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General Dermatology Flashcards

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1
Q

Which medications can induce a flare of pustular psoriasis (8)?

A 
Beta-blockers
Lithium
IFN
Antimalarials (plaquenil)
TNF-inhibitors
NSAIDs
Terbinafine
CCBs
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2
Q

Erythema gyratum repens is associated with which malignancies (5)?

A 
Lung = #1
Breast
Cervical
Bowel
Bladder
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3
Q

Name the 3 longitudinal sections of the hair follicle and an associated disease with each section.

A
  • Infundibulum (surface of skin to sebaceous gland opening): LPP
  • Isthmus (sebaceous gland opening to insertion of arrestor pili): DLE
  • Inferior segment (the rest): alopecia areata
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4
Q

What is the most common mutation in mucosal melanoma? In uveal melanoma?

A

Mucosal melanomas: KIT

Uveal melanomas and blue nevi: GNAQ

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5
Q

Which cutaneous manifestations are more common with Ulcerative Colitis than Crohn’s? …more common in Crohn’s than UC?

A

UC > Crohns: erythema nodosum, pyoderma gangranosum, pyoderma vegetabs

Crohns > UC: oral disease, fissures, fistulae, metastatic disease to skin, PAN

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6
Q

Verruciform xanthomas are seen in which conditions? What is the most common location?

A

CHILD syndrome, EBA, GVHD, lymphedema syndromes

Most common location = oral mucosa

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7
Q

How do you calculate the dose of UVR a phototherapy patient should receive?

A

Irradiance (Watts, which is power/unit area) x time (seconds) = UV dose (Joules, which is energy/unit area)

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8
Q

What to DSAP and Hyper IgD have in common? What are manifestations of Hyper IgD?

A

MVK mutation (melavonate kinase gene) - regulates calcium-induced keratinocyte differentiation and may protect from UVA-induced apoptosis

HIDS: periodic fevers (induced by vaccines, etc), nausea/vomiting/diarrhea, LAD, rash

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9
Q

What are the mutations and distinguishing features of the following auto inflammatory conditions: Muckle-Wells, Familial Mediterranean Fever, TRAPS?

A

*All have periodic fevers!

Muckle-Wells: CIAS1 mutation (cryopyrin); AD; urticaria, deafness, renal amyloidosis (AA), abd pain, myalgia/arthralgia, conjunctivitis
– Tx = Anakinra, steroids

Familial Mediterranean Fever: MEFV mutation (pyrin); AR; polyserositis, erysipelas-like erythema of legs
– Tx = colchicine

TNF Receptor Associated Periodic Syndrome: TNFR1 mutation; AD; erythematous serpiginous patches/plaques on extrems, abd pain, arthralgia/myalgia
– Tx = TNF-alpha inhibitor, steroids

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10
Q

Name the porphyrias that “HAVE” abdominal pain.

A

Hereditary coproporphyria
Acute Intermittent Porphyria
Variegate Porphyria
Erythropoietic Porphyria (also has cholelithiasis)

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11
Q

Androgens:

    • Most potent? How is it made?
    • Where are androgen receptors that are relevant to acne?
    • Which androgens are made in the adrenals?
A
  • Dihydrotestosterone (DHT) = most potent.
  • Testosterone is made in gonads and converted to DHT by 5-alpha-reductase.
  • Dehydroepiandrosterone sulfate (DHEA-S) and 17-hydroxyprogesterone = weak androgens made in adrenals

Androgen receptors on sebaceous glands and outer root sheath of hair follicle

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12
Q

How does estrogen help acne?

A

Decreases sebum production
Directly opposes effects of androgens on sebaceous glands
Inhibits production of androgens by gonads

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13
Q

In psoriasis, which cytokine stimulates Th1? Th17? Which cytokine correlates with disease severity

A

IL-12 stimulates Th1

IL-23 stimulates Th17

IL-22, a Th17 cytokine, correlates with disease severity

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14
Q

Which medications can cause drug-induced lichen planus (typically NO Wickam’s striae)?

