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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
What infectious trigger classically leads to **guttate psoriasis**?
**Group A strep (GAS) infection** (oropharynx or perianal)
26
Name this condition. * Clinical finding buzzword
**Acrodermatitis continua of Hallopeau** * "Lakes of pus" on distal fingers, toes and nail beds * Nail shedding
27
Name this condition. * This is a variant of what other condition? * How should the pregnancy be managed?
**Impetigo herpetiformis** * **Pregnancy associated** variant of generalized pustular psoriasis * Begins in flexures and generalizes with toxicity * Early delivery recommended
28
Name the condition. * What is the associated symptom? * What lab abnormalities are often present on CBC and CMP?
**Generalized pustular (von Zumbusch) psoriasis** * Rapid and generalized * Painful skin * Fever, **leukocytosis, hypoalbuminemia** * Associated with **hypocalcemia**
29
What are nail changes associated with **psoriasis**?
* **Nail pitting** * **Oil spots, salmon patches** * **Onycholysis**
30
Name the diagnosis.
**Prurigo nodularis**
31
Name the diagnosis.
**Psoriasis vulgaris**
32
What are notable systemic treatments for **psoriatic arthritis**?
* Biologics * Methotrexate * Apremilast (PDE-4 inhibitor) * Cyclosporine * Tofacitinib (JAK-1 and -3 inhibitor)
33
Name the diagnosis. RF negative or positive? HLA type?
**Psoriasis with psoriatic arthritis** * Typically **RF-negative** * Strong genetic predisposition (**50% HLA-B27 positive**)
34
What is the first line therapy for: **mild to moderate** psoriasis? **moderate to severe** psorasis?
* Mild to moderate: **topical corticosteroids** * Moderate to severe: **phototherapy (NB-UVB)** * Note, most effective wavelenth for treatment is **311 - 313 nm**.
35
What is the classic histopathology of the **psoriasis**? * What happens in the corneum and epidermis?
* **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)
36
Name the diagnosis.
**Pyoderma gangrenosum** * Starts as tender indurated papulopustule * Leads to bulla or ulcer * **Violaceous/grey border** * Heals with **cribriform scar** * **Pathergy**
37
What are notable associations with **pyoderma gangrenosum**?
* **IBD** * Hematologic disorders (e.g. **IgA monoclonal gammopathy, AML and CML**) * **Inflammatory arthritis**
38
Debridement for **pyoderma gangrenosum** is contraindicated for this reason.
**Pathergy** * Insult to the tissue can lead to worsening and expanding
39
What is the treatment of choice for **pyoderma gangrenosum**? * What are treatments for recalcitrant disease?
* Topical, ILK or systemic steroids * **Treatment of choice for recalcitrant disease is infliximab or cyclosporine**
40
What is the histopathology for **pyoderma gangrenosum**? * Is the epidermis intact? * Where is the infiltrate and what is it composed of?
* Epidermal ulceration with dense underlying **superficial and deep dermal neutrophilic infiltrate** (inflammation deeper than in Sweet's syndrome), leukocytoclasis, epidermal pustules, and dermal edema
41
What are the four main subtypes of **rosacea**?
* Erythematotelangiectatic * Papulopustular * Phymatous * Ocular
42
Name the diagnosis.
**Rosacea**
43
What is the pathogenesis of **rosacea**?
* Chronic vascular inflammatory disorder * Vascular hyperreactivity, solar damage, heat sensitivity * Possible association with *Demodex* mites
44
How do you tell **papulopustular rosacea** from **acne vulgaris**?
**No comedones in rosacea!**
45
What are the topical and oral treatment options for **rosacea**? * What kind of procedures can be done? * How do you treat ocular rosacea?
* Topical: metronidazole, sulfacetamide-sulfur, azelaic acid * Oral: **tetracyclines,** amoxicillin, isotretinoin * PDL, CO2 laser, electrosurgery * Always need oral therapies for ocular symptoms!
46
Name the diagnosis and describe the key findings. * Who is classically affected by this? * What is the treatment?
