin mutations, hyperhomocysteinemia)
  • Autoimmune conditions (SLE, scleroderma, APLS)
  • Atherosclerosis and stasis
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3
Q

What are the early and late histopathology findings of livedoid vasculopathy and atrophie blanche?

  • What happens to the vessels?
  • What happens to the epidermis?
A
  • Segmental hyalinization (“pink-red crayon”) and thrombosis of small vessels in the upper and mid dermis
  • Late stage with epidermal atophy and hyalinized vessels
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4
Q

What are the treatment options for livedoid vasculopathy?

  • First line?
  • In recurrent/recalcitrant cases?
A
  • Aspirin
  • Pentoxyfilline
  • Dipyridamole
  • In recurrent or recalcitrant cases:
    • Anticoagulants (warfarin, heparin, etc.)
    • Oral steroids
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5
Q

What labs should be obtained in suspected livedoid vasculopathy?

  • What is part of the coagulopathy work up?
A
  • Coagulopathy workup
    • Cryoglobulins
    • Homocysteine
    • Protein C and S
    • Anti-thrombin III
    • ANA
    • Anti-cardiolipin antibody
    • Factor V mutation
    • Prothrombin mutation
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6
Q

Name the diagnosis.

  • What do early lesions look like? Late lesions?
  • How is hair and sweat affected?
  • What indicates persistent disease activity with respect to lesion appearance?
A

Plaque morphea (localized scleroderma)

  • Begin as erythematous to violaceous patches on trunk and proximal extremities
  • Evolve to indurated hyperpigmented or ivory plaques
  • Often hairless and anhidrotic
  • Violaceous border indicates persistent disease activity
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7
Q

What is the most common subtype of morphea (localized scleroderma) in adults and in children?

A
  • Plaque in adults
  • Linear in children
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8
Q

What is the suspected pathogenesis of morphea (localized scleroderma)?

  • What cytokines are involved?
  • What happens to vessels and the dermis?
A
  • Genetic predisposition + environmental trigger
  • Vascular injury leads to inflammation
  • Triggers profibrotic Th2 cytokines (IL-4, IL-6 and TGF-beta)
  • Fibroblast proliferation and collagen deposition
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9
Q

What are classic triggers of morphea (localized scleroderma)?

  • What types of infections?
  • What are general iatrogenic causes?
A
  • Infections with Borrelia spp. (in Europe and Japan mainly; Borrelia afzelii and Borellia garinii)
  • Radiation
  • Medications
  • Trauma
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10
Q

Name the diagnosis.

  • What do early lesions look like? Late lesions?
  • How is hair and sweat affected?
  • What indicates persistent disease activity with respect to lesion appearance?
A

Plaque morphea (localized scleroderma)

  • Begin as erythematous to violaceous patches on trunk and proximal extremities
  • Evolve to indurated hyperpigmented or ivory plaques
  • Often hairless and anhidrotic
  • Violaceous border indicates persistent disease activity
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11
Q

Name the diagnosis.

  • in which population is this the most common subtype?
  • What autoantibodies is most common in this condition?
  • What are possible complications of this condition?
A

Linear morphea (localized scleroderma)

  • Associated with significant morbidity (especially in kids, in whom it is the most common subtype)
  • Look for linear distribution often along Blaschko’s lines
  • Legs (#1 site) > arms > head/trunk
  • Anti-ssDNA autoantibodies most common
  • Undergrowth of limbs, joint restriction/contractures
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12
Q

Name the diagnosis.

A

En coup de sabre

  • Indentation of frontal, frontoparietal or parasagittal forehead or scalp
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13
Q

Name the diagnosis.

  • What is the other term for this condition?
  • What are other associations with this condition?
A

Parry-Romberg syndome (a.k.a. progressive hemifacial atrophy)

  • Unilateral atrophy of face involving dermis, subcutaneous tissue, muscle and bone
  • Can be associated with epilepsy, headache, exophthalmos, cerebral atrophy, alopecia
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14
Q

Name the diagnosis.

  • What is the buzzword for this condition?
  • What does the dermis look like on histology?
A

Atrophoderma of Pasini and Pierini

  • Brownish-gray hyperpigmented oval, atrophic, well-demarcated plaques with sharp sloping borders (“cliff drop” edges)
  • Begins as persistent single lesion with additional lesions over time
  • Histology: significantly decreased dermal thickness compared to normal skin (biopsy at lesion edge)
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15
Q

Name the diagnosis.

A

Necrobiosis lipoidica

  • Yellow to red-brown atrophic to indurated plaques typically over pretibial areas; prominent telangiectasis, +/- ulceration
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16
Q

Name the diagnosis.

A

Necrobiosis lipoidica

  • Yellow to red-brown atrophic to indurated plaques typically over pretibial areas; prominent telangiectasis, +/- ulceration
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17
Q

How can you tell the difference between morphea and systemic sclerosis on rheumatologic serologies?

A
  • All forms of morphea lack anti-Scl70 (Topo I) and anti-centromere antibodies (in contrast to systemic sclerosis)
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18
Q

What is the suspected pathogenesis of necrobiosis lipoidica?

  • What happens to the vessels and dermis?
  • What kind of inflammation occurs?
A
  • Vascular compromise from immunodeposition in vessel walls or diabetes-related microangiopathic changes
  • Subacute dermal ischemia leads to dermal collagen degeneration
  • Secondary granulomatous inflammatory response
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19
Q

What are the key histopathology findings of necrobiosis lipoidica?

  • What is the special “sign” on biopsy?
  • What is the inflammatory pattern and how is it arranged in the dermis?
  • How does its histology compare with granuloma annulare?
  • What immune cells are abundant? What stromal component is absent?
A
  • “Square biopsy” sign
  • Horizontally arranged (“layered”) palisaded granulomatous inflammation with horizontal tiers of degenerated collagen fibers and dermal sclerosis
  • Process diffusely involves entire dermis (vs. GA which is mainly superficial)
  • Lacks mucin
  • Plasma cells and multinucleated giant cells are abundant
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20
Q

What are the treatments for necrobiosis lipoidica?