A 
Beta-blockers
Captopril
Penicillamine
HCTZ
Anti-malarials
Quinidine
NSAIDs
Tetracyclines
Gold
Sulfonylureas
Methyldopa
Carbamazepine 
5-FU
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15
Q

Type of Amyloid deposited in these conditions: Macular, Lichen, Nodular, Secondary, Primary Systemic, Secondary Systemic, Dialysis-Associated, Familial, Senile Systemic

A 
Macular -- AA
Lichen -- AA
Nodular -- AL
Secondary -- AA (derived from liver)
Primary Systemic -- AL
Secondary Systemic -- AA (periodic fevers, RA, other inflammatory states)
Dialysis - Beta-2 Microglobulin 
Familial -- ATTR (transthyretin)
Senile -- ATTR
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16
Q

Muckle Wells Syndrome

    • Mutation
    • Treatment options
A

Mutation: CIAS1 (cryopyrin)

Treatment:

    • steroids
    • Anakinra (IL-1 receptor antagonist)
    • Canakinumab (mAb against IL-1)
    • Rilonacept (IL-1 -TRAP fusion protein)
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17
Q

Familial Mediterranean Fever

    • Mutation and Inheritance
    • Features
    • Treatment
A

MEFV mutation (Pyrin)

AD inheritance

Features: hives, polyserositis, fever, erysipelas-like erythema on legs

Tx: Colchicine

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18
Q

TNF Receptor Associated Periodic Syndrome (TRAPS)

    • Mutation and Inheritance
    • Features
    • Treatment
A

TNFR1 mutation; AD

Features: fevers, red patches/plaques on extremities, and pain, arthralgias/myalgias

Tx: TNF-inhibitors, glucocorticoids

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19
Q

Scleredema

    • What are the 3 forms?
    • Treatment?
A

I: infection-related – often strep; self-limited induration of cervicofacial area and proximal extremities
II: Gammopathy associated – IgG kappa; insidious onset
III: Diabetes-related – slow onset of induration on neck/back in obese men with IDDM; sharply demarcated normal skin; treating DM does NOT improve.

Tx: Phototherapy, cyclophosphamide, steroids, cyclosporine

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20
Q

Erythropoietic Protoporphyria

    • Mutation and inheritance
    • Features
    • Treatment
A

Ferrochetolase (AD)

EPP = “empty PP but gallbladder full of stones”

Features: photosensitivity with burning, scars, milia, gallstones, hepatic damage

Tx: light avoidance, beta-carotene

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21
Q

Porphyria Cutanea Tarda

    • Mutation and inheritance
    • Features and Triggers
    • Treatment
    • AR form’s name and features
A

Uroporphyrinogen decarboxylase (AD or acquired)

    • Features: bullae, erosions, milia, hypertrichosis, scleroderma-like changes
    • Triggers: alcohol, HCV, estrogen, polychlorinated hydrocarbons, iron overload (hemochromatosis), HIV
    • Tx: phlebotomy, plaquenil
    • AR form = Hepatoerythropoietic Porphyria (features of PCT and congenital erythropoietic protoporphyria; Tx = photo protection)
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22
Q

Variegate Porphyria

    • Mutation and Inheritance
    • Features
    • Treatment
A

Ptoroporphyrinogen deaminase (AD)

    • Features: combo of PCT and Acute Intermittent (neuro/psych findings, abdominal pain; AIP has no skin findings); plasma fluoresces at 626 nm
    • Tx: during attacks glucose load, hematin infusion; avoid triggers (alcohol, drugs, stress, fasting, hormone change, infection)
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23
Q

Familial Hyperlipidemia

– Mutation, lipid levels and characteristic skin findings of Type I, Type IIa, Type IIb, Type III, Type IV, Type V

A

Type I: LPL deficiency, elevated TG, Eruptive xanthomas and acute pancreatitis
Type IIa: LDL receptor defect (either LDLR or Apo-B mutated); elevated LDL; tendinous/tuberous xanthomas (interdigital webspace pathoglomonic); statins dont help b/c no LDLR
Type IIb: Familial combined; LDL receptor defect; elevated chol/TG; tendinous/tuberous xanthomas
Type III: ApoE protein defect (chylomicrons not cleared); elevated Chol and TG; Xanthoma striatum palmare pathognomonic; tuberous xanthomas
Type IV: Increased production of VLDL; elevated TG; eruptive xanthomas; assoc w/ DM, obesity, alcoholism
Type V: apolipoprotein C-II defect; increased TG/chol; Eruptive xanthomas, pancreatitis, DM

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24
Q

What mediators are pre-formed in mast cells (5)?

