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

Group 1, Column 2 Flashcards

1
Q

What are treatments for molluscum contagiosum?

  • What are topical and oral treatments?
A
  • Cryotherapy
  • Cantharidin
  • High-dose oral cimetidine
  • Candida antigen immunotherapy
  • Topical retinoids
  • Imiquimod
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2
Q

What are the path findings of molluscum contagiosum?

A

Henderson-Patterson molluscum bodies (intracytoplasmic inclusion bodies)

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3
Q

What is the expected onset after drug initiation of a morbilliform drug eruption?

A

7-14 days

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4
Q

Name some of the most common culprit drugs of morbilliform drug eruptions.

A
  • Beta-lactams (PNCs and CSNs)
  • TMP/SMX
  • Anticonvulsants
  • Allopurinol
  • Classically occurs within 7-14 days
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5
Q

Name the diagnosis.

A

Morbiliform drug eruption

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6
Q

What are some notable triggers/mutations that lead to the development of common acquired melanocytic nevi?

A
  • UV exposure
  • BRAF mutations (found in up to 80%; more common than NRAS mutations)
  • Immunosuppression
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7
Q

How are congenital melanocytic nevi divided by size?

A
  • < 1.5 cm = small
  • 1.5 cm - 20 cm = medium
  • > 20 cm = large

Note: > 40 cm by adulthood has recently been termed “giant”

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8
Q

What does FAMMM Syndrome stand for and what are the key features?

  • Inheritance type
  • Clinical features, family history
  • Genetic mutation
A

Familial Atypical Multiple Mole Melanoma Syndrome

  • AD inheritance
  • Characterised by:
    • 50+ melanocytic nevi
    • Family history of melanoma
    • CDKN2A gene (encodes p16 and p14)
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9
Q

How should large congenital nevi be treated?

  • After what age?
  • When should you screen the patient with an MRI - brain and for what potentially fatal condition?
A
  • Surgical resection should be attempted if possible after 6 months of age
  • If not possible, perform serial examinations with early biopsies of nodular areas
  • If large posterior axial congenital nevi or multiple satellites, then obtain an MRI to screen for neurocutaneous melanosis, a potentially fatal condition
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10
Q

What are the classic histological features of dysplastic nevi?

  • What is seen at the edges?
  • How are the junctional nests arranged?
  • What does the cytologic atypia look like?
A
  • Asymmetry
  • Junctional “shoulder” (extends > 3 rete ridges beyond dermal component)
  • Irregular size and placement of junctional nests with bridging or lentiginous pattern
  • Papillary dermal concentric and/or lamellar fibrosis
  • Cytologic atypia: nuclei enlarged, “dirty grey” cytoplasm
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11
Q

What should you consider if an elderly patient has a new “atypical/dysplastic nevus” of a sun-damaged site?

A

It is most likely well-nested lentigo maligna!

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12
Q

Name the diagnosis.

A

Nummular dermatitis

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13
Q

Name the diagnosis.

  • What is the most common cause of this in adults and children, respectively?
A

White superficial onychomycosis, due to:

T. mentagrophytes (adults) or T. rubrum (children)

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14
Q

What is the classic histology of a dermatophyte infection, including tinea or onychomycosis?

  • What does the corneum and dermis look like?
A
  • Septate hyphae in stratum corneum or nail plate
  • May have brisk dermal infiltrate (versus minimal in tinea versicolor)
  • +/- neutrophilic microabscesses in epidermis or corneum/nail plate
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15
Q

Name the diagnosis.

  • What part of the face is usually spared?
  • What is usually the associated symptom?
A

Perioral dermatitis

  • Look for clusters of small, pink discrete scaly papules/pustules in perioral region with clear zone around vermilion border
  • Can also involve nasolabial folds and cheeks
  • Burning sensation, minimal itching
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16
Q

What is perioral/periorificial dermatitis most commonly attributed to?

A
  • Topical fluorinated corticosteroids
  • Facial cosmetics
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17
Q

What is the treatment of perioral/periorificial dermatitis?

  • What are the oral medications used for adults and kids, respectively?
  • What topical medications can be used?
  • What should be avoided?
A
  • Tetracyclines (or erythromycin in pediatrics) for 6-8 weeks with gradual tapering
  • TCIs, topical metronidazole and other antibacterials
  • Avoid cosmetics, steroids and other irritants
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18
Q

What parts of the face can perioral/periorificial dermatitis involve?

