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

Group 1, Column 1 Flashcards

1
Q

Name the diagnosis.

  • What is the most common associated malignancy?
  • This is histologically identical to what three other things?
  • How do you treat this?
A

Acanthosis nigricans

  • Most common underlying malignancy is GI adenocarcinoma, especially with palmar involvement
  • Derm path buzzword: epidermal papillomatosis
  • Histologically identical to CARP, acrokeratosis verruciformis of Hopf and SK
  • Can be treated with topical retinoids and AmLactin
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2
Q

What are the four components of acne vulgaris?

A
  1. Abnormal follicular keratinization
  2. Sebum overproduction
  3. Propionibacterium acnes overgrowth
  4. Inflammation
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3
Q

Topical retinoids downregulate which receptor?

A

TLR-2

P. acnes activates this on macrophages, causing inflammation and attracting neutrophils

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4
Q

Describe key findings of actinic keratosis (AK).

  • What kind of genetic damage/mutation has occurred?
A
  • UVB causes AKs by inducing thymidine dimers and causing p53 mutations, impairing apoptosis
  • Look for “flag sign” with overlying parakeratosis (looks pink) alternating with orthohyperkeratosis (looks blue)
  • Rate of transformation to SCC: less than 0.1%
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5
Q

What kinds of immune cells target the hair follicles in alopecia areata and where?

What type of cytokines are involved?

A

CD8+ T-cells attack bulb, involving type 1 cytokines (IL-2, IL-12, IFN-gamma and TNF-alpha)

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6
Q

What is important to know about the prognosis of ophiasis pattern alopecia areata?

A

There is a poor prognosis.

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7
Q

What is the opposite of ophiasis pattern?

A

Sisapho pattern

(This is basically ophiasis spelled backward.)

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8
Q

What are the nail findings in alopecia areata?

A
  • Regular (geometric) nail pitting
  • Trachyonychia (or 20-nail dystrophy), where nails are sandpaper-like
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9
Q

What findings on dermoscopy are classically seen with alopecia areata?

A
  • Exclamation point hairs
  • Perifollicular yellow dots
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10
Q

What are other disease associations with alopecia areata?

A
  • Atopy (a poor prognostic factor)
  • Autoimmune thyroid
  • Vitiligo
  • SLE
  • IBD
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11
Q

What are classic histology findings in alopecia areata?

  • What kind of inflammatory pattern is seen?
  • What kind of hairs are present?
A
  • Peribulbar lymphocytic infiltrate (“swarm of bees”)
  • Catagen-telogen shift
  • Increased miniaturized hairs (i.e., nanogen hairs)
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12
Q

What does anagen mean?

  • What proportion of hairs are in this phase?
  • How long does this last?
  • What medicine recreates this phase?
A
  • Hair growth phase and determines length of hair
  • 85% of hairs at any particular time
  • Lasts 2-6 years (genetically determined)
  • Minoxidil recreates anagen phase
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13
Q

What does catagen mean?

  • What happens to the hair in this phase?
  • What proportion of hair are in this phase?
  • How long does this last?
A
  • Transitional phase after anagen
  • The bulb regresses and the inner root sheath (IRS) is lost
  • 2% of hairs at any particular time
  • Lasts 2-4 weeks
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14
Q

What does telogen mean?

  • How long does this last?
  • What proportion of hairs are in this phase?
A

“Telogen is tired and resting.”

  • Resting phase
  • Lasts 3 months
  • 15% of hairs at any particular time
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15
Q

Name the layers of the hair follicle from outer to inner.

A
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16
Q

What is the gene implicated in atopic dermatitis?

A

Fillagrin mutations, causing alterations in the epidermal barrier

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17
Q

Where is filaggrin located in the epidermal cell and in what layer of the epidermis?

  • What does filaggrin do in the cell?
A
  • In the keratohyalin granules of the stratum granulosum
  • Filaggrin binds to intermediate filaments, also known as keratin filaments, causing structural integrity
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18
Q

Is atopic dermatitis Th1 or Th2 mediated?

A

Th2

  • Important in allergies, humoral immunity
  • Think IL-4, IL-5, IL-6, IL-10, IL-13
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19
Q

Name the Th1 cytokines.

A
  • IL-2
  • IL-12
  • IFN-γ (downregulates Th2 pathway)
  • TNF-α

Important in cell-mediated immunity, delayed-type hypersensitivity reactions

Think ACD, psoriasis

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20
Q

Name the Th2 cytokines.

A
  • IL-4
  • IL-5
  • IL-6
  • IL-10
  • IL-13

Important in allergies, humoral immunity

Think atopic dermatitis

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21
Q

Name the diseases associated with Th1 cytokine profile.