A 
histamine
heparin
tryptase
chymase
serotonin
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25
Q

Types of Hereditary Angioedema and what is dysfunctional.

A

Type I: Decreased C1-INH level (85% of cases)
Type II: normal C1-INH level but dysfunctional (15% of cases)
Type III: estrogen dependent; activating mutation in factor XII; normal C1-INH level (rare)

Labs for all show decreased C4 (type III has normal C4!), Decreased/Normal C1-INH, normal C1q

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26
Q

Expected lab values in hereditary vs acquired angioedema

A

Hereditary Angioedema: low C4, low/normal C1-INH, normal C1q

Acquired Angioedema: low C4, low/normal C1-INH, LOW C1q
*Acquired due to anti-C1 INH Abs OR is secondary to a lymphoproliferative process in which immune complexes are consuming C1q

If C4 normal, angioedema is drug-induced or idiopathic

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27
Q

Causes of Drug-Induced Pemphigus Vulgaris (many)

A

Thiol drugs (penicillamine (PF > PV), captropril, enalapril, lisinopril, prioxicam); pyrazolone derivatives (phenylbutazone, oxyphenylbutazone); antibiotics (penicillin derivatives, cephalosporin, rifampicin)

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28
Q

Causes of drug-induced pemphigus foliaceous

A

Penicillamine, nifedipine, ACEIs

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29
Q

Malignancies associated with paraneoplastic pemphigus, in order of frequency (6)

A 
Non-Hodgkin's Lymphoma (40%)
Chronic lymphocytic leukemia (30%)
Castleman's (10%)
Thymoma (6%)
Waldenstrom macroglobulinemia (6%)
Sarcomas
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30
Q

Autoantigens implicated in paraneoplastic pemphigus

A

All plakins + BPAG1…

Desmoglein 3, periplakin, envoplakin, desmoplakin, BPAG1, plectin, alpha-2 macroglobulin-like 1 (A2ML1 - 170 kDa)

NOT BPAG2! Must have Abs to either Dsg1 or Dsg3 which initiates blister formation

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31
Q

causes of drug-induced Bullous Pemphigoid?

A

Furosemide, NSAIDs, phenactin, PCN-derivatives, gold, potassium iodide, captopril, enalapril, penicillamine, sulfasalazine

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32
Q

Autoantigens in cicatricial pemphigoid and implications…

A 
BPAG2 (c-terminus): mucosa and skin 
Beta4 subunit of a6b4-integrin: OCULAR
Laminin 332 (epiligrin): cancer risk (adenocarcinoma)! -- binds DERMAL side of SSS
Laminin 6
BP230
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33
Q

Paraneoplastic Pemphigus vs Cicatricial Pemphigus and the lip…what differentiates the two?

A

PNP involves vermilion lip; CP does NOT.

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34
Q

Gluten is found in…

It is NOT found in…

A

Found in: wheat, rye, barley

NOT: rice, oats, corn

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35
Q

What are Anti-Ro (SSA) and Anti-La (SSB) associated with in Lupus? In Sjogren’s?

A

Lupus: mild SLE, photosensitivity, SCLE, neonatal LE/congenital heart block

Sjogrens: increased risk of systemic disease and lymphoma

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36
Q

Which antibody is most specific for Sjogrens?

A

Anti-alpha-fodrin (actin binding protein) is 93% specific

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37
Q

What are the following antibodies associated with in dermatomyositis? What is their target antigen?