  • What are topical and systemic treatments?
  • What does not affect disease course?
A
  • Potent topical steroids and/or ILK (into inflammatory rim), TCIs
  • Systemic treatments include PO steroids, colchicine, cyclosporine, TNF-alpha inhibitors and pentoxifylline for chronic/recalcitrant cases
  • Note: none of these is borne out in the literature
  • Glycemic control does not affect disease course
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21
Q

What is the inheritance pattern and genetic mutation of NF-1?

A
  • Autosomal dominant inheritance (but can occur as a sporadic mutation)
  • Mutation of neurofibromin (NF1), a tumor suppressor gene that downregulates Ras activation
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22
Q

What is another name for NF1?

A

von Recklinghausen’s disease

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23
Q

What is the diagnostic criteria for NF1?

Hint: think of the mnemonic!

A

“CA NN OT FAI L2 B 1ST”

Must have >2 of the following:

  • ​CA: CAfe-au-lait (six lesions)
  • NN: Neurofibromas
  • OT: OpTic glioma
  • FAI: Freckles (Axillary, Inguinal)
  • L2: Lisch nodules x 2
  • B: Bone (sphenoid or tibial wing dysplasia)
  • 1st: (affected 1st degree relative)
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24
Q

Name the clinical finding and disease association.

A

Lisch nodules found in NF1

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25
Q

Name the diagnosis.

Hint: think of the mnemonic!

A

NF1

Must have >2 of the following:

  • ​CA: CAfe-au-lait (six lesions)
  • NN: Neurofibromas
  • OT: OpTic glioma
  • FAI: Freckles (Axillary, Inguinal)
  • L2: Lisch nodules x 2
  • B: Bone (sphenoid or tibial wing dysplasia)
  • 1st: (affected 1st degree relative)
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26
Q

Name the diagnosis.

Hint: think of the mnemonic!

A

NF1

Axillary freckling is also called “Crowe’s sign.”

Must have >2 of the following:

  • ​CA: CAfe-au-lait (six lesions)
  • NN: Neurofibromas
  • OT: OpTic glioma
  • FAI: Freckles (Axillary, Inguinal)
  • L2: Lisch nodules x 2
  • B: Bone (sphenoid or tibial wing dysplasia)
  • 1st: (affected 1st degree relative)
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27
Q

What is the strong triple association that includes NF1?

A
  1. NF1
  2. Juvenile xanthogranulomas (JXGs)
  3. Juvenile myelomonocytic leukemia (JMML)
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28
Q

What is the inheritence pattern and genetic mutation (and its gene product) seen in NF2?

A
  • AD
  • Caused by mutations in SCH gene (encodes schwannomin/merlin)
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29
Q

What are the key cutaneous (2) and neurologic (1) findings in NF2?

  • Where are the neurofibromas located, and how is this different than NF1?
A
  • Subcutaneous neurofibromas (overlying pigment/hair, rather than intradermal like in NF1; see photo)
  • Cafe au lait macules (two or fewer)
  • Bilateral vestibular schwannomas (acoustic neuromas)
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30
Q

What is the classic histopathology of nevus sebaceus?

  • How is the epidermis affected? Follicles?
  • What glands are present? (2)
  • With what other condition is the histology similar to?
A
  • Verrucous epidermis with malformed, dimunitive hairs
  • Lacks fully formed terminal hairs within lesion
  • Sebaceous glands open directly onto skin surface
  • Dilated apocrine glands
  • Histology is similar to an epidermal nevus
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31
Q

Name the diagnosis.

  • What are the typically present along?
A

Nevus sebaceus

  • Present at birth along Blaschko’s lines
  • Becomes more yellow and verrucous after puberty
  • Scalp/face most common sites
  • Alopecia of affected area
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32
Q

Name the diagnosis.

  • What are they typically present along?
A

Nevus sebaceus

  • Present at birth along Blaschko’s lines
  • Becomes more yellow and verrucous after puberty
  • Scalp/face most common sites
  • Alopecia of affected area
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33
Q

What secondary adnexal neoplasms are known to arise within nevus sebaceus?

  • There are three of them.
A
  1. Trichoblastoma (#1)
  2. SPAP (syringocystadenoma papilliferum)
  3. BCC
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34
Q

What is the other name for nevus spilus?

A

Speckled lentiginous nevus

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35
Q

Name the diagnosis.

  • What is this also known as?
A

Nevus spilus

(Speckled lentiginous nevus)

  • Homogeneous tan patch within which develops small pigmented macules and papules
  • Presents within first year of life
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36
Q

What is the name of the condition where a nevus spilus/speckled lentiginous nevus is associated with port-wine stains?

  • What other type of spots/nevi may also be found in this condition?
A

Phakomatosis pigmentovascularis

  • May also have dermal melanocytosis (Mongolian spots) and nevus of Ota or Ito
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37
Q

Name the diagnosis.

  • How does this differ from a nevus spilus?
A

Agminated nevus

  • Presents in teenage years
  • Cluster of nevi over a skin-colored background (rather than tan background in nevus spilus)
  • Probably what Addison has on his neck
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38
Q

What is the most common form of pemphigus worldwide?

A

Pemphigus vulgaris

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39
Q

Which desmoglein plays a major role in mucosal epithelial adhesion?

  • Where is this Dsg present in the epidermis and mucosal epithelium?
  • If autoantibodies only targeted this Dsg, then where would blisters form?
A

Desmoglein 3 (Dsg3)

  • Expressed in lower portion of epidermis and throughout mucosal epithelium
  • If only Dsg3 is targeted by autoantibodies, then mucosal blisters form but the skin is intact because of Dsg1
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40
Q

What are the (3) autoimmune conditions that are associated with pemphigus vulgaris?

A
  • Myasthenia gravis
  • Thymoma
  • Autoimmune thyroiditis
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41
Q

Name the diagnosis.