A
  1. Allergic contact dermatitis
  2. Psoriasis
  3. Tuberculoid leprosy
  4. Cutaneous leishmaniasis
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22
Q

Name the diseases associated with Th2 cytokine profile.

A
  • Atopic dermatitis
  • Lepromatous leprosy
  • Disseminated leishmaniasis
  • Sezary syndrome
  • Parasitic infections
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23
Q

What is the classic histopathology of acute atopic dermatitis?

  • What happens in the epidermis?
  • What kind of inflammatory pattern and what immune cells are present?
A
  • Prominent spongiosis
  • Intraepidermal vesicles/bullae
  • Perivascular lymphohistiocytic infiltrate with eosinophils
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24
Q

What is the classic histopathology of chronic atopic dermatitis?

  • What happens in the epidermis?
A
  • Psoriasiform acanthosis with little spongiosis
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25
Q

What are the two most common genetic mutations in BCCs?

A
  • PTCH (chromosome 9q), most common
  • p53 point mutations, second most common
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26
Q

List the (8) subtypes of BCCs

A
  1. Nodular
  2. Superficial
  3. Morpheaform/sclerotic
  4. Micronodular
  5. Fibroepithelioma of Pinkus
  6. Pigmented
  7. Infundibulocystic
  8. Basosquamous
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27
Q

List the genetic syndromes associated with multiple BCCs.

Hint: “Green Berets Rarely Buy eXtra Shoes”

A

“Green Berets Rarely Buy eXtra Shoes…but they get a lot of BCCs from being in the sun!”

  • Gorlin’s
  • Bazex-Dupre-Christol
  • Rombo
  • Brooke-Spiegler
  • Xeroderma pigmentosum
  • Schopf-Schulz-Passarge
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28
Q

What is the classic histology of BCC?

  • What do the cells look like? How do they organize? How do they interact with the stroma?
A
  • Nests of basaloid and uniform cells with high N:C ratio (i.e., look blue)
  • Peripheral palisading
  • At least focal epidermal connection
  • “Retraction spaces” between epithelium and stroma
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29
Q

What is the chemotherapy used for inoperable or metastatic BCC?

A

Vismodegib, a hedgehog pathway inhibitor (and the first of its kind)

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30
Q

Describe candidal diaper dermatitis.

  • Are the intertriginous areas and scrotum involved?
  • What does Candida look like on histology?
A
  • Bright red patches with pustules and satellite papules with possible intertriginous involvement, including the scrotum
  • May also have thrush
  • Look for pseudohyphae and budding yeast on histology
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31
Q

What are the two most common causes of cellulitis?

A

Group A beta-hemolytic strep (GAS)

Followed by S. aureus (the most common cause in children)

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32
Q

What are the (3) antibiotics of choice for uncomplicated cases of cellulitis?

A
  • Oral cephalexin, dicloxacillin or clindamycin for 10 days
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33
Q

What is the antibiotic of choice for cellulitis associated with decubitus or diabetic ulcers? (2 regimens)

  • What kinds of bacteria must these antibiotics cover?
A

Piperacillin-tazobactam (Zosyn) or ciprofloxacin-metronidazole (Flagyl)

This covers GPs, GNs and anaerobes, as these ulcers tend to be polymicrobial.

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34
Q

What is the antibiotic of choice for MRSA cellulitis? (4)

A
  • Bactrim
  • Minocycline
  • Doxycycline
  • Clindamycin
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35
Q

State the one-liner for hypersensitivity reactions:

  • Type I
  • Type II
  • Type III
  • Type IV
A
  • Type I: IgE-mediated (anaphylaxis)
  • Type II: IgG-mediated cytotoxic (i.e., autoimmune hemolytic anemia, Goodpasture syndrome, myasthenia gravis)
  • Type III: immune complex-mediated
  • Type IV: delayed, cell-mediated
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36
Q

What is the most common cause of allergic contact dermatitis in the U.S. and the world?

A
  • US: poison ivy
  • Worldwide: nickel
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37
Q

What is the classic histology of ACD?

  • What is the inflammatory pattern, and what cells are notably present in the dermis?
  • Are necrotic keratinocytes present?
A
  • Spongiotic dermatitis with dermal eosinophils
  • Lacks necrotic keratinocytes (found in ICD)
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38
Q

What is the classic histology of ICD?

  • What is the inflammatory pattern, and what cells are notably present in the dermis?
  • Are necrotic keratinocytes present?
A
  • Mild spongiosis
  • Scattered necrotic keratinocytes (in contrast with ACD)
  • Mild perivascular inflammation
  • Probably not eosinophils (compared to ACD)
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39
Q

How do you discriminate between an irritant and allergic response on patch testing?

A
  • Irritant reactions will fade between the first and second readings
  • Allergic reactions will persist or progress
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40
Q

Name the diagnosis.

A

Dermatofibroma

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41
Q

Name the diagnosis.