A
  • Basically any part of face
  • Variants include periorbital and periorificial (perioral + periorbital)
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19
Q

What are the notable causes of pityriasis rosea?

  • What infections?
  • What medications?
A
  • HHV-6 and -7
  • Drugs like ACE inhibitors (most common), gold, beta-blockers, NSAIDs and isotretinoin
  • Note that ACE inhibitors, beta-blockers and gold salts are also triggers of drug-induced LP.
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20
Q

Name the diagnosis.

A

Pityriasis rosea

  • Papulosquamous eruption
  • Herald patch followed 1-2 weeks later with patches and plaques with trailing scale in “Christmas tree” pattern
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21
Q

What is the treatment for pityriasis rosea?

  • What oral medication may hasten clearance?
A
  • Not necessarily required
  • Symptomatic treatment with topical steroids, antipruritics
  • Oral erythromycin may hasten clearance
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22
Q

What is the notable histopathology of pityriasis rosea?

  • What changes are seen in the corneum? In the epidermis?
  • What may be present in the dermal papillae?
  • Where is the infiltrate and what composes it?
A
  • Non-adherent thin mounts of parakeratosis (wound be thicker in guttate psoriasis)
  • Spongiosis
  • RBC extravastion
  • Perivascular lymphohistiocytic infiltrate
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23
Q

What are the treatments of prurigo nodularis?

  • Oral and topical medications
A
  • SSRIs/TCAs for underlying psychiatric conditions
  • Doxepin
  • Cryotherapy, ILK, TCS/TCI
  • Methotrexate and cyclosporine have even been used!
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24
Q

Name notable triggers of psoriasis.

  • Namely, what infection, electrolyte disturbance and drugs?
A
  • Koebner phenomenon
  • Infections (streptococcal pharyngitis #1)
  • Hypocalcemia (pustular psoriasis)
  • Pregnancy (impetigo herpetiformis)
  • Drugs (lithium, beta-blockers, TNF-alpha inhibitors, steroid tapers, excess imiquimod use)
  • TNF-alpha inhibitors may cause plaque or palmopustular psoriasis
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25
Q

What infectious trigger classically leads to guttate psoriasis?

A

Group A strep (GAS) infection (oropharynx or perianal)

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26
Q

Name this condition.

  • Clinical finding buzzword
A

Acrodermatitis continua of Hallopeau

  • “Lakes of pus” on distal fingers, toes and nail beds
  • Nail shedding
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27
Q

Name this condition.

  • This is a variant of what other condition?
  • How should the pregnancy be managed?
A

Impetigo herpetiformis

  • Pregnancy associated variant of generalized pustular psoriasis
  • Begins in flexures and generalizes with toxicity
  • Early delivery recommended
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28
Q

Name the condition.

  • What is the associated symptom?
  • What lab abnormalities are often present on CBC and CMP?
A

Generalized pustular (von Zumbusch) psoriasis

  • Rapid and generalized
  • Painful skin
  • Fever, leukocytosis, hypoalbuminemia
  • Associated with hypocalcemia
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29
Q

What are nail changes associated with psoriasis?

A
  • Nail pitting
  • Oil spots, salmon patches
  • Onycholysis
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30
Q

Name the diagnosis.

A

Prurigo nodularis

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31
Q

Name the diagnosis.

A

Psoriasis vulgaris

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32
Q

What are notable systemic treatments for psoriatic arthritis?

A
  • Biologics
  • Methotrexate
  • Apremilast (PDE-4 inhibitor)
  • Cyclosporine
  • Tofacitinib (JAK-1 and -3 inhibitor)
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33
Q

Name the diagnosis.

RF negative or positive?

HLA type?

A

Psoriasis with psoriatic arthritis

  • Typically RF-negative
  • Strong genetic predisposition (50% HLA-B27 positive)
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34
Q

What is the first line therapy for:

mild to moderate psoriasis?

moderate to severe psorasis?

A
  • Mild to moderate: topical corticosteroids
  • Moderate to severe: phototherapy (NB-UVB)
  • Note, most effective wavelenth for treatment is 311 - 313 nm.
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35
Q

What is the classic histopathology of the psoriasis?

  • What happens in the corneum and epidermis?
A
  • Confluent parakeratosis
  • Regular (psoriasiform) acanthosis with elongated rete ridges
  • Decreased/absent stratum granulosum
  • Dilated capillaries of dermal papillae
  • Microabscesses of Munro (stratum corneum)
  • Micropustules of Kogoj (stratum spinosum)
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36
Q

Name the diagnosis.