  • Where are the most common sites for lesions?
A

Pemphigus vulgaris

  • All patients have painful oral erosions
  • Most common sites = buccal and palatine mucosa
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42
Q

Where does desmoglein 1 play a major role in epithelial adhesion?

  • Where does this Dsg occur in the epidermis and mucosal epithelium?
A

Desmoglein 1 (Dsg1)

  • Expressed in all levels of epidermis (top > bottom)
  • No significant role mucosal epithelial adhesion (Dsg3 does this)
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43
Q

Name the diagnosis.

  • What are the two “signs” that are positive in this condition?
A

Pemphigus vulgaris

  • Flaccid vesicles/bulla easily rupture, erode and form crust
  • Kodachromes are usually open erosions because vesicles/bulla rupture so easily
  • Positive Nikolsky and Asboe-Hansen signs
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44
Q

What desmogleins are targeted in mucosal-dominant pemphigus? Mucocutaneous pemphigus?

A
  • Mucosal-dominant pemphigus: Dsg3
  • Mucocutaneous pemphigus: Dsg3 and Dsg1
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45
Q

Name the diagnosis.

  • What areas are usually involved?
  • What do early lesions look like? More developed lesions?
  • This is thought to be a reactive phenonemon to what?
A

Pemphigus vegetans

  • Usually involves intertriginous areas
  • Early lesions are flaccid pustules that progress to erosions then ultimately vegetative plaques
  • Reactive phenomenon to friction
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46
Q

Name the diagnosis.

  • What areas are usually involved?
  • What do early lesions look like? More developed lesions?
  • This is thought to be a reactive phenonemon to what?
A

Pemphigus vegetans

  • Usually involves intertriginous areas
  • Reactive phenomenon to friction
  • Early lesions are flaccid pustules that progress to erosions then ultimately vegetative plaques
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47
Q

Neonatal skin has what Dsg expression pattern?

  • This is the same as what tissue in adults?
A

Dsg3

  • The same expression pattern as adult mucosa
  • This is why neonates whose mothers have pemphigus foliaceus (anti-Dsg1 autoantibodies) are unaffected
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48
Q

Maternal autoantibodies against which desmoglein can cross the placenta and cause transient blistering of the infant?

A

Dsg3

  • Neonatal skin has same Dsg expression pattern as adult mucosa
  • This is why neonates whose mothers have pemphigus foliaceus (anti-Dsg1 autoantibodies) are unaffected
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49
Q

What will DIF look like in pemphigus vulgaris?

  • What immunoglobulin and complement is present?
  • What part of the epidermis is most strongly stained?
A
  • Intercellular “chicken wire” staining with IgG (100%) +/- C3
  • Lower epidermis most strongly stained
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50
Q

What is the classic histopathology of pemphigus vulgaris?

  • What is the earliest finding?
  • What is the buzzword?
  • What is present in the blister cavity?
A
  • Eosinophilic spongiosis (earliest finding)
  • Suprabasilar acantholysis
  • “Tombstoning” of basal cells (vertically oriented basal keratinocytes attached to BMZ but not surrounding keratinocytes)
  • Individual rounded-up acantholytic keratinocytes within blister cavity
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51
Q

What are the treatment options for pemphigus vulgaris?

  • First line? Second line?
  • For mild cases?
  • What lab(s) can be used to monitor treatment response?
A
  • First line: oral steroids (1 mg/kg/day) + steroid-sparing immunosuppresive (azathioprine most effective)
  • Tetracycline + nicotinamide for mild cases
  • Second line: plasmapheresis, IVIg, rituximab
  • Monitor treatment response with IIF or ELISA levels
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52
Q

Dsg1 is cleaved by what bacterial toxin in what two infection-related disorders?

A

S. aureus exfoliatoxins

  • Seen in bullous impetigo and SSSS
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53
Q

Name the diagnosis.

  • What is the classic distribution? Is the mucosae involved?
  • What is the clinical exam buzzword?
A

Pemphigus foliaceus

  • Well-demarcated transient impetigo-like crusted erosions on erythematous base
  • Favors seborrheic distribution
  • Look for “cornflake” scale
  • Lacks mucosal involvement
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54
Q

Name the diagnosis.

  • What is the classic distribution? Is the mucosae involved
  • What is the clinical exam buzzword?
A

Pemphigus foliaceus

  • Well-demarcated tranient impetigo-like crusted erosions on erythematous base
  • Favors seborrheic distribution
  • Look for “cornflake” scale
  • Lacks mucosal involvement
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55
Q

What lab work can be used to monitor treatment response in pemphigus vulgaris?

  • What is the substrate used?
  • Which desmoglein do the autoantibodies target?
A
  • IIF: assesses serum IgG against monkey esophagus substrate
  • ELISA: assesses serum anti-Dsg1 and anti-Dsg3 IgG
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56
Q

What are autoantibodies targeting in pemphigus foliaceus?

A

Dsg1

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57
Q

What is the classic histopathology of pemphigus foliaceus?

  • What is the earliest finding?
  • Where in the epidermis does acantholysis occur?
  • What cells are in the blister cavity?
A
  • Eosinophilic spongiosis (early)
  • Subcorneal acantholysis (granular layer >> midlevel epidermis)
  • Look for acantholytic keratinocytes +/- neutrophils and eosinophils in blister cavity
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58
Q

Pemphigus foliaceus has identical histology findings with what three other disorders?

A
  1. Pemphigus erythematosis (i.e., essentially lupus + PE)
  2. Bullous impetigo
  3. SSSS
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59
Q

What is the difference between phototoxic and photoallergic reactions?

  • Which is more common?
  • Which commonly occurs due to topical medications? Systemic medications?
A
  • Phototoxic: common and predictable; occurs in anyone who receives enough drug and UVR; most commonly due to systemic medications
  • Photoallergic: less common but more chronic; occurs only in sensitized patients (delayed-type hypersensitivity); most commonly due to topical photoallergens
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60
Q

Name the diagnosis.