A

Dermatomyositis

  • Gottron’s papules are over MCP joints
  • Versus Gottron’s sign (which is reddish scaling over knuckles, knees and elbows)
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42
Q

Name the diagnosis.

A

Dermatomyositis (shawl sign)

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43
Q

Name the diagnosis.

  • What are three nail findings of these condition?
A

Dermatomyositis

  • Ragged cuticles (Samitz sign)
  • Nailfold telangiectasias
  • Periungual erythema
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44
Q

Name the diagnosis.

A

Dermatomyositis (heliotrope rash)

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45
Q

Name the diagnosis.

A

Dermatomyositis

(Ragged cuticles, a.k.a. “Samitz sign”)

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46
Q

Name the diagnosis.

A

Dermatomyositis

  • Gottron’s sign (reddish scaling over knuckles, knees and elbows)
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47
Q

Name notable causes of drug-induced dermatomyositis.

A
  • Hydroxyurea (a chemotherapy for SCC and treatment for sickle cell disease; most common, > 50% of cases)
  • Statins
  • Cyclophosphamide
  • TNF-alpha inhibitors
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48
Q

Describe the classic muscle and activity problems in dermatomyositis.

A
  • Symmetric proximal muscle weakness without myalgias
  • Difficulty walking up stairs or brushing hair
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49
Q

Describe the classic skin findings of dermatomyositis.

Hint: think about face, chest and arms.

A
  • Gottron’s papules (lichenoid papules overlying knuckles)
  • Gottron’s sign (maculary erythema overlying joints)
  • Facial erythema with malar involvement AND melolabial involvement (versus lupus)
  • Heliotrope sign (lid erythema and edema)
  • Holster sign (erythema of lateral hips/thighs, see photo)
  • V-sign/”shawl” sign
  • Poikiloderma
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50
Q

Why does the heliotrope sign arise?

A

It is the result of inflammation of underlying orbicularis oculi muscle and NOT the skin.

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51
Q

What is mechanic’s hands of dermatomyositis associated with?

A

Anti-synthetase syndrome

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52
Q

What are the notable nail changes of dermatomyositis?

A
  • Ragged cuticles (Samitz sign)
  • Proximal nail fold with dilated capillary loops, as well as other areas with vessel dropout
  • Periungual erythema
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53
Q

What is one way to help differentiate dermatomyositis from lupus or psoriasis based on pruritus?

A

Dermatomyositis is often very pruritic (especially on the scalp), while the others are usually NOT

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54
Q

What are the associated malignancies of dermatomyositis in men and women?

A
  • Lung and GI cancer most common in men
  • Ovarian and breast most common in women
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55
Q

Name the findings of anti-synthetase syndrome.

Hint: think about clinical findings, symptoms and rheumatologic serologies.

A
  • Mechanics hands
  • ILD (pulmonary fibrosis)
  • Antisynthetase autoantibodies (Anti-Jo1)
  • Acute disease onset (myositis)
  • Constitutional symptoms
  • Raynauds
  • Arthritis
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56
Q

Name the diagnosis.

  • What is the buzzword for this diagnosis?
  • In patients with which other skin conditions is this diagnosis seen?
A

Eczema herpeticum

  • Monomorphic, umbilicated vesiculopapules or punched-out ulcerations
  • Disseminated HSV (usually HSV-1) mainly seen in atopics, Darier, Hailey-Hailey
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57
Q

What is the classic histopathology of dermatomyositis?

  • What is the inflammatory pattern? What is abundant in the dermis?
A
  • Subtle vacuolar interface dermatitis
  • Very abundant mucin
  • Mild inflammation
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58
Q

What are the most common causes of erythema multiforme?

A

HSV is by far the most common cause of EM (HSV-1 > HSV-2) in general

  • HSV is the most common cause of EM minor
  • Mycoplasma pneumoniae is the most common cause of EM major (simulates SJS)
59
Q

Name the diagnosis.

A

Erythema multiforme

60
Q

Describe the three zones of a typical target lesion of EM.

A

Three zones

  1. A dusky, vesicular or necrotic center
  2. Elevated, edematous pale surrounding ring
  3. Outer rim of macular erythema
61
Q

Describe the papular (elevated) atypical target lesion of EM.

A

Only two zones, but is palpable

  • Note that macular atypical lesions are seen in SJS/TEN but NOT EM
62
Q

Describe the components of EM minor.

A
  • Targetoid lesions (palpable)
  • Minimal mucosal involvement
  • No systemic symptoms
63
Q

Describe the components of EM major.

A
  • Target lesions (palpable)
  • Severe mucosal involvement (mouth > eyes > genitals)
  • Systemic symptoms (fever, arthralgias)
64
Q

What infectious lab testing is often positive in EM patients?