A

Pyoderma gangrenosum

  • Starts as tender indurated papulopustule
  • Leads to bulla or ulcer
  • Violaceous/grey border
  • Heals with cribriform scar
  • Pathergy
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37
Q

What are notable associations with pyoderma gangrenosum?

A
  • IBD
  • Hematologic disorders (e.g. IgA monoclonal gammopathy, AML and CML)
  • Inflammatory arthritis
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38
Q

Debridement for pyoderma gangrenosum is contraindicated for this reason.

A

Pathergy

  • Insult to the tissue can lead to worsening and expanding
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39
Q

What is the treatment of choice for pyoderma gangrenosum?

  • What are treatments for recalcitrant disease?
A
  • Topical, ILK or systemic steroids
  • Treatment of choice for recalcitrant disease is infliximab or cyclosporine
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40
Q

What is the histopathology for pyoderma gangrenosum?

  • Is the epidermis intact?
  • Where is the infiltrate and what is it composed of?
A
  • Epidermal ulceration with dense underlying superficial and deep dermal neutrophilic infiltrate (inflammation deeper than in Sweet’s syndrome), leukocytoclasis, epidermal pustules, and dermal edema
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41
Q

What are the four main subtypes of rosacea?

A
  • Erythematotelangiectatic
  • Papulopustular
  • Phymatous
  • Ocular
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42
Q

Name the diagnosis.

A

Rosacea

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43
Q

What is the pathogenesis of rosacea?

A
  • Chronic vascular inflammatory disorder
  • Vascular hyperreactivity, solar damage, heat sensitivity
  • Possible association with Demodex mites
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44
Q

How do you tell papulopustular rosacea from acne vulgaris?

A

No comedones in rosacea!

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45
Q

What are the topical and oral treatment options for rosacea?

  • What kind of procedures can be done?
  • How do you treat ocular rosacea?
A
  • Topical: metronidazole, sulfacetamide-sulfur, azelaic acid
  • Oral: tetracyclines, amoxicillin, isotretinoin
  • PDL, CO2 laser, electrosurgery
  • Always need oral therapies for ocular symptoms!
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46
Q

Name the diagnosis and describe the key findings.

  • Who is classically affected by this?
  • What is the treatment?
A

Pyoderma faciale (a.k.a. rosacea fulminans)

  • Females in 20s-30s
  • Rapid onset of intense inflammatory lesions
  • Most develop scarring
  • Treatments: prednisone (with a slow taper), isotretinoin
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47
Q

Name the diagnosis and describe key findings.

  • Who is classically affected by this?
  • Involvement of what part of the face is characteristic of this condition?
A

Lupus miliaris disseminatus faciei

  • Young adults; more common in Asians
  • Smooth firm yellow-brown to red monomorphic papules on butterfly region
  • Eyelid involvement is characteristic (see photo)
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48
Q

Describe key findings in granulomatous rosacea.

  • How do you treat this condition?
A
  • Discrete yellow/brown-red firm papules or nodules on a background of diffusely reddened thickened skin on butterfly area
  • Treatment: TCNs and isotretinoin
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49
Q

Name the condition.

  • What is the cause of this?
  • How might it fluctuate during the day?
  • What is the treatment?
A

Solid facial edema in rosacea

(Morbihan disease or rosacea lymphedema)

  • Chronic inflammation leads to obstruction of lymphatics and fibrosis
  • Hard non-pitting swelling of forehead, glabella, nose and cheeks
  • May be more pronounced in early morning
  • Treatment of choice: isotretinoin +/- ketotifen (an antihistamine)
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50
Q

Name the diagnosis.

A

Scabies

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51
Q

Name the diagnosis.

A

Sebaceous hyperplasia

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52
Q

Name the diagnosis.

A

Seborrheic dermatitis

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53
Q

Name the diagnosis.

A

Seborrheic dermatitis

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54
Q

What is the classic histopathology of seborrheic dermatitis?

  • What occurs in the epidermis? Corneum?
  • Where is the inflammation?
A
  • Irregular to psoriasiform acanthosis
  • Spongiosis
  • “Shoulder parakeratosis”
  • Superficial perivascular and perifollicular infiltrate
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55
Q

What other conditions is seborrheic dermatitis associated with?