  • What are risk factors for this condition?
A

Pitted keratolysis

  • Small crateriform/cribriform pits and foul odor
  • Risk factors include hyperhidrosis and occlusion
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61
Q

What bacteria causes pitted keratolysis?

  • What can it digest?
A

Caused by Kytococcus sedentarius (a gram-positive bacteria)

  • Digests keratin in the stratum corneum
62
Q

What are possible treatments for pitted keratolysis? (4)

A
  • Topical erythromycin
  • Topical clindamycin
  • Mupirocin
  • Azole antifungals
63
Q

What is the classic histology of pitted keratolysis?

  • What occurs in the stratum corneum?
  • What is the name of the bacteria that causes this?
A
  • Sharply demarcated, deep pits in stratum corneum with gram-positive bacteria (Kytococcus sedentarius) at base of pits
64
Q

Name the diagnosis.

  • What is found on histology?
  • Where is the infiltrate? What is notably deposited in the dermis?
A

Schamberg’s disease

  • Cayenne-pepper purpura on the lower extremities that can extend; middle aged to older adults
  • Histology: hemosiderin containing macrophages with RBC extravasation, endothelial swelling and perivascular lymphocytic infiltrate
65
Q

Name the diagnosis.

  • What is found on the palms and soles? The nails?
A

Pityriasis rubra pilaris

  • Folliculocentric keratotic papules on erythematous base (“nutmeg-grater” papules)
  • Papules coalesce into orange to salmon-colored plaques with “islands of sparing”
  • Orange-red waxy keratoderma of palms and soles (“sandal-like palmoplantar keratoderma [PPK]”)
  • No nails pits (to differentiate from psoriasis)
66
Q

Name the diagnosis.

  • What is found on the palms and soles? The nails?
A

Pityriasis rubra pilaris

  • Folliculocentric keratotic papules on erythematous base (“nutmeg-grater” papules)
  • Papules coalesce into orange to salmon-colored plaques with “islands of sparing”
  • Orange-red waxy keratoderma of palms and soles (“sand-like PPK”)
  • No nails pits (to differentiate from psoriasis)
67
Q

What is the classic histopathology of pityriasis rubra pilaris (PRP)?

  • What occurs in the stratum corneum?
  • What occurs at and around the follicles?
A
  • Alternating vertical and horizontal orthohyperkeratosis and parakeratosis (“checkerboard pattern”)
  • Follicular plugging
  • “Shoulder parakeratosis” (parakeratosis at edges of hair follicle orifice)
68
Q

What are the treatments for pityriasis rubra pilaris (PRP)?

A
  • Acitretin
  • Isotretinoin
  • High-dose vitamin A
  • MTX
  • TNF-alpha inhibitors (infliximab, adalimumab, etanercept)
  • Phototherapy (though note that this may cause flares, so phototesting is recommended)
69
Q

Name the diagnosis.

A

Pityriasis rubra pilaris (PRP), type IV

a.k.a. circumscribed juvenile PRP

70
Q

Name the diagnosis.

  • Where does this occur? What area is usually spared?
A

Poikiloderma of Civatte

  • Reticular reddish-brown telangiectatic patches on neck (central submental region usually spared)
71
Q

What are classic triggers of polyarteritis nodosa (PAN)?

  • Diseases?
  • Medications?
  • Infections?
A
  • Hairy cell leukemia
  • Hepatitis B
  • Autoimmune diseases
  • Medications, including minocycline
  • Infections, including streptococcal infection in children

(Thought to be immune-complex mediated)

72
Q

Name the diagnosis.

  • What other finding may this be associated with?
A

Polyarteritis nodosa

  • Painful single or multiple subcutaneous nodules on lower extremities that may ulcerate
  • +/- livedo reticularis
73
Q

What are the two classic subtypes of medium vessel vasculitis?

A
  1. Polyarteritis nodosa (PAN)
  2. Kawasaki disease
74
Q

What are systemic associations with polyarteritis nodosa (PAN)?

  • What other vasculitis is it associated with?
  • What arteries are affected in PAN?
  • What can happen in the brain?
  • What is the most common cause of death in PAN?
A
  • LCV
  • Necrotizing arteritis of medium-sized arteries (coronary, renal, celiac and mesenteric arteries) of subcutis and dermopannicular junction
  • Microaneurysms, leading to thrombosis, ischemia and necrosis
  • Can lead to HTN and renal failure (most common cause of death)
75
Q

What are the treatment options for the cutaneous-only subtype of polyarteritis nodosa?

  • What should be considered in children?
A
  • ILK, NSAIDs and oral steroids for 3-6 months, if severe skin involvement
  • In children, consider PCN given Streptococcal association
76
Q

What are the treatment options for the multi-system form of polyarteritis nodosa?

A
  • Cyclophosphamide + oral steroids
  • MTX
  • IVIg
  • Need to treat the underlying infection, if present
77
Q

What is the most common photosensitive dermatosis?

A

Polymorphic light eruption (PMLE)

78
Q

What is the onset after UVA exposure when PMLE classically occurs?

A

Arises 1-4 days after UVA

79
Q

Name the diagnosis.

  • What is the primary associated symptom?
A

Polymorphous light eruption (PMLE)

  • Erythematous, itchy papules/vesicles/plaques on sun-exposed areas on sun-exposed areas (malar face, V of neck, outer arms, dorsal hands)
80
Q

What is the classic histopathology of polymorphous light eruption (PMLE)?

  • What occurs in the dermis?
  • Where is the infiltrate located and what composes it?
A
  • Marked papillary dermal edema
  • Dense perivascular dermal lymphocytic inflammation
81
Q

What type of hypersensitivity reaction is PMLE?

A

Delayed (type IV) hypersensitivity reaction

82
Q

What is the treatment for polymorphous light eruption (PMLE)?