A

80% have detectable HSV DNA by PCR in early erythematous papules or outer rim of targets

65
Q

What is the classic histopathology of EM?

  • What is the inflammatory pattern?
  • Where is the inflammatory infiltrate?
  • Are necrotic keratinocytes and eosinophils present?
A
  • Prominent basal vacuolar change and spongiosis
  • Moderately dense superficial dermal perivascular lymphohistiocytic infiltrate
  • Necrotic keratinocytes
  • Absent/rare eosinophils (as opposed to SJS/TEN)
66
Q

Name the diagnosis.

A

Granuloma annulare

67
Q

What is the classic histopathology for granuloma annulare?

  • What is more abundant in the dermis?
  • Are eosinophils present?
A
  • Granulomas in the dermis
  • Increased mucin
  • Scattered eosinophils
68
Q

Describe the three common histologic patterns of GA.

A
  1. Interstitial (most common; 70% of cases): subtle, singly-arrayed histiocytes between collagen fibers intermixed with increased dermal mucin, perivascular eosinophils
  2. Palisaded granulomas (25%)
  3. Sarcoidal pattern (5%)
69
Q

What is the classic histopathology of HSV?

  • What are the epidermal changes? What is the buzzword for the keratinocyte change?
  • What is the name of the viral inclusions seen within keratinocyte nuclei?
A
  • Intraepidermal vesicles with slate-gray enlarged keratinocytes (ballooning degeneration) that are multinucleated
  • +/- Cowdry A inclusions (eosinophilic) within nucleus
70
Q

Name the diagnosis.

A

HSV

“Dew drops on a rose petal”

71
Q

What do you use to treat eczema herpeticum, neonatal HSV, or severe HSV in immunosuppressed?

  • What do you use in refractory cases?
A
  • First line: IV acyclovir
  • If acyclovir-resistant, use foscarnet or cidofovir
72
Q

What constitutes disseminated herpes zoster?

  • What patients tend to have this?
  • What other organs may be affected when this occurs?
A
  • Dermatomal disease and > 20 lesions outside of the dermatome
  • Seen in the immunosuppressed
  • Increased risk of pneumonitis and encephalitis
73
Q

Describe Ramsey-Hunt syndrome.

  • What are the cause and clinical symptoms?
A
  • Reactivation of varicella infection
  • Geniculate ganglion of CN VII is affected
  • Ipsilateral facial nerve paralysis
  • Hearing loss
  • Anterior 2/3 tongue taste loss
74
Q

What is Hutchinson’s sign?

  • What is involved/affected?
  • What does this raise special concern for?
A
  • Involvement of the side and tip of nose with herpes zoster, indicating disease of CN V1 (ophthalmic nerve)
  • Raises concern for uveitis and vision loss
75
Q

Name the diagnosis.

A

Bullous impetigo

76
Q

Name the diagnosis.

A

Impetigo

77
Q

What is the pathophysiology of bullous impetigo?

  • What are the toxins involved and desmoglein is targeted?
A

Phage group II (types 55 and 77) S. aureus –> produce exfoliatoxins A and B –> cleaves desmoglein 1 –> subcorneal/intragranular acantholysis

78
Q

True or false?

Streptococcal impetigo can lead to rheumatic fever.

A

False

Only streptococcal pharyngitis leads to rheumatic fever.

79
Q

Bullous impetigo plus renal insufficiency or immunodeficiency can lead to what serious condition? Why?

A

Staph scalded skin syndrome

  • Due to disseminated exfoliatoxin
80
Q

Bullous impetigo has nearly identical histology with which other disorder because the target is the same?

A

P. foliaceus

Both involve cleavage of desmoglein 1

81
Q

Name the diagnosis.

A

Keloid

82
Q

What is the histopathology of lentigo simplex?

  • What are the epidermal changes?
A
  • Basal layer hyperpigmentation
  • Elongated rete ridges with mild increased melanocyte density
83
Q

What (6) conditions are associated with multiple lentigines?

A
  1. LEOPARD
  2. Carney complex (LAMB/NAME)
  3. Peutz-Jeghers (especially oral/perioral)
  4. Bannayan-Riley-Ruvalcaba (penile)
  5. Cowden syndrome
  6. Xeroderma pigmentosum
84
Q

Name the diagnosis.

A

Lentigo simplex

85
Q

Name the diagnosis.

A

Lichen planus

86
Q

What are classic viral triggers of lichen planus?

A
  • HBV (oral or bullous LP)
  • HCV (oral ulcerative/erosive LP)
87
Q

Name the diagnosis.

A

Lichen planus

88
Q

What are classic contact allergen triggers of LP? (3)

A
  • Mercury amalgam (tooth fillings; oral LP)
  • Gold
  • Copper
89
Q

Name the diagnosis.

