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PGY2-General Dermatology Flashcards

1
Q

List 6 clinical variants psoriasis

A
  • Plaque
  • Pustular-multiple subtypes
  • Guttate
  • Erythrodermic
  • Special locations-scalp, inverse, nail, oral
  • Psoriatic arthritis: 5 subtypes
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2
Q

List 5 variants pustular psoriasis

A
  • Generalized pustular psoriasis VEAL
    o Von Zombusch
    o Exanthematic
    o Annular of lapier
    o Localized
    -Gestational/Impetigo herpetiformis
  • Acrodermatitis continua of Hallopeau
  • Acrodermatitis repens of Crocker
  • Pustular psoriasis of palms and soles

VEALGAAP

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3
Q

List psoriasis triggers

A

PITTED NAILS

  • Psychogenic stress
  • Infection (e.g., streptococcus)
  • Trauma/koebner
  • Terrible habits (e.g., EtOH and smoking)
  • Endocrine (e.g., pregnancy, hypocalcemia)
  • Drugs= NAILS (see below)
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4
Q

List 5 systemic associations with psoriasis

A

a. Metabolic dz
b. Diabetes
c. Obesity
d. IBD
e. PG
f. RA
g. Celiac

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5
Q

List 10 causes drug induced psoriasis

A
  • NSAIDS-e.g. indomethacin
  • Anti-malarial -CQ/HQ
  • Anti-hypertensive (ACEi, betablockers)
  • Infliximab and other anti-TNFs
  • Interferon
  • Imiquimod
  • Lithium
  • Steroids withdrawl

Others:
* Quinidine
* Gemfibrozil
* Clonidine
* Rapid taper of cyclosporine
* GM-CSF/G-CSF
* SSKI
* Bupropion/Wellbutrin

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6
Q

What are the variants of PsA

A

SODAS:
Spondylitis + sacroiliitis (5%): often HLA-B27 + (w/ IBD, uveitis)

Asymmetric Oligoarthritis + Mono (70%)

DIPs (OA-like, 5%): exclusively DIPs, classic, but uncommon

Arthritis Mutilans: (5%, least common)

Symmetric RA-like (MCPs, PIPs, 15%): sym polyarthritis of small-med joints

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7
Q

What 3 psoriasis sites in a patient are high risk for arthritis

A
  • Scalp
  • Nails
  • Gluteal cleft
  • Severe psoriasis
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8
Q

Name 10 histological signs in psoriasis

A
  • Regular acanthosis
  • Confluent parakeratosis
  • Munroe’s micro abscesses (stratum corneum)
  • Spongiform pustules of Kojog (stratum spinosum)
  • Squirting papillae (neutrophils discharge from papillary dermal tips)
  • Thinning supra-papillary plates
  • Dilated and tortuous capillaries in dermal papillae
  • Elongation dermal papillae
  • Superficial perivascular infiltrate w/ lymphocytes and macrophages
  • Decreased or absent granular layer
  • Elongated and squared off rete ridges
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9
Q

What does PASI stand for? What min and max score?

A

a. Psoriasis Area and Severity Index
b. Erythema, scale, thickness/induration
c. Minimum: 0, Max: 72

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10
Q

Name 4 cytokines elevated in psoriasis

A
  • IL-17
  • IL-23
  • IL-22
  • TNF
  • Also: IFN, IL-2, Il-1, IL-6
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11
Q

Name 5 classes of medications used for psoriasis

A
  • PDE-4 inhibitor (Apremilast)
  • Retinoids (Acitretin)
  • Immunosuppressants (MTX, Cyclosporine)
  • Biologics (TNF, 12/23, 23, 17)
  • JAK inhibitor (Tofacitinib)
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12
Q

Name 4 systemic associations with prp

A

celiac sprue
myositis
MG
hiv

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13
Q

According to the Griffith classification, what are the 5 variants of pityriasis rubra? What is the 6th additional variant?

A

Type I- Classic adult (scalp erythema, keratitis follicular papules on red base, salmon plaques, islands sparing, orange-red waxy keratoderma)
Type II- Atypical adult (itchyosiform leg lesions, eczema and lamellate coarse ppt)
Type III-Juvenile classic
Type IV-Juvenile circumscribed (knees, elbows follicular pap)
Type V-Juvenile atypical (sclerodermoid hands and feet)
Type VI-HIV associated
Type VII-Facial discoid dermatosis

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14
Q

What are 6 morphological variants of Pityriasis Rosea?

A

Gigantea – confined to herald patch
Urticarial
Vesicular
Pustular
Inverse
Purpuric
EM-like

GUV PIPE:

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15
Q

What are 5 medications known to cause drug induced PR?

A

KFC BAGS TOH

Ketotifen
Flagyl
Clonidine

Beta blockers, bismuth, barbiturates, BCG vaccine
ACEi, Aresnic, accurate
Gold
Salvarsan

TNF in
omeprazole
HCTZ

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16
Q

Name top 5 causes erythroderma per Scott Walsh

A

Dermatitic- AD>contact>SD>actinic
Psoriasis
drug rxn
MF
idiopathic

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17
Q

List 10 causes of Erythroderma (please ensure that the first 5 are listed most common to least common)

A
  • Dermatitis
  • Psoriasis
  • Drugs
  • CTCL
  • Idiopathic
  • Seborrheic dermatitis
  • Stasis dermatitis with autosensitization
  • PRP
  • Ichthyosis
  • Bullous dermatoses-e.g. Bullous pemphigoid
  • GVHD
  • AI-CTD: e.g. Dermatomyositis
  • Infestation-scabies
  • Paraneoplastic
  • Chronic actinic dermatitis
  • Papuloerythroderma of ofuji
  • Mastocytosis
  • PER SCOTT WALSH
    o Dermatitic -24% (AD>contact>seb>actinic)
    o Psoriasis -20%
    o Drug rxn -19%
    o CTCL -8%
    o Idiopathic
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18
Q

List 5 variants pustular psoriasis

A
  • Generalized pustular psoriasis of von Zumbusch
  • Exanthematous pustular psoriasis
  • Annular pustular psoriasis of LaPierre
  • Localized pustular psoriasis
  • Gestational (Impetigo herpetiformis)
  • Acrodermatitis continua of Hallopeau
  • Acrodermatitis repens of Crocker
  • Pustulosis palmaris et plantaris
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19
Q

Name which findings in psoriasis are due to what parts of nail bed?
Salmon patch
Oil drop sign
Splinter hemmorhages
Pitting
Beaus lines
Leukonycia
Erythema of lunula
Distal onycholysis
Sublingual hyperkeratosis

A
  • Salmon patch/oil drop – NB
  • Splinter hemorrhages – NB
  • Distal onycholysis – NB
  • Subungual hyperkeratosis – NB or distal matrix
  • Pitting – PNM
  • Beau’s lines – PNM
  • Leukonychia – Distal nail matrix
  • Erythema of lunula – DNM

Key:
* PNM - proximal nail matrix
* DNM - distal nail matrix
* NB - nail bed
* H - hyponychium

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20
Q

What are the HLA associations for each of the following? HLA Cw6, HLA B27, HLA B13/B17

A
  • HLA-Cw6: early onset psoriasis, increased severity, fmhx
    o Increased risk Caucasians (13x), Japanese (25x)
  • HLA-B27: reactive arthritis, sacroiliitis, pustular PsO
  • HLA-B13/HLA-B17: erythrodermic PsO
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21
Q

From epidemiologic studies, what is the risk of psoriasis in an offspring if:
1 parent
both parents
1 sibiling
No parent/sibling

A
  • One parent is affected? 14%
  • Both parents are affected? 41%
  • One sibling is affected? 6%
  • No parent or sibling is affected? 2%
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22
Q

Define the following:
Auspitz sign
Woronoff ring
Koebner phenomenon

A

Woronoff: hypopigmented ring surrounding individual psoriasis lesions possibly due to inhibition of prostaglandin synthesis by treatments.

Koebner: traumatic induction of psoriasis on non-lesional skin.

The Auspitz sign: focal bleeding points that appear when the scale is removed due to dilated capillaries and thinned suprapapillary plates

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23
Q

Name 5 systemic associations w/ LP

A

Hep C
Dental amalgams
Drug
GVHD
paraneoplastic

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24
Q

List 10 variants lichen Planus

A

Annular
Actinic
Atrophic
Bullous
Eruptive/exanthematous
Hypertrophic
Linear
Lichen planopilaris
Lichen Plans pigmentosus
LP pemphigoides
Ulcerative
Oral
Inverse
Nail
Vulvovaginal
DLE/LP overalp

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25
Q

List 8 classes of drugs known to cause lichenoid drug eruptions.

Name

A

Anti 6 PANG (6 Antis then PANG)

Anti-hypertensives: ACEi, BB, methyl dopa, HCTZ
Anti-malarial: HCQ, Chloroquine, Quinacrine, quinidine
Anti-depressants: Amitryptiline, lithium
Anti-fungal: ketoconazole
Anti-TNFs: Etanercept, infliximab
Anti-cancer: Pembrolizumab, Nivolumab,, trosine kinase inhibitors e.g. matinib

PANG
Penicllamine
Allopurinol
NSAIDS
Gold salts

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26
Q

Name 10 features seen on histology for LP

A

Orthokeratosis
Hyperkeratosis
Irregular acanthosis
Saw tooth rete ridges
Wedge shaped hypergranulosis
Hypereosinophilia of keratinocytes at Malphigian layer
Lymphocytic band like infiltrate DEJ
Basal layer vacuolar degeneration
Colloid bodies papillary dermis
Civatte bodies basal layer
Pigment incontinence
Subepidermal clefts between epidermis and dermis: Max-Joseph spaces

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27
Q

Name 4 associations with PLCA and PLEVA

A

Hodgkins, B cell lymphoma
HIV
CTCL

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28
Q

Name 10 porokeratos variants

A

a. DSAP
b. DSP (non-actinic)
c. Porokeratosis palmaris et plantaris disseminate
d. Porokeratosis plantaris discrete
e. Punctate porokeratosis
f. Linear porokeratosis
g. Porokeratosis of Mibelli
h. Porokeratosis psychotropica
i. Porokeratoma
j. Pruritic papular porokeratosis
k. Porokeratotic adnexal ostial nevus

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29
Q

Name 4 mutations in porokeratosis

A

a. MVK-mevalonate kinase, PMVK phosphomevalonate kinase, MVD mevalonate diphosphate decarboxylase, FDPS farnesyl diphosphate synthase.
b. *End up with deficiency in cholesterol
c. Treat with topical statin (cholesterol inhibitor) and cholesterol

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30
Q

What is the highest risk porokeratosis for scc

A

linear porokeratosis

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31
Q

18) Name 5 conditions caused by malessizia furfur/sympodialis in yeast form and 1 in mycelium form

A

Yeast:
seb derm
head neck AD
pityrosporum folliculitis
CARP
Neonatal cephalic pustolosis

Mycelium
PV

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32
Q

19) EDV: Name the 2 HPV subtypes, the 2 clinical presentations, the genetics predispositions

A

EVER 1 and 2- regulate zinc transport in nucleus
HPV 5/8
PV like, flat wart like
Risk SCC in PV-like if photo exposed

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33
Q

Name 2 associations w; nekams

A

heme malig
IDA

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34
Q

Name 4 presentations/additional features seen in nekams

A

Seb derm like lesions
Aphthous ulcers
PPK
Blepharitis/conjuctivitis
*alopecia in children

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35
Q

How is drug induced lichen planus different from classic lichen planus

A

Older age in lichenoid drug eruption (65 vs. 50)

More generalized distribution on the trunk, often spares classic LP sites (forearms, wrists, genitals)

Whickam’s striae less common

Larger lesions, more eczematous, psoriasiform or PR-like morphology

Mucous membranes usually spared

Frequently photo distributed

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36
Q

What are 5 morphological variants of systemic ACD to nickel?

A

Eyelid dermatitis
Widespread nummular dermatitis
Hand dermatitis
Popmpholyx
Intertriginal dermatitis
Anogenital baboon syndrome
Erythroderma

a. Symmetrical eyelid dermatitis
b. Hand dermatitis
c. Pompholyx (dishydrotic eczema)
d. Dermatitis in skin folds
e. Anogenital baboon syndrome (peri-anal/genital)
f. Widespread nummular dermatitis
g. Erythroderma
h. Generalized mac pap
i. Recall dermatitis
j. Flare up genital site
k. Peri-orbital/perioral

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37
Q

List 5 allergens that can lead to systemic ACD.

A

Metals: nickel

Plants:
Poison ivy (Mangos/cashew exposure)
Balsam of Peru (sodas, citrus foods, spices like cloves, vanilla, toothpaste)
Sesqueterpene lactone –>chamomile tea

Meds:
Topical steroids (systemic steroids)
Neomycin–>aminoglycosides,
Quinolones
Ampicillin
Ethylenediamine hydrochloride –> aminophyline

Foods:
Sorbic acid–> sorbic acid
Formaldehyde –> aspartame

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38
Q

6 allergens that can lead to contact anaphylaxis

A

BAN PCR

Bacitracin
Ammonium peruslfate
Neomycin
PPD
Chlorehexidine
Rubber-latex

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39
Q

Describe the grading system for patch testing

A

i. +/- macular erythema/doubtful reaction
ii. + weak, non-vesicular with erythema, papules and infiltration
iii. ++ strong vesicular reaction with erythema, infiltration and papules
iv. +++ spreading bullous reaction
v. IR= irritant
vi. – is negative rxn

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40
Q

If a patient is unable to perform patch testing, what other alternatives exist and how is it performed?

A

Repeat open application test:
Apply product to unaffected area e.gg forearm for 1-22 weeks

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41
Q

List 6 contraindications to patch testing

A

a. History of severe allergic reaction
b. Generalized active dermatitis or angry back already
c. Immunosuppressive treatment (up to 15 mg pred ok)
d. Pregnancy/lactation
e. Potent topical steroids on site of application within 2 days prior
f. Recent sunburn -extensive
g. Infection at site of intended application
h. Unreliable patient/unwilling to comply with protocol

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42
Q

List 7 reasons for a false positive reading.

A

a. Irritant contact dermatitis
b. Concentration too high
c. Contamination
d. Adjacent to a strong positive reaction
e. Plaster reaction or allergy to finn chamber (aluminum)
f. Angry back syndrome (often in patient with severe or widespread dermatitis)
g. External manipulation or pressure artefact (e.g. scratching, bra strap)
h. Uneven dispersion

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43
Q

List 6 reasons for a false negative reading.

A

a. Oral immunosuppression
b. Recent sun exposure/sun burn
c. Too weak dilution
d. Patch falls off/poor placement
e. Sweating or getting patched areas wet
f. Reading results too early (e.g. no delayed reading for gold, drugs, steroids)
g. Topical immunosuppression within days before test

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44
Q

What are 7 adverse reactions that can occur from patch testing that the patient must be counseled about.

A

a. Blistering reaction
b. May trigger eczema flare
c. Infection
d. Pruritus
e. Anaphylaxis
f. Sensitization to new allergen
g. Pigmentation to clothes (dye allergens)
h. Hypopigmentation
i. Scarring
j. Angry back reaction

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45
Q

Name 5 formaldehyde-releasing preservatives

A

a. DMDM hydantoin
b. Quaternium-15
c. Imidazolidinyl urea
d. Diazolidinyl urea
e. 2-bromo-2-nitropronane-1,3-diol (Bronopol)
f. Tris(hydroxymethyl)nitromethane
DQ BDI T

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46
Q

Name 6 potential cross-reacting substances to paraphenylene diamine

A

Sulfonamide antibiotics (TMP-SMX)
Sulfonamide diuretics (HCTZ)
Sulfonamide anti-diabetics (Glyburide)
Benzacaine, procain, tetracaine
PABA-para-aminobenzoic acid
PTDA-paratoluene diamine
Celecoxib
Black rubber mix
Disperse yellow, disperse orange

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47
Q

What are 3 co-sensitizers with nickel allergy?

A

Cobalt
Chromate
Palladium

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48
Q

what are 5 cross reactors with poison ivy

A

Cashew oil
Mango rind
Poison sumac
Poison oak
Japanese lacquer tree
Gingko Balboa tree-fruit bulp
Brazilian pepper tree
Hawaiian Kahlil tree

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49
Q

What are 3 reasons why allergic contact dermatitis in leg ulcer patients is so prevalent?

A

Broken skin barrier
Multiple topical preparations used
Application under occlusion
Chronic wounds

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50
Q

Top 5 allergens in patients with chronic leg ulcers

A

Fragrances: Balsam of peru, colophony
Topical steroids HC, budesonide
Anti-septics: chlorhexidine
Antibiotics-bacitracin, neomycin
Preservatives-MCI/MI, formaldehyde, paraben
Vehicles-propylene glycol, lanolin

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51
Q

What are 4 groups of accelerators used in vulcanization of rubber that can result in allergic contact dermatitis

A

Thiurams
Thioureas
Carbamates
Benzothiazoles

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52
Q

What are 3 antioxidants used in vulcanization that can cause allergic contact dermatitis to rubber?

A

Amines–> Diphenyl-p-phenylenediamine, IPPD
Phenols–> Hydroquinone
Dithioacids–> dibutyldithiocarbamate

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53
Q

What are 6 plant-derived food allergens that comprise the “latex-fruit syndrome” of cross reaction?

A

a. Bananas
b. Avocado
c. Bell pepper
d. Potatoe
e. Chestnut
f. Kiwi
g. Passionfruit
h. Mango

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54
Q

What are the top 3 allergens causing non-occupational airborne allergic contact dermatitis?

A

a. Fragrances
b. Sesquiterpene lactone
c. Methylchloroisothiazolinone

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55
Q

What are the top 3 allergens causing occupational airborne allergic contact dermatitis?

A

Epoxy resins
MCI/MI (cleaning)
Formaldehyde
Chrome
Nickel

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56
Q

What are the top 3 allergens causing occupational airborne allergic contact dermatitis?

A

Epoxy resins
MCI/MI (cleaning)
Formaldehyde
Chrome
Nickel

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57
Q

12) What are 4 areas that you would examine to distinguish an airborne contact dermatitisfrom a photocontact/phototoxic dermatitis?

A

Retroauricular (Wilkinsons triangle)
Eyelids
Nasolabial fold
submental

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58
Q

13) What are the 2 major species of poison ivy and their differences?

A

Toxicodendron radicans
-eastern
-clinbing vine

Toxicodendron rydbergii
-western
-sprawling shrub

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59
Q

1) What does LASER stand for? What are the 3 C’s which characterize lasers?

A

a. Light amplification by stimulated emission of radiation
b. Monochromicity (single or well-defined wavelength), coherence (light waves travel in phase), collimation (parallel beams)

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60
Q

2) What are the 3 different LASER media that exist and determine the laser wavelength?

A
  • Gas (e.g argon, krypton, CO2)
  • Liquid (e.g. dye )
  • Solid (e.g ruby, ND:YAG, alexandrite)
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61
Q

3) What are the 4 main safety concerns when using LASERS?

A

Cutaneous burns
Fires
Eye injury
Biohazardous plume production from laser

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62
Q

4) List the 12 LASERS from Figure 9-1 in Alikhan, along with their wavelength (nm)

A

EAK PRAD NETEC
Excimer: 308
Argon 488-514
KTP 532
PDL 585-600
Ruby 695
Alex 755
Diode 800
Nd:YAG 1064
Erbium: glass 1540
Thulium 1927
Erbium yağ 2940
CO2: 10600

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63
Q

5) List 3 chromophores that are frequent targets for LASERS.

A

Melanin
Hb
Water

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64
Q

List 2 vascular lasers

A

PDL
Long pulse ND:Yag
IPL
Diode

I love pulsed dye (IPL, Long pulse ND yag, PDL, Diode)

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65
Q

List 2 hair removal lasers

A

i. Diode, Nd:YAG (safest in richer skin tones), Alex, IPL

DANI
Diode, alex, nd , ipl

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66
Q

List 2 resurfacing lasers

A

Ablative: CO2, Er:YAG
Non-ablative: PDL, diode, NdYaG, Erbium glass
PEND)

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67
Q

Name 2 tattoo removing lasers

A

Q switch:
Ruby
Alexandrite
ND-YAG

  • Again think melanin
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68
Q

List 4 commercially available botulinum toxins available. Provide both the generic name and the trade name for each.