    • Anti-155 kDa Ab
    • Anti-Jo1
    • Anti-SRP
    • Anti-Mi2
    • Anti-Ku
    • Anti-CADM
A
    • Anti-155 kDa Ab (uncharacterized): Amyopathic DM, cancer-associated DM
    • Anti-Jo1 (Hidtidyl tRNA synthetase): Antisynthetase syndrome with Raynayd’s, mechanic hands, pulm fibrosis
    • Anti-SRP (signal recog protein): Cardiac disease, severe DM/PM, poor prognosis
    • Anti-Mi2 (nuclear helicase): good prognosis, classic skin findings
    • Anti-Ku (p70/80 protein): DM/PM overlap with SLE or scleroderma
    • Anti-CADM (?): skin ulcerations, poor prognosis, possible malignancy assoc
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38
Q

What % of SCLE patients have a positive ANA? Positive Anti-Ro (SSA)? What HLA types are associated with SCLE?

A

ANA 60-80%
Anti-Ro 60-90%
HLA types: HLA-B8 strongest, HLA-DR3, HLA-DRw52, HLA-DQ1

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39
Q

What are the diagnostic criteria for SLE?

A

Need 4 of 11: malar erythema, discoid LE, photosensitivity, oral ulcers, + ANA, Arthritis, Serositis, Hematologic disorder, Immunologic (sDNA, Sm), Neuro disorder, Nephropathy

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40
Q

What are the most common malignancies associated with dermatomyositis in men / women?

A

Men: Lung, GI cancer

Women: Ovarian, Breast

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41
Q

If a dermatomyositis patient has anti-MDA5 antibodies, what does this mean?

A

MDA5 = melanoma differentiation associated gene 5

Associated with cutaneous manifestations including ulcerations, interstitial lung disease, malignancy. Do more intense malignancy evaluation (CT c/a/p)

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42
Q

What are the features of Mixed Connective Tissue Disease? Characteristic, but not specific, antibody?

A

Must have – Raynaud’s, Dactylitis, Arthritis
Can Have – fever, sclerodermoid/poikiloderma of trunk, esophageal dysmotility, pulm HTN

Ab: Anti-U1RNP

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43
Q

What differentiates Brunsting and Baker types of Dermatomyositis?

A

Brunsting: slow, progressive with weakness and calcinosis; steroid responsive

Baker is evil: vasculitis of muscle/GI tract; rapid onset severe weakness; steroid resistant –> Death

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44
Q

Which antibody is most specific for Sjogren’s? Which other antibodies (2) are commonly found?

A

Anti-alpha-fodrin (antigen = actin binding protein) = 93% specific

Also see Anti-Ro, Anti-La

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45
Q

What malignancy are patients with Sjogren syndrome at risk for?

A

B-cell lymphomas, including MALT and non-Hodgkins

Increased risk of present with vasculitis.

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46
Q

Which cells are increased in nephrogenic systemic sclerosis?

A

CD34+ T-cells

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47
Q

Which conditions is relapsing polychondritis associated with (3)? HLA-association? Antibodies?

A

Myelodysplastic syndrome, Behcet’s disease, MAGIC (Mouth And Genital ulcers with Inflamed Cartilage)

HLA-DR4

Antibodies to type II collagen (same in MAGIC)

48
Q

Which medications can cause accelerated cutaneous nodulous in RA patients? Affected sites? Treatment?

A

MTX&raquo_space;> etanercept, infliximab, leflunomide

  • Rapid onset on hands/feet/ears and can also occur in lungs, heart, meninges
  • Treatment: Colchicine, D-penicillamine
49
Q

What is the differential diagnosis of panniculitis with neutrophils (7)?

A

pancreatic panniculitis, alpha-1-antitrypsin, Weber-Christian, infectious conditions, cold panniculitis (mixed), subcutaneous Sweets, early erythema nodosum (lymphs later)

50
Q

What differentiates Pemphigoid Gestations from PUPPP?

A

PG: involves umbilicus, starts 2nd trimester - immediate postpartum, + IF and NC16A ELISA, fetal risk of prematurity and SGA; treat with systemic steroids. Maternal risk of Graves! Typically recurs with subsequent press/OCPs/menstruation.