A

HIV and Parkinson’s disease

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56
Q

What is the classic histopathology of seborrheic keratosis?

  • What happens in the epidermis? Corneum?
A
  • Orthohyperkeratosis with pseudohorn cysts
  • Flat base (“string sign”)
  • Acanthosis and papillomatosis
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57
Q

Name the diagnosis.

A

Inflamed SK

58
Q

Name the diagnosis.

A

Small vessel vasculitis (specifically LCV)

  • Look for partially blanchable, symmetric, palpable purpura on the lower extremities (dependent areas)
59
Q

What is the pathophysiology of cutaneous small vessel vasculitis?

  • What type of vessels are affected?
A
  • Immune complex deposition in post-capillary venules activates complement, leading to neutrophilic inflammation
  • Ultimately vessel damage (fibrinoid necrosis), hemorrhage and tissue necrosis occurs
60
Q

Name examples of small vessel vasculitis.

A
  • Henoch-Schonlein purpura (HSP)
  • Acute hemorrhagic edema of infancy
  • Urticarial vasculitis
  • Erythema elevatum diutinum (EED)
  • Granuloma faciale
  • Secondary vasculitis to drug, infection, malignancy or autoimmune
61
Q

Name the diagnosis and key features of this condition.

  • What causes it, and when is its onset?
  • What red flags should be watched out for?
A

Henoch-Schonlein purpura

  • Most common pediatric vasculitis
  • IgA vascular deposition in blood vessels leads to neutrophilic inflammation
  • Occurs 1-2 weeks after URI or Streptococcus infection
  • Look for palpable purpura on buttocks/legs, arthralgias, abdominal pain, blood in stool, hematuria and even ESRD
62
Q

What are infectious causes of secondary small vessel vasculitis?

A
  • Bacterial: group A beta-hemolytic Streptococcus (GAS), Neisseria
  • Viral: hepatitis C > B >> A, HIV
  • Candida
63
Q

What are common causes of drug-induced small vessel vasculitis?

A
  • Beta-lactams
  • Sulfonamides
  • TNF-alpha inhibitors
  • Levimasole-tainted cocaine
  • NSAIDs
  • Propylthiouracil
  • BP medications
64
Q

Name the diagnosis and key features of this condition.

  • What age range is affected typically?
  • What causes it?
  • How do you treat it?
A

Acute hemorrhagic edema of infancy

  • In children <3 years; not ill appearing
  • Immune complex deposition in small vessels (a small vessel vasculitis)
  • Look for annular or targetoid edematous hemorrhagic plaques on head (cheeks and ears) or extremities
  • Treatment: supportive care with antihistamines
  • Spontaneous resolution within 1-3 weeks
65
Q

Name the diagnosis and key features of this condition.

  • How is the complement level affected?
  • What are the associated symptoms?
  • How long do lesions last?
A

Urticarial vasculitis

  • Either normal complement level (70-80%; usually idiopathic) or low complement level (20-30%; associated with systemic disease)
  • See painful/burning urticarial lesions lasting > 24 hours
  • Recurrent episodes lasting months to years
66
Q

Name the diagnosis.

A

Granuloma faciale

  • Red-brown papules, plaques and nodules of face, especially nose, malar prominence, forehead and ear
  • Follicular prominence, “peau d’orange” appearance
  • A small vessel vasculitis
67
Q

Name the diagnosis and key features.

  • What infection is this associated with?
  • What is the cause?
  • What is the treatment?
A

Erythema elevatum diutinum (EED)

  • A small vessel vasculitis
  • Associated with HIV
  • Immune complex deposition with repeat inflammation leads to perivascular fibrosis
  • Early lesions: red-brown violaceous nodules and plaques on extensor surfaces
  • Later lesions: firm nodules
  • Dapsone is treatment of choice
68
Q

What is the classic histopathology of small vessel vasculitis?

  • What inflammatory cell is primarily involved?
  • What occurs at vessel walls?
  • What does DIF show?
A
  • Perivascular neutrophilic infiltrate with leukocytoclasis at post-capillary venules
  • Fibrinoid necrosis of vessel walls
  • RBC extravasation
  • DIF with perivascular C3 and IgM
69
Q

Adults who present with fever, elevated ESR and purpura above the waist are more likely to have what condition?

A. HSP

B. IgA glomerulonephritis

A

IgA glomerulonephritis

70
Q

What are treatments for Henoch Schonlein purpura?