A

a. Botox: Onabotulinumtoxin A
b. Dysport: Abobotulinumtoxin A
c. Xeomin: Incobotulinumtoxin A
d. Nuceiva: prabobotulinumtoxi A
e. Myobloc: Rimabotulinumtoxin B

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69
Q

List 5 broad categories of dermal fillers (based on material) and provide 1 example of each.

A

HA: Juvederm, restyle, parlance, beloetero
Calcium hydroxyapatite: Radiesse
Poly-L-Lactic acid: Scultpra
Silicone: Silikone 1000
PMMA/bovine: Bellafill/Artefill
Autologous fat
Autologous fibroblasts

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70
Q

9) What type of dermal filler is each of the following (based on material)
a. Zyderm:
b. Restylane:
c. Perlane:
d. Belotero:
e. Juvederm:
f. Artefill:
g. Sculptra:
h. Radiesse:

A

a. Zyderm: Bovine collagen
b. Restylane: HA
c. Perlane: HA
d. Belotero: HA
e. Juvederm: HA
f. Artefill: PMMA in Bovine collagen
g. Sculptra: Poly-L-Lactic acid
h. Radiesse: Calcium hydroxyapatite

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71
Q

List 5 complications that can occur with dermal fillers.

A

Blindness
Necrosis/ulceration
Ecchymoses
Nodules
Blue nodules
Anaphylaxis

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72
Q

3 categories sclerotherapy agents and 2 examples of each

A

a. Hyperosmotic: Hypertonic saline (12-23%), Hypertonic saline 10% + dextrose 25%
b. Chemical irritants: Glycerin, Polyiodide iodide
c. Detergents: Sodium tetradecyl sulfate, Polidocanol

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73
Q

4 contraindications to sclerotherapy

A

a. Allergy to sclerosants
b. DVT
c. Advanced arterial occlusive disease
d. Syptomatic PFO (for foaming sclerosants only)

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74
Q

What are 8 complications of sclerotherapy?

A

Urticaria
Intraterial injection
Ulceration/cutaneous necrosis
Telangiectatic swelling
Swelling
Anaphylaxis
Pain
Ecchymoses
PIH

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75
Q

What are the different categories of peels (based on depth)? Give 1 examples of each.

A

a. Superficial (papillary dermis)
i. Salycyclic acid, glycolic acid, TCA 10-25%, Jessner’s

b. Medium (upper reticular dermis)
i. TCA 35-50%

c. Deep (Deep reticular dermis)
i. TCA >50%

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76
Q

15) What are components of Jessner’s solution?

A

LESR
Lactic acid
Ethanol
Salicyclic acid
Resorcinol

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77
Q

1) List the 4 motor nerve danger zones on the head and neck.

Describe the following: i) Nerve affected; ii) Associated Adverse Events; iii) How to localize/landmark each danger zone.

A

a. Zygomatic arch/temple: Temporal nerve  brow ptosis (unilateral frontalis paralysis). Draw a line from 0.5 cm below the tragus diagonally to 1.5 cm above the lateral brow, third line from lateral orbital rim along the zygoma, forms a triangle
b. Malar cheek: Zygomatic nerve inability to close eye, corneal desiccation. Mark highest point malar eminence, mandibular angle, oral commissure, forms a triangle.
c. Mandible: Marginal mandibular nerve Inability to raise mouth to smile, drooling. 2-3 cm inferolateral to lateral oral commissure as traverses over mandible.
d. Erb’s point: Spinal accessory nerve winged scapula, unable to abduct arm. 6.5 cm inferior to mastoid process in belly of SCM.

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78
Q

List 9 absorbable sutures (generic name and trade name).

A

-Fast absorbing gut
-Plain gut
- chromic gut
- Fast absorbing polyglactin (Vicryl rapide)
- Polyglactin 910 (Vicryl)
- Polyglecaprone (Monocryl)
-Polyglycolic acid (Dexon)
-Polyglyconate
-Polydioxanone (PDS 11)

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79
Q

List 5 non-absorbable sutures (generic name and trade name).

A

a. Silk
b. Nylon (Ethilon)
c. Polyprolene (Prolene)
d. Polyester (Ethibond)
e. Polybutester (Novafil)

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80
Q

Which absorbable suture has highest tissue reactivity? Which has the lowest?

A

Surgical gut > monocryl (polyglecaprone)

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81
Q

Which non-absorbable suture has highest tissue reactivity? Which has the lowest?

A

Silk > prolene

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82
Q

Which absorbable suture has initial tensile strength? Which has the lowest?

A

Monocryl (polyglecaprone) > plain surgical gut

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83
Q

Which non-absorbable suture has initial tensile strength? Which has the lowest?

A

Ethibond (of the non-metals)> silk

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84
Q

List 8 antiseptic used in dermatologic surgery. List 2-3 key points about each (bolded items in table 8-12).

A

a. Alcohol – fastest onset, broad spectrum, but inactive against spores and soiled hands, flammable
b. Chlorhexidine - rapid onset, broad spectrum, but toxic to eyes and ears, inactive against spores, longest acting
c. Iodine and iodophors- broad spectrum including bacterial spores, inactivated by blood and sputum, need to be dry to be effective, skin irritation
d. Soap and water- best for hands, great for norwalk and c.diff
e. Triclosan – binds enoyl-acyl carrier protein reductase, not overly effective
f. Quaternary ammonium compounds (Benzalkonium) – slow, inactivated by organic compounds (e.g. gauze), used in eyedrops
g. Chloroxylenol- slow, ineffective against pseudomonas
h. Hexachlorphene – NO LONGER USED-neurotoxic, teratogenic

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85
Q

9) What is the difference between electrosurgery and electrocautery?

A

a. Electrosurgery: high frequency alternating current to conduct energy through cold tipped electrode, relies on poor conductance of human tissue to halt the current and convert electrical energy into thermal energy, which allows for hemostasis

b. Electrocautery: direct application of heat to tissue through a hot tipped electrode generated by a direct current, there is no current flowing through the patient

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86
Q

Name 4 examples electrosurgery and 1 use for each, and whether biterminal or monoterminal

A

Mono:
Electrofulguriation- zap off seb k
Electrodescciation- ED&C

Biterminal:
Electrocoagulation -hemostasis
Electrosection- surgery

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87
Q

What is mono vs. biterminal

A

Mono=no grounding terminal
Biterminal= grounding terminal (grounding pad or biterminal forceps)

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88
Q

Safest method to use in ICD/pacemakrers?

A

Electrocautery
If electrosurgery-biterminal

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89
Q

11) What are the 4 stages in graft uptake physiology (include timings).

A

Imbibition: 24-48 hours
Inosculation-48-27, continues for 7-10 days
Neovascularization- finished by day 7
Renervation- 2mo-years

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90
Q

Differentiate full thickness skin graft from split thickness skin graft on:
Tissue match
durability
infection risk
Nutritional requirments
Adnexal structure function
Wound contraction
Sensation

A

FSTG better/good/higher in:
-better tissue match, slightly better durability, better sensation, better adnexal function
-higher nutritional requirements than STSG
-less wound contraction

Both low infection risk

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91
Q

List 7 surgical complications and the time frame when they usually occur.

A

Infection: 3-4 days
Bleeding: first 24-48 hours
Dehiscence: highest risk suture removal, first 1-2 weeks
Poor wound healing/abnormal: variable
Hematoma: 0-3 weeks
ischemia/necrosis: flaps first 24-48 hours
Nerve impairment-?immediate

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92
Q

List 7 surgical complications and the time frame when they usually occur.

A

Infection: 3-4 days
Bleeding: first 24-48 hours
Dehiscence: highest risk suture removal, first 1-2 weeks
Poor wound healing/abnormal: variable
Hematoma: 0-3 weeks
ischemia/necrosis: flaps first 24-48 hours
Nerve impairment-?immediate

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93
Q

List 6 broad categories of non-surgical modalities for scar improvement.

A

Massage
Pressure therapy
Topicals- e.g. silicone
Injection-ILK
Laser
Radiofrequency

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94
Q

15) List 4 broad categories of surgical modalities used for scar improvement.

A

Dermabrasion
Subcision
Excision
Re-orienting/lengthening

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95
Q

What is the scar tensile strength at 1 week, 3 weeks, 3 mo, 1 yr

A

5% at 1 week
20% at 3 weeks
40% at 3 months
80% 1 yr

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96
Q

List 5 streptococcal skin infections

A

Eryispelas
Cellulitis*
Non bullous impetigo
Blistering dactylitis
Necrotizing fascitis
Ecthyma
Perianal strep
Scarlet fever
Toxic shock syndrome

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97
Q

List 5 staphylococcal infections

A

Impetigo-bullous/non-bullous
Cellulitis
Abscess/furuncle/carbuncle
Folliculitis
Staph scalded skin syndrome
Toxic shock syndrome
Pyomyositis
Botryomycosis

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98
Q

List 5 pseudomonal skin infections.

A

Green nail syndrome
Otitis externa, malignant otitis externa
Psuedomonal folliculitis
Psuedomonal pyoderma
Psuedomonal hot foot
Ecthyma gangrenosum

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99
Q

List 10 different forms of cutaneous tuberculosis (broad categories: exogenous, endogenous, and tuberculid)

A

Exogenous:
1. Tuberculous chancre
2. Tuberculosis verruca cutis (high)

Endogenous:
3. Lupus vulgaris (high)
4. Scrofuloderma
5. Miliary TB
6. Tuberculous gumma
7. Oroficial TB

Tuberculid: All high immunity
8. Lichen scrofulosum
9. Papulonecrotic tuberculids
10. Erythema induratum of basin

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100
Q

5) List the types of leprosy according to the Ridley and Jopling classification system.

A

Tuberculoid (th1/high cell immunity)
Bordeline tuberculoid
Borderline borderline
Borderline lepormatous
Lepromatous (Th2, low cell)

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101
Q

List 6 cutaneous nerves that run superficially and should be palpated to assess for thickening in leprosy patients:

A

Medial
radial
ulnar
Greater auricular
CN 5
CN 7
Posterior tibial
Common perineal

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102
Q

List 6 dermatophytes that demonstrate endothrix growth during hair infection

A

Ringo Gave Yono Two Squeaky Violins

Trichophyton rubrum, T.Gourvilli, T.Yaounde, T.Tonsurans, T.Soudanense, T.Violaceum

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103
Q

8) List 5 dermatophytes (ectothrix) that fluoresce on Woods lamp examination due to the presence of what substance:

A

Pteridine

Cats And Dogs Fight and Growl Sometimes

M. canus
M. audouinii
M. Distortum
M. Ferrugenium
M. Gypseu,
T. Schloenni

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104
Q

What causes favus

A

T Schloenni
*May fluoresce dull gray green

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105
Q

Most common causes tinea wapitis:
-us
-worldwide
-favus
-kerion

A

Trichophyton tonsurans (#1 cause in
United States)
Microsporum canis (#1 cause worldwide; more inflammatory)
T. violaceum (East Africa)

Endothrix (black dot; arthroconidia within hair shaft): Ringo

Ectothrix (arthrospores around hair shaft)
1. Fluorescent (green via Wood lamp – pteridine): “Cats And Dogs”

  1. Nonfluorescent: MMR NGV
    T. mentagrophytes, T. rubrum, M. nanum, T. megninii, T. gypseum, and T. verrucosum
  2. Favus – T. schoenleinii mainly
  3. Kerion – M. canis, T. verrucosum,
    T. mentagrophytes, and T. tonsurans
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106
Q

What are 4 clinical variants or presentations of tinea capitis?

A

Non inflam:
Grey Patch (ecto)
Black dot (endo)
Diffuse scale

Inflammatory:
Kertion
Favus
Diffuse pustular

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107
Q

What are 4 clinical presentations of tinea pedis?

A

Moccasin
Interidigital
Acute ulcerative
Acute vesiculobullous

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108
Q

List 4 clinical types of onychomycosis:

A

DLSO
Proxima white subungual
Superficial white
Total dystrophic
Endonyx

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109
Q

What are the vectors for leishmaniasis

A

Sand flies
Old world-Phlebotomus
New world-Lutzomyia

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110
Q

List 3 species that cause old world leishmaniasis

A

Major Tropical Infants in Ethiopia

a. Leishmania major, L. Tropica, L. infantum, aethiopica

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111
Q

List 3 species that cause new world leishmaniasis

A

a. L. mexicana, L. brasiliensis, L. amazonensis

BAM

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112
Q

15) What are 5 broad clinical variants of leishmaniasis?

A

Cutaneous-new and old
Diffuse cutaneous
Mucocutaneous
Visceral (Kala Azar)
Post Kala Azar

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113
Q

What are 5 risk factors for cutaneous larva migrans (CLM)?

A

Male, young/children, barefoot/bum, travelers to tropical climates (jamiaca, Dominican, Thailand), swimmers, broken skin, wet sand, beach with many cats/dogs

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114
Q

What is one major difference between new and old world leish?

TOC visceral and cutaneous leash

A

Not confirmed
a. Old world cutaneous–> typically presents with single ulcer verrucous w/ sporotrichoid spread, new world usually more varied: ulcerations (Chiclero ulcer = ear lesion in workers who harvest chicle gum in forest), impetigo-like, lichenoid, sarcoid-like, nodular, vegetating, and miliary
b. Mucocutaneous is almost always new world
c. Most cases of old world resolve in 15 months. 75% of L. Mexican new world resolve ) Mucocutaneous (new world) does NOT self resolve ((L. braziliensis and L. panamensis) does NOT self-resolve and requires treatment to prevent progressive destruction)

Visceral more old world

Cutaneous/mucocutaneous: pentavalent antimony
Visceral leishmaniasis: Amphotericin B (ToC)

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115
Q

18) List 2 organisms responsive for CLM.

A

Ancylostoma brasiliensis
Ancylsotoma caninum

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116
Q

19) List 5 treatment options for CLM.

A

Albendazole
Ivermectin
Thiabendazole-topical and oral
Liquid nitrogen

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117
Q

20) What is the classic cutaneous eruption seen in strongyloides? What is the treatment of choice for strongyloides?

A

Thumbprint purpura
Ivermectin

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118
Q

List 5 genodermatoses that can be associated with CALMS

A

a. NF I, NF II, Mosaic NF I (NF 5)
b. Legius syndrome
c. McCune Albright syndrome
d. Bloom syndrome
e. Noonan syndrome (Allelic w/ LEOPARD syndrome/Noonan with multiple lentigines)
f. Tuberous sclerosis
g. Fanconi
h. Ataxia telangiectasia
i. MENI
j. Constitutional mismatch repair
k. Ring chromosome syndrome
l. Cowdens
m. Proteus syndrome
n. Watson syndrome

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119
Q

List 5 syndromes associated with multiple lentigines.

A

a. Noonan syndrome with multiple lentigines (Formerly known as LEOPARD)
b. Carney complex (LAMB/NAME)
i. Lentigines, atrial myxoma, blue nevus
ii. Nevi, atrial myxoma, myxoid neurofibromas, Ephelids
c. Laughier-Hunziker (Oral, genital, melanonychia, r/o peutz Jegher)
d. Peutz Jegher (intra-oral)
e. Cowdens (penile-PTEN)
f. Bannayan-Riley-Ruvalcaba (penile-PTEN)
g. Xeroderma pigmentosum

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120
Q

What does LEOPARD stand for

A

L stands for (L)entigines
(E)lectrocardiographic conduction defects (abnormalities of the electrical activity and the coordination of proper contractions of the heart);
(0)cular hypertelorism (widely-spaced eyes);
(P)ulmonary stenosis (obstruction of the normal outflow of blood from the right ventricle of the heart); (A)bnormalities of the genitals; (R)etarded growth resulting in short stature;
(D)eafness or hearing loss due to malfunction of the inner ear (sensorineural deafness).

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121
Q

List 5 variants of dermal melanocytosis

A

a. Congenital dermal melanocytosis (Mongolian spots)
b. Nevus of ota
c. Nevus of ito
d. Hori’s nevus (acquired)
e. Sun’s nevus (acquired, unilateral Hori’s)

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122
Q

Which mutations are often associated with Blue Nevus

A

GNAQ
GNA11

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123
Q

Which gene is associated with inherited form of melanoma? Which proteins does it code for?

A

CDKN2A–> FAMM
Familial atypical multiple melanoma

P14-ARF and P16–> modulate cell cycle progression through P53 and Rb pathways, respectively

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124
Q

Name 8 mutations seen in melanomas

A

BRAF –> V600E MC (sup spreading)
NRAS
C-KIT (mucosal and acral)
CCND1/CDK4
TERT
GNAQ/GNA11: uveal melanoma, blue nevi, and nevus of Ota

BAP-1: Cutaneous melanoma, uveal melanoma, malignant cellular blue nevus, epithelia spitzoid nevi, MESOTHELIOMA, and renal cell carcinoma may be seen in a syndrome which is associated with which mutation?

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125
Q

List 5 variants melanoma

A

a. Nodular
b. Superficial spreading
c. Lentigo maligna melanoma
d. Acral lentiginous melanoma
i. Uveal melanoma
ii. Mucosal melanoma
iii. Desmoplastic melanoma
iv. Spitzoid melanoma
v. Malignant blue nevus

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126
Q

Acral and mucosal melanomas are associate with which mutations

A

C-KIT

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127
Q

Superficial spreading melanomas are associated with which mutation

A

BRAF-V600E

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128
Q

10) Uveal melanomas and blue nevi are associated with which mutation

A

GNAQ/GNA11

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129
Q

11) Cutaneous melanoma, uveal melanoma, malignant cellular blue nevus, MESOTHELIOMA, and renal cell carcinoma may be seen in a syndrome which is associated with which mutation?

A

BAP-1

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130
Q

12) According to AJCC 8, what do the following correspond to:
Name the T stages for melanoma

A

T1a- <0.8 mm no ulceration (1A)
T1b- <0.8 mm w/ ulceration, or 0.8-1.0mm (1B)
T2a- >1-2.0 m w/out ulceration (1B)
T2b- >1-2.0 mm w/ ulceration (2A)
T3a- >2-4.0 mm w/out ulceration
T3b- >2-4.0 w/ ulceration
T4a- > 4 mm w/o ulceration
T4b- > 4 mm w/ ulceration

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131
Q

Name the clinical staging for melanoma according to AJCC 8 edition

A

IA: T1a (anything <0.8 mm w/out ulcer)
IB: T1b, T2a (anything < 1mm w/ ulceration, 0.8-2 w/out ulceration
2A: T2b, T3a
2B: T3b, T4a
2C: T4b
3: Any T N>1 M0
4: Any T any N M >1

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132
Q

Which two gene mutation have been associated with seborrheic keratoses? List 7 clinical variants of SKs. List 6 histological variants of SKs.

A

PIK3CA
FGFR3

Variants:
-inverted follicular keratosis
-lichenoid keratosis
-stucco keratosis
-acrokeratosis verruciformis of hopf
-dermatosis papulosa nigra
-clear cell acanthoma
-large cell acanthoma

6 path variants: “CHRAIM”
-hyperkeratotic
-acanthotic
-clonal
-irritated
-reticulate
- melanoacanthoma

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133
Q

List 10 risk factors for invasive SCC

A

Ia. Immunosuppressed, CLL
b. Older age
c. Male
d. Fair skin
e. Genetic conditions: e.g. XP
f. UV- chronic>intermittent
g. HPV
h. Radiation
i. Chronic non healing wounds-Marjolin ulcer
j. Inflammatory dermatoses such as DLE, erosive oral LP, chronic LSA
k. Medications: BRAF inhibitors, voriconazole

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134
Q

List 6 genetic syndromes associated with SCC.