PUPPP: starts late 1st trimester of 1st pregnancy; does not recur. SPARES umbilicus. No fetal risk. Tx topical steroids and antihistamines; resolves 7-10 days after delivery.

51
Q

Which drugs are often culprit of drug-induced cutaneous small vessel vasculitis?

A

Common: NSAIDs, COX-2 inhibitors, leukotriene inhibitors, penicillins, quinolones, anti-TNF, G-CSF, hydralazine, propylthiouracil

Others: ACEIs, allopurinol, furosemide, quinine, macrolides, thiazides, sulfonylureas, TMP-SMX, vancomycin, IFN, beta-blockers, penicillamines, MTX, OCPs, cocaine with levamisole, retinoids, sirolimus, warfarin, SSRIs, contrast media

52
Q

Diagnostic criteria for Henoch-Schonlein Purpura

A

Palpable Purpura + 1 of the following:

    • Arthritis / Arthralgia
    • Diffuse abdominal pain
    • Predominant IgA deposition on biopsy
    • Renal involvement
53
Q

Three phases of Churg-Strauss (Eosinophilia with granulomatosis and polyangiitis)? Lab abnormalities?

A

Labs: elevated IgE and eos; p-ANCA positive (anti-myeloperoxidase)

1st Phase: allergic rhinitis, nasal polyps, asthma

2nd: peripheral eosinohpilia, resp infections, GI symptoms
3rd: systemic necrotizing vasculitis with granulomas

54
Q

Common presenting signs of Granulomatosis with Polyangiitis (Wegeners)? Expected Lab?

A

Skin: strawberry gingiva, oral ulcers, painful nodules/ulcers that mimic PG
Other: nose/sinus/ear complaints typical because upper and lower respiratory tracts involved

C-ANCA positive in 80%

55
Q

Which 5 factors predict increased risk of mortality in Polyarteritis Nodosa?

A

Creatinine > 1.58, Proteinuria > 1g/day, GI tract involvement (bleeding/perforation/infarction/pancreatitis), CNS involvement, Cardiac involvement

*Whether HBV alters mortality is up for debate (KW and Jean Bologna are debating…). Orchitis is more common if HBV+.

56
Q

Name the lupus anticoagulants (3)

A

Anti-beta2-glycoprotein
Lupus anticoagulant
Anti-cardiolipin

57
Q

What is Degos Disease?

A

Malignant Atrophic Papulosis

  • LETHAL small vessel angiopathy of skin, GI tract and CNS
    • crops of small erythematous papules –> porcelain white scars
    • Ischemic infarcts cause death (GI > CNS)
  • Patients often present with stroke, GI bleed or acute abdomen
58
Q

Diagnostic criteria for Behcet’s disease.

A

Oral ulcers 3x/12 months + at least 2 of the following:

    • recurrent genital ulcers
    • positive pathergy test
    • ocular (uveitis, retinal vasculitis)
    • skin findings (ulcerations that can be acneniform, papulopustular, EN-like, pseudofolliculitis)
59
Q

Diagnostic criteria for Sweets syndrome.

A

Abrupt onset of typical eruption with histopath findings + 2 of the following:

    • Preceded by associated infxn, vaccination, drug, malignancy, inflammatory condition, pregnancy
    • fever and constitutional symptoms
    • leukocytosis
    • excellent response to systemic corticosteroids
60
Q

Drugs associated with Sweet’s syndrome

A

G-CSF, ATRA, hydralazine, carbamazepine, levonorgestrel/ethinyl estradiol, TMP-SMX, minocycline

61
Q

Systemic diseases associated with pyoderma gangrenous

A

IBD (UC > Crohn’s), arthritis, hematologic disorders (IgA monoclonal gammopathy; multiple myeloma), HCV

62
Q

What are patients with Vogt-Koyanagi-Harads syndrome at risk for? Skin findings?

A

Blindness from bilateral granulomatous uveitis (systemic steroids can prevent).