  • What about when abdominal pain, arthritis or nephritis occurs?
  • What can treat the skin findings? Abdominal pain?
  • What can be used for RPGN?
A
  • Supportive measures
  • Prednisone +/- azathioprine or cyclosporine if abdominal pain, arthritis or severe nephritis
  • Dapsone (for skin findings)
  • Ranitidine (for abdominal pain)
  • IVIG if having rapidly progressive glomerulonephritis (RPGN)
71
Q

What lab testing should be done for Henoch Schonlein purpura?

  • What does DIF show
    What kind of follow up is needed?
  • What should be obtained if there is abdominal pain?
A
  • DIF shows IgA in blood vessel walls
  • Long term follow up with serial UAs
  • Guaiac if abdominal pain or GI bleed suspected
72
Q

What is the classic histopathology of Henoch Schonlein purpura?

  • What kind of vasculitis is present?
  • What does DIF show?
  • What biopsy finding is associated with renal disease?
A
  • LCV
  • DIF with IgA, C3 and fibrin in dermal small blood vessels
  • No eosinophils in biopsy is associated with renal disease!
73
Q

What is the classic histopathology of granuloma faciale?

  • What kind of vasculitis is present?
  • What occurs at the superficial dermis?
  • What kind of infiltrate is present?
  • What is notably NOT present?
A
  • LCV
  • Grenz zone (narrow area of papillary dermis that is normal)
  • Dense mixed dermal infiltrate with eosinophils, neutrophils, lymphocytes and plasma cells
  • Despite the name, there are no granulomas in the tissue
74
Q

Name the diagnosis.

A

SCC

75
Q

How do you treat granuloma faciale?

  • What are the oral treatments for refractory disease?
A
  • ILK
  • Cryotherapy
  • Topical steroids and steroid-sparing agents
  • If unresponsive, dapsone, colchicine or Plaquenil
76
Q

Name the diagnosis.

A

Keratoacanthoma (SCC)

77
Q

Name the diagnosis.

A

SCC in situ

  • Also known as Bowen’s disease
78
Q

What is the classic histopathology of Bowen’s disease (SCCis)?

  • What happens to the epidermis? Corneum?
  • Are follicles involved?
A
  • Full-thickness keratinocyte atypia (often involving follicles)
  • Disorganized (“windblown”) architecture with loss of normal maturation
  • Acanthosis, parakeratosis
  • Dyskeratotic keratinocytes
79
Q

Name the two variants of SCCis of the penis.

  • Which has higher malignant potential?
A
  1. Bowenoid papulosis: multiple hyperpigmented penile papules with lower malignant potential)
  2. Erythroplasia of Queyrat: juicy red, erosive plaques on the glans penis with higher malignant potential
80
Q

What are the risk factors for developing SCC?

A
  • Chronic sun-exposure, male, age, fair skin
  • Immunosuppression, HPV
  • Radiation
  • Chronic non-healing wounds (i.e., Marjolin’s ulcer)
  • Hypertrophic LE/LP
  • Arsenic exposure
  • Chronic LS&A
  • CLL
  • Vemurafenib, long-term voriconazole
  • Transplant patient (65x increased risK)
81
Q

What is the classic histopathology of invasive SCC?

A
  • Full-thickness keratinocytic atypia with dermal invasion
82
Q

Describe the clinical findings of stasis dermatitis.

A
  • Pitting edema and hemosiderin deposits
  • Lipodermatosclerosis (“inverted wine bottle” appearance of lower legs)
  • Atrophie blanche (white stellate scars)
83
Q

Name the clinical finding.

A

Lipodermatosclerosis

  • “Inverted champagne bottle”
  • Tight circular cuff over distal leg from chronic inflammation
84
Q

Name the clinical finding.

A

Atrophie blanche

  • Typically seen in medial supramalleolar region
85
Q

Name the #1 cause of tinea capitis in the U.S. and worldwide.

A
  • In the U.S., Trichyophyton tonsurans
  • In the world, Microsporum canis
86
Q

Name the 3 types of tinea pedis.

A
  • Moccasin
  • Interdigital
  • Vesiculobullous
87
Q

Name the diagnosis.

A

Tinea pedis

88
Q

Name the diagnosis.

A

Tinea capitus (complicated by kerion)

89
Q

How do you treat tinea versicolor?