A

a. Photosensitive:
i. Oculocutaneous albinism
ii. Xeroderma pigmentosum
iii. Rothmund thompson

b. The D’s:
i. EDV
ii. Dystrophic EBA
iii. Dyskeratosis congenita
iv. KID syndrome-keratitis, ichthyosis, deafness

c. Misc:
i. Porokeratosis-linear
ii. Werner syndrome
iii. Chronic mucocutaneous candidiasis

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135
Q

What is verrucous carcinoma? Which HPV subtype is it associated with? What are the 3 clinical variants and where on the body does each variant present?

A

Low grade, locally destructive SCC

HPV 6/11

Clinical variants:
Buschke lowenstein Tumor - perianal
Epithelium cuniculatum - foot
Oral florid papillomatosis - oral cavity
Papillomatosis cutis carcinoides of Gottron

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136
Q

List 6 clinical variants of keratoacanthoma. What are 2 KA specific syndromes?

A

Variants:
Solitary
Multiple
Intraoral
Subungual
Giant
Keratoacanthoma centrifigum marginatum

KA syndromes:
Gryzbowski
Ferguson-Smith

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137
Q

Describe the two KA syndromes- acquired vs. genetic, onset, appearance

A

Ferguson-Smith-AD, rapid onset multiple large KAs, resole spont. 3rd decade

Gryzbowski: Sporadic, thousands milia-like KAs, later in life, can have airway involvement, scarring, ectropion

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138
Q

What is the most common mutation identified in BCCs. List 8 variants of BCCs. List 6 genetic syndromes associated with BCCs.

A

a. PTCH most common mutation
b. Variants
i. Superficial
ii. Nodular
iii. Morpheaform
iv. Fibroepithelioma of Pinkus
v. Micronodular
vi. Basosquamous
vii. Infundibulocystic
viii. Pigmented

Genetic syndromes
i. Basal cell nevus syndrome, Brooke Spiegler
ii. OCA, XP, Bloom syndrome, Rothmund Thomson, Werner
iii. Bazex Dupre Christol, Rombo syndrome, Schopf Shulz Passarge

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139
Q

Which syndrome is associated with multiple epidermoid cysts.

What are other features of this syndrome?

A

a. Gardner’s syndrome-APC (adenomatous polyposis coli)

i. Skin: Epidermoid cysts w/ pilomatricoma features, lipomas, fibromas (skin, subcutaneous, mesentery, retroperitoneal), osteomas
ii. GI manifestations: Desmoid tumors, premalignant polyposis
iii. Eyes: CHRPE
Cancer: colon duodenal , brain liver adrenals thyroid
iv. Others: Osteomas (subcutanesous), odontomas, supernumary teeth, sarcoma, papillary thyroid cancer (women), adrenal adenomas, brain tumors (gliblastomas and medulloblastoma in Turcot syndrome), pancreatic carcinomas

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140
Q

Who most frequently gets dermoid cysts and where are they most commonly located?

A

a. Along embryonic fusion lines, most common lateral eyebrow
b. Infants

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141
Q

Which syndrome is steatocystoma multiplex associated with? What are the gene mutations and other features of this syndrome?

A

a. Pacyhonychia congenita Type II
b. Gene mutations: KRT17»KRT6B

c. *In general: PPK, painful heels, thickened nails

d. Features:
i. Natal teeth
ii. Oral leukokeratosis
iii. Steatocystoma or other cysts
iv. Palmar plantar keratoderma-milder than type I

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142
Q

What are the 3 main findings in Brooke Spiegler

A

Trichoepithelioma
Spiradenoma
Cylindroma
Trichoblastoma

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143
Q

Which syndrome is cylindroma associated with? What is the gene mutation? What are the other features of this syndrome?

A

Brooke Spiegler
Gene mutation: CYLD

Features
i. Cylindroma (papules/nodules scalp)
ii. Trichoepithelioma (facial papules)
iii. spiradenoma (painful nodules head neck)
iv. Trichoblastomas,

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144
Q

What are 5 cancers that can occur in Brooke Spiegler

A

BCC
Spiradenocarcinoma
Cylindrocarcinoma
Salivary and parotid gland tumors

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145
Q

What syndrome is associated with multiple fibrofolliculomas/trichodiscomas?

What is the gene mutation?

List all cutaneous and 4 non-cutaneous features.

A

Birt-Hogg-Dube
Gene: FLCN (folliculin)

Cutaneous:
i. Fibrofolliculoma
ii. Trichodiscoma
iii. Achrocordons
iv. Angiofibromas

Non cutaneous features:
i. RCC
ii. Spont. Pneumothorax
iii. Pulmonary cysts
iv. Medullary thyroid cancer
v. Parotid gland onycocytomas

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146
Q

Which secondary adnexal neoplasms can arise in a nevus sebaceous? Which is the most common?

A

2 S’s, 2 T’s and a B

a. Trichoblastoma -most common
b. Trichilemmoma
c. Syringocystadenoma papilliferum
d. Sebaceoma
e. BCC

f. Others:
i. Eccrine poroma
ii. Tubular apocrine adenoma

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147
Q

List 2 syndromes with multiple trichoepitheliomas.

A

Brooke Spiegler
Rombo

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148
Q

Which gene/protein mutation is associated with pilomatricomas? List 4 syndromes associated with pilomatricomas.

A

CTNNB1 Gene–> B catenin

Myotonic dystrophy

Rubinstein Taybes

Gardner-pilomatricoma features in epidermoid cysts

Turners

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149
Q

What syndrome are multiple trichilemmomas associated with

What gene is mutated in this syndrome?

What are other features of this syndrome? List malignancies that are associated with this syndrome.

A

a. Cowden’s
b. PTEN mutation

i. LA HAS TOPS BET
1) Lipomas, angiolipomas, hemangiomas, acral keratoses, skin tags, trichelommomas, oral papillomas (cobble stoning to lips/gingival/oral mucosa), sclerotic fibromas

Malignancy: Breast, thyroid, endometrial

Others: Fibrocystic breasts, thyroid goiter, GI tract hamartomous polyps (low risk), ovarian cysts, uterine leiomyomas, menstrual irregularities,

bony cysts, kyphoscoliosis, craniomegaly, large hands/feet, adenoid facies, angiod streaks, myopia

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150
Q

What is the inheritance pattern for Muire-Torre syndrome (MTS)?

Which genes are associated with this?

What is the clinical presentation for MTS?

Which malignancies are patients with MTS at an increased risk for?

A

a. Inheritance pattern: AD
b. Phenotypic variant of Lynch
c. Genes: MLH1, MSH2 (90%), MSH6, PMS2
Sebaceous adenoma, sebaceous carcinoma, sebaceoma *Esp non facial, multiple KAs often w/ sebaceous differentiation (strong)

At risk for: Colon cancer #1, GU #2 (bladder, kidney, ureter etc.), gastric, ovarian, endometrial

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151
Q

17) Differential for painful skin tumors

A

BLEND AN EGG

Blue rubber bleb nevus
Leiomyoma
Eccrine spiradenoma
Neuroma
Dermatofibroma
Angiolipoma, angioleiomyoma
Neurilemmoma
Endometrioma
Gloms tumor
Granular cell tumor

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152
Q

18) Which syndrome is associated with multiple cutaneous leiomyomas? What is the gene mutation? What are the other clinical features?

A

Hereditary Leiomyomatosis and RCC syndrome/Reed syndrome

Fumarate hydratase

RCC
Leiomyomas-cutaneous and uterine

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153
Q

List 5 path variants of dermatofibroma.

A

Cellular DF
Hemosiderotic
Aneurysmal
Monster cells (DF with monster cells)
Xanthomatous

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154
Q

b. List 4 clinical (superficial) variants of fibromatosis.

A

Palmar
Plantar
Peyronies
Knuckle pads

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155
Q

List 3 clinical differences between and infantile hemangioma and vascular malformation.

A

a. Growth: IH rapidly proliferate for 4-6 mo, VM do not
b. Resolution: IH can spont. Resolve, VM either persist or resolve
c. Onset: IH not present at birth, VM present at birth
d. Appearance: IH are usually bright red but can be purple-blue if deeper; VM have variable clinical appearances but tend to persist and become more verrucous over time

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156
Q

Compare the epidemiology of infantile hemangiomas and vascular malformation.

A

IH: 4-5% of infants, more in Caucasians, F>M

Vascular malformation: F=M, most common are CMs, least common AV, low flow more common

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157
Q

What are the three phases in the natural history of an infantile hemangioma

A

Proliferating, plateau, involution

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158
Q

List 5 risk factors for infantile hemangiomas.

A

female sex
multiple gestations-twins
placental anomalies
premature
advanced maternal age
low birth weight

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159
Q

5) What are 4 potential complications of infantile hemangiomas?

A

a. Ulceration
b. Disfigurement – e.g. nasal tip, breast asymmetry, fibrofatty residual
c. Interference with function from location- e.g. periocular and vision loss
d. Extracutaneous involvement-e.g. internal hemangiomas, PHACES, beard hemangioma and laryngeal hemangiomatosis

Also death from airway involvement or high output cardiac failure

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160
Q

List 3 immunohistochemical markers that can be used to differentiate infantile hemangioma from vascular malformation.

A

a. GLUT-1
b. Lewis Y-Antigen
c. Merosin
d. Wilm tumor protein (WT-1)
e. FcγRII
f. *All positive in IH, negative in vascular malformation

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161
Q

What are the 4 segmental hemangioma patterns?

A

Frontotemporal
Maxillary prominence
Mandibular prominence
Frontonasal

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162
Q

What does PHACES stand for

A

a. P: Posterior fossa malformations (e.g., Dandy-Walker and cerebellar hypoplasia)
b. H: Hemangioma, segmental
c. A: Arterial anomalies (internal carotid arteries and cerebral arteries)
d. C: Cardiac anomalies (coarctation of aorta, ventral and atrial septal defects, and patent
e. ductus arteriosus)
f. E: Eye anomalies (microphthalmos, optic atrophy, cataracts, strabismus, and exophthalmos)
g. S: Sternal cleft or supraumbilical raphe

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163
Q

What is LUMBAR syndrome

A

Lower body/lumbosacral/lipoma /hemangioma
Ulceration/urogenital anomalies
Myelopathy (spinal dyspraphism)
Bony deformities (hip dysplasia, scoliosis)
Anorectal anomalies
Renal anomalies (hypo plastic single kidneys, bladder/ureter anomalies)

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164
Q

What does SACRAL stand for?

A

a. Spinal dysraphism
b. Anogenital anomalies
c. Cutaneous anomalies
d. Renal/urologic anomalies
e. Angioma in Lumbosacral area

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165
Q

What does PELVIS stand for?

A
  • P: Perineal haemangioma
  • E: External genitalia malformations
  • L: Lipomyelomeningocele
  • V: Vesicorenal abnormalities
  • I: Imperforate anus
  • S: Skin tag
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166
Q

List 3 clinical differences between infantile hemangiomas and RICH/NICH.

A

o Onset: IH develops in the first few months of life; RICH/NICH is apparent at birth
o Growth: IH undergoes rapid growth for 4-6 months followed by slow involution over years; RICH/NICH are fully developed at birth
o Resolution: RICH will involute over 1 year, IH will involute over several years, NICH will not involute

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167
Q

List 2 histopath differences in RICH/NICH vs. IH

A

IH: GLUT-1, WT-1, Lewis-Y-antigen POSITIVE (vs. RICH/NICH negative)

  1. striking lobularity with densely fibrotic stroma
  2. stromal hemosiderin deposits,
  3. focal thrombosis and sclerosis of capillary lobules,
  4. fewer mast cells
  5. coexistence of proliferating vasculature with multiple thin-walled vessels
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168
Q

What are 4 reasons to consider systemic therapy for infantile hemangioma?

A

a. Threaten vital function- vision, airway
b. Threatent life e.g. High output heart failure, airway involvement
c. Potential for disfigurement: columella, nasal tip, ear, rapidly growing lesion on face
d. Ulceration-severe or recalcitrant

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169
Q

What are the 5 major goals of management of infantile hemangiomas?

A

a. Preventing or reversing life or function- threatening complications
b. Preventing potential disfigurement
c. Treating ulcerations
d. Minimizing psychosocial impairment to patient and families
e. Avoiding overly aggressive procedures that could cause scarring

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170
Q

What are 6 extractable antigens

A

SSA-ro
SSB-la
Smith
SCL-70
RNP (U1RNP)–> high titers → MCTD; lower titles → SLE
J0-1

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171
Q

What are 3 non ENA targets

A

Centromere
dsDNA
Histone

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172
Q

List 3 antibody targets that are highly specific for SLE. What are they associated with?

A

dsDNA: lupus nephritis and activity, lupus disease activity, sun-protected non lesional skin lupus band

Smith- not much, more prevalent in Asian/African American patients

rRNP (ribosomal)–>neuropsychiatric

*NB
1. rRNP with lupus/neuropscyh lupus
2. RNA polymerase I/III with systemic sclerosis
3. U1RNP with MCTD

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173
Q

List 5 dermatomyositis associated antibodies, not including anti-synthetase syndrome. What are they associated with?

A

4) List 5 dermatomyositis associated antibodies, not including anti-synthetase syndrome. What are they associated with?
a. Mi-2: Classic DM findings, good tx response, no malig or ILD risk

Tiff-1-gamma (P155/P140): A/hypomyopathic, ++ malignancy, GI w/ severe dysphagia, severe skin (ovoid patch, psoriasiform lesions, palmar hyperkeratosis, atrophic hypopigmented patches w/ telangiectasias), No RP/ILD/arthritis
i. JDM: no malignancy, treatment refractory, lipodystrophy

MDA-5: Amyopathic, rapidly progressive ILD specific skin (cutaneous vasculopathy with oral/skin ulcers, tender palmar papules, mechanics hands, panniculitis)
- JDM ulcers, ILD, arthritis, mild muscle (i.e. similar)

NXP2 (P140, MJ): Malignancy in adults, calcinosis, peripheral edema,
-JDM: Severe calcinosis, severe muscle involvement, vasculopathy w/ gi bleeds

SRP: fulminant PM/DM, cardiac involvement, poor prognosis

SAE: Severe cutaneous dz, progressive muscle disease w/ dysphagia, fever/weight loss, erythroderma if given HCQ
g. Anti-synthetase: Jo-1, PL7, PL-12, OJ, EJ
i. Others include ARS, KS, HA, ZA

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174
Q

Which antibody is most specific for CREST? What is it associated with?

A

a. Anti-centromere–> Calcinosis, raynauds, esophageal dysmotiliy, sclerodactyly, telangiectasias
b. Associated with pulmonary HTN

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175
Q

Which antibody is most strongly associated with primary systemic sclerosis? What is it associated with?

A

a. SCL-70/Topoisomerase
b. Associated with ILD/pulm fibrosis

*RNA polymerase III is the third ab and related to renal crisis and severe skin

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176
Q

7) Which two antibodies are associated with linear morphea?

A

ssDNA (correlated w/ disease activity)
Anti-histone (lin and generalized, correlated w/ dz activity)

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177
Q

Which two antibodies can be detected in patients in RA? What are they associated with?

A

RF:
-high levels associated with severe erosive RA, vasculitis and neuropathy, can also be seen in mixed cryoglobulinemia
-Low level RF non specific

CCP: severe RA, development of RA

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178
Q

List 3 autoantibodies associated with Sjogren’s syndrome. What are they associated with?

A

SSA (neonatal LE and SCLE)
SSB
alpha fodrin (actin binding product)

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179
Q

Which antibody is detected in neonatal lupus?

A

RO/ssA

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180
Q

11) Which antibody is associated with mixed connective tissue disease?

A

U1RNP

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181
Q

List the components of the newest (EULAR/ACR) criteria for SLE (more recent than the SLICC criteria).

A

*Need 10 points
Must have + ANA for entry criteria

Constitutional domain: Fever

Cutaneous: ACLE, SCLE/DLE, non scarring alopecia, oral ulcers

Arthritis: synovitis or tenderness in 2+ jonts

Renal: Lupus nephritis, proteinuria

Serositis: Pleural or pericardial effusion, acute pericarditis

Neurologic: Delirium, psychosis, seizure

Labs: Leukopenia, thrombocytopenia, hemolytic anemia

Immunologic
i. dsDNA or smith
ii. APLS: ACA or LAC or B2GP
iii. Low C3 and/or C4

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182
Q

List the classification for dermatomyositis.

A

Adult
-Classic
-DM overlap
-Amyo
-Hypomyo
-Malignancy assoc.

Juvenile
-classic
-hypomyo
-amyopathic

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183
Q

List 5 variants of morphea

A

Localized: plaque, superficial, atrophoderma passini and piereni, , guttate, nodular, bullous

Linear: en coup de sabre, Perry-romberg, trunk-limb, atrophoderma of moulin

Generalized
Pansclerotic
Mixed

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184
Q

Skin findings in RA

A

a. Rheumatoid nodules

b. Rheumatoid vasculitis
i. Small, medium, EED, Bywaters lesions

c. Livedo reticularis and livedoid vasculopathy

d. Neutrophilic dermatoses
i. PG
ii. Sweet’s
iii. Rheumatoid neutrophilic dermatitis
iv. Palisading neutrophilic granulomatous dermatitis
v. Interstitial granulomatous dermatitis
vi. Superficial ulcerating rheumatoid necrobiosis

MTX induced papular eruption

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185
Q

List 5 entities on the ddx for systemic sclerosis.

A

GVHD
Nephrogenic systemic fibrosis
Scleredema, scleromyxedema, pretibial myxedema
Morphea
Eosinophilic fasciitis

Others:
Mucinoses
Localized: radiation induced, injection site (vitamin K, bleomycin)
Generalized: toxic oil syndrome, polyvinyl chloride, belomycine, taxanes, eosinophilic-myalgia (L tryoptophan)

Paraneoplastic: POEMS, carcinoma en cuirasse, amyloidosis, carcinoid

Metabolic: PCT, diabetic cheiropathy (diabetic stiff hand syndrome)

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186
Q

What are the different types of scleredema and their associations?

A

Post infectious- Type I

Monoclonal gammopathy related – Type II

Diabetic related -Type III

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187
Q

3) What is POEMS syndrome?

A

Polyneuropathic
organomegaly
endocrinopathy
monoclonal gammopathy
Skin changes-melanoderma/hyperpigmentation, hemangioma, hypertrichosis

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188
Q

List 4 major perforating disorders and 1 association with each.

A

a. Elastosis perforans serpiginosa (EPS):
i. MAD PORES
1. Marfans
2. Acrogeria
3. Downs
4. Penicillamine, PXE
5. OI
6. Rothmund Thompson
7. EDS
8. Scleroderma

b. Acquired perforating dermatosis (APD): Diabetes, renal failure

c. Reactive perforating collagenosis (RPC); Childhood onset, minor trauma

d. Perforating calcific elastosis (PCE): Obese, hypertensive, multiparous women

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189
Q

What are 4 broad categories of cutaneous crohn’s disease?

A

a. Specific lesions:
i. metastatic chrons, contiguous perianal or oral chrons

ii. Oral: cobblestoning of the buccal mucosa, tiny gingival nodules, gingival hyperplasia, aphthae-like ulcers, linear, knife-like ulcerations, angular cheilitis and ulceration, cheilitis granulomatosa, diffuse oral swelling, or indurated fissuring of the lower lip

b. Non-specific lesions/reactive
i. erythema nodosum, PG (UC>chrons), pyostomatitis vegetans (UC>chrons), erythema multiforme, finger clubbing, cutaneous small vessel vasculitis, epidermolysis bullosa acquisita, vitiligo, palmar erythema, a pustular response to trauma (pathergy),

c. Nutritional skin changes e.g. acrodermatitis enteropathica

d. Treatment related skin change

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190
Q

What are the 5 clinical findings seen in Lofgren’s syndrome?