Skin finding: vitiligo

Other finding: aseptic meningitis

63
Q

Thiamin (vitamin B1) Deficiency

    • Skin findings
    • Other findings
    • Function
    • Who gets it
A

Berberi

    • Skin: glossitis
    • peripheral neuropathy (dry Beriberi), congestive heart failure (wet Beriberi), Korsakoff’s syndrome, Wernicke’s encephalopathy
    • Function: coenzyme in carbohydrate metabolism
    • Who: polished rice diet, alcoholics, Gi disease, hyperthyroid, diarrhea, malnutrition
64
Q

Riboflavin (vitamin B2) Deficiency

    • Skin findings
    • Other findings
    • Function
    • Who gets it
A

Oral-Ocular-Genital Syndrome

    • Skin: angular cheilitis, magenta colored tongue, seb derm, genital dermatitis, photophobia
    • Conjunctivitis
    • Function: energy prod, fatty acid / amino acid synthesis
    • Who: Celiac disease, alcoholics, malnutrition
65
Q

Niacin (vitamin B3) Deficiency

    • Skin findings
    • Other findings
    • Function
    • Who gets it? Associated meds?
A

Pellagra (4Ds – dermatitis, diarrhea, dementia, death)

    • Skin: photosensitive eruption, Casal’s necklace, angular cheilitis, perianal dermatitis
    • Other: stomatitis, diarrhea, disorientation, coma
    • Function: red-ox reactions; tryptophan precursor amino acid
    • Who: corn diet, alcohol, isoniazid use, colitis, diarrhea, carcinoid syndrome; azathioprine and 5-FU can induce as well.
66
Q

Pyridoxine (vitamin B6) deficiency

    • Skin findings
    • Other findings
    • Function
    • Who gets it
A
    • Skin: seb derm, atrophic glossitis, angular cheilitis, conjunctivitis
    • Other: dementia, peripheral neuropaths
    • Function: amino acid and fatty acid synthesis
    • Who: cirrhosis, uremia, INH therapy, malnutrition
67
Q

Cobalamin (vitamin B12) deficiency

    • Skin findings
    • Other findings
    • Function
    • Who gets it
A
    • Skin: hyperpigmentation, glossitis, premature gray hair
    • Other: megaloblastic anemia, paresthesias, peripheral neuropaths, irritability
    • Function: DNA synthesis, neuro function
    • Who: GI absorption issues, vegetarians
68
Q

Folic Acid Deficiency

    • Skin findings
    • Other findings
    • Function
    • Who gets it
A
    • Skin: patchy diffuse hyperpigmentation, cheilitis, glossitis
    • Other: megaloblastic anemia (similar to B12 but without neuro findings)
    • Function: DNA synthesis
    • Who: elderly, MTX treatment, malnutrition
69
Q

Biotin Deficiency

    • Skin findings
    • Other findings
    • Function
    • Who gets it
A
    • Skin: similar to zinc def…periorificial eruption, conjunctivitis, alopecia; most common nutritional deficiency to be secondarily infected with CANDIDA
    • Other: depression, paresthesias, seizures
    • Function: essential cofactor for carboxylases
    • Who: acquired / inherited; ingesting raw egg whites, short gut and malabsorption
70
Q

Vitamin A Deficiency

    • Skin findings
    • Other findings
    • Function
    • Who gets it
A

Phrynoderma

    • Skin: keratotic follicular papules (KP-like), xerosis, keratomalacia
    • Other: night blindness, Bitot’s spots (white spots on conjunctiva), bone changes
    • Function: normal keratinization of epithelial structures
    • Lab: check serum retinol to evaluate
71
Q

Vitamin C Deficiency

    • Skin findings
    • Other findings
    • Function
    • Who gets it
A

Scurvy

    • Skin: follicular hyperkeratosis, corkscrew hairs, perifollicular hemorrhage, petechiae, epistaxis, gingivitis, slow wound healing,
    • Other: IM and intraarticular hemorrhage –> pseudo paralysis due to pain
    • Function: collagen/ground substance formation
    • Who: alcoholics, fad diets, malnutrition
72
Q