A

Lichen planus

90
Q

What are classic triggers of drug-induced LP?

A
  • HCTZ (often photo-exacerbated)
  • Beta-blockers
  • ACE inhibitors
  • Antimalarials
  • “Gold salts” (used for RA)
  • Note that ACE inhibitors, beta-blockers and gold salts are also drug triggers of pityriasis rosea.
91
Q

What is the classic histopathology of LP?

  • How are the granular layer and rete ridges affected?
  • What are the special cells found in the superficial dermis?
  • Are eosinophils and parakeratosis present?
A
  • Wedge-shaped hypergranulosis
  • Saw-toothed rete ridges
  • Apoptotic keratinocytes of basal layer with some falling into superficial dermis (eosinophilic, a.k.a. civatte or colloid bodies)
  • Usually lacks eosinophils and parakeratosis (except drug-induced LP)
  • “Shaggy” fibrinogen along BMZ
92
Q

Name the diagnosis and nail finding.

A

Lichen planus (dorsal pterygium)

  • Can also see 20-nail dystrophy (trachyonychia; children >> adults) in LP
93
Q

Name the diagnosis.

A

Livedo reticularis

94
Q

What inherited genetic mutation raises risk for familial melanoma?

  • What syndromes is this seen in? (2)
  • What tumor suppressor genes are involved? (2)
A

Inherited CDKN2A mutations

Seen in FAMMM syndrome, dysplastic nevus syndrome

  • Tumor suppressor genes p14 (via p53) and p16 (via Rb) stop working
95
Q

Name the diagnosis.

A

Melanoma

96
Q

Name the four subtypes of melanoma.

A
  1. Superficial spreading
  2. Nodular
  3. Lentigo maligna
  4. Acral lentiginous
97
Q

What is the most common subtype of melanoma?

A

Superficial spreading

98
Q

What are factors associated with a poor prognosis for melanoma?

  • Some are clinical and some are histologic
A

Clinical:

  • Ulceration
  • Lymph node or visceral metastasis
  • Head/neck/trunk location

Histologic:

  • Breslow > 1 mm
  • Increased mitotic rate
99
Q

Name this clinical sign.

  • What condition is this seen in?
A
  • Hutchinson’s sign: extension of pigment from the nail bed, matrix, and nail plate to the adjacent cuticle and/or nail folds
  • Seen in nail matrix lesions of acral lentiginous melanoma
100
Q

What are indications for sentinel lymph node biopsy?

A
  • Breslow > 1 mm (which is why you want a biopsy at least 1 mm deep)
  • Ulcerated
  • >/= 1 mitosis
101
Q

Name the diagnosis.

A

Discoid lupus

(Chronic cutaneous lupus erythematosus, CCLE)

  • Red macules and plaques develop scale, atrophy and scarring
  • Central hypopigmentation
  • Peripheral hyperpigmentation
102
Q

Name the diagnosis.

A

Discoid lupus

(Chronic cutaneous lupus erythematosus, CCLE)

  • Red macules and plaques develop scale, atrophy and scarring
  • Central hypopigmentation
  • Peripheral hyperpigmentation
103
Q

Name the diagnosis.

A

Discoid lupus

(Chronic cutaneous lupus erythematosus, CCLE)

  • Red macules and plaques develop scale, atrophy and scarring
  • Central hypopigmentation
  • Peripheral hyperpigmentation
104
Q

Name the diagnosis.

  • What is there an increased risk for?
  • What part of the body is favored in this condition, compared with another similar condition?
A

Hypertrophic (verrucous) lupus erythematosus

  • Thick, hyperkeratotic and verrucous scaling plaques with indurated border
  • Increased risk of SCC
  • Favors upper half of body (versus hypertrophic LP, which favors lower half)
  • Usually accompanies typical discoid lupus lesions
105
Q

Name the diagnosis.

  • What can trigger this?
A

Chilblains lupus erythematosus

  • Red or dusky purple papules and plaques on fingertips, rims of ears, heels and toes
  • Precipitated by cold, moist climates but can persist year-round
  • Note: Chilblains can occur by itself (without lupus)
106
Q

Name the diagnosis.

  • This looks similar to what other condition?
A

Tumid lupus erythematosus

  • Edematous, indurated, erythematous, often annular or arcuate plaques without epidermal change
  • Favors face and trunk
  • Similar in appearance to Jessner’s lymphocytic infiltrate (see photo)
107
Q

What is the classic histopathology of discoid lupus?

  • What happens in the epidermis?
  • What is the inflammatory pattern?
  • Where is the infiltrate and what composes it?
  • Is follicular plugging present?
  • What is present in the stroma?
A
  • Epidermal atrophy
  • BMZ thickening
  • Vacuolar interface dermatitis
  • Follicular plugging
  • Superficial and deep perivascular and periadnexal lymphohistiocytic inflammation with plasma cells
  • Mucin deposition
  • DIF: Lupus band test positive (IgG and complement deposits at DEJ)
108
Q

What is the suspected pathogenesis of subacute cutaneous lupus erythematosus (SCLE)?