A

EN
Fever
hilar LAD
migrating polyarthritis
uveitis

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191
Q

7) What are the clinical findings seen in Heerfordt’s syndrome?

A

Uveitis
Fever
parotid gland enlargement
CN palsies

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192
Q

8) What are the clinical findings seen in Mikulicz’s syndrome?

A

Salivary gland (parotid, submandibular) and lacrimal gland swelling

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193
Q

What are 5 examples of palisaded granulomas? (Figure 3-64)

A

a. GA (central mucin)
b. RA nodule (Central fibrin)
c. Necrobiotic xanthogranuloma (degenerative collagen)
d. Necrobiosis lipoidica diabeticorum
e. Annular elastolytic giant cell granuloma
f. Uric acid crystals gout

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194
Q

List 6 different types of cutaneous xanthomas.

A

Eruptive
Tendinous
Tuberous
Plane
Xanthelasma-plane xanthoma on eyelids
verruciform xanthoma

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195
Q

11) List 6 different types of physical urticarias.

A

a. Dermatographism
b. Aquagenic
c. Cholinergic
d. Solar
e. Vibratory
f. Delayed pressure
g. Cold-induced

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196
Q

12) What is the clinical criteria for Sweet’s syndrome?

A

c. Major:
i. Skin: abrupt onset painful cutaneous lesions
ii. Path: consistent with sweets

d. Minor
i. Leukocytosis
ii. Response to steroids
iii. Associated Dz: infection, vaccinations/drugs, inflammatory condition (IBD, AI-CTD, sarcoid, bechets), malignancy, pregnancy
1. Drug induced: GO SHLAM
a. G-CSF/GM-CSG
b. OCP
c. Septra
d. Hydralazine
e. Lasix
f. ATRA
g. Minocycline

iv. Fever or constitutional symptoms

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197
Q

13) What is the clinical criteria for pyoderma gangrenosum?

A

a. 2 Major + 2 Minor

b. Major:
i. Skin: Rapidly progressive painful cutaneous ulcer (50% growth in 1 mo), undermined, irregular violaceus border
ii. Causes: Other causes excluded

c. Minor
i. Pathergy- Hx suggestive pathergy (minor trauma) or cribiform base scarring
ii. Associated dz (IBD, IgA gammopathy, arthritis, malignancy)
iii. Response to treatment (rapid response to steroids)
iv. Path findings

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198
Q

What are 4 variants of pyoderma gangrenosum?

A

Bullous
Ulcerative
Pustular
Superficial granulomatous/
vegetans

Pyostomatitis vegetans/pyoderma also mentioned

Peristomal

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199
Q

What is the clinical criteria for Behcet’s disease?

A

a. Major (1/1):
Recurrent apthosis 3+ episodes for year

b. Minor (2/4)
i. Pathergy
ii. Eyes-anterior or posterior uveitis
iii. Genital ulcers
iv. Skin findings -EN, folliculitis

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200
Q

16) What do the following acronyms stand for: i) PAPA; ii) PASH; iii) PAPASH; iv) PASS; v) SAPHO

A

a. PAPA: Pyogenic arthritis, Pyoderma gangrenosum and Acne

b. PASH: Pyoderma gangrenosum, Acne and HS

c. PAPASH: Pyoderma gangrenosum, pyogenic arthritis, Acne, and HS

d. PASS: PG, Acne, HS, Ankylosing spondylitis

e. SAPHO: Synoviits, acne, pustulosis, hyperostosis and osteitis

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201
Q

17) What are 3 different types of miliaria?

A

Cyrstalina-corneum
Rubra-mid epidermis
Profunda - DEJ

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202
Q

18) List 5 causes of drug-induced acne:

A

18) List 5 causes of drug-induced acne:
a. Prednisone
b. Anabolic steroids
c. Androgens-Testosterone
d. JAK inhibitors
e. Halogens
f. Lithium
g. Isoniazid
h. Phenytoin
i. EGFR inhibitors, MEK inhibitors, Mtor inhibitors
j. IUD
k. OCP
l. Vitamin B2, B6,B12, biotin

SHIELD yourself from Vitamin T
i. “Steroids (anabolic, corticosteroids), Halogens, Isoniazid, EGFR inhibitors, Lithium, Dilantin (phenytoin), Vitamin B2, B6, B12, Testosterone and babies (OCP, IUD)

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203
Q

19) How is acne fulminans different from acne conglobate?

A

a. Systemic symptoms in fulminans-fevers, arthralgia, myalgias, malaise, osteolytic bone lesions

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204
Q

20) List 10 acne variants.

A

a. Acne vulgaris
b. Acne conglobata
c. Acne fulminans
d. Acne excoriee
e. Neonatal acne
f. Infantile acne
g. Acne cosmetica
h. Pomaid acne
i. Chloracne
j. Radiation acne

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205
Q

Name 5 GA variants

A

a. Generalized
b. Annular
c. Patch
d. Perforating
e. Subcutaneous/Deep

GAPPS

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206
Q

Ddx for eosinophilic spongiosis

A

BAD CHIP PIGS

BP
AD
Drug
Contact derm
herpes gestationis/pempigoid
IP
PV
PF
Grovers
scabies
infestation

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207
Q
  1. What clinical sign is associated with papuloerythroderma of ofuji? What histological finding is characteristically seen with Well’s syndrome?
A

Deck chair sign
Flame figures

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208
Q

What is the criteria for hypereosinophilic syndrome and what are the 2 major subtypes

A

peripheral eosinophils >1500/mm3 x 6 months or < 6 mo w/ end organ damage

No evidence underlying cause (parasite, allergy, drug etc.)

End organ damage

i. Myeloproliferative: MC FIP1L1A-PDGFRA translocation, tyrosine kinase, can tx w/ imatinib, , elevated tryptase, b12, constitutional symptoms, endomyocardial fibrosis, Hepatosplenomegaly, bad prognosis
ii. Lymphocytic: clonal proliferation that produced Th2 Il5, benign course but cardiac complications can occur still and increase risk T cell lymphoma,

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209
Q

What is the # 1 cause death HES

A

CHF

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210
Q

What are 5 common causes of flushing?

A

MR FAB D

Menopause
Rosacea
Fever
Alcohol
Benign cutaneous flushing-emotion, hot, spicy foods, exercise

Drugs:
niacin, alitretinoin, ACEi, BB, CCB, doxorubicin, opioids, vanco, eicosanoids, rifampicin, steroids, gold, sildenafil

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211
Q

What are 4 serious causes of flushing

A

A spicy red pineapple made me cry violently

Anaphylaxis
Scombroid poisoning
RCC
Pheo
medullary thyroid cancer
mastocytosis
carcinoid
ViPoma

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212
Q

What are 3 variants of eosinophilic folliculitis?

A

Eosinophilic pustular folliculitis of ofujii

Neonatal eosinophilic pustular folliculitis

HIV-associated

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213
Q

What is the follicular occlusion tetrad?

A

HS
Acne conglobata
Pilnodal sinus
Dissecting cellulitis

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214
Q

What are the clinical findings seen in Hurley stage 1, 2 and 3 HS

A

a. Stage 1: Solitary or multiple isolated abscesses, with no scarring or sinus tracts
b. Stage 2: Recurrent abscesses, with sinus tract or scarring
c. Stage 3: multiple interconnected sinus tracts and abscesses throughout an affected region; more extensive scarring (entire area usually)

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215
Q

What are the 3 diagnostic criteria for HS

A
  1. typical lesions of deep-seated painful nodules (known as “blind boils” without a purulent point) in early lesions and abscesses, sinuses, bridged scars, and “tombstone” open comedones (pseudocomedones) in secondary lesions.

Lesions occurring in at least 1 typical body location such as the axillae, groin, perineal and perianal region, buttocks, and inframammary and intermammary folds.

Chronic nature of disease, relapses, and recurrences.

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216
Q
  1. List 5 medications that can cause DRESS
A

a. Allopurinol
b. Antibiotics (septra, minocycline)
c. Anti-inflammatory- NSAIDS
d. Anticonvulsants (carbamazepine, phenobarbital, phenytoin, VPA, lamotrigine)
e. AZA, abacavir and nevirapine
f. Dapsone

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217
Q
  1. List 5 medications that can cause AGEP.
A

LiT BECA

Lamisil/terbinafine
Tetracycline
Beta lactam
Erythromycin/macrolides
CCB-diltiazem
Anti-malarial

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218
Q
  1. List 5 medications that can cause pseudoporphyria:
A

LATINO

Lasix
Amiodarone
Tetracycline
Isotretinoin
Naproxen
OCP

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219
Q
  1. List 5 medications that can cause a morbilliform drug eruption.
A

a. Penicillins
b. Cephalosporin
c. Anticonvulsants
d. Allopurinol
e. TMP-SMX

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220
Q
  1. List 5 medications that can cause SJS/TEN.
A

5 A’s

a. Antibiotics- septra, B-lactams
b. Anti convulsants – carbamazepine, VPA, phenytoin, phenobarb, lamotrigine
c. Anti-inflammatory - NSAIDS
d. Anti-retrovirals- abacavir, nevirapine
e. Allopurinol

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221
Q

What are 7 components of the SCORTEN score? (include specific values)

A

CA2B3S
CAABBBS

Cancer
Age >40
Area of body > 10%
Bicarb <20
BUN >10
Beats per minute >120
Sugar >14

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222
Q
  1. What are 5 medications that cause fixed drug eruption?
A

PAST

Psuedoephedrine
Anti-inflammatories: ASA, saids, acetaminophen, naproxen
Sulfonamides
Tetracycinlines

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223
Q

What are 5 conditions associated with photoaging

A

a. Solar elastosis, cutis rhomboidalis nuchae
b. Poikiloderma of civatte
c. Favre racouchot syndrome
d. Colloid millium
e. Erosive pustular dermatosis

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224
Q

List 5 photodermatoses.

A

PMLE
Solar urticaria
Actinic prurigo
Hydro vacciniforme
Actinic dermatitis

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225
Q

What are 3 cutaneous forms of amyloid? Which one has the highest risk of progression to systemic amyloidosis? Which one overlaps with notalgia paresthetica?

A

lichen Amyloid
Macular -notalgia
Nodular-highest risk, 7%

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226
Q

What are 5 categories of triggers for CSVV

A

Infection- strep, hep C>B
Autoimmune
Malignancy
Drug
Other-cryoglobulinemia, emboli, thrombi

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227
Q

List 5 causes of urticarial vasculitis

A

a. AI-CTD: lupus, sjogrens
b. Drug – Nsaids, MTX, TNF alpha, cimetidine, fluoxetine, SSKI
c. Infection-viral (hep)
d. Malignancy -leukemia/lymphoma, malignancies
e. Other-serum sickness

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228
Q
  1. List the systemic findings and symptoms of Granulomatosis with polyangiitis, microscopic polyangiitis and eosinophilic granulomatous with polyangiitis. Which ANCA type is associated with each?

GPA

A

i. Nasal/sinus: sinusitis, rhinorrhea, epistaxis
ii. Pulmonary: cough, hemoptysis, SOB
iii. Renal: GN w/ hematuria
iv. Other: Arthralgias, ocular findings
v. CNS: Peripheral neuropathy, CVA
vi. Skin: Palpable purpura, PG-like nodules and ulcers, gingival hyperplasia with strawberry gums, oral ulcers
vii. ANCA (PR3, C-ANCA)

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229
Q
  1. List the systemic findings and symptoms of Granulomatosis with polyangiitis, microscopic polyangiitis and eosinophilic granulomatous with polyangiitis. Which ANCA type is associated with each?

EGPA

A

i. Nasal/sinus: Allergic rhinitis, nasal polyps
ii. Pulmonary: Asthma
iii. Cardiac: cardiomyopathy, valvular disease
iv. GI: N/V abdo pain
v. Renal: Limited
vi. CNS: mononeuritis multiplex
vii. Cutaneous: Palpable purpura, painful subcutaneous nodules
viii. Labs: Peripheral Eos
ix. ANCA: P-ANCA > C-ANCA

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230
Q

List the systemic findings and symptoms of Granulomatosis with polyangiitis, microscopic polyangiitis and eosinophilic granulomatous with polyangiitis. Which ANCA type is associated with each?

MPA

A

c. MPA
i. Pulmonary: Alveolar hemorhage
ii. Renal: GN
iii. Neuro: Neuropathy, mononeuritis multiplex
iv. Cutaneous: Palpable purpura, livedo reticularis, ulcers, retiform purpura
v. ANCA: (MPO, P-ANCA)

231
Q

List 5 pathology features of eczematous dermatitis.

A

a. Focal parakeratosis
b. Acanthosis if more chronic
c. Epidermal spongiosis (hallmark)
d. Intraepidermal vesicle and bullae formation if acute
e. Superficial perivascular lymphocytic infiltrate
f. Variable eosinophilic infiltrate

232
Q
  1. List 7 pathology features of lichen simplex chronicus.
A

a. Hyperkeratosis
b. Focal parakeratosis
c. Impressive irregular acanthosis
d. Hypergranulosis
e. Vertical orientation of collagen in the dermal papillae
f. Perivascular lymphocytic infiltrate
g. Prominent fibroblasts, occasionally multi-nucleated fibroblasts (Montogmery giant cells)
h. Enlarged nerves

233
Q

List 6 pathology features of pityriasis rosea

A

SAMPLER- spongiosis, acanthosis, mounded parakeratosis, perivascular lymphocytes, extravasated reds

a. Mounds of parakeratosis
b. Occasional mild acanthosis
c. Mild epidermal spongiosis
d. Occasional dyskeratotic keratinocytes
e. Superficial lymphocytic perivascular infiltrate
f. Eosinophilic infiltrate sometimes present
g. RBC extravasation in dermis

234
Q

List 7 pathology features of psoriasis.

A

a. Confluent parakeratosis, hyperkeratosis
b. Neutrophilic abscesses in the stratum corneum (Munro microabscesses)
c. Neutrophils in spinous layer (spongiform pustules of Kojog)
d. Regular acanthosis
e. Elongated and clubbed rete ridges
f. Hypogranulosis
g. Suprapapillary thinning
h. Dilated capillaries
i. Superficial perivascular lymphocytic infiltrate

235
Q

List 5 pathology features of PRP

A

a. Follicular plugging
b. Shoulder parakeratosis-adjacent to follicular plugs
c. “Checkerboard” parakeratosis alternating with orthokeratosis
d. Irregular acanthosis
e. Acantholysis, focal, occasionally
f. Perivascular lymphocyte
2. Shortened, fat rete pegs
3. Dilated hair follicles
4. Follicular plugging
6. Hypergranulosis
Focal acantholysis with dyskeratosis

236
Q

List 7 pathology features of Lichen Planus.

A

a. Compact hyperkeratosis, usually no parakeratosis
b. Acanthosis-irregular
c. Wedge shaped hypergranulosis
d. Saw tooth rete ridges
e. Lymphocytic infiltrate at DEJ (lichenoid)
f. Basal cell layer liquefactive degeneration
g. Colloid bodies often
h. Melanin incontinence
i. DIF reveals IgM, complement, fibrin staining of colloid bodies

237
Q

List 3 pathology features of lichen nitidus

A

a. Epidermal atrophy, parakeratosis, overlying ball of papillary dermal lymphocytes, with epidermal rete ridges forming collarette = “ball in clutch”
b. Focal liquefactive degeneration of basal layer
c. Multinucleated giant cells

238
Q

List 5 pathology features of PLEVA

A

P-parakeratosis focally w/ scale crust
Lichenoid infiltrate w/ basal cell layer vaculoization, lymphocytic exocytosis into the epidermis
Extravasated reds
V-shaped/wedge shaped infiltrate
A-apoptotic KCs
S-Spongiosis w/ epidermal vesicles and papillary dermal edema

239
Q

List 3 pathology features of urticaria.

A

a. Normal epidermis
b. Papillary dermal edema
c. Sparse perivascular and interstitial infiltrate of eosinophils, lymphocytes, neutrophils and/or mast cells

240
Q

List 6 pathology features of Erythema multiforme.

A

a. Basal layer degeneration, sometimes subepidermal bullae
b. Perivascular and interface infiltrate of lymphocytes, sometimes eos
c. Necrotic keratinocytes
d. Spongiosis, rarely intraepidermal vesicles
e. Papillary dermal edema
f. Extravasated RBCs, sometimes

241
Q

List 5 pathology features of sweet’s syndrome.

A

a. Epidermal necrosis
b. Superficial derma edema, sometimes subepidermal blister
c. Diffuse dermal neutrophils (also lymphocytes, histiocytes, eosinophils)
d. Nuclear dust, no true vasculitis
e. Sometimes extravasated erythrocytes

242
Q

List 6 pathology features of erythema ab igne.

A

a. Epidermal atrophy
b. Keratinocyte atypia
c. Basal cell layer degeneration
d. Dilated dermal blood vessels
e. Elastosis in the dermis
f. Melanin incontinence
g. Hemosiderin the dermis

243
Q
  1. List 5 pathology features of LCV.
A

a. Epidermis varies from normal to necrotic, sometimes with vesicles or pustules
b. Fibrinoid necrosis of vessel wall
c. Nuclear dust
d. Superficial and mid perivascular infiltrate, predominantly neutrophils
e. RBC extravasation
f. Thrombi

244
Q
  1. List 4 pathology features of granuloma annulare.
A

a. Normal epidermis
b. Palisading granulomas (histiocytes) around foci of necrobiosis and mucin
c. Often single filing or subtle interstitial pattern of histiocytes or giant cells between collagen bundle
d. Perivascular lymphocytes

245
Q

List 3 features NLD

A

a. Epidermis normal, atrophic or ulcerated
b. Palisading granulomas in the dermis, often oriented parallel to the epidermis, surrounding necrobiotic collagen, often with sclerosis
c. Dermal interstitial infiltrate of histiocytes, multinucleated giant cells, lymphocytes, plasma cells

246
Q
  1. List 3 pathology features of Erythema nodosum.
A

a. Septal panniculitis of lymphocytes, histiocytes, neutrophils
b. Multinucleated giant cells in older lesions, without caseation
c. Septal fibrosis in older lesions
d. Mild fat necrosis sometimes with foamy histiocytes

247
Q

List 7 path findings MF

A

a. Atypical lymphocytes with angulated nuclei
b. Haloed cells (perinuclear halo)
c. Epidermotropism with minimal spongiosis
d. Lymphocytes in epidermis larger than ones in dermis
e. Lining up of lymphocytes along the DEJ
f. Pautriers microabscesses-lymphocytes in epidermis
g. Thickening of collagen in papillary dermis
h. Lichenoid infiltrate

248
Q

List 2 calcium stains

A

von kossa
alizarin red

Von kossa all read calcium

249
Q

List 1 iron/hemosiderin stain.

A

Prussian blue

“Russia made of iron

250
Q

List 5 mucin stains

A

a. Alcian blue PH 0.5, 2.5
b. Colloidal iron
c. Toluidine blue
d. PAS
e. Mucicarmine

CAT-PM

251
Q

List 3 amyloid stains.

A

a. Congo red
b. Thioflavin T
c. Cresyl Violet

252
Q

List 3 fungal stains.

A

a. PAS
b. PAS-Diastase
c. GMS (Gormori methenamine silver)

253
Q

What stain is used for leprosy?

A

a. FITE

FITE LEPROSY

254
Q

What stain is commonly used for acid fast bacteria?

A

a. Zhiel-Neelson

255
Q

What are 2 silver stains and what are they used for?