  • First line? Second line?
  • What type of UVR causes PMLE?
  • What can be done for prophylaxis? (2)
A
  • Photoprotection (first line): broad-spectrum sunscreens that block UVA (avobenzone, titanium dioxide and zinc oxide)
  • Topical or oral steroids
  • Antimalarial prophylaxis
  • Prophylactic phototherapy in the early spring
83
Q

Is PMLE caused by UVA or UVB?

A

UVA

84
Q

Name the (6) subtypes of porokeratosis.

  • Which three classically affect the palms/soles?
  • What is the name of the subtype that looks like a nevus comedonicus of the palm/sole? What does histology show?
A
  1. Porokeratosis of Mibelli: onset in infancy/childhood; extremities; large circinate plaques with keratotic borders
  2. Disseminated superficial actinic porokeratosis (DSAP): numerous brown-red macules with keratotic borders on sun-exposed areas
  3. Linear porokeratosis: onset in newborns; linear lesions following Blaschko lines; highest SCC risk
  4. Punctate porokeratosis: onset in adolescence; small, “seed-like papules” on palms/soles; no SCC risk
  5. Porokeratosis palmaris, plantaris, et disseminata (PPPD): onset childhood/teens; initially of palms/soles
  6. Porokeratotic eccrine ostial and dermal duct nevus: looks like nevus comedonicus of palm/sole (see photo); histology shows abundant cornoid lamellae arising from acrosyringium
85
Q

Name the diagnosis.

  • When is classic onset?
  • What part of body is usually involved?
A

Porokeratosis of Mibelli

  • Onset in infancy or childhood
  • Extremities
  • Large circinate plaque with keratotic border
86
Q

Name the diagnosis.

  • When is classic onset?
  • What part of body is usually involved?
A

Disseminated superficial actinic porokeratosis (DSAP)

  • Onset in middle age
  • Numerous brownish-red macules with keratotic borders in sun exposed areas
  • Most common on legs
87
Q

What is the classic histology of porokeratosis?

  • What is notable about the stratum corneum and granular layer?
  • How may the epidermis otherwise appear?
A
  • Cornoid lamella (angled column of parakeratosis with underlying hypogranulosis and dyskeratotic cells)
  • Between two cornoid lamellae, the epidermis may otherwise appear atrophic, hyperplastic, normal or BLK-like
88
Q

What syndromes are seen in association with port-wine stains? (6)

A
  1. Maffucci Syndrome
  2. Klippel-Trenaunay
  3. Sturge-Weber
  4. Blue Rubber Bleb
  5. Kasabach-Merritt
  6. Proteus
89
Q

Describe the clinical course of a port-wine stain.

  • When is its onset?
  • How does it progress over time?
  • Do they resolve?
A
  • Present at birth
  • Does not rapidly enlarge (because it is a malformation and NOT a neoplasm), unlike infantile hemangiomas
  • Tend to persist and become more verrucous over time
90
Q

Are port-wine stains GLUT-1 positive or negative?

A

GLUT-1 NEGATIVE

91
Q

Name the diagnosis.

A

Port-wine stain

92
Q

Name the diagnosis.

  • What are other skin findings?
  • What areas are classically afected?
A

Porphyria cutaneous tarda (PCT)

  • Skin findings include: fragility, vesicles, bullae, erosions, milia, scarring, hyperpigmentation, hypertrichosis in photodistributed areas (dorsal hands/forearms)
  • Classic photo is hemorrhagic blisters on dorsal hands
93
Q

Name the diagnosis.

  • What are other skin findings?
  • What areas are classically affected?
A

Porphyria cutaneous tarda (PCT)

  • Skin findings include: fragility, vesicles, bullae, erosions, millia, scarring, hyperpigmentation, hypertrichosis in photodistributed areas (dorsal hands/forearms)
  • Classic photo is hemorrhagic blisters on dorsal hands
94
Q

What enzyme is affected in porphyria cutanea tarda (PCT)?

A

Decreased hepatic uroporphyrinogen decarboxylase (UROD)

95
Q

What are classic triggers of porphyria cutanea tarda?

  • What dietary habits?
  • What hormone?
  • What infections?
A
  • Alcohol abuse
  • Hemochromatosis, high iron/red meat diets
  • Estrogen
  • Hepatitis C
  • HIV
96
Q

Describe the classic histology findings of porphyria cutanea tarda (PCT)?

  • What is inside the blister cavity?
  • What occurs in the epidermis?
  • What buzzword may be found in the blister cavity and epidermis?
A
  • Cell poor subepidermal bulla with “festooning” of dermal papillae
  • “Caterpillar bodies” (pink BMZ material in blister cavity and epidermis; click on photo)
97
Q

What is classically seen on DIF of porphyria cutanea tarda (PCT)?

  • What is deposited (4) and in what pattern?
  • Where is it deposited? (2)
A

IgG, IgM, fibrinogen and C3 linearly along BMZ AND in superficial dermal vessels

98
Q

What is the treatment for porphyria cutanea tarda?

  • What is the classic treatment?
  • What things should be avoided?
  • What medications could be given?
A
  • Phlebotomy
  • Avoid precipitating factors (alcohol, estrogen)
  • Photoprotection/sun avoidance
  • Low-dose hydroxychloroquine
  • Defasirox (iron reducer)
99
Q

Name the diagnosis.

  • How do you describe the normal skin at the margin of the lesion?
  • What are common sites? What about during pregnancy?
A

Pyogenic granuloma

  • Rapidly growing, exophytic, and hemorrhagic papule with epidermal collarette
  • Common sites: gingiva (pregnancy), lips, digits
100
Q

Name the diagnosis.

  • How do you describe the normal skin at the margin of the lesion?
  • What are common sites? What about during pregnancy?
A

Pyogenic granuloma

  • Rapidly growing, exophytic, and hemorrhagic papule with epidermal collarette
  • Common sites: gingiva (pregnancy), lips, digits
101
Q

What are notable associations with pyogenic granuloma?