A
  • UVR-induced apoptosis releases high levels of nuclear antigens (Ro, La, DNA)
  • Reduced clearance of apoptotic cells leads to loss of immune tolerance
  • Release of pro-inflammatory cytokines and production of ANAs (especially anti-Ro/La auto-Ab)
109
Q

What are genetic associations with SCLE?

A
  • HLA-B8 (strongest association), HLA-DR3
  • Hereditary complement deficiencies (especially those involving the early intrinsic pathway: C1q/r/s, C2 and C4)
110
Q

What two autoimmune diseases are strongly associated with anti-Ro/SS-A autoantibodies?

A
  1. Sjogren syndrome
  2. Subacute cutaneous lupus erythematosus (SCLE)
111
Q

Name the diagnosis.

  • What are the two clinical variants of this condition?
  • What parts of the body are usually involved?
A

SCLE

  • May occur as two clinical variants:
    • Papulosquamous SCLE (psoriasiform plaques)
    • Annular SCLE (scaly polycyclic annular plaques with central clearing)
  • Involves sun-exposed areas of lateral face (central face spared), V-chest, upper back, neck and extremities
  • Arthritis/arthralgias is most common systemic finding (up to 70%)
112
Q

Name the diagnosis.

  • What are the two clinical variants of this condition?
  • What parts of the body are usually involved?
A

SCLE

  • May occur as two clinical variants:
    • Papulosquamous SCLE (psoriasiform plaques)
    • Annular SCLE (scaly polycyclic annular plaques with central clearing)
  • Involves sun-exposed areas of lateral face (central face spared), V-chest, upper back, neck and extremities
  • Arthritis/arthralgias is most common systemic finding (up to 70%)
113
Q

Name the diagnosis.

  • What are the two clinical variants of this condition?
  • What parts of the body are usually involved?
A

SCLE

  • May occur as two clinical variants:
    • Papulosquamous SCLE (psoriasiform plaques)
    • Annular SCLE (scaly polycyclic annular plaques with central clearing)
  • Involves sun-exposed areas of lateral face (central face spared), V-chest, upper back, neck and extremities
  • Arthritis/arthralgias is most common systemic finding (up to 70%)
114
Q

What rheumatologic serologies are found in SCLE?

  • Also, what else might be abnormal on CBC?
A
  • Anti-Ro/SS-A (75% - 90%)
  • Anti-La/SS-B (30% - 40%)
  • ANA (60% - 80%): speckled/particulate pattern
  • Leukopenia (20%)
115
Q

What is the classic histopathology of SCLE?

Hint: Think about its findings regarding the corneum, epidermis, dermatitis pattern, and whether mucin, eosinophils and follicular plugging are present.

A
  • Compact hyperkeratosis
  • Prominent epidermal atrophy
  • Vacuolar interface dermatitis with pigment incontinence
  • Perivascular and periadnexal lymphoid aggregates of the superficial dermis with scattered plasma cells
  • Mucin deposition
  • Lacks eosinophils and follicular plugging
  • DIF: Positive lupus band test in 60 - 80%
116
Q

What are the first and second line treatments for SCLE?

A
  • First line: TCS, antimalarials (hydroxychloroquine-quinacrine; requires annual eye exams) and sun protection
  • Second and third line: oral retinoids (acitretin, isotretinoin), dapsone, methotrexate, mycophenolate mofetil
117
Q

What are the most important implicated drugs of drug-induced SCLE?

A
  • HCTZ (most common; same as drug-induced LP)
  • Terbinafine
  • Griseofulvin
  • Calcium channel blockers
  • ACE inhibitors
  • TNF-alpha inhibitors (most commonly etanercept)

Think HCTZ, oral antifungals and CCBs.

118
Q

Name the diagnosis.

  • Are the lesions usually present at birth?
  • What is this condition the result of?
  • The baby should be evaluated for what other serious congenital condition?
A

Neonatal lupus erythematosus

  • Lesions arise within first weeks of life but not at birth
  • Photosensitivity
  • Periorbital erythema = “raccoon eyes”
  • Annular, polycylic erythematous plaques with central clearing and raised red border, fine scale favoring head and neck (looks similar to SCLE)
  • Resolves without scarring but with dyspigmentation and telangiectasias by around 6 months old
  • Result of transplacental passage of anti-Ro/SS-A autoantibodies, which can lead to congenital third-degree heart block
119
Q

Name the diagnosis.