A

a. Gormori methenamine (GMS fungal)
b. Warthin Starry Spirochetes-syphillis, borrelia

256
Q
  1. Which stain is used for leishmania?
A

a. Giemsa

We fite leprosy
We get “GIET after” leishmania

257
Q

3 mast cells stains

A

toluidine blue, Giemsa, Leder

Take M (for mast cells) to your Great Leader

258
Q

What is the direct method? The indirect method? List the substrate and reagent for each and 3 examples of each

A

i. Direct: Look at patient’s tissue direct to see if ab or complement bound.
1. Substrate: Patient perlesional skin
2. Reagent: Fluorescently labeled anti-human IgM, IgG, IgA and C3 that bind to pathogenic ab’s attached to skin targets
3. E.g. DIF, salt split skin with DIF, direct immunoelectron microscopy, FOAM

Indirect: Look at patients serum and see if ab’s present that bind to substrate
1. Substrate: Tissue (rat bladder, monkey esophagus, guinea pig esophagus)
2. Reagent: Patients serum w/ ab’s against antigen , then 2nd ab added that is anti human and fluorescently labelled
3. IIF, IIF with salt split skin, indirect immunoelectron microscopy, immunoprecipitation, immunoblotting, ELISA

259
Q

Where is the split in salt split skin

A

lamina lucida

260
Q

What are 4 reasons DIF can be negative despite the patient having the disease

A

Media expired
Sat in media too long
Leg lesion samples
Perilesional or too far from lemon sampled

261
Q

d. How does Direct immune electron microscopy work

A

Patients perilesional skin mixed with anti human Fc ab’s labelled with gold , examined with electron microscopy

262
Q

What is FOAM

A

“Fluorescence overlay antigen mapping”

Anti-human ab’s labelled with specific coloured label, also colour eith different label collagen typ 4, type 7, laminin 332, integrin

Conofocal laser microscopy to examine

263
Q

Name 5 types of substrate for IIF

A

i. Human skin
ii. Guinea pig esophagus
iii. Monkey esophagus
iv. Rat bladder epithelium
v. Keratinocyte culture

264
Q

Name the 4 intercellular junctions and what they anchor

A

Desmosomes- keratin
Gap junctions
Adherens junctions- actin
Tight

265
Q

Name the 3 protein families that make up intercellular junctions

A

Cadherens: Desmoglein, desmocollin, cadherin
Armadillo proteins: Plakoglobin, plakophilin, alpha beta catenin
Plakins: Desmoplakin, periplakin, envoplaikin, BPAG1/2, pectin
Connexins

266
Q

From inside to out name the proteins in desmosomes

A

DSG/DSC

Plakoglobin, plakophilin

Desmoplakin

267
Q

From top to bottom name the proteins on hemi-desmosome

A

BPAG1/180, plectin

Lamina lucida: BPAG2/230, integrin subunit alpha and beta

Lamina densa: Collagen type IV, Laminin 332

Sublamina densa: Collagen type VII, collagen type II and type I, elastin

268
Q

Where is DSG-1 present vs. DSG-3 ? Explain DSG compensation

A

a. DSG1 present in skin, superficial>deep, less in mucosal. DSG-3 is deeper in epidermis and high prevalence in both skin and mucosa
b. Compensation: If DSG3 is lost in skin, DSG1 can compensate, but NOT in mucosal surfaces. If DSG-1 is lost, DSG3 cannot compensate. SO, PF always skin, but PV is sometimes only mouth, with skin in 50-80%
i. *Can get epitope spreading from ab to DSG 1 to DSG 3 so PF PV

269
Q

DSG-1 affected causes?

270
Q

DSG-3 affected causes?

A

PV-mucosal

271
Q

DSG-1/3 affected?

A

PV-mucosa and skin

272
Q

What is the ab in pemphigus

273
Q

Where is the split in PF? PV?

A

PF –> granular layer

PV–> spinous layer

274
Q

List 5 pemphigus variants

A

Pemphigus Folicaceous:
PF
IgA pemphigus foliaceous
Fogo selvagem
Pemphigus erythematous
Pemphigus herpetiformis
Drug induced PF

275
Q

List the 5 PV variants

A

i. PV: Mucosal (DSG3), Mucocutaneous (DSG 1/3)
ii. Pemphigus vegetans-Neuman, Hallopeau
iii. Paraneoplastic (plakins, cadherins)
iv. IgA pemphigus/Intraepithelial neutrophilic (DSG 3, DSC)
v. Drug induced PV
vi. Pemphigus herpetiformis (DSG 1>3)

276
Q

How does PF present

A

a. Well demarcated crusted erosions, impetigo like on erythematous base in seborrheic areas, “cornflake” like scale, + nikolsky, no oral

277
Q

What is the difference between thiol and non-thiol drugs

A

b. Most induced by thiol drugs (e.g. sulfhydryl containing), which can cause DIRECT acantholysis (Penicillamine, ACE, ARBs)
–> MORE PF LIKE
c. Non-thiol drugs can induce an immune phenomenon causing more a PV presentation
-B, B, C, G PR
(Beta lactams, gold, CCB, B-blocker, piroxicam, rifampin)

278
Q

Name 3 drugs that can cause drug induced PF

A

penicillin, penicillamine, captopril

279
Q

How does pemphigus herpetiformis present

A

polycyclic urticarial plaques, ocasional herpetiform vesicles, minimal acantholysis

280
Q

Which substrate do Ab’s bind best to in IIF for PF? PV? PNP PV

A

PF–> guinea pig esophagus
PV–> monkey esophagus
PNP PV–> rat bladder

281
Q

13) What is the difference between pemphigus vegetans of hallopeau vs. neumann

A

Neumann-flaccid bullae and erosions that develop vegetating plaques, similar course to PV

Hallopeau –> Crops of pustules turn into crusted plaques. May remit spont.

282
Q

14) List 10 clinical differences that PNPV differs from PV

A

a. Polymorphous rash (PV, PF, lichenoid, GVHD, BP) > flaccid bullae/oral erosions
b. Vermillion lip border involved> buccal mucosa
c. Extensive erosive stomatitis
d. Scalp usually spared
e. Palmar/plantar involvement>palms/soles spared
f. Non scarring conjunctivitis > periocular involvement
g. Asboe hansen/nikolsky usually negative
h. Suprabasal acantholysis + lichenoid, subepidermal bullae
i. IgG and C3 intercellular and linear at BMZ > only intercellular
j. Indirect IF on rat bladder possibly positive vs. negative in PV
i. Helpful to use rat bladder epithelium, should be + in PNP and negative in PV
ii. Contains plakins but NO desmogleins
k. Bronchiolitis obliterans > no systemic
l. Mortality 90% >minimal mortality
m. Fails typical PV therapies

283
Q

What are the 5 different presentations (based on B and T-cell predominance) of PNPV
a

A

B-cell:
pemphigus like
BP-like
EM like
GVHD like
LP like
T-cell

284
Q

5 malignancies associated with PNPV

A

a. CLL
b. Non hodgkin lymphoma
c. Castlemans
d. Thymoma
e. Sarcoma
f. Waldenstroms
g. Adenocarcinomas-breast, prostate, lung , pancreas
h. *Lichenoid variant usually Castlemans

285
Q

17) Name 6 antigens seen in PNPV

A

Plectin, periplakin, envoplakin, desmoplakin, BPAG1, DSG-3, 1

286
Q

why does rat bladder help distinguish PNPV

A

contains plakins and no DSGs

287
Q

19) What type of B cell is typically producing abs in PV/PF

A

B lymphocytes > long lasting memory cells

288
Q

First line treatments for PF/PV

A

Prednisone alone
Pred + ritux
Prednisone + steroid sparing- AZA or MMF

289
Q

What is the rituxumab dosing for PV

A

1 gram day 1 and 14, 500 mg at month 12 and 18

290
Q

Treatment of choice pemphigus herpetiformis

291
Q

List 2 epidermal and 10 sub epidermal blistering d/o

A

a. PF and variants
b. PV and variants
c. Paraneoplastic PV

1.Bullous pemphigoid
2. Pempigoid/herpes gestationis
3.Anti-laminin gamma1 pemphigoid
4. Mucous membrane pemphigoid (MMP),
5. Ocular predominant MMP
6. Anti-Laminin 5 MMP
7. Dermatitis herpetiformis
8. Linear IgA disease
9. EBA
10. Bullous SLE

292
Q

List the variants of Bullous Pemphigoid per Scott Walsh- there are 20

A

Localized:
1. Pretibial
2. Dyshidrosiform
3. Stomal
4. Radiation aggravated
5. Hempiplegic (stroke site)
6. Stump
7. Vulvar
8. Umbilical

Generalized:
1. Urticarial (classic)
2. Eczematous
3. Pemphigoid nodularis
4. Invisible
5. Erythrodermic
6. Vegetans
7. Seborrheic
8. TEN-like
9. Erosive
10. Ecthyma gangrenosum like
11. Palmar-plantar purpuric
12. Lichen planus pemphigodes
13. Neonatal
14. childhood
15. drug induced

293
Q

Name 4 causes pemphigoid gestations/herpes gestations and 2 associations

A

PRegnancy
Choriocarcinoma
HYatidiform mole
Trophoblatic tumor

Association HLA DR4, thyroid dz

294
Q

When does herpes gestationis appear in pregnancy? Where does it occur?

A

2nd trimester > 3rd,
improves with delivery then flares

Periumbilical- involves the umbilicus

295
Q

Name 3 reasons for pemphigoid gestationis to recur

A

subsequent pregnancy with same dad
ocp
menses

296
Q

27) Name 3 treatments for pemphigoid gestationis

A

a. Pred, CsA, IVIG

297
Q

28) What is the autoantibody and antigen in BP

A

BP180 (BPAG2)* and BP230 (BPAG1)

IgG1 against NC16A of BPAG-2 (180 or COL17)

Can see IgG4 against BPAG1/230 but non pathogenic

298
Q

What % BP have mucous membrane involvement

299
Q

What is most common location BP

300
Q

3 diseases associated with BP

A

MS
Parkinsons
stroke
dementia
epilepsy

301
Q

5 drugs that cause BP

A

Enalapril
Furosemide
Spironolactone
Gliptins
PD-1

302
Q

Name 5 biochemical requirements other than Ab’s for BP disease

A

a. Mast cells
b. Complement
c. Granulocytes-eos, neuts
d. Gelatinase causes blister
e. IgE then class switch to IgG (prevent conversion, prevent disease?)

303
Q

Name 4 methods of treating BP, broadly

A

a. Inhibit auto-antibody production: Pred, MMF, AZA, etc.
b. Catabolize autoantibodies: IVIG, omalizumab
c. Inhibit mast cells: Cetirizine, omalizumab
d. Inhibit inflammatory infiltrate; dapsone, sulfasalazine, colchicine ,doxycycline, nicotinamide

304
Q

35) What is Anti-Laminin Gamma 1 Pemphigoid? Name its other name its target, its clinical presentation, path differences/SSS, tx differences

A

Anti p200 pemphigoid

200 kd antigen in lamina lucida, which is the C-terminus of laminin 1 gamma in deep lamina lucida

a. Anti-P200 pemphigoid
b. Antigen: C-terminus of laminin 1 gamma in 90% (DEEP laminin)
c. BP like eruption in males, younger (50-70), concomitant psoriasis, have palmar-plantar involvment, mucosal erosions, milia and scarring can occur
d. Floor of SSS, more neutrophilic infilitrate
e. Tx: Dapsone, sulfasalazine, colchicine

305
Q

How to tell the difference MMP with skin involvement vs. BP with mucosal involvement

A

a. No OCULAR involvement in BP

306
Q

How does MMP differ from BP

A

a. Predominantly mucosal, can have ocular, tendency to scar, chronic course
b. Deeper antigenic targets generally
c. A disease phenotype

307
Q

38) What are the antigenic targets in MMP

A

i. Lamin 332
ii. BP-180 C-terminus, BP 230
iii. Integrin
iv. Type 7 collagen

308
Q

39) List 3-5 variants of mucous membrane pemphigoid and their antigenic target (includes another scarring that could be on its own)

A

a. Anti-Epiligrin MMP/Anti-laminin 5/Laminin 332 cicatricial pemphigoid
b. Pure ocular pemphigoid (B4 integrin)
c. Classic form: BP-180 C terminus
d. Variable mucosal but no skin involvement
e. Brunsting perry variant
f. Anterior oral pemphigoid

Laminin 332 (Anti epiligrin)
BP-180 C-terminus (classic)
Integrin (pure ocular)
Collagen 7?

309
Q

40) What are is the most common site of MMP and 3 other sites,

A

a. Oral in 85%  gingival, buccal, palate
b. Conjuctiva blindness
c. Esophagus  can lead to strictures, resp distress
d. Genitals anal, vaginal

310
Q

TOC for anterior oral MMP

311
Q

Treatment for MMP if ocular, airway or genital dz

A

Pred
cyclo
leflunomide or MMF

312
Q

What are the 3 types of LABD

A

Adult LABD
-laminda lucida - BP like
-sublamina densa- EBA like

CBDC: chronic bullous disease of childhood

Drug induced

313
Q

44) Name 4 drugs that can induce LABD

A

vancomycin, penicillin, cephalosporins
amiodarone
sulfamethaxazole

C-VAPS

314
Q

Which antigens targeted in LABD

A

Shed ectodomain of BP-180
Split products of BP180–> 120 KD= LAD1 or 97 KD LAd97

Collagen 7 in LABD like

315
Q

3 tx for LABD

A

Dapsone
Colchciine
Sulfasalzine

316
Q

NAme 4 ddx for neutrophilic sub epidermal blistering diseases

A

LABD
DH
Anti laminin gamma 1
bullous SLE

317
Q

Name two variants of acquired EBA

A

a. Classic mechanobullous EBA (non-inflammatory-acral blisters, scarring, milia, mitten deformities, pauci inflammatory) supress ab>inflammation
b. Inflammatory (BP-like) EBA  flexural/intertriginous bullae that heal w/out scarring, eosinophils, misinterpreted often
c. Inflammatory EBA (CP-like) brunsting perry w/ scarring alopecia, may have scarring oropharyngeal,

318
Q

49) What is EBA associated with?

A

chrons
asians

319
Q

Antigen target EBA

A

a. Collagen 7

320
Q

4 diagnostic criteria for bullous SLE

A

a. Diagnosis of SLE
b. Vesicles/bullae arising on, but not limited to, sun exposed skin
c. Subepidermal blistering w/ predominant neutrophils
d. DIF showing linear or granular IgG (90%), C3 (90%) or IgM (60%), IgA (60%) in the BMZ.

321
Q

TOc bullousSLE

A

dapsone colchicine sulfa

322
Q

53) What is the clinical presentation DH

54) What is antigen target in DH? What is target in gut?

A

a. Grouped herpetiform and urticarial and excoriation on buttocks, knees, elbows

IGA to TTG-3 in skin
TTG 2 in gut

323
Q

55) What do we see on path for DH

A

a. Subepidermal blisters/absceses at the dermal papillae tips with ++ neutrophils
b. “Squirting papillae”

324
Q

What do you order for a celiac profile

A

a. IgA and IgG to: Gliadin, TTG, EMA
b. IgA level
c. Biopsy and DIF

325
Q

57) Describe the antigen, DIF pattern and salt split skin pattern for: PF, PV, PNPV, pemphigus erythematous, IgA pemphigus, BP, pemphigoid gestations, MMP, laminin 332, DH, LABD, EBA, bullous SLE

A

PF/PV: DSG1/3, linear IgG +-C3, intercellular

IgA pemphigus: DSC1 (SPD), DSG1/3 (IEN), Linear IgA intercellular

Pemphigus erythematous: DSG1/3, Granular to linear IgG and C3

PNPV:
Antigen: Many-plakin family, DSG1/3, BPAG180, plectin, Linear IgG/C3 intercellular and BMZ

BP: BPAG2/180, linear IgG/C3, n serrated, roof salt split

Pemphigoid gestationis: Linear C3

MMP: laminin-5, ocular, classic, variable mucosa
-DIF for all: Linear IgG and C3
Salt split skin:
-laminin-5: floor
-ocular: roof or both
-classic: roof or both
-variable mucosal: roof or both

EBA:
Linear IgG > C3
Salt split: Floor

Bullous SLE
i. DIF: Linear IgG, C3, can also see IgM, IgA
1. *Can also see granular IgG, M, A, C3 =lupus band
ii. Salt split: Floor

LABD
i. DIF: Linear IgA
ii. Salt split: Roof or floor

DH
i. DIF: Granular IgA in dermal papillae

326
Q

Ab target for bullous impetigo

327
Q

Ab target for SSSS

328
Q

Ab target for PF

329
Q

Ab target for PV

330
Q

IgA pemphigus

A

DSC- SPD

DSG1/3 - IEN

331
Q

Ab for pemphigus herpetiformis

332
Q

6) PV:

A

6) PV: DSG3 or DSG1+3,

333
Q

BP

A

BP180/BPAG2-> N16CA domain non collagenous

334
Q

Pemphigoid gestationis

A

BPAG 180/2

335
Q

LABD

A

LAD-1 (120 KD cleaved portion of BP180 antigen) and LABD97 (97 Kd portion of LAD-1)

336
Q

MMP antigen

A

BP180 c-terminus

337
Q

Ocular predominant

A

B4 integrin

338
Q

Anti-epiligrin

A

Laminin 5/332/Epiligrin

339
Q

13) p200 pemphigoid:

A

Laminin gamma 1

340
Q

EBA

A

Collagen 7

341
Q

Bullous SLE

A

Collagen 7

342
Q

Where does the split occur in the following conditions:
a) EB simplex;
b) Junctional EB;
c) Dystrophic EB.