**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**
47
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?
**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)
48
Describe key findings in **granulomatous rosacea**. * How do you treat this condition?
* Discrete **yellow/brown-red firm papules** or nodules on a background of diffusely reddened thickened skin on butterfly area * Treatment: TCNs and isotretinoin
49
Name the condition. * What is the cause of this? * How might it fluctuate during the day? * What is the treatment?
**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)
50
Name the diagnosis.
**Scabies**
51
Name the diagnosis.
**Sebaceous hyperplasia**
52
Name the diagnosis.
**Seborrheic dermatitis**
53
Name the diagnosis.
**Seborrheic dermatitis**
54
What is the classic histopathology of **seborrheic dermatitis**? * What occurs in the epidermis? Corneum? * Where is the inflammation?
* Irregular to psoriasiform acanthosis * **Spongiosis** * **"Shoulder parakeratosis"** * Superficial perivascular and perifollicular infiltrate
55
What other conditions is **seborrheic dermatitis** associated with?
**HIV and Parkinson's disease**
56
What is the classic histopathology of **seborrheic keratosis**? * What happens in the epidermis? Corneum?
* Orthohyperkeratosis with **pseudohorn cysts** * **Flat base ("string sign")** * Acanthosis and papillomatosis
57
Name the diagnosis.
**Inflamed SK**
58
Name the diagnosis.
**Small vessel vasculitis (specifically LCV)** * Look for **partially blanchable, symmetric, palpable purpura on the lower extremities** (dependent areas)
59
What is the pathophysiology of cutaneous **small vessel vasculitis**? * What type of vessels are affected?
* Immune complex deposition in **post-capillary venules** activates complement, leading to neutrophilic inflammation * Ultimately vessel damage (fibrinoid necrosis), hemorrhage and tissue necrosis occurs
60
Name examples of **small vessel vasculitis**.
* 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
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?
**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
What are infectious causes of _secondary_ **small vessel vasculitis**?
* Bacterial: group A beta-hemolytic Streptococcus (GAS), Neisseria * Viral: hepatitis C \> B \>\> A, HIV * Candida
63
What are common causes of **drug-induced small vessel vasculitis**?
* **Beta-lactams** * **Sulfonamides** * **TNF-alpha inhibitors** * **Levimasole-tainted cocaine** * NSAIDs * Propylthiouracil * BP medications
64
Name the diagnosis and key features of this condition. * What age range is affected typically? * What causes it? * How do you treat it?
**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
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?
**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
Name the diagnosis.
**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
Name the diagnosis and key features. * What infection is this associated with? * What is the cause? * What is the treatment?
**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
What is the classic histopathology of **small vessel vasculitis**? * What inflammatory cell is primarily involved? * What occurs at vessel walls? * What does DIF show?
* Perivascular **neutrophilic infiltrate** with **leukocytoclasis at _post-capillary venules_** * **Fibrinoid necrosis of vessel walls** * **RBC extravasation** * **DIF with perivascular C3 and IgM**
69
Adults who present with fever, elevated ESR and purpura above the waist are more likely to have what condition? ## Footnote A. HSP B. IgA glomerulonephritis
**IgA glomerulonephritis**
70
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?
* 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
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?
* DIF shows IgA in blood vessel walls * Long term follow up with serial UAs * Guaiac if abdominal pain or GI bleed suspected
72
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?
* LCV * DIF with **IgA, C3 and fibrin** in dermal small blood vessels * No eosinophils in biopsy is associated with renal disease!
73
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?
* 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
Name the diagnosis.
**SCC**
75
How do you treat **granuloma faciale**? * What are the oral treatments for refractory disease?
* **ILK** * Cryotherapy * Topical steroids and steroid-sparing agents * If unresponsive, dapsone, colchicine or Plaquenil
76
Name the diagnosis.
**Keratoacanthoma** (SCC)
77
Name the diagnosis.