  • What other parts of the body are classically involved with this rash?
A

Acute cutaneous lupus (ACLE)

  • Most strongly associated with systemic lupus erythematosus (SLE) of all cutaneous subtypes
  • Malar erythema (“butterfly rash”) for hours to weeks after sun exposure
  • Classically involves the nasal bridge and bilateral malar eminence
  • Sparing melolabial folds (in contrast to facial erythema of dermatomyositis)
  • May develop scaling, papules, erosions, poikiloderma
  • May be accompanied by generalized photodistributed eruption of the V-neck, upper back, extremities but classically sparing the knuckles (unlike dermatomyositis)
120
Q

Name the diagnosis.

  • What other parts of the body are classically involved with this rash?
A

Acute cutaneous lupus (ACLE)

  • Most strongly associated with systemic lupus erythematosus (SLE) of all cutaneous subtypes
  • Malar erythema (“butterfly rash”) for hours to weeks after sun exposure
  • Classically involves the nasal bridge and bilateral malar eminence
  • Sparing melolabial folds (in contrast to facial erythema of dermatomyositis)
  • May develop scaling, papules, erosions, poikiloderma
  • May be accompanied by generalized photodistributed eruption of the V-neck, upper back, extremities but classically sparing the knuckles (unlike dermatomyositis)
121
Q

What is the classic histopathology of acute cutaneous lupus erythematosus (ACLE)?

Hint: think about what the dermatitis pattern is and where/what the infiltrate is.

A
  • Vacuolar interface dermatitis
  • Sparse perivascular lymphocytic infiltrate limited to upper dermis
  • Dermal edema
  • DIF: Positive lupus band test
122
Q

Name the diagnosis.

  • What autoantibody is involved?
  • What parts of the body may be involved with this rash?
  • What is the treatment?
A

Bullous SLE

  • Anti-type VII collagen autoantibodies (same as EBA)
  • Widespread, symmetric eruption of dense, subepidermal bullae on erythematous-to-urticarial base
  • Involves both sun-exposed and non-exposed areas, including the mucosa
  • Patients must meet ACR criteria for SLE to term it bullous SLE
  • Treat with dapsone
123
Q

Name the diagnosis.

  • What autoantibody is involved?
  • What parts of the body may be involved with this rash?
  • What is the treatment?
A

Bullous SLE

  • Anti-type VII collagen autoantibodies (same as EBA)
  • Widespread, symmetric eruption of dense, subepidermal bullae on erythematous-to-urticarial base
  • Involves both sun-exposed and non-exposed areas, including the mucosa
  • Patients must meet ACR criteria for SLE to term it bullous SLE
124
Q

What is the classic histopathology of bullous SLE?

  • What occurs at the DEJ?
  • What is found on DIF?
A
  • Subepidermal bullae with neutrophils at DEJ and dermal papillae
  • DIF: granular to linear deposition of IgG, IgM, IgA and/or C3 along BMZ (also called “a full house”)
125
Q

What laboratory testing is notable in bullous SLE?

  • What is found on salt-split skin testing?
  • An ELISA tests for what autoantibodies?
  • Is ANA positive?
A
  • Dermal reactivity (i.e., floor pattern) on salt-split skin
  • ELISA: autoantibodies to type VII collagen (same as EBA)
  • ANA positive
126
Q

What is the treatment of choice for bullous SLE?

  • A quick response differentiates it from what other condition?
A

Dapsone

  • Dramatic response within 1-2 days, differentiating bullous SLE from EBA
127
Q

What are the general ACR criteria for diagnosis of systemic lupus erythematosus (SLE)?

Hint: think about the clinical, immunologic and serologic features, as well as a biopsy of a specific organ.

A

Need to satisfy four items (at least one clinical and one immunological item) OR have biopsy-proven nephritis compatible with SLE in the presence of ANA or anti-dsDNA antibodies

  • Malar or discoid rash
  • Photosensitivity
  • Oral ulcers
  • Arthritis
  • Serositis (pleuritis, pericarditis)
  • Renal disorder (proteinuria, cellular casts)
  • Neurologic disorders (seizures, psychosis)
  • -cytopenias
  • Anti-DNA, Anti-Sm, antiphospholipid antibodies (i.e., anti-cardiolipin, lupus anticoagulant, false positive RPR)
  • ANA
128
Q

How should pregnant women with systemic lupus erythematosus be managed in terms of medicine and clot prophylaxis?

A
  • Continue with hydroxychloroquine and low-dose steroids
  • Consider azathioprine
  • Anticoagulation for antiphospholipid syndrome (APLS)
129
Q

What laboratory testing is seen in systemic lupus erythematosus?