A

EB simplex: Intraepidermil

JEB:lamina lucida

DEB: sub lamina densa

Kindler: Mixed

343
Q

Which protein is mutated in each of the following conditions (this is on your exam):

EBS localized, generalized intermediate, generalized severe, mottled-pigmentation

EBS w/ muscular dystrophy

JEB

JEB w/ pyloric atresia

Dominant DEB

Recessive DEB

Kindler

A

EBS localized/generalized intermediate/generalized severe/mottled-pigmentation: KRT5/KRT14= Keratin 5 and 14

EBS with muscular dystrophy: PLEC- Plectin

Junctional EB – generalized severe/generalized intermediate: LAMA3/LAMB3/LAMC2/COL17A1- Laminin 332 and Collagen XVII (BPAG2/180)

JEB with pyloric atresia: ITGA6/ITGB4- Alpha-6 Beta-4 integrin
o 15% plectin mutation

Dominant Dystrophic EB: COL7A1- Collagen VII (missense mutation)

Recessive Dystrophic EB: COL7A1- Collagen VII (premature termination =complete lack anchoring fibrils)

Kindler Syndrome: FERMT1- Fermitin family homolog 1

344
Q

What disease states associated with:
BPAG1

345
Q

What disease states associated with:
BPAG2

A

N16A terminus: Bullous pemphigoid, Pemphigoid gestationis, LABD

Carboxy terminus: Mucous membrane pemphigoid

346
Q

alpha6-beta4 integrin:

A

JEB w/ pyloric atresia
Ocular MMP (B4 subunit)

347
Q

Laminin 332/Laminin5/Epiligrin

A

Anti epiligrin MMP

348
Q

Plectin

A

EBS w/ muscular dystrophy,
EB w/ pyloric atresia -15%

349
Q

Type IV collagen

A

Goodpasture
Alport syndrome

350
Q

Collagen 7

A

EBA
Bullous SLE
dystrophic EB

351
Q

Which disease states are associated with mutations in the following:
Keratin 1

A

i. Epidermolytic ichthyosis
ii. Epidermolytic and non-epidermolytic PPK
iii. Icthyosis hystrix of curth-macklin

352
Q

Which disease states are associated with mutations in the following:
Keratin 2

A

Superficial epidermolytic icthyosis

353
Q

Which disease states are associated with mutations in the following:
Keratin 4

A

white sponge nevus

354
Q

Keratin 5

A

EBS
Dowling degos

355
Q

Keratin 6a/keratin 16

A

Pachyonychia congeenita type I

356
Q

Keratin 6b/17

A

Pachyonychia congeenita type II

357
Q

Name the 5 indolent primary cutaneous T cell lymphomas

A

MF

Primary cutaneous CD30+ lymphoproliferative d/o
-Anaplastic large cell lymphoma
-Lymphomatoid papulosis
Subacute panniculitis-like T-cell lymphoma

EBV+ lymphoproliferative disorder in childhood
-Hydro vacciniforme like LPD
-Hypersensitivity reations to mosquito bites

Primary cutaneous peripheral T-cell lymphoma, rare subtypes

Primary cutaneous CD4+ small/medium t-cell LPD

Primary cutaneous Acral CD8+ T-cell lymphoma

358
Q

Name the 5 aggressive CTCLs

A
  1. Sezary syndrome
  2. Extranodal NK/T-cell lymphoma, nasal type
  3. aggressive epidermotropic cd8+ cytotoxic CTCL
  4. Gamma-delta T-cell lymphoma
  5. peripheral T-cell lymphoma NOS
359
Q

What are the 3 known subtypes of MF? Which are aggressive, which indolent

A

Granulomatous slack skin
Pagetoid reticulosis
Folliculotropic-aggressive w/ 75% 5 yr survival

360
Q

What are the 2 variants of folliculotropic MF? Which has worse prognosis

A

Acneiform/cyst like = worse prog
Follicular papules

361
Q

4) Where is the classic location for pagetoid reticulosis? What is the life expectancy? How does it present

A

Hands, foot (bottom), face
100%
Solitary plaque, psoirrasiform, slow growing
“worringer dollop”

362
Q

What is the variant of pagetoid reticulosis that can be systemic and aggressive

A

Ketron Goodman

363
Q

What is granulomatous slack skin associated with in 1/3 of cases

A

Hodgkin’s lymphoma

364
Q

What is common but least specific cd change in MF

365
Q

What is the specific change in CD, MF

A

Loss of CD5 and 2

366
Q

Is the typical pattern of CD in MF, what is the exception

A

CD3+ CD4+ CD8- CD30-

hypopigmented MF tends to be CD8+. CD4-

367
Q

9) How does the ratio of CD4:CD8 change as MF progresses

368
Q

10) What is the diagnostic criteria of Sezary syndrome

A

Ertyrhoderma >80%
TCR clonality
>1000 sezary cells/ul
-CD4:8 ratio >10
-Abberant expression T-cell antigens (loss of t-cell markers like CD7 and CD26 most commonl)

369
Q

Name 11 morphological variants MF

A

Hypopigmented
Hyperpigmented

Poikilodermatous
Telangiectatic
Atrophic

Acral
Palmoplantar

Lichenoid
Granulomatouos

pigmented purpuric dermatosis
Purpric

370
Q

Name 10 morphological variants MF

A

Hypopigmented
Hyperpigmented
Poikilodermatous
Telangiectatic
Atrophic
Purpric
Acral
Palmoplantar
Lichenoid
Granulomatouos
pigmented puru0ric dermatosis

371
Q

What is the staging for MF

A

Stage IA- patch or plaque <10% BSA
Stage IB-patch or plaque >10% BSA
Stage IIA- palpable reactive lymphadenopathy, can have histological involvement but with normal architecture.
Stage IIB- tumors w/up to palpable LN but no histo
Stage III- Erythroderma with up to histo LN
Stage IVA1- Sezary cells > 1000, any T, up to histo LN
Stage IVA2- histologically involved nodes with architecture effaced, anyB
Stage IVB-Mets, any B

*All can have up to 1000 cells/ul and >5%, even stage IA

372
Q

What is the 5 year survival based on stage of MF

A

1A- same as age match controls

1B/2A- 73% (>10%BSA/palpable lymphadenopathy)

2B/III-44% (tumor or erythroderma)

IV-27% (Mets)

373
Q

What is the best way to diagnose Sezary

A

Blood flow cytometry with TCR
CT or PET
+- LN biopsy

374
Q

What are the two variants of extranodal NK t-cell lymphoma

A

BOTH EBV +
a. Nasal type – “lethal midline granuloma”
b. Extranasal type – skin, GI, spleen

375
Q

What are 8 treatments for Stage IA/B, 2A disease

A

a. Topical steroids
b. Topical retinoids
c. Topical Imiquimod
d. Topical Nitrogen mustard
e. Phototherapy-PUVA, nbUVB
f. Total skin electron beam
g. Systemic +- phototherapy
-Oral retinoid (alitretinoin)
-Interferon + PUVA
-Methotrexate + PUVA

376
Q

What are 8 systemic therapies for Stage 2B and higher

A

*Phototherapy and TSEB as adjuncts

b. Retinoids-Alitretinoin
c. Targeted radiation
d. Histone deacetylase inhibitors:
i. Vorinostat (Zolinza), Romidepsion (Istodax)
e. MTX
f. Interferon
g. ECP if circulating clone
h. Chlorbuxil
i. Brentximab vedotin
Mogalizumab

377
Q

21) What are the immune changes sen in progression of MF?

A

a. Increasing TH2 response, decreasing TH1
b. Dsyregulated cytokine production and inability to fight infection
c. Accumulation genetic mutations and epigenetic changes in lymphoma cells, possibility of large cell transformation

378
Q

Most common cause death MF

379
Q

23) Name 8 anti-itch therapies for MF

A

a. Camphor/menthol
b. Pramoxine
c. Doxepin (TCA)
d. Mirtazapine
e. Gabapentin/pregabalain
f. Naltrexone
g. Butorphanol
h. Aprepitant

380
Q

What is the morphological change on histopathology seen in large cell transformation? What is a clinical sign of this change? What is median survival post LCT?

A

Small/medium sized cerebriform cells->CD30+ or CD30- large cells 4x size make >25% of total lymphoid infiltrate

ulceration of tumor or nodule

12-22 months

381
Q

What is TOC for PC CD4+ small/medium pleomorphic T-cell lymphoproliferative d/o

A

surgical excision or radiation

382
Q

How does CD8+ acral T-cell lymphoma present

A

a. Slowly progessive papulonodules- ear>nose>foot

383
Q

How does CD4+ small/medium pleomorphic T-cell lymphoproliferative d/o present

A

b. Presents as small solitary plaque head/neck

384
Q

27) What is the Sezary triad

A

LAD
erythroderma
sezry cells

385
Q

28) What is the cell type in Sezary

386
Q

29) Name 9 histopath signs of MF

A

a. Atypical lymphocytes with angulated nuclei
b. Lymphocytes lined up at DEJ
c. Epidermotropism
d. Haloed cells
e. Minimal spongiosis in relation to the lymphocytic epidermotropism
f. Darier-Pautrier’s micro abscesses
g. Lymphocytes in epidermis larger than demis
h. Thickening of collagen in papillary dermis
i. Lichenoid infiltrate

387
Q

30) Name 7 conditions where CD30+ cells can be seen

A

a. Reactive: arthropod bite, viral (HSV, orf), infestations, drug reaction
b. Malignant-primary cutaneous:
i. LyP, Anaplastic large cell lymphoma
ii. MF large cell transformation, Sezary, pagetoid reticulosis, extra-nodal NK/T cell , peripheral T-cell lymphoma
c. Malignant-systemic: HODKGINS lymphoma, systemic anaplastic large cell

388
Q

31) Name 3 CD4 markers in LyP

A

CD30+, CD4+, CD7 decreased

389
Q

32) Name 3 conditions associated with LyP

A

a. MF (75%)
b. Hodgkins (1%)
c. Systemic anaplastic large cell lymphoma (24%)

20%* have preceding, concurrent or subsequent lymphoma

390
Q

Name 7 treatments for LYP

A

a. Observation
b. Topical steroids-class I/II -usully not helpful
c. ILK
d. Phototherapy- PUVA
e. Imiquimod
f. MTX- helpful
g. MMF
h. doxycycline -usually not helpful

Aggresive would be systemic chemo or TSEB

topical mechlorethamine or carmustine, and low-dose etoposide.

Excision, radiation

391
Q

35) How does LyP present? Anaplastic large cell lymphoma?

A

a. LYP: recurrent crops ulcerated red-brown papulonodules, usually multiple (40ish), heal with varioliform scars, self resolve then recur

b. Anaplastic large cell: single rapidly growing ulcerated nodule, doesn’t come and go,

392
Q

36) Name 2 differences between primary and secondary anaplastic large cell lymphoma

A

Secondary evolves from another lymphoma

  • Secondary often has T2;5 ALK translocation
    -secondary is EMA positive with ALK expression
    -primary better prognosis

*must exclude MF in transformation

393
Q

Treatment for CD30+ ALCL

A

brentuximab

394
Q

37) Hydro vacciniforme-like LPD (CD8+) and hypersensitivity reaction to insect bites (EBV related lymphoproliferative d/o) (NK-type, CD56+) are associated with increased risk of what?

A

Systemic EBV+ NK or T-cell lymphoma

395
Q

What is subacute panniculitis like T-cell lymphoma often signed out as

A

lobular lymphocytic ppanniculitis
confused often wth lupus panniculitis

396
Q

how does primary cutaneous CD4+ small/medium pleomorphic T cell lymphporpilferatice d/o present? Name 3 T-cell markers

A

solitary plaque on head/neck trunk
CD4+. BCL6+. CXCL13+

397
Q

What are the T-cell markers in subacute panniculitis like t cell lymphoma

A

CD4 -, CD8+, TIA+, granzyme B+ with alpha/beta phenotype CD56-,

398
Q

T-cell markers in cd8+ acral

A

CD8+, TIA+, granzyme and perforin neg

399
Q

What % of cutaneous lymphomas are B-cells

400
Q

What are the 5 L’s

A

lupus tumidus
pmle
jessners
lymphoma
psuedolymphoma

401
Q

Name the 5 major types of primary cutaneous B-cell Lymphoma

A

a. Primary cutaneous follicle center lymphoma (PCFCL)
b. Primary cutaneous marginal zone B cell lymphoma (PCMZL)
i. Includes previously called plasmacytoma or immunocytoma
c. Primary cutaneous diffuse large b-cell lymphoma, leg type (PCDLBCL, LT)
d. Intravascular large B-cell lymphoma
e. Diffuse large B-cell lymphoma, NOS

402
Q

Name 5 less common B-cell lymphomas

A

a. B-cell lymphoma with secondary cutaneous involvement
b. Precursor B-cell lymphoblastic lymphoma/leukemiakids/young adults
c. EBV-associated DLBCL of elderly
d. Immunosuppressive induced lymphoproliferative disorders
e. EBV mucocutaneous ulcer (often immune suppressed)

403
Q

43) Which B-cell lymphomas are aggressive? What are their 5 year disease specific survivials

A

intravascular diffuse

404
Q

45) What is the most common to least common B-cell lymphoma

A

a. Most common: PCFCL>PCMZL >LT > EBV = intravascular

405
Q

46) Which is the best lab predictor of systemic lymphoma

406
Q

48) What is the clinical presenation of PcFCL. Who gets it?

A

H/N of middle age patients (60s)
Solitary often
Male=Female

Pink/plum nodules

Sometimes peripheral patch erythema (Crostis), sometimes acneiform or agminated papules nearby.

407
Q

What is Crust’s lymphoma

A

a. Primary cutaneous follicular center lymphoma w/surrounding erythematous patch, papules and plaques

408
Q

51) What are 3 histologic patterns in FCL

A

a. Follicular
b. Follicular diffuse
c. Diffuse (must differentiate DLBCL-LT)

409
Q

52) What is the status of CD20, BCL6, CD10, BCL-2

A

a. CD20 +, BCL6+, CD10 + (follicle cell markers), BCL-2 -

410
Q

53) Who gets PCMZL?

A

Male predominant
40s

411
Q

What is clinical presentation of PCMZL

A

a. Pink-violet or red-brown papules, plaques nodules
b. Often multifocal
c. upper extremities (Arms, trunk, head, neck)>lower
d. Asymptomatic, indolent, no B-symptoms, almost never progresses

412
Q

55) What are the two distinct entities of marginal zone lymphoma

A
  1. Express class switched Igs: More benign
    i. IgA, G, E,
    ii. Show many T-cells, no risk transformation into diffuse large b-cell, thought to be more lymphoid hyperplasia
    iii. Do not express CXRC3
  2. Non class switched : More aggressive
    Express IgM and often CXCR3 positive
    ii. Share features with MALT lymphoma
    iii. More like to have extracutaneous disease
    iv. Risk transformation to DLBCL
413
Q

56) Name 4 cell markers in MZL

A

CD20+, BCL2+, CD10-, BCL6-

414
Q

57) What is the cell type characterized by in DLBCL-LT.

A

a. Centroblastic and immunoblastic

415
Q

58) What are the cell markers for DLBCL-LT: CD20, BCL2, BCL6, CD10, MUM-1, FOX-P!?

A

a. Positive for CD20, BCL-2, MUM-1, FOX-P1, +- BCL6, CD10-

*BCL-2 + and MUM-1

416
Q

59) What is the presentation of primary cutaneous DLBCL-leg type

A

a. Primary elderly women
b. Solitary or clustered red-brown nodules on distal lower leg, uniltateral, often ulcerate
c. *20% may arise other places, but still call leg-type

417
Q

60) What is the 5 yr survival for DLBCL-LT

418
Q

Name 4 poor prognostic factors for DLBCL-LT

A

Both legs
Multople tumors
apoptotic cells
Loss p16

419
Q

62) What is presentation IVDLBCL

A

a. Painful telangectatic nodules or subcutaneous nodules
b. *Must differentiate from secondary disease

420
Q

63) What are 5 other skin lesions that can be seen in up to 1/3 of systemic IV lymphomas>? 3 lab findings?

A

Livedo
Purpura
Nodules
Panniculitis
Painful telangiectasis

Anemia, LDOH, inflammatory markers

421
Q

64) What are the 2 major forms of intravascular large B cell lymphoma

A

Western form–> skin/cns or skin only

Asian–> multiorgan and HLH

422
Q

65) What is the 5-year survival fro primary vs. Systemic intravascular lymphoma

A

a. 72% primary vs. 33% systemic

423
Q

66) What is lymphocytoma cutis/psuedolymphoma/cutaneous lymphoid hyperplasia? Name 5 triggers. Where does it occur:

A

a. Benign reactive proliferation lymphocytes which mimicks cutaneous lymphoma clinically, thought to be from antigen stimulation
b. arthropod bites, tick bites, contact allergen (gold, nickel, cobalt), vaccinations, tattoo allergens, drugs (phenytoin, MTX, clozapine, doxepin)
c. face, earlobes, nipples, and scrotum

424
Q

67) What % of cutaneous lymphoid hyperplasia will transform to lymphoma? Clonal vs. non?

A

a. Clonal: 25%
b. Non clonal: 5%

425
Q

69) Name 6 treatments for low grade B-cell lymphoma: MZL, FCL

A

69) Name 6 treatments for low grade B-cell lymphoma: MZL, FCL
a. Active non-intervention
b. ILK
c. Surgical excision
d. Radiation
f. Subcutaneous/intralesions interferon-alpha-2a (e.g. multifocal lesions)
g. Rtixumab: Intralesional (few localized) OR systemic (many)

426
Q

70) What is TOC for PCMZL

427
Q

71) What is a risk of radiation in follicle centre lymphoma

A

a. Recurrences in the field not included, eg. Crostis lymphoma  need 10-20 cm

428
Q

What is TOC in PCDLBCL-LT and IVDLBCL

429
Q

73) Name 5 plasma cell dyscrasias

A

a. MGUS
b. Smoldering myeloma
c. Multiple myeloma
d. Light chain deposition disease
e. Amyloidosis

430
Q

74) What are the main symptoms of MM: CRAB

A

a. Hypercalcemia
b. Renal dysfunction
c. Anemia
d. Bone-pain and lytic>sclerotic lesions

431
Q

Name 2 conditions where there is a proliferation of lymphoplasmacytic cells in the skin:

A

a. Extramedullary cutaneous plasmocytoma (marginal zone lymphoma now)
b. Cutaneous Waldenstroma macroglublinemia (IgM monoclonal gammopathy present by definition

432
Q

76) Name 7 conditions where there is deposition of monoclonal protein in the skin

A

a. Primary systemic amyloidosis-light chains
b. Cryoglobulinemis occlusive vasculopathy (Type I)
c. Follicular hyperkeratotic spicules
d. Crystal storing histiocytosis
e. Crystalglobulinemia
f. IgM storage papules (cutaneous macroglublinosis)
g. Subepidermal bullous dermatosis associated with IgM gammopathy

433
Q

Name 5 conditions almost always asspociated with monoclonal gammopathy and 4 frequently associated

A

a. Always
-Scleromyxedema
-POEMS syndrome
-AESOP: Adenopathy and Extensive skin patch overlying plasmacytoma
-Schnitzler
-Necrobiotic xanthrogranuloma

d. Frequently
i. Scleredema type 2
ii. Normolipemic plane xanthoma
iii. Clarksons syndrome-idiopathic systemic capillary leak
iv. Angioedema secondary to acquired C1 esterase inhibitor

434
Q

78) Name 3 conditions associated primarily IgA gammopathy

A

a. EED
b. Subcorneal pustular dermatosis
c. Pyoderma gangrenosum

435
Q

Name the Hanifin and Raja criteria

A

a. Need 3 major and 3 minor
b. Major: Itch, Typical distribution, Chronic/relapsing dermatitis, Hx-fam or personal
c. Minor:
i. Early age of onset
ii. Allergic salute
iii. Allergic shiners
iv. Cheilitis
v. Anterior neck folds
vi. Dennie morgan lines
vii. Perifollicular papules
viii. Keratosis pilaris
ix. Xerosis
x. Centrofacial paleness or erythema
xi. White dermographism
xii. Pityriasis alba
xiii. Itchyosis/hyperlinear palms
xiv. Hand/foot dermatitis
xv. Nipple eczema
xvi. Pruritus when sweating
xvii. Elevated IgE
xviii. Keratoconus
xix. Anterior subcapsular cataract
xx. Recurrent conjucitivtis
xxi. Type I hypersensitivity/allergies
xxii. Food intolerance
xxiii. Intolerance to wood and lipid solvents
xxiv. Course influenced by environmental and emotional factors

436
Q
  1. Name 6 variants of hand eczema
A

a. Dishydrotic
b. Pompholyx
c. Chronic fissured
d. Hyperkeratotic
e. ID reaction
f. ICD
g. ACD
h. Pulpitis
i. Nummular
j. Interdigital

437
Q

Name 3 reasons higher risk ACD in venous stasis

A

a. Broken skin barrier
b. Chronic wounds
c. Occlusive or semi-occlusive

438
Q

Name top 9 categories ACD in venous stasis patients

A

a. Fragrances - balsam of peru, colophony
b. Rubbers- carbamates, thiurams
c. Abx – neomycin, bacitracin, fusidic acid
d. Anti-septics – chlorhexidine, BPO, povidone
e. Textiles and dyes
f. Corticosteroids
g. Preservatives- formaldehyde
h. Vehicles – propylene glycol, lanolin
i. Analgesic- esters like benzocaine

439
Q

paraben paradox

A

a. ACD to paraben often tolerated unless skin is broken or compromised

440
Q
  1. How can you test if a product has nickel
A

Dimethyl dioxide

441
Q

Allergen in poison ivy

442
Q

What are the 3 stages of pruritus pigmentosa

A

a. Early: Urticarial papules
i. Neutrophilic spong

b. Fully developed: crusted red papules, smooth papulo- vesicles or bullae
i. Lymphocytic patchy interface pattern

c. Late: Reticulated pigmentation
i. Prominent melanophages

443
Q

3 associations with prurigo pigmentosa

A

keto diet
irritation from occluded swat
ACD-nickel chrom textiles

444
Q
  1. What is the first treatment for pruritus pigmentosa
445
Q

Name 4 underlying causes/RF for asteatotic eczema

A

a. Nutritional deficiency e.g. vitamin A
b. Aging-lose oil glands
c. Hypothyroid
d. Retinoids

446
Q

Name 5 associations w/ nummular dermatitis

A

a. AD
b. xerosis
c. Id rxn to dermatophyte
d. Id rxn venous stasis
e. Id rxn ACD-nickel, PPD
f. *often staph