A
  • Topical or systemic -azole antifungals
  • Selenium sulfide shampoo
  • Topical ciclopirox
90
Q

Name the diagnosis.

A

Tinea corporis

91
Q

Describe the clinical presentation of tinea versicolor.

  • What is the classic distribution the body?
  • What is hypopigmentation due to?
  • What physical exam findings can aid diagnosis?
A
  • Hyper- and hypo-pigmented macules and patches in a sebaceous distribution
  • Hypopigmentation is due to melanocyte inhibition by azelaic acid, a byproduct of Malassezia
  • Use a Woods lamp
  • Scratching may accentuate fine scale
92
Q

Name the diagnosis.

A

Tinea versicolor

93
Q

Name the diagnosis.

A

Tinea versicolor

94
Q

Name the diagnosis.

A

Tinea cruris

95
Q

Name the diagnosis

A

Tinea faciei

96
Q

Name the diagnosis.

A

Bullous tinea manuum

97
Q

What are the most common culprit medications in SJS/TEN?

A
  • Allopurinol
  • Anticonvulsants (safe ones to use are valproic acid or lamotrigine)
  • Antibiotics (sulfonamides)
  • NSAIDs
  • NNRTIs (nevirapine, abacavir)
98
Q

What is the suspected pathogenesis of SJS/TEN?

  • What MHC and T-cells are involved?
  • What cell mediators are involved?
A
  • Drug binds to MHC I complex, forming antigen recognized by cytotoxic CD8+ T-cells
  • Granulysin released by immune cells leads to keratinocyte apoptosis
  • FasL-Fas complex is formed on target keratinocytes, leading to activation of caspases and triggering apoptosis
99
Q

How can you differentiate between SJS and TEN based on BSA involvement of desquamation?

A
  • SJS: < 10%
  • SJS-TEN overlap: 10-30%
  • TEN: > 30%
  • Mucosal involvement in 92-100% of SJS patients and 100% of TEN patients
100
Q

What is Nikolsky’s sign?

A

Tangential pressure induces dermal-epidermal cleavage

101
Q

What is the single most important risk factor in predicting mortality from SJS/TEN?

A

Serum bicarbonate (< 20 mmol/L)

102
Q

What is the classic histopathology of SJS/TEN?

  • What cells are present in dermis?
A
  • Early: apoptotic keratinocytes scattered among all epidermal layers with scant dermal lymphohistiocytic infiltrate with eosinophils
  • Later: confluent full-thickness epidermal necrosis again with scant dermal lymphohistiocytic infiltrate with eosinophils
  • Note: eosinophils are not usually seen in erythema multiforme
103
Q

What is the treatment for SJS/TEN?

A
  • Discontinue medication culprit
  • Early administration of high dose IVIg (2-4 gm/kg over 3-4 days)
  • Systemic steroids and other immunosuppressants are controversial
104
Q

What are the two possible sequelae for a baby that can occur due to a primary varicella eruption (chicken pox) during pregnancy?

  • When does primary infection occur in each?
  • How do they compare in terms of mortality risk?
A
  • Congenital varicella syndrome: infection within first 20 weeks of gestation
    • Cutaneous scarring
    • CNS/ocular/limb anomalies
    • Baby prone to shingles in childhood
  • Neonatal varicella: infection within 5 days prior to delivery to 2 days post-delivery
    • ​30% mortality due to lack of protective maternal antibodies
105
Q

What is the treatment of choice for a primary varicella infection?

  • How do you treat healthy versus immunocompromised patients?
A
  • Systemic acyclovir or valacyclovir within 3 days of lesion onset will decrease duration/severity of disease
  • Oral treatment appropriate in healthy patients
  • IV treatment needed in the immunocompromised
106
Q

What is the difference in presentation between a primary varicella infection and subquent reactivation of the virus?

A
  • Primary varicella infection: chicken pox
  • Reactivation: herpes zoster, a.k.a. shingles
107
Q

What is the post-exposure prophylaxis recommended for those exposed to primary varicella?

  • Immunocompetent
  • Immunocompromised, pregnant females and neonates
A
  • Varicella vaccine within 3-5 days of exposure in the non-immune, immunocompetent individuals > 12 months
  • VZIg or IVIg within 4 days of exposure in immunocompromised, pregnant females and neonates
    • Then oral acyclovir can be administered within 7-10 days of exposure
108
Q

Name the diagnosis.