  • What about medications?
A
  • Trauma
  • Pregnancy
  • OCPs
  • Oral retinoids
  • Indinavir (HIV protease inhibitor)
  • EGFR-inhibitors (lung cancer therapy)
102
Q

Describe the histological findings of pyogenic granuloma.

  • What is this also known as?
  • What happens to the vessels and RBCs?
  • What is the dermis packed with?
  • What may be seen in the epidermis circumscribing the lesion?
A
  • Also known as a lobular capillary hemangioma
  • Well-circumscribed, lobular proliferation of small capillaries with RBC extravasation
  • Dermis with solidly packed endothelial cells, ectatic vessels
  • Epidermal collarette common; erosion, crust, impetigo
103
Q

What is the other term for pyogenic granuloma?

A

(Eruptive) Lobular capillary hemangioma

104
Q

What are the medications implicated in drug-induced sarcoidosis?

  • Patients with what viruses taking what drugs?
A
  • Hepatitis C patients on treatment (IFN-alpha, ribavirin)
  • HIV patients on HAART
  • Other meds: TNF-alpha inhibitors, vemurafenib and ipilimumab (both for melanoma), alemtuzumab (leukemias/lymphomas)
105
Q

What is the suspected pathogenesis of sarcoidosis?

  • What immune cells are involved?
  • What MHC class is involved?
  • What cytokines are involved?
A
  • Genetic predisposition + unknown antigen trigger
  • MHC class II on monocytes binds to unknown antigen and activates CD4+ Th1 cells
  • Increased IL-2, interferon-gamma, TNF-alpha and monocyte chemotactic factor (MCF)
  • Monocytes enter peripheral tissues and form granulomas
106
Q

Patients with cutaneous sarcoidosis should be worked up with what other studies? (3)

A
  1. CXR
  2. PFTs
  3. Regular eye exams
107
Q

Name the diagnosis.

  • What special physical exam finding may be found?
  • What areas of the body does this have a predilection for?
A

Sarcoidosis

  • Look for red-brown or erythematous papules and plaques with “apple jelly” color with diascopy (especially in light skinned patients)
  • Predilection for face (especially lips and nose)
108
Q

Name the diagnosis.

  • What special physical exam finding may be found?
  • What areas of the body does this have a predilection for?
A

Sarcoidosis

  • Look for red-brown or erythematous papules and plaques with “apple jelly” color with diascopy (especially in light skinned patients)
  • Predilection for face (especially lips and nose)
109
Q

Name the diagnosis.

  • What special physical exam finding may be found?
  • What areas of the body does this have a predilection for?
A

Sarcoidosis

  • Look for red-brown or erythematous papules and plaques with “apple jelly” color with diascopy (especially in light skinned patients)
  • Predilection for face (especially lips and nose)
110
Q

What are notable non-cutaneous complications of sarcoidosis?

  • What might occur in the chest cavity?
  • Eyes?
  • Blood?
  • Kidneys?
A
  • Lung disease (“honeycombing” of lung, fibrosis, bronchiectasis)
  • Hilar and/or paratracheal lymphadenopathy
  • Anterior uveitis
  • Hypercalcemia due to calcitriol synthesis by sarcoidal granulomas
  • Nephrocalcinosis due to hypercalcemia
111
Q

Describe the histopathology of sarcoidosis.

  • What is the dermis packed with?
  • What type of granulomas are involved?
  • What special “bodies” may be found within granulomas?
A
  • Superficial and deep dermis packed with nodules of well-formed, non-caseating “naked epithelioid granulomas”
    • ​Lacking significant inflammatory ring
  • Asteroid bodies (star shaped eosinophilic inclusions of collagen) and Schaumann bodies (basophilic calcium and protein inclusions) are commonly seen within granulomas
112
Q

What tests can be performed when suspecting sarcoidosis?

  • What “historical” test could be used?
  • What imaging or testing could be obtained?
  • What lab work could be obtained?
A
  • Kveim-Siltzbach test (mostly historical; injection of suspension of sarcoidal spleen into the skin leads to granuloma formation at injection site)
  • CXR or CT - chest (hilar/paratracheal lymphadenopathy)
  • PFTs (restrictive lung disease pattern)
  • Increased angiotensive converting enzyme (ACE) level (useful for monitoring response to therapy)
  • Increased ESR
113
Q

What is the first line treatment for systemic sarcoidosis?

AND

What is the most effective treatment option for chronic skin involvement?

A
  • First line: oral prednisone for systemic involvement +/- TCS/ILK for skin involvement
  • Most effective treatment for chronic skin involvement: HCQ or CQ
114
Q

Name the (6) major granulomatous dermatitides.

A
  1. Sarcoidosis
  2. Classic granuloma annulare (GA)
  3. Necrobiosis lipoidica
  4. Cutaneous Crohn’s disease
  5. Rheumatoid nodule
  6. Annular elastolytic giant cell granuloma (AEGCG)
115
Q

Name the diagnosis.

A

Spitz nevus

  • ​Most commonly present as pink papules on the face/scalp of a child
116
Q

Name the diagnosis.

A

Spitz nevus

  • ​​Most commonly present as pink papules on the face/scalp of a child
117
Q

What is the suspected pathogenesis of a Spitz nevus?

  • What genetic mutation is suspected?
  • What is the name of the recently described subset of atypical epithelioid Spitz nevi, and what mutation do they have?
A
  • HRAS mutations/11p gains
  • No BRAF mutations (usually)
  • There is also a recently described subset of atypical epithelioid Spitz nevi with loss of BAP-1 tumor suppressor gene (“BAPomas,” which have BRAF mutations)
118
Q

What is the classic histopathology of a Spitz nevus?