447
Q
  1. Name 4 associations with prurigo nodules
A

a. CKD
b. IDA
c. AD
d. ACD
e. Insect bite reactions

448
Q
  1. What isMC cause gionotti crostti
A

a. EBV> CMV, enteroviruses, hep B, RSV

449
Q
  1. Compare and contrast swimmers itch vs. sea bathers eruption in terms of : Causative agent, distribution, time to onset, fresh vs. salt
A

i. Sea bathers:stings from nematocysts (stinging cells) from jelly fish and sea anemones

ii. Swimmers itch: Parasitic flat worms called “shistomomes”, their larval stage, go into skin and die
b. Time course
i. Sea bathers: 4-24 hrs, can have fever/systemic sx
ii. Swimmers itch: 30 minutes

c. Rash distribution
i. Sea bathers: covered skin
ii. Swimmers itch: exposed skin

d. Salt or fresh water
i. Sea bathers: salt
ii. Swimmers itch: fresh

450
Q
  1. Causative agent CLM
A

Ancylstoma braziliensis

451
Q

Compare and contrast HES subtypes

A

a. Lympho-small clonal pop’n lymphocytes making IL-5 or 13 driving EOS elevation, more dermatitic, more lung involvement
b. Myelo- mutation (FIPL/PDGF translocation) causing proliferation in eosinophils, ulcerative lesions predominate, cardiac

452
Q

Approach to urticaria from pathophys syandpoint

A

a. Immunologic
i. Antibodies-CSU
ii. IgE dependent- allergy (drugs, food, envrionemtnal, contact)
iii. Immune complexes-serum sickness
iv. Chronic infection H pylori, Hepatitis, other viral, bacterial parasitis
v. hereditary fever syndromes
vi. AI diseases
b. Non immunologic
i. Direct mast cell releasing agents- contrast, opiates
ii. Exogenous- stinging nettle (contains histamine)
iii. Leukotriene production -ASA, nsaids
iv. Bradykinin production - ACE

Physical/inducible (see below)

453
Q

Approach to urticaria:

A

Acute < 6 weeks
i. Allergic -drugs, food, environment, contact
ii. Infection-MC viral
iii. Serum sickness
iv. Non immunologic (direct mast, external, leukotriene, bradykinin, contact-benzoic acid, balsam Peru

Chronic > 6 weeks
Immunologic:
-Spontaneous
1. Autoantibody- CSU
2. Autoinflammatory- herecitary fever syndromes
3. Infections- HIV, hepatitis B/C, H.pylori, helminthic
4. AI disorders

Non immunologic:
Meds-Bradykinin, LKTRN
Inducible
1. Aquagenic, solar, cold, cholinergic, delayed pressure, dermatographism, vibratory

454
Q
  1. Explain the difference between white and black dermographism
A

a. White – blanching response from vasoconstriction with stroking of skin, often in atopics
b. Black-black/green colour on skin due to metal deposits on skin

455
Q

What is the triple response of lewis

A

a. Red line – capillary dilation
b. Wheal- edema from histamine release
c. Flare – neurogenic response causing arteriolar dilation

456
Q
  1. Name 5 causes of contact urticaria
A

a. Latex
b. PPD
c. Benzoic acid
d. PEG
e. Parabens
f. Exogenous-stinging nettle (non immunologic), sorbic acid, cinnamic aldehyde, balsam of peru

457
Q

What is urticarial multiforme

A

a. Acute annular urticaria in children with preceding fever/cough, lesions < 2 hours
b. Associated angioedema of hands, feet, no arthralgias/arthritis
c. Dusky ecchymotic centre, no true target lesions, no mucous membrane lesions
d. Dermographism often present
e. Resolved 7-10 days
f. Often responds to anti-histamines

458
Q

Name 5 sources of bite reactions

A

a. Pediculosis pubis or capitis
b. Cheyletiella (cat mites)
c. Groups of 3
i. Fleas
ii. Bed bugs
iii. Cone nose bugs

459
Q

Name 6 causes exaggerated bite reactions

A

a. CLL
b. Mantle Cell lymphoma
c. NK cell lymphoproliferative
d. B-cell lymphoblastic lymphoma
e. EBV
f. Well’s
g. HIV

460
Q

What is papular urticaria

A

Insect, arthropod or parasite reaxctions that can persist e.g. post scabies

461
Q

What is eosinophilic dermatosis of hematological malignancy (EDHM)

A

a. Edematous/urticarial papules, vesicles or bullae on patients with heme malig mimicking insect bite rxn
b. Associated with: CLL, mantle cell lymphoma, ALL, AML, B-cell lymphoma, MM, MGUS,

462
Q

Describe the 3 types of eosinophilic folliculitis

A

a. Classic- recurrent clusters of follicular papules and pustules on annular plaques, often in japanese
b. Infancy associated – pustular scalp folliculitis
c. Immunosuppression- intensely pruritic discrete edematous follicular papules w/ head and neck predominance often seen <250 CD4 or 3-6 months post HART

463
Q

3 types of eosinophilic folliculitis

A

a. Classic- recurrent clusters of follicular papules and pustules on annular plaques, often in japanese
b. Infancy associated – pustular scalp folliculitis
c. Immunosuppression- intensely pruritic discrete edematous follicular papules w/ head and neck predominance often seen <250 CD4 or 3-6 months post HART

464
Q
  1. Name the stages of lyme disease and the rash associated
A

a. Early localized- erythema migrans
b. Early disseminated
Skin- erythema migrans chronicum (multiple erythema migrant spots), . Borrelia lymphocytoma is a rare presentation of early Lyme disease that has been reported in Europe. It presents as a nodular red-bluish swelling that usually occurs on the ear lobe or areola of the nipple. The lesions can be painful to touch.

“SCORN: skin, cardiac, ocular, rheumatologic, neurologic”
-CN palsies, meningitis, peripheral neuropathy, keratitis, AV block

c. Chronic
i. ANCS- arthritis, neuro, skin
-arthritis, cognitive inmpairment, mononeuropathy,
Skin in chronic
3. Acrodermatitis chronica atrophicans- reddish purple atrophic on dorsal hands/feet

465
Q
  1. What are the most common locations for scabies? What are the clinical presentations?
A

a. Webspaces, wrists, axillae, groin
b. Crusted scabies, nodular scabies, papular urticaria
c. *Often dermatitic and nodular

466
Q
  1. What are the 2 groups of urticarial vasculitis
A

a. Neutrophilic
i. Hypocomplementic: Low C1q/C3/C4, high C1q antibodies, often associated w/ systrmic symptoms and other AI dz
ii. Normocomplementimic: often post URTI, can also be seen with EBV, HEP B/C, serum sickness, NSAIDS/SSKI
b. Lymphocytic

467
Q
  1. Name 4 associated diseases with Hypocomplementemic UV
A

a. Sjogrens, Lupus, paraproteinemias, multiple myeloma,

468
Q
  1. What syndromes can you see UV?
A

a. Muckle Wels- hereditary CAPS
b. Cogans- hearing loss, systemic vasculitis, keratitis
c. Schniztler- IgM paraproteinemia, fever, bone pain,
d. Jacouds- UV with GN

469
Q
  1. What is acute hemorrhagic edema of infancy
A

a. LCV found in young children 4 mo- 2 years, often post viral, staph/strep, HSV, medications like penicillins, vaccinations
b. Prev. thought to be similar to HSP but no IgA deposition, no GI or tenal effects
c. On path C1q an IgM deposition
d. Clincially- abrupt onset, annular, targetoid or nummular and pften purpuric plaques on FACE, EARS, extremities, often spares the trunk
e. Child usually well, arthralgias in 56%, SIGNIFICANT edema
f. Self resolving 1-3 weeks

470
Q
  1. What is one distinguishing feature of the urticaria in autoinflammatory syndromes
471
Q
  1. Name 3 congenital autoinflammatory syndromes
A

a. CAPS: Muckle-wells, NOMID, FCAPS  NLRP3
b. TNF-receptor associated periodic syndrome (TRAPS) = TNFR1
c. Hyperimmunoglublinemia D syndrome with. Periodic fevers. (HIDS)- mevalonate kinase

472
Q
  1. Name 2 acquired autoinflammatory syndromes
A

Stills
Schnitzler

473
Q
  1. Name 4 differences between neutrophilic urticaria (variant of common urticaria) and NUD.
    *mostly path

Neutrophilic urticaria shows:

A

i. Presence of dermal edema, neutrophils confined to the upper dermis, limited leukocytoclasia, similar numbers neuts:eos:monocytes
ii. No association systemic dz
vs.

i. significant interstitial distribution of the neutrophilic infiltrate, along the collagen bundles (“en file indienne”) and also in the deep part of the reticular dermis
ii. significant leukocytoclasia is a constant feature in our experience.
iii. Limited dermal edema
iv. Eos/monocytes usually sparse
v. Systemic disease

474
Q

What is neutrophilic urticarial dermatosis? name 3 assoc. diseases

A

a. Variant of urticaria with neutrophilic infiltrate, LCV but no fibrin, minimdal dermal edema
b. Painful > itchy
c. Strongly associated with Stills, SLE, Schnitzlers

475
Q
  1. What is the 2 main cutaneous finding in Schnitzler
A

Neutrophilic urticarial dermatosis
U

476
Q
  1. What are the diagnostic criteria for Schnitzlers
A

IgM monoclonal gammopathy
urticarial lesions <24 hrs
+ 2 of following:
1. Bone pain-distal femur, prox tib
2. Abnormal bone scintirgraphy
3. Arthralgia, arthritis
4.LAD
5. HPS
6. ESR
7. Leukocytosis
8. Fever

477
Q
  1. What canSchnitzler progress to? What is the % progression to these diseases in Schnitlzers
A

i. 15% progress to Waldenstroms, Others include IgM myeloma, marginal b cell lymphoma, lymphoblastic lymphoma over 10-20 yrs

478
Q
  1. What is the most common trigger EM?
A

a. HSV-1 >2, precede out break by 1 week ish in 80%
b. Also reported from covid

479
Q
  1. What is the clinical presentation EM
A

a. Start out monomorphic edematous papules on extremities, nay show actinic predilection and Koebner
b. Develop into targetoir with dark/dusky ventre/ulcer, pale ring, then red inflammatory exterior
c. Mild fever, mild mucosal sometimes,

480
Q
  1. Compare and contrast PEP and pemphigoid/gestationis
A

a. PEP:
i. 3rd trimester more than pemphigoid is
ii. Can flare at delivery but usually not after
iii. Assoc w/ rapid weight gain, multiple gestations
iv. Spares umbilicus
v. May blister
vi. Involves striae
vii. No risk to baby for prematurity
viii. Baby won’t get lesions
ix. Does NOT rend to recur with future pregnancies, occurs at 1st pregnancy
x. No association w/ thyroid ab’s
xi. No HLA association
xii. Path shows eosinophils and eos spong, negative DIF
xiii. Responds to prednisone
b. Pemphigoid gestationis
i. 2nd trimester > 3rd
ii. Can flare at delivery and often post partum
iii. Involves umbilicus, no striae
iv. Can occur with choriocarcinoma
v. Recurs in subsequent pregnancies (or menses, OCP)
vi. Risk prematurity
vii. Baby can develop blisters
viii. HLA DR4 association, Thyroid ab association
ix. Path shows eos, eos spong, IgG1 and C3 deposition along BMZ
x. Responds to pred

481
Q
  1. What is the UV thought to trigger PMLE
482
Q
  1. Where does PMLE occur? How long does it take for onset and offset?
A

a. V-neck, facial in kids
b. Minutes, 7-10 days to improve
c. Variants:
i. Papular, papular-vesicular, plaque, urticarial, hemorrhagic, eczematous, vesiculobullous, EM like, prurigo like,

483
Q
  1. What is Wells syndrome
A

a. Eosinophilic cellulitis
b. Granulomatous dermatitis with eosinophilia

484
Q
  1. What are the 3 stages Wells
A

a. Early- striking dermal edema with eos sup and deep
b. Middle – eos, flame figures (eosinophilic MBP on collagen bundles), histiocytes
c. Late – histiocytes and giant cells around flame figures, lesions gray-blue hue as resolve

485
Q

Name 7 associations w/ Wells

A

a. Arthropod bite
b. EGPA
c. Hematological syndromes – polycythemia, lymphoma, leuk
d. Hypereosinophilic syndromes
e. Infection- dermatophyte, HSV, bacterial
f. Drugs
g. Solid tumors

486
Q
  1. Name 7 clinical variants of wells
A

a. Classic plaque- children
b. Anular granuloma- adults
c. Urticaria-like
d. Pap-vesicular
e. Pap-nodular
f. Bullous
g. FDE like

487
Q
  1. What is the DDX for flame figures:
A

I HATE BPH

a. Insect bite
b. Herpes/pemphigoid gestationois
c. Atopic dermatitis
d. Tinea pedis
e. Eosinophilic cellulitis, EGPA
Bulloous pemphgioi
f. Psuedolymphoma
g. Hypereosinophilic syndrome

488
Q

What is eosinophilc annular erythema? How does it compare to Wells

A

a. Annular erythema with tissue eosinophilia without granulomatous inflammation or flame figures
b. Often lethargy, fatigue
c. Tx colchicine, sulfasalazine, plaquenil

Both can have peripheral Eos

489
Q

Name the different associations of Sweets

A

a. Drugs - GO SHLAM
b. Post infectious- viral URTI, strep, yersinia
c. Post vaccination
d. Malignancy- AML, MDS, solid organ tumors,
e. Inflammatory: IBD > RA, lupus, behcets
f. IDIOPATHIC 70%

490
Q
  1. What are the associations with palisaded neutrophilic and granulomatous dermatitis / IGND
A

VIMID

a. Vasculitis-ANCAs, takayasaus, EED, cryo
b. Infection- subacute IE, hepatitis, strep
c. Malignancy- lymphoma
d. Inflammatory: IBD, RA, SLE, PMR, scleroderma , stills, sarcoid
Drugs

*RA and SLE

491
Q
  1. Name the 2 things on the ddx for PNGD/INGD
A

EED
Granulomatous drug re

492
Q
  1. Name the 5 most common drugs to cause serum sickness like rxn
A

a. Cefaclor
b. Minocycline
c. Bupropion
d. Infliximab
e. Rituximab

B-CRIM

493
Q

Name 5 drugs associated with IGND

A

Hypertension-CCBs, BBs, ACE inh
Diuretics- Furosemide
Statins
TNFa inh *
Antihistamines
Thalidomide
Anakinra

HD STAAT

494
Q

Name 4 subtypes of miliaria

A

crystalina
rubra
pustulosa
profunda

495
Q
  1. What is urticarial dermatitis
A

a. Hypersensitivity syndrome, dermal lympho-eosinophilic infiltrate with minimal epidermal change
b. Very common
c. Reaction drugs, supplements,food, id reactions

Urticarial + dermatitic morphology in same plaque or

496
Q
  1. What is neutrophilic eccrine hidradenitis
A

a. Neutrophilic infiltration of eccrine glands
b. Often painful papules plaques and nodules +- fever
c. Associated w/ AML/CML, cytrabine, cetuximab, imatinib, antrhacyclin

MC situation is acute myelogenous leukemia patients receiving chemotherapy, most commonly with cytarabine.

497
Q

What is major and minor criteria of papuloerythroderma of ofuji? How does it present?

A

Urticarial to dermatitic polygonal flat topped papules and plaques that spares the folds, often erythrodermic and sometimes flat topped papules, most common in Japan

Major
-Erythrodermic eruption of flat topped coalescent red brown papules with cobblestone appearance
-Spares skin folds
-Pruritus
-Pathological picture excludes lymphoma and other skin diseases
-Absence of triggering factors like neoplasms, infections, drugs

Minor
-> 55
-Male
-Peripheral or tissue eos
-Elevated IgE
-Peripheral lymphopenia

498
Q
  1. Name 2 Large vessel vasculitidies and 2 medium vessel vasculitides
A

Large: GCA, takayasaus
Medium: PAN, KD

499
Q

2.Describe the chapel hill vasculitis approach, highlight which are immune complex mediated

A

Large/medium as above

b. Small vessel
i. IgA/HSP
ii. Urticarial vasculitis Hypocomplementemic/AntiC1Q
iii. Cryoglobulinemic
iv. EGPA
v. GPA
vi. MPA
vii. Anti-GBM

Variable vessel
i. Behcets, cogans

Vasculitis associated w/ systemic disease
i. SLE, sarcoid, RA, Sjogrens

Vasculitis w/ probable etiology
i. Drugs, infections, sepsis, AI

Cutaneous SOV
i. IgG/IgM
ii. Nodular vasculitis/ Erythema induratum of bazin
iii. EED
iv. Granuloma faciale
v. Hypergammaglobulinemic macular vasculitis
vi. Normoclomplementic urticarial vasculitis

500
Q

Name 6 cutaneous features of PAN

A

a. Livedo reticularis or racemosa
b. Subcutaneous nodules
c. Punched out ulcers
d. Hemorrhagic macules
e. Retiform purpura
f. Erythema

501
Q
  1. What are 3 systemic features that can be seen in cutaneous PAN
A

a. Fever
b. Arthralgia
c. Peripheral neuropathy in that limb

502
Q
  1. What genetic syndrome can you see PAN or cPAN-like features
A

ADA2 deficiency or :dada2

503
Q
  1. Name 4 underlying causes/triggers for PAN
A

a. Infections-HBV, HCV
-Strep, Parvo, HIV with cutaneous PAN

b. AI disease – IBD, SLE, familial med fever
c. Malignancy – Hairy cell leukemia*
d. Drugs (MTS)
-Minocycline, tnf alpha, sulfasalazine

For cutaneos PAN most commonly is chonric infections, AI CTD also often cutaneous

504
Q

When might a PAN have a + P-ANCA

A

drug induced

505
Q
  1. What is KD diagnostic criteria
A

a. Fever 5 days + 4/5 of:
i. Conjuctivitis (non purulent, bilat)
ii. Rash-polymorphous
iii. Adenopathy >1.5 cm
iv. Strawberry tongue and mucosal changes (fissured lips)
v. Hands and feet- palmar erythema/edema and desquamation

506
Q

What are the 3 phases of EGPA? Name 3 cutaneous manifestations EGPA? What ANCA is most associated with EGPA and how often is it + and what does it mean? What systems are involved?