**SCC in situ** * Also known as Bowen's disease
78
What is the classic histopathology of **Bowen's disease (SCCis)**? * What happens to the epidermis? Corneum? * Are follicles involved?
* Full-thickness keratinocyte atypia (often involving follicles) * Disorganized ("windblown") architecture with loss of normal maturation * Acanthosis, parakeratosis * Dyskeratotic keratinocytes
79
Name the two variants of **SCCis of the penis**. * Which has higher malignant potential?
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
What are the risk factors for developing **SCC**?
* 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
What is the classic histopathology of **invasive SCC**?
* Full-thickness keratinocytic atypia with dermal invasion
82
Describe the clinical findings of **stasis dermatitis**.
* Pitting edema and hemosiderin deposits * Lipodermatosclerosis ("inverted wine bottle" appearance of lower legs) * Atrophie blanche (white stellate scars)
83
Name the clinical finding.
**Lipodermatosclerosis** * "Inverted champagne bottle" * Tight circular cuff over distal leg from chronic inflammation
84
Name the clinical finding.
**Atrophie blanche** * Typically seen in **medial supramalleolar region**
85
Name the #1 cause of **tinea capitis** in the U.S. and worldwide.
* In the **U.S.**, ***Trichyophyton tonsurans*** * In the **world**, ***Microsporum canis***
86
Name the 3 types of **tinea pedis**.
* Moccasin * Interdigital * Vesiculobullous
87
Name the diagnosis.
**Tinea pedis**
88
Name the diagnosis.
**Tinea capitus** (complicated by kerion)
89
How do you treat **tinea versicolor**?
* Topical or systemic -azole antifungals * Selenium sulfide shampoo * Topical ciclopirox
90
Name the diagnosis.
**Tinea corporis**
91
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?
* 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
Name the diagnosis.
**Tinea versicolor**
93
Name the diagnosis.
**Tinea versicolor**
94
Name the diagnosis.
**Tinea cruris**
95
Name the diagnosis
**Tinea faciei**
96
Name the diagnosis.
**Bullous tinea manuum**
97
What are the most common culprit medications in **SJS/TEN**?
* **Allopurinol** * Anticonvulsants (safe ones to use are valproic acid or lamotrigine) * Antibiotics (**sulfonamides**) * NSAIDs * NNRTIs (**nevirapine, abacavir**)
98
What is the suspected pathogenesis of **SJS/TEN**? * What MHC and T-cells are involved? * What cell mediators are involved?
* 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
How can you differentiate between **SJS** and **TEN** based on BSA involvement of **_desquamation_**?
* SJS: \< 10% * SJS-TEN overlap: 10-30% * TEN: \> 30% * Mucosal involvement in 92-100% of SJS patients and 100% of TEN patients
100
What is **Nikolsky's sign**?
**Tangential pressure** induces dermal-epidermal cleavage
101
What is the single most important risk factor in predicting mortality from **SJS/TEN**?
**Serum bicarbonate** (\< 20 mmol/L)
102
What is the classic histopathology of **SJS/TEN**? * What cells are present in dermis?
* 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
What is the treatment for **SJS/TEN**?
* 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
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?
* **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
What is the treatment of choice for a **primary varicella infection**? * How do you treat healthy versus immunocompromised patients?
* 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
What is the difference in presentation between a **primary varicella infection** and subquent reactivation of the virus?
* Primary varicella infection: chicken pox * Reactivation: herpes zoster, a.k.a. shingles
107
What is the post-exposure prophylaxis recommended for those exposed to **primary varicella**? * Immunocompetent * Immunocompromised, pregnant females and neonates
* 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
Name the diagnosis.
**Varicella (chicken pox)** "Dew drops on a rose petal"
109
Name the diagnosis.
**Vitiligo**
110
What is the pathogenesis of **vitiligo**?