A

Varicella (chicken pox)

“Dew drops on a rose petal”

109
Q

Name the diagnosis.

A

Vitiligo

110
Q

What is the pathogenesis of vitiligo?

A
  • Multifactorial with genetic and non-genetic causes
  • Absence of functional melanocytes due to melanocyte destruction
  • Many theories for how destruction occurs:
    • Autoimmune; autoreactive T-cells
    • Intrinsic defect in melanocytes
    • Oxidative stress
    • Dysregulation of nervous system
    • ……….??? Unknown!
111
Q

What are the known associations with vitiligo?

Hint: think endocrine, other skin findings, eyes

A

Other autoimmune diseases!

  • Thyroid dysfunction (most common)
  • Halo nevi
  • T1DM
  • Addison’s disease
  • Alopecia areata
  • Uveitis
112
Q

What are the treatments available for vitiligo?

  • Topicals
  • Lasers
  • Oral medications
A
  • Topical steroids
  • Calcineurin inhibitors
  • Topical vitamin D analogs
  • NB-UVB or excimer laser
  • Systemic immunosuppressants
  • Depigmentation
113
Q

What are the bad prognostic indicators of vitiligo?

A
  • Mucosal involvement
  • Family history
  • Koebnerization
  • Non-segmental disease
114
Q

Name the diagnosis.

A

CTCL

115
Q

Name the diagnosis.

A

CTCL

116
Q

What are the different clinical stages of mycosis fungoides?

A
  • Patch: irregular erythematous scaly patches in non sun-exposed/bathing suit distribution
  • Plaque: Well-demarcated violaceous to red-brown plaques
  • Tumor: rapidly growing nodules with frequent ulceration; arises in a backgroun of patch and plaque lesions
117
Q

What are the histologic features of patch stage MF?

  • Where are the lymphocytes located?
  • What are the clusters of lymphocytes called?
A
  • Epidermotropic atypical lymphocytes (enlarged with cerebriform, hyperchromic nuclei) predominantly in the epidermis in clusters (Pautrier’s microabscesses) and lined up at the DEJ with clear halos surrounding the cells
118
Q

What are the histopathologic features of plaque stage MF?

  • Where are the lymphocytes located?
A
  • More prominent epidermotropism than patch stage with more atypical lymphocytes in the dense dermal band-like infiltrate
119
Q

What are the histopathologic features of tumor stage MF?

  • Where are the lymphocytes located?
  • How does the epidermotropism compare with patch or plaque stage MF?
A
  • Increased density and depth of dermal infiltrate of atypical lymphocytes with decreased/absent epidermotropism
120
Q

What is the typical immunophenotype for MF?

  • I.e., what kind of CDs are present on the T-cells?
A
  • CD3 positive
  • CD4 positive
  • CD8 negative
  • Look for CD4:CD8 ratio of 10:1
121
Q

What are the treatment options for MF?

  • What medications are often added for progressive/advanced disease?
A
  • Patch/plaque stage: TCS/ILK, nitrogen mustard, phototherapy, radiotherapy
    • Can add IFN-alpha or retinoids for progressive disease
  • Systemic chemotherapy: reserved for advanced/rapidly progressive disease (increased risk of secondary infections)
122
Q

Describe Sezary syndrome.

  • What are the clinical features and symptoms?
  • What lab finding is needed to diagnose this condition?
A
  • Neoplastic Sezary cells present in skin, blood and nodes
  • Erythroderma, lymphadenopathy
  • Intensely pruritic
  • Must have circulating populations of CD4 positive T-cells with absolute count of > 1000 cells/µL
  • Poor prognosis
123
Q

Name the diagnosis.

A

Tumor stage MF

124
Q

What are the strains of HPV that classically cause common warts and palmar/plantar warts?

A
  • HPV-1
  • HPV-2
  • HPV-4
125
Q

What is the classic histopathology of palmar/plantar warts?

  • What happens in the epidermis? Corneum?
  • What keratinocyte structural change is present?
A
  • “Church spire” papillomatosis
  • Hyperkeratosis
  • Acanthosis with elongated rete ridges
  • Hypergranulosis
  • Koilocytosis (nuclear enlargement and hyperchromasia)
  • Increased dermal vessels
126
Q

Name the diagnosis.

  • What infection causes this?
A

Plantar wart

  • Usually caused by HPV-1, HPV-2 or HPV-4
127
Q

Name the diagnosis.