A

i. Adult onset asthma, allergic rhinitis, nasal polyps
ii. Eosinophilic phase- pneumonia, GI, eosinophilia
iii. Systemic vasculitis with granulomatous inflammation- cardiac, neurologic

b. Skin findings
i. Palpable purpura
ii. Nodules
iii. Ulcers
iv. Urticaria early on

c. ANCA?
i. P-ANCA (MPO) in 40%
ii. + indicates more neuropathy, - more cardiac

d. Systems
i. , cardiac, GI, upper and lower airway, neuropathy
ii. NO RENAL

507
Q
  1. What are the 3 main systems involved in GPA? Name 5 cutaneous findings? How often cutaneous findigns? How often/what ANCA?
A

a. Upper and lower airway, renal
b. Cutaneous in 46%-66%
c. Skin
i. Palpable purpura
ii. Ulcerations resembling PG
iii. Oral/nasal ulceration
iv. Strawberry gums – gingival hyperplasia with friable tissue
v. Papulonecrotic lesions
vi. Subcut nodules
d. C-anca/PR3 in 80%

508
Q
  1. How does MPA present? Who gets it? Name 3 lab findings?
A

a. Prodrome constitutional then explosive into pulm hemorrhage + renal

RF+ often, P-ANCA/MPO in 90%,

509
Q
  1. What type of cryoglobulinemia is vasculopathic?
A

a. Type I- Monoclonal IgM, causes ulcers and infarcts

510
Q

Describe the differences between Type I and Type II/III cryoglobulenemia

A

Mixed MONOCLONAL IgM (type I) OR POLYCLONAL (type II) IMMUNOGLOBULINS bind to polyclonal IgG (Fc portion)

Type 1: Caused by monoclonal IgM>IgG (mono)
Type 2: Monoclonal IgM or IgG against polyclonal IgG (mono-poly)
Type 3: Polyclonal IgM against polyclonal IgG

511
Q
  1. What is cryoglobulinemia assoc with most often
512
Q
  1. Name the systemic findings of cryoglobulinemia? Name the cutaneous findings
A

a. SKIN, NERVES, KIDNEYS
b. Skin-palpable purpura 90%, rarely erythematous papules, ecchymoses, and dermal nodules;
i. rarely, urticaria, livedo reticularis, necrosis, ulcerations, and bullae are observed
c. Systemic-peripheral neuropathy, GN

513
Q

what is a RF

A

a. Antibodies directed against the Fc portion of IgG

514
Q
  1. Compare and contrast HSP in children and adults
A

a. KIDS- URTI MC cause vs. Adults-drugs and malignancy
b. Renal involvement more common in adults (8-70%) > kids (2-15%)
c. Abdo pain in kids vs. diarrhea in adults

515
Q
  1. What specifically is the immunoglobulin in HSP? Why is it different
A

IgA1-deficient in galactose in hinge region, makes it precipitate more easily

516
Q
  1. What systemic features can be seen in HSP?
A

a. Abdo pain
b. Orchitis
c. Arthralgias and arthritis
d. GI- abdo pain, diarrhea, intussuception
e. Peripheral edema
f. GN

517
Q

What are the 3 variants of hypocomplementic UV

A

a. Skin only
b. As part of AI disease (Sjogrens, RA, SLE)
c. Pulmonary, renal, eyes and arthritis

518
Q
  1. What is the diagnostic criteria for behcets
    (name both)
A

a. Need 4 points
i. Oral apthae- 2
ii. Genital apthae-2
iii. Ocular involvement (uveitis) - 2
iv. Skin manifestations 1
v. CNS 1
vi. Vascular1
vii. Pathergy 1 point

Vs. 3 of following:
Skin-EN like, necrotic folliculitis, acneiform
Oral apthae-3x/yr
Genital ulcers
Neuro
Ocular- uveitis, vasvulitis retina
Vascular -venous thrombosis, arterial thrombosis or aneurysms

519
Q
  1. What are the non ulcer skin mainfestations of behcets
A

a. Acneiform rash
b. Necrotic folliculitis
c. EN-like lesions  v speific
d. EN

520
Q
  1. What is the MC SOV?
A

a. IgG/IgM vasculitis
b. Often triggered by infection

521
Q
  1. What is the demographic for nodular vasculitis/erythema induratum? What is it
A

a. Lobular panniculitis w/ vasculitis
b. Nodular lesions Backs of legs, women, 30-60, venous stasis, obese

522
Q
  1. What is erythema induratum of bazin
A

a. Lobular panniculitis with vasculitis
b. Indicative of active Tb

523
Q
  1. How does EED present? What is it associated with
A

-Red–violet to red–brown papules, plaques, and nodules that favor extensor surfaces (elbows, dorsal hands, knees, ankles)
-Nodular lesions, palmoplantar, that progress to form bulky masses –> consider HIV infection

*High association IgA monoclonal gammopathy, AI CTD
b. Associated with infection (strep, HIV, HBV, syphilis, tb), monoclonal gammopathy (esp IgA) and other heme malignancy, AI disease (GPA, RA, IBD, celiac, polychondritis)

524
Q

What does granuloma faciale show on path? Who gets it ? triggers?

A

a. Mixed vasculitis with neutrophils, eosinophils, lymphocytes, plasma cells
b. Grenz zone
c. Perivascular infiltrate, +- vasculitis, +- IgG on DIF
Telangiectasias

Who gets it? Males, older/middle age
Sun exposure

525
Q
  1. What is hypergammaglobulinemic macular vasculitis
A

( golfers/exercise induced
vasculitis may also be a form of this)
c. Macular purpura lower extremities, monoclonal or more often polyclonal gammoapathy , often associated w/ Sjogrens
IgG
e. Labs: ESR, poly/monoclonal gammopathy, Non igM RF

526
Q
  1. What is diagnostic criteria for HUVS (hypocomplement)
A

a. two major criteria : (1) urticaria for 6 months and (2) hypocomplementemia +
b. two or more minor criteria: (1) vasculitis on skin biopsy; (2) arthralgia or arthritis; (3) uveitis or episcleritis; (4) glomerulonephritis; (5) recurrent abdominal pain; or (6) positive C1q precipitin test with a low C1q level.

527
Q

What is the workup/ddx for LCV?

A

Viral (hep B/C)
i. Hep B/C, HIV serology
Autoimmune
i. ANA, RF, ENA, UA, ANCAs,
Strep, Staph, hSp, Skin bx w/DIF
i. Throat swab, SPEP
Cryoglobulinemia, cryofibrinogens
i. Cryoglobulins, cryofibrinogins, creatinine
UV Hypocomplementemic, UC/IBD
i. C3/C4
ii. +- colonoscopy if indicated
Lymphoproliferative-hairy cell
i. CBC, LDH, SPEP, smear
Infectious-endocarditis, meningococcemis, gonoccoal arthritis, RMSF
i. Blood cultures,
ii. Gram stain and culture bx
Thiazide diuretics + other drugs, traumatic
Immune complex, immune sera
Septra and other abx

528
Q

3 phases of raynauds

A

white blue red, sometimes no blue

529
Q

8 RF for primary raynauds

A

Thin
Smoking
cold climate
cv disease
manual occupation
drugs
older age

female gender,
family history of PRP, migraine,
smoking, CVD
, oestrogren replacement therapy

530
Q

10 features of primary raynauds vs. contrast to secondary:
Sex
Age
Frequency
Precipitants
Ischemic injury
Capillaroscopy
Other vasomaotor instability
ANA +
In vivo PLT activation
Fam hx

A

Sex: Strong female predominance vs. only 4:1 M:F
Age: puberty vs. >25
<5 vs. >5 attacks daily
Precipitants: cold or stres vs. cold
Ischemic injury and abnormal capillaroscopy absnet in primary

Other vasomotor phenomenon present in both

All ab’s absent in primary
ANA + in almost all secondary:
i. CREST -ACA+
ii. Diffuse systemic SCL70
iii. SLE sm+
iv. Sjogrens SSA/SSB

Others:
Fam hx strong in primary
Progressivr disease in secondary

531
Q
  1. Percent of people healthy with ANA 1:80, 1:160, 1:320
A

13%, 5%, 3.3%

532
Q

Name 3 general causes for seconday raynauds and give 5 examples of each

A

a. Vasculopathy
i. CTD (scleroderma>SLE>sjogrens), traumatic (frost bite, vibration), drug (chemo), buergers, vasculitis, thpracic outlet, brachiocephalic trunk dz e.g. takayasaus, athero
b. Vasospastic
i. Drugs (ergots, sympathetic agonists), endocrine (pheo, carcinoid, hypothyroid), neuro (nerve root entrapment)
c. Coagulation
i. Cryoglob, cryofirin, paraproteins, macroglobulins, cold agglutinin, PCV, thromboembolism

533
Q
  1. Name 3 1st, second and third line tx for raynauds
A

a. 1st: nifedipine/amlodipine, topical nitro, ASA, dipyramidole
b. 2nd: PDE-5 (sildenafil), ARB, pentoxifylline
c. 3rd: Endothelin receptor antagnoists (Bosentan), Prostaglandin E1 infusion, biofeedback, LMWH

534
Q

5 general tx for digital ulcers

A

a. Pain control
b. Soak BID in ½ strength H202
c. Abx ointment and occlusive dressing
d. Hydrocolloids/gels
e. Max CCB therapy

535
Q

Name the 6 types of scleroderma

A

a. Morphea-localized scleroderma
b. Prescleroderma
c. Systemic sclerosis-limited
d. Systemic sclerosis-diffuse
e. Sine scleroderma
f. MCTD

536
Q
  1. Limited systemic sclerosis: which ab most associated? What systemic finding do they often get? What nailfold change?
A

a. Anti centromere
b. Pulm htn
c. Tortuous capillaries, but no dropout

537
Q
  1. In systemic sclerosis diffuse, what nailfold changes are seen? Name 2 other cutaneous features? Name 5 internal organ findings and the most common Ab
A

a. Ptergyium unguis inversum, confetti leukoderma
b. Tortious capillaries with dropout
c. Internal
i. Cardiac, GI, ILD, oliguric renal failure, tendon friction rubs, polyarticular synovitis
d. Ab: SCL-70/topoisomerase in 30%

538
Q
  1. Name 4 new treatments for scleroderma
A

a. Tocilizumab (anti-IL-6)
b. Rituximab +- MMF
c. PDE-5 inhibitors, endothelin receptor antagonists, prostacyclin analogues
d. Antifibrotics: Nintendanib

539
Q
  1. List the 12 SLICC criteria (need 4 or more)
A

a. ACLE or SCLE
b. Chronic LE
c. Non scarring alopecia
d. Oral ulcers
e. Serositis
f. Arthritis/arthralgias
g. Lupus cerebritis/neuro
h. Lupus nephritis
i. Hemolytic anemia
j. Leukopenia or lymphopenia
k. Thrombocytopenia
l. Immunologic: ANA, dsDNA, smith, low complement, APLAS, DAT)

540
Q
  1. What are 4 changes on path that help distinguish lupus specific skin changes and 2 more in general
A

a. Increased mucin
b. BMZ thickening
c. Perivascular and periadnexal lymphocytic sup and deep infiltrate
d. Interface dermatitis

e. General: hyperkeratosis, follicular plugging , epidermal atrophy

541
Q
  1. Name the Lupus specific lesions
A

ACLE-malar and generalized
SCLE- psoarisiform or annular, TEN-like
CCLE- DLE, panniculitis, profundus, tumid, chilblains

542
Q
  1. Name 10 non lupus specific lesions
A

Vasculitis
APLS changes/vasculopathy( nodules, ulcers, atrophie blanche)
livedo
RP
non-scarring alopecia,
oral ulcers,
periungual telangiectasias, erythromelalgia,
bullous lupus,
rheumatoid nodukes, dermatofibromas,
lupus mucinosis,

sclerodactylyl,
acanthosis nigricans,
anetoderma,
CSU,
alopecia areata

543
Q
  1. Name 7 drugs that can cause SLE, what ab’s associated, and 1 clinical difference, and 1 drug that’s different
A

a. Drugs “HIP MC”
i. Hydralazine #1
ii. Isoniazid #2/3, interferon
iii. Procainamide #2/3, phenytoin , penicillamine (unmasks dz)
iv. Minocycline (anti MPO), Methyldopa
v. Chlorpromazine
vi. TNF-inhibitors
b. Ab: anti-histone in 95%
c. No skin involvement usually
d. TNF dsDNA +, skin present often, more CNS and more renal

544
Q
  1. What are MC Abs in SCLE? Name 5 causative drugs . What % SCLE is drug induced
A

a. Ab: SSA 90%, SSB40%, ANA 70%
b. Drug induced also usually SSA/SSB + in
c. 50% drug induced

d. Drugs: THIN DRAGS
i. Terbinafine, TNF alpha, taxanes
ii. HCTZ #1
iii. Interferon
iv. NSAIDS
v. Diliazem/CCBs
vi. Ranidtinde/PPI/PUVA
vii. Acei/antiepileptics
viii. Griseofulvin
ix. Spironoloactone, sulfonylureas

545
Q
  1. Name 4 RF for SLE in SCLE, and what % of SCLE pts have SLE?
A

a. ANA+
b. dsDNA
c. Papsquam>annular variant
d. Leukopenia

546
Q
  1. Name 4 internal organ systems present in neonatal lupus? What Ab is in them? Which RO subtype is more associated with lupus? Sjogrens?
A

a. Organs
i. Heart block
ii. Transamninitis/cholestasis/hepatic failure
iii. Cytopenias
iv. Macrocephaly
v. *annular skin lesions
b. SSA >SSB
c. SSA 52 KD w/ SJOGRENS  may have higher risk heart block
d. SSA 60 KD w/ LUPUS

547
Q
  1. What is risk SLE with DLE localized, generalized, chilblains and profundus
A

a. Localized- 20%
b. Generalized- 50-70%
c. Chillblains 20%
d. Profundus 50%

548
Q
  1. Name 6 tx for cutaneous lupus
A

a. SPF 50 +
b. TCS, TCI, crisaborole, topical retinoids, topical dapsone
c. ILK
d. Anti-malarials
e. Acitretin if hyperkeratotic
f. Immune suprresants: AZA, MMF, mtx, apremilast, csa, leflunomide.
g. Biologics: ustekunumab, ritux,

MC: Rituximab, Belimumab

549
Q
  1. What is dosing for HCQ, chloroquine and quinacrine
A

a. HCQ 5 mg/kg actual BW
b. Chloroquine 2.3 mg /kg actual BW
c. Quinacrine 100-200 mg po daily

550
Q
  1. Name 8 RF for ocular toxicity in HCQ or chloroquine
A

a. Dosing > 5 m/kg or 2.3 for chloroquine
b. > drug 5 yrs
c. Renal disease
d. Hepatic disese
e. Macular degeneration, retinal dystrophy
f. > 60
g. Obese
h. Tamoxifen

551
Q

Name treatments for: livedoid vasculopathy

A

a. Compression
b. clopidogrel
c. Topical steroids or ILK
d. Pentoxyfilline
e. Nicotinamide

552
Q
  1. What is seen on path for bullous Lupus
A

Linear or granular IgG and C3, +- IgM and IgA at DEJ
Floor on SSS
Lesions and perilesional

553
Q
  1. Top 3 tx bullous SLE
A

dapsone colchicine sulfasalazine

554
Q

Name 9 features of JDM more prevalent in juvenile than adult

A

a. Vasculitis
b. Vasculopathy
c. Calcinosis
-superficial nodules and plaques
-Calcinosis circumscripta
-calcinosis universalis
-exoskeleton pattern
d. Dystrophic calcification
e. Gingival telangiectasia
f. Arthritis
g. Muscle atrophy and contracture
h. Retinopathy
i. Large bowel infarction/perf secondary to vasculitis

555
Q
  1. Name top 5 cancers seen in adult dM? what is the RR in the first year
A

a. Ovarian, breast, lung, gastric, nasopharyngeal
b. 26 x risk in 1st year

556
Q

What is the workup required for DM in adults cancer screening wise

A

a. CT CAP
b. Colonoscopy
c. TVUS
d. Mammogram
e. CBC, LDH
f. Tumor markers

557
Q
  1. Name the pathognomonic findings of DM, characteristic findings, and suggestive findings
A

Pathognomonic: Gottrons papules, gottrons sign

Characteristics
i. Shawl sign, Holster sign
ii. Heliotrope
iii. Periungual erythema +- cuticular dystrophy
iv. Mechanics hands

c. Suggestive
i. Calcinosis cutis
ii. Seb-like dermatitis
iii. Flagellate erythema
iv. Lymphocytic lobular panniculitis
v. Poikiloderma vasculare atrophicans

558
Q
  1. Name 5 features anti synthethase syndrome
A

a. Mechanics hands
b. ILD
c. RP
d. Arthritis
e. Fever

559
Q
  1. Name 4 DM treatments pre malignancy and once malignancy ruled out
A

Pre-malig
i. Prednisone
ii. HCQ
iii. IVIG
iv. MTX

Malig rules out
i. AZA, MMF, Csa, Ritux * esp if vasculitis

560
Q
  1. How often to repeat malignancy workup
A

a. At 1-2 years
b. If no malignancy in first 2 years, decreased risk, at baseline at 5 yrs

561
Q
  1. Name 10 organs sarcoid can affect and 1 manifestation of each
A

a. Skin- specific vs. reactive
b. Constitutional-fever, weight loss, sweats
c. Lung (90%)- SOB, cough
d. Liver- increase ALP
e. Eye -uveitis
f. Lymph nodes-asymptomatic
g. Spleen
h. Heart- heart block, cardiomyopathy
i. Hematologic – lymphopenia, eosinophilia
j. Hypercalcemia- kidney stones
k. Brain – CN palsies, seizures
l. Joints- ankles, knees, wrists, cysts

562
Q
  1. What type of granulomas are sarcoid?
A

non caseating
naked often

563
Q
  1. What % sarcoid in skin will go on to have systemic involvement
564
Q

Approach to sarcoid in the skin

A

a. Reactive/non specific: no granulomas, usually acute and self limited sarcoid
i. E.g. EN, pruritus, EM, nummular dermatitis, calcinosis cutis, clubbing, prurigo

Specific: Granulomas present
Acute
1. Maculopapular
2. Nodular

Chronic: AAAPPI
1. Lupus pernio
2. Angiolupoid
3. Plaque
4. Annular
5. Alopecic
6. Icthyotic

No association with acute or chronic
1. Darier roussy nodules
2. Scar sarcoid
3. Tattoo sarcoid
4. Drug induced
5. Follicular
6. Ulcerative
7. Psoriasiform
8. Hypopigmented
9. Rarer-erythrodermic, lichenoid, perfortating, hypertrophic, imbilicated

565
Q

iv. What are the 4 major organs to screen for in sarcoid

A

Heart
Lungs
Eyes
Brain

566
Q

What is the workup for sarcoid

A

i. H+P including neuro, eyes, heart, lungs
ii. Biopsy for H+E and culture
iii. Labs: CBC, LE, Ca, ACE level, CD4:CD8 level, serum immunoglobilins
iv. EKG and TTE +- cardiac MRI
v. CXR and PFTs
vi. TBST
viii. Refer: Optho, resp, IM, cardio

567
Q
  1. What is the prognosiss for sarcoid
A

a. 60% spont. Resolution
b. 30% progressive/chronic

568
Q
  1. Name 5 tx for EN lesions in sarcoid (reactive)
A

a. Bed rst
b. NSAIDS
c. ILK
d. Pred
e. SSKI

569
Q
  1. Name 8 tx options for specific lesions of sarcoid
A

a. TCS
b. ILK
c. Anti malarials
d. Tetracyclines
e. Allopurinol
f. Pentoxyfilline
g. Pred
h. MTX
i. AZA

570
Q

What are the diagnostic criteria for Sjogrens

A

Inclusion: dry eyes or mouth x 3 months, not explained by something else

Need 4 points or more
i. Salivary gland bx showing focal lymphocytic sialdenitis and focus score of 1 FS/ 4 mm2 or greater (3)
ii. SSA + (3)
iii. Schirmer test <5 mm/5min in one eye (1)
iv. Ocular staining score (>5) in one eye (1)
v. Unstimlated whole saliva flow rate <0.1 ml/min

Exclusion criteria:
i. Hep C, AIDS, head/neck radiation, sarcoid, amyloid, GVHD, IgG4 related disease

571
Q
  1. Name the 3 most common glandular manifestations of sjogrens
A

a. Xerostomia
b. Keratoconjuctivitis sicca
c. Vaginal tract dryness

572
Q
  1. Name 8 systemic manifestations Sjogren
A

a. Fatigue
b. MSK- arthralgia, non erosive arthritis
c. Neuro- small fibro neuropathy, peripheral neuropathy, transverse myelitis, , dementia, psych)
d. Pulmonary- xerotrachea, ILD, lymphocytic pneumonitis
e. Vascular- vasculitis
f. GI- gastroparesis,
g. Liver-PBC, AI hepatitis
h. Nephro- tubuluinterstialn nephritis
i. Heme- lymphopenia, B cell lymphoma, polyclonal gammopathy

573
Q

NAme the 12 cutaneous features Sjogrens

A

a. Xerosis
“Vasculitis”
b. LCV
c. Waldenstroms benign hypergammaglobulinemic purpura
d. UV
e. Cryoglobulinemic vasculitis
“Urticarial”
f. Annular erythema of sjogrens
g. Urticaria

“AI-CTD”
h. RP
Neonatal lupus
i. Livedo reticularis

“Infiltrative”
j. Marginal zone lymphoma
k. Nodular amyloid

MyDermatology-Bolognia (31 decks)

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