* 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
What are the known associations with **vitiligo**? Hint: think endocrine, other skin findings, eyes
Other autoimmune diseases! * **Thyroid dysfunction (most common)** * **Halo nevi** * T1DM * Addison's disease * Alopecia areata * Uveitis
112
What are the treatments available for **vitiligo**? * Topicals * Lasers * Oral medications
* Topical steroids * Calcineurin inhibitors * Topical vitamin D analogs * NB-UVB or excimer laser * Systemic immunosuppressants * Depigmentation
113
What are the bad prognostic indicators of **vitiligo**?
* Mucosal involvement * Family history * Koebnerization * Non-segmental disease
114
Name the diagnosis.
**CTCL**
115
Name the diagnosis.
**CTCL**
116
What are the different clinical stages of **mycosis fungoides**?
* **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
What are the histologic features of **patch stage MF**? * Where are the lymphocytes located? * What are the clusters of lymphocytes called?
* **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
What are the histopathologic features of **plaque stage MF**? * Where are the lymphocytes located?
* **More prominent epidermotropism than patch stage** with more atypical lymphocytes in the dense dermal band-like infiltrate
119
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?
* Increased density and depth of dermal infiltrate of atypical lymphocytes with **decreased/absent epidermotropism**
120
What is the typical immunophenotype for **MF**? * I.e., what kind of CDs are present on the T-cells?
* **CD3 positive** * **CD4 positive** * CD8 negative * Look for CD4:CD8 ratio of 10:1
121
What are the treatment options for **MF**? * What medications are often added for progressive/advanced disease?
* **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
Describe **Sezary syndrome**. * What are the clinical features and symptoms? * What lab finding is needed to diagnose this condition?
* 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
Name the diagnosis.
**Tumor stage MF**
124
What are the strains of HPV that classically cause common warts and palmar/plantar warts?
* **HPV-1** * **HPV-2** * **HPV-4**
125
What is the classic histopathology of palmar/plantar warts? * What happens in the epidermis? Corneum? * What keratinocyte structural change is present?
* **"Church spire" papillomatosis** * Hyperkeratosis * Acanthosis with elongated rete ridges * **Hypergranulosis** * **Koilocytosis (nuclear enlargement and hyperchromasia)** * Increased dermal vessels
126
Name the diagnosis. * What infection causes this?
**Plantar wart** * Usually caused by **HPV-1, HPV-2 or HPV-4**
127
Name the diagnosis. * What infection causes this?
**Common wart** * Usually caused by **HPV-1, HPV-2 or HPV-4**
128
Name the diagnosis. * What infection causes this?
**Palmar/plantar wart** * Usually caused by **HPV-1, HPV-2 or HPV-4**
129
Name the diagnosis. * What infection causes this?
**Plantar wart** * Usually caused by **HPV-1, HPV-2 or HPV-4**
130
Name the diagnosis. * What infection causes this? * What parts of the body are usually affected?
**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
Name the diagnosis. * What infection causes this? * What parts of the body are usually affected?
**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
Name the diagnosis. * What infection causes this? * What parts of the body are usually affected?
**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
What is the most common STD?
**Genital warts (condyloma acuminata)**
134
Name the diagnosis. * What infection causes this? * What reagent can be applied to the area to visualize lesions?
**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
Name the diagnosis. * What infection causes this? * What reagent can be applied to the area to visualize lesions?
**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
What are treatments for genital warts? * Topicals * Procedures
* Cryotherapy * TCA peel (high concentrations) * Electrosurgery * Scissors/shave removal * CO2 laser or PDT * Podophyllin (Podofilox) * Imiquimod * Cidofovir gel/intralesional
137
Name the diagnosis. * What infection can lead to this? * What is another term for how this lesion appears histologically?
**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
Name the diagnosis. * What infection can lead to this? * What is another term for how this lesion appears histologically?
**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
Name the diagnosis. * What infection can lead to this? * What invasive neoplasm can this progress to?
**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
Name the diagnosis. * This is part of what group of skin neoplasms? * What infection can cause this? * What is the treatment?
**Buschke-Löwenstein tumor** * Part of group of verrucous carcinomas * Cauliflower-like tumors * **HPV-6 and -11** * Treat with excision
141
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?
**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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