  • How does the overall lesion and epidermis appear from the lowest magnification?
  • How are the cells in nests arranged? What occurs around nests?
  • What do the cells in the nests look like in terms of their cytoplasm and nucleoli?
  • What are the special “bodies” present in the epidermis?
  • What should occur as you go from the superficial to deep dermis?
  • What is allowable in the superficial dermis?
A
  • Symmetric and circumscribed
  • Epidermal hyperplasia
  • Large junctional nests with clefting around entire nest
  • Parallel, vertically-oriented nests (“bananas on a tree”) that have vertically-oriented melanocytes
  • Kamino bodies (pink clumps of BMZ material [collagen IV] within epidermis)
  • “Spitzoid” cytology (large epithelioid/spindled cells with abundant pink-purple [amphophilic] cytoplasm and prominent lilac-colored nucleoli [versus cherry-red nucleoli in melanoma])
  • Dermal component “matures” with depth (reduction in density and cell size)
  • Superficial mitoses allowable
119
Q

What is the classic histopathology of a Spitz nevus?

  • How does the overall lesion and epidermis appear from the lowest magnification?
  • How are the cells in nests arranged? What occurs around nests?
  • What do the cells in the nests look like in terms of their cytoplasm and nucleoli?
  • What are the special “bodies” present in the epidermis?
  • What should occur as you go from the superficial to deep dermis?
  • What is allowable in the superficial dermis?
A
  • Symmetric and circumscribed
  • Epidermal hyperplasia
  • Large junctional nests with clefting around entire nest
  • Parallel, vertically-oriented nests (“bananas on a tree”) that have vertically-oriented melanocytes
  • Kamino bodies (pink clumps of BMZ material [collagen IV] within epidermis)
  • “Spitzoid” cytology (large epithelioid/spindled cells with abundant pink-purple [amphophilic] cytoplasm and prominent lilac-colored nucleoli [versus cherry-red nucleoli in melanoma])
  • Dermal component “matures” with depth (reduction in density and cell size)
  • Superficial mitoses allowable
120
Q

What is the classic histopathology of a Spitz nevus?

  • How does the overall lesion and epidermis appear from the lowest magnification?
  • How are the cells in nests arranged? What occurs around nests?
  • What do the cells in the nests look like in terms of their cytoplasm and nucleoli?
  • What are the special “bodies” present in the epidermis?
  • What should occur as you go from the superficial to deep dermis?
  • What is allowable in the superficial dermis?
A
  • Symmetric and circumscribed
  • Epidermal hyperplasia
  • Large junctional nests with clefting around entire nest
  • Parallel, vertically-oriented nests (“bananas on a tree”) that have vertically-oriented melanocytes
  • Kamino bodies (pink clumps of BMZ material [collagen IV] within epidermis)
  • “Spitzoid” cytology (large epithelioid/spindled cells with abundant pink-purple [amphophilic] cytoplasm and prominent lilac-colored nucleoli [versus cherry-red nucleoli in melanoma])
  • Dermal component “matures” with depth (reduction in density and cell size)
  • Superficial mitoses allowable
121
Q

What immunostains would be positive in a Spitz nevus? (4)

A
  • S100A6+
  • p16+
    • Note: p16+ is frequently lost/diminished in atypical Spitz tumors and Spitzoid melanomas
  • S100+
  • Melan-A+
122
Q

Name the disease with this histology.

  • How are the cells arranged?
A

Spitz nevus

  • Nests of cohesive spindled and epithelioid melanocytes with clefts between the nests and a hyperplastic epidermis
123
Q

Name the infections that cause sporotrichoid spread.

A

“No SALT”

Nocardia

Sporotrichosis

Atypical mycobacteria

Leishmaniasis

Tularemia

124
Q

Name the disease.

  • In whom is this classically seen?
A

Sporotrichosis

  • Multiple ascending ulcerated nodules or subcutaneous abscesses
  • Most frequently in gardeners, farmers, veterinarians
125
Q

Name the diagnosis.

  • In whom is this classically seen?
A

Sporotrichosis

  • Multiple ascending ulcerated nodules or subcutaneous abscesses
  • Most frequently in gardeners, farmers, veterinarians
126
Q

What is the treatment for sporotrichosis? (3)

  • What is the treatment of choice?
  • What can be used in disseminated disease?
A
  • Itraconazole (treatment of choice)
  • SSKI (potassium iodide oral solution)
  • Amphotericin B in disseminated disease
127
Q

Name the diagnosis.

  • What is the other name for this condition?
  • What is the buzzword descriptor for these lesions?
  • What areas of the body are favored?
A

Sweet’s syndrome (acute febrile neutrophilic dermatosis)

  • Tender/burning, red, well-demarcated, expanding, edematous/”juicy” papules and plaques
  • Favors head/neck and arms
  • Can have oral lesions
  • May be vesiculobullous, pustular or targetoid
128
Q

What is another name of Sweet’s syndrome?

A

Acute febrile neutrophilic dermatosis

129
Q

Name the diagnosis.

  • What is the buzzword descriptor for these lesions?
  • What areas of the body are favored?
A

Sweet’s syndrome (a.k.a. acute febrile neutrophilic dermatosis)

  • Tender/burning, red, well-demarcated, expanding, edematous/“juicy” papules and plaques
  • Favors head/neck and arms
  • Can have oral lesions
  • May be vesiculobullous, pustular or targetoid
130
Q

Name the triggers of Sweet’s syndrome.

  • ​Infections?
  • Cancers?
  • Diseases?
  • Drugs?
  • Other triggers?
A
  • Infections: mainly Streptococcus, yersiniosis
  • Cancer: AML plus other hematologic and solid malignancies
  • IBD
  • Drugs: G-CSF, GM-CSF, ATRA, TMP/SMX, minocycline, OCPs, furosemide, hydralazine
  • Other: autoimmune CTDs, pregnancy, HIV, HCV
131
Q

What are extracutaneous features of Sweet’s syndrome (acute febrile neutrophilic dermatosis)?