Hint: think about how it affects a CBC with diff, complement levels, inflammatory markers, UA, as well as autoantibodies (5)

A
  • Hemolytic anemia (Coombs positive)
  • -Cytopenias
  • Decreased total complement levels (CH50)
  • Increased inflammatory markers (CRP, ESR)
  • Proteinuria, hematuria
  • Anti-C1q Ab (associated with severe SLE nephritis)
  • ANA (99%)
  • Anti-dsDNA (60%; highly specific)
  • Anti-Smith (10% - 30%; highly specific)
  • Anti-histone (seen in drug-induced SLE)
130
Q

What is the treatment for mild SLE without visceral involvement?

A

Hydroxychloroquine + NSAIDs

131
Q

What is the treatment for moderate-to-severe SLE without renal involvement?

A

Prednisone + steroid-sparing agent (e.g., azathioprine, MTX or MMF)

132
Q

What is the treatment for severe SLE with renal involvement?

A

High dose prednisone + pulsed IV cyclophosphamide or MMF

133
Q

What is the treatment for moderate-to-severe and recalcitrant SLE?

A

Rituximab or belimumab

134
Q

How long after drug initiation does drug-induced lupus classically occur?

  • How long does it take to resolve?
A
  • Onset is usually > 1 year after drug initiation
  • Typically resolves within 4 - 6 weeks of stopping the drug
135
Q

What rheumatologic serologies characterize drug-induced SLE? (2)

A
  • Positive anti-histone antibody (> 95%)
  • Negative dsDNA antibody
136
Q

What are the most important implicated drugs for drug-induced lupus?

Hint: for high risk medications, think about the heart.

A
  • High risk: procainamide, hydralazine
  • Medium to low risk: methyldopa, isoniazid, D-penicillamine, minocycline, TNF-alpha inhibitors
137
Q

In children, what are the most common causes of urticaria?

A
  • Viral
  • Idiopathic
  • Infectious (UTI, URI, GI infection)
  • Allergic (foods, meds, environmental allergens)
  • Physical stimuli (pressure, solar, cold)
  • Arthropod bite reactions (“papular urticaria”)
  • Malignancy (most commonly lymphoma)
138
Q

What are the most common causes of acute urticaria?

A
  • Idiopathic (#1)
  • URIs (#2)
  • Drugs (beta-lactams most common)
139
Q

What are different types of physical urticaria?

A
  • Dermatographism
  • Delayed pressure
  • Heat-induced
  • Cold (“ice cube test” for primary cold contact urticaria, PCCU)
  • Cholinergic (exercise, hot bath, emotions)
  • Adrenergic (reproduced by norepinephrine injection)
  • Solar
  • Aquagenic (associated with cystic fibrosis)
140
Q

How can urticaria and urticarial vasculitis be distinguished?

Hint: think about lesion duration, specific associated symptoms and histology.

A
  • Any given urticarial lesion lasts < 24 hours
  • Urticarial vasculitis (UV) lesions last > 24 hours
  • UV burns/hurts and leaves behind bruises rather than itches (like urticaria)
  • UV shows mild LCV +/- eosinophils
141
Q

Name the diagnosis (these lesions have been present for > 24 hours).

  • What are associated symptoms, lab findings and treatments for this?
  • What broad family of diseases is associated with this diagnosis?
A

Urticarial vasculitis

  • Pain/burning > itch (unlike acute urticaria)
  • Usually chronic
  • Angioedema in one-third of patients
  • Arthralgias (50%), GI issues (20%), asthma (20%)
  • Increased ESR, decreased complement, (+) ANA
  • Treat with NSAIDs (first line), colchicine, dapsone, MTX, steroids
  • Associated with autoimmune CTDs
142
Q

What is the classic histopathology of urticaria?

A
  • Superficial dermal edema
  • Vasodilation
  • Scant perivascular and interstitial infiltrate seen in lesions at least an hour old
    • Predominantly neutrophils ( > eosinophils, lymphocytes)
143
Q

What kind of testing can be performed for acute and recalcitrant chronic urticaria?

Hint: think about specific allergy testing and blood work, including antibody testing.

A
  • For acute urticaria:
    • Radioallergosorbent (RAST) test (20% false negative rate)
    • Skin prick (intradermal) test
  • For recalcitrant chronic urticaria
    • CBC with diff
    • ESR/CRP
    • Anti-thyroid Ab, TFTs
    • Anti-FcεRI and anti-IgE Ab
144
Q

What is the treatment of urticaria?

  • What oral and topical medications can be used?
  • What can be used in recalcitrant cases?
  • What should be avoided?
A
  • First-line treatment = H1 antihistamines (cetirizine [Zyrtec], diphenhydramine [Benadryl])
  • Recalcitrant cases: doxepin, PO steroids, montelukast, phototherapy, colchicine, dapsone, omalizumab
  • Soothing lotions (pramoxime, menthol)
  • Avoidance of triggers
  • Avoid aspirin, NSAIDs and opiates

BASIC Exam Study Guide (11 decks)

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