  • What infection causes this?
A

Common wart

  • Usually caused by HPV-1, HPV-2 or HPV-4
128
Q

Name the diagnosis.

  • What infection causes this?
A

Palmar/plantar wart

  • Usually caused by HPV-1, HPV-2 or HPV-4
129
Q

Name the diagnosis.

  • What infection causes this?
A

Plantar wart

  • Usually caused by HPV-1, HPV-2 or HPV-4
130
Q

Name the diagnosis.

  • What infection causes this?
  • What parts of the body are usually affected?
A

Flat/plane warts

  • Light pink/brown, soft/smooth, sometimes linear papules
  • HPV-3, HPV-10
  • Prefers dorsal hands and face
  • More common in children, adult women
131
Q

Name the diagnosis.

  • What infection causes this?
  • What parts of the body are usually affected?
A

Flat/plane warts

  • Light pink/brown, soft/smooth, sometimes linear papules
  • Prefers dorsal hands and face
  • More common in children, adult women
  • HPV-3, HPV-10
132
Q

Name the diagnosis.

  • What infection causes this?
  • What parts of the body are usually affected?
A

Flat/plane warts

  • Light pink/brown, soft/smooth, sometimes linear papules
  • HPV-3, HPV-10
  • Prefers dorsal hands and face
  • More common in children, adult women
133
Q

What is the most common STD?

A

Genital warts (condyloma acuminata)

134
Q

Name the diagnosis.

  • What infection causes this?
  • What reagent can be applied to the area to visualize lesions?
A

Condyloma acuminata (genital warts)

  • HPV-6, HPV-11, HPV-16, HPV-18, HPV-31, HPV-33 and HPV-45 (underlined are hi-risk for CA)
  • Condyloma plana (flat warts) best seen with acetic acid (whitening of warts)
135
Q

Name the diagnosis.

  • What infection causes this?
  • What reagent can be applied to the area to visualize lesions?
A

Condyloma acuminata (genital warts)

  • HPV-6, HPV-11, HPV-16, HPV-18, HPV-31, HPV-33 and HPV-45 (underlined are hi-risk for CA)
  • Condyloma plana (flat warts) best seen with acetic acid (whitening of warts)
136
Q

What are treatments for genital warts?

  • Topicals
  • Procedures
A
  • Cryotherapy
  • TCA peel (high concentrations)
  • Electrosurgery
  • Scissors/shave removal
  • CO2 laser or PDT
  • Podophyllin (Podofilox)
  • Imiquimod
  • Cidofovir gel/intralesional
137
Q

Name the diagnosis.

  • What infection can lead to this?
  • What is another term for how this lesion appears histologically?
A

Bowenoid papulosis

  • ​Multiple red-brown or white papules/smooth plaques
  • Associated with hi-risk HPV subtypes (16, 18, 31, 33, 45)
  • “High-grade squamous intraepithelial lesions (HSIL)”
  • Progression to invasive SCC very rare
138
Q

Name the diagnosis.

  • What infection can lead to this?
  • What is another term for how this lesion appears histologically?
A

Bowenoid papulosis

  • ​Multiple red-brown or white papules/smooth plaques
  • Associated with hi-risk HPV subtypes (16, 18, 31, 33, 45)
  • High-grade squamous intraepithelial lesions (HSIL)
  • Progression to invasive SCC very rare
139
Q

Name the diagnosis.

  • What infection can lead to this?
  • What invasive neoplasm can this progress to?
A

Erythroplasia of Queyrat

  • Red smooth plaque on glabrous genitals
  • A/w hi-risk HPV types (16, 18, 31, 33, 45)
  • Either an HSIL or SCCis
  • Can progress to invasive SCC
140
Q

Name the diagnosis.

  • This is part of what group of skin neoplasms?
  • What infection can cause this?
  • What is the treatment?
A

Buschke-Löwenstein tumor

  • Part of group of verrucous carcinomas
  • Cauliflower-like tumors
  • HPV-6 and -11
  • Treat with excision
141
Q

Name the diagnosis.

  • What infection can cause this? What other condition is caused by the same infection?
  • What other infectious disease looks similar to this condition?
A

Oral warts

  • Soft pink-white papules
  • HPV-6 and -11 (same as in Buschke-Lowenstein tumor)
  • Also see Heck’s disease (focal epithelial hyperplasia; see photo), caused by HPV-13 and -32

BASIC Exam Study Guide (11 decks)

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