  • Clinical findings?
  • Symptoms?
  • Lab finding?
  • What about the HPI?
A
  • Fever
  • Leukocytosis
  • Arthralgias
  • Ocular involvement
  • Malaise
  • Preceding URI or flu-like symptoms
132
Q

What lab abnormalities are seen with Sweet’s syndrome (acute febrile neutrophilic dermatosis)? (3)

A
  • Leukocytosis with neutrophilia and bandemia
  • ESR and CRP elevation
133
Q

What are the classic histological findings of Sweet’s syndrome?

  • What occurs in the dermis? What cells are abundant?
  • What is generally not present?
A
  • Diffuse dermal neutrophilic infiltrate with karyorrhexis (fragmentation of nuclei) + massive papillary dermal edema
  • Generally lacks LCV
134
Q

What is the treatment for Sweet’s syndrome (acute febrile neutrophilic dermatosis)?

  • Hint: there are several of them.
A
  • Systemic steroids (prednisone 0.5-1.0 mg/kg daily for 4-6 weeks)
  • SSKI (potassium iodide oral solution)
  • Dapsone
  • Colchicine
135
Q

What is the classic histopathology of a syringoma?

  • What do the sweat ducts look like?
  • What is inside the lumen of the sweat ducts? What is lining the inside of them?
  • What does the surrounding stroma look like?
  • Where in the dermis is the lesion?
A
  • Paisley-tie pattern of tadpole or comma-shaped sweat ducts lined by a thin two cell layer of cuboidal cells
  • Eosinophilic cuticle within sweat ducts
  • Amorphous sweat within lumen
  • Surrounding sclerotic stroma
  • Confined to upper half of dermis
136
Q

Name the diagnosis.

  • Where is this typically found?
  • In what patients is this associated with?
A

Syringomas

  • Translucent-skin colored papules on periorbital region (eyelids #1), trunk, genitals
  • Associated with females, Asians, Down syndrome
137
Q

What are the important autoantibodies and cytokines associated with scleroderma (systemic sclerosis)?

  • Think of three anti-nuclear antibodies
A
  • Anti-centromere, anti-Scl70 (anti-topoisomerase I) and anti-RNA polymerase antibodies
  • Profibrotic Th2 cytokines and growth factors (especially TGF-beta)
138
Q

Describe CREST Syndrome.

A
  • Calcinosis cutis
  • Raynaud’s phenomenon
  • Esophageal dysmotility
  • Sclerodactyly
  • Telangiectasias
139
Q

Name the diagnosis.

  • What is the initial presenting sign in 50% of cases?
A

Scleroderma (systemic sclerosis)

  • Skin thickening of fingers of hands extending proximal to MCP joints
  • Note in photo the pitting edema of digits (the initial presenting sign in 50% of cases)
140
Q

Name the diagnosis.

  • What is this finding called?
A

Scleroderma (systemic sclerosis)

This finding is called sclerodactyly.

141
Q

Name the diagnosis.

  • What is this physical exam finding?
A

Scleroderma (systemic sclerosis)

  • This is called microstomia.
142
Q

What are extracutaneous findings of scleroderma (systemic sclerosis)?

  • What occurs in the lungs, heart, esophagus and kidneys?
  • What is the most common cause of death?
A
  • Interstitial lung disease (pulmonary disease is most common cause of death; screen with high-res CT - chest and PFTs)
  • Restrictive cardiomyopathy
  • Esophageal dysmotility
  • Scleroderma renal crisis (help avoid by giving ACE inhibitors)
143
Q

Name the diagnosis.

  • What is the size cut off for this diagnosis?
  • Where on the body do lesions mostly occur?
A

Small plaque parapsoriasis

  • Hyperpigmented or yellowish red scaling patches, round to oval in configuration, with sharply defined, regular borders
  • Lesions should be smaller than 5 cm
  • Can be hypopigmented
  • Mostly occurs on trunk
144
Q

Name the diagnosis.

  • What is the size cut off for this diagnosis?
  • Where on the body do lesions mostly occur?
A

Small plaque parapsoriasis

  • Hyperpigmented or yellowish red scaling patches, round to oval in configuration, with sharply defined, regular borders
  • Lesions should be smaller than 5 cm
  • Can be hypopigmented
  • Mostly occurs on trunk
145
Q

Name the diagnosis.

  • What is the size cut off for this diagnosis?
  • Where on the body do lesions mostly occur?
A

Small plaque parapsoriasis

  • Hyperpigmented or yellowish red scaling patches, round to oval in configuration, with sharply defined, regular borders
  • Lesions should be smaller than 5 cm
  • May be hypopigmented
  • Mostly occurs on trunk
146
Q

Name the diagnosis.

  • What is the size cut off for this diagnosis?
  • Where on the body do lesions mostly occur?
A

Large plaque parapsoriasis

  • Large brown-red, ovoid or irregular plaques with minimal scale
  • Usually asymptomatic or minimally pruritic
  • “Bathing suit” distribution
  • Lesions should be at least 5 cm
  • Resembles patch stage MF (and can progress to MF)
147
Q

Name the diagnosis.

  • What is the size cut off for this diagnosis?
  • Where on the body do lesions mostly occur?
A

Large plaque parapsoriasis

  • Large brown-red, ovoid or irregular plaques with minimal scale
  • Usually asymptomatic or minimally pruritic
  • “Bathing suit” distribution
  • Lesions should be at least 5 cm
  • Resembles patch stage MF (and can progress to MF)
148
Q

Name the diagnosis.

  • What is the size cut off for this diagnosis?
  • Where on the body do lesions mostly occur?
A

Large plaque parapsoriasis

  • Large brown-red, ovoid or irregular plaques with minimal scale
  • Usually asymptomatic or minimally pruritic
  • “Bathing suit” distribution
  • Lesions should be at least 5 cm
  • Resembles patch stage MF (and can progress to MF)
149
Q

What is the rare but important clinical progression of (large plaque) parapsoriasis that we worry about?

A

Progression to cutaneous lymphoma

150
Q

What are the treatment options for parapsoriasis? (2)

A
  • Topical steroids
  • Phototherapy

BASIC Exam Study Guide (11 decks)

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