Vitamin D Deficiency

    • Skin findings
    • Other findings
    • Function
    • Who gets it
A
    • Skin: alopecia
    • Others: rickets in kids, osteomalacia in adults
    • Function: regulates calcium-phosphate metabolism
73
Q

Vitamin K Deficiency

    • Skin findings
    • Other findings
    • Function
    • Who gets it
A
    • Skin: purpura, ecchymosis, hemorrhage
    • Other: prolonged PT
    • Function: synthesizes coagulation factors II, VII, IX, X and protein C and S
74
Q

Describe Vitamin D metabolism and skin’s role

A

dehydrocholesterol absorbs UVB –> vitamin D3 (cholecalciferol) –> hydroxylated by liver to 25-OH-D3 –> hydroxylated by kidney to 1,25-OH2-D3 (calcitriol, the active form)

75
Q

What is Bazex Sign? What does it signify?

A

Acrokeratosis neoplastica

    • psoriasiform plaques on palms, soles, nose, helices; NAILS INVOLVED! Can look eczematous
    • Upper aerodigestive tract SCC
76
Q

Carcinoid Syndrome

    • Skin findings
    • Lab findings
    • Where is tumor?
    • Medical Tx
A
    • Skin: head/neck flushing, pellagra-like dermatitis (photosensitive, Casal’s necklace, perianal dermatitis, etc), erythema, hyperhidrosis
    • Labs: elevated 5-HIAA in urine (serotonin metabolite)
    • Mid-gut tumors with liver and LN mets; #1 site is appendix but Ileum is most common location to cause Carcinoid syndrome
    • Tx: somatostatin, methylsergide, cyproheptadine, beta-blockers
77
Q

Excess growth of lanugo hair is associated with which tumors?

A

Hypertrichosis lanuginosa acquisita

– Lung, Colon, Breast

78
Q

Thick, velvety palms are associated with…

A

Tripe Palms

– lung cancer (if only palms); gastric cancer if palms + acanthosis nigricans

79
Q

What is AESOP?

A

“Adenopathy and Extensive Skin patch Overlying Plasmacytoma”

– enlarging violaceous patch with local andenopathy, usually around osseous structures on thorax

80
Q

What can hyperkeratotic follicular papillose on the nose be a sign of?

A

Multiple myeloma

81
Q

What is POEMS?

    • Skin findings?
    • Cancers (3)?
A

“Polyneuropathy, Organomegaly, Endocrinopathies, M-protein, Skin changes”

    • Skin: glomeruloid hemangioma (pathognomonic but rarely seen), other angiomas, hyper pigmentation, hypertrichosifs, hyperhidrosis, sclerodermatous changes, digital clubbing
    • Cancers: osteosclerotic myeloma, Castleman’s, plasmacytoma
82
Q

What is the chromophore for most of UVB’s effects?

A

DNA

83
Q

What is the UVB signature mutation? Most common DNA photoproducts (in order)?

A

Cytosine –> Thymine

TT > CT > TC and CC = cyclobutane-pyrimidine dimers

84
Q

Cytokine expression induced by UVR?

A

Increased IL-1, IL6, IL-10, TNF-alpha

85
Q

Role of UVA in…

    • sunburn
    • skin penetration
    • darkening
    • drug-induced photosensitivity
    • carcinogenesis
    • Vit D3 production
    • Glass penetration
A
    • Sunburn: minor role; causes immediate erythema and delayed erythema 6-24 hours later
    • Penetrates to deep dermis
    • Darkening: immediate pigment darkening due to melanin oxidation
    • Major contributor to drug-induced photosensitivity
    • Carcinogenesis: minor role; causes ROS production
    • NO role in vitamin D production
    • Penetrates window glass
  • causes phytophotodermatitis
  • causes photoaging
86
Q

Role of UVB in…

    • sunburn
    • skin penetration
    • darkening
    • drug-induced photosensitivity
    • carcinogenesis
    • Vit D3 production
    • Glass penetration
A
    • Sunburn: Major role 6-24 h later; UVB 1000X more erythemogenic than UVA and causes apoptotic “sunburn” cells
    • Penetrates epidermis only
    • Darkening: delayed melanogenesis 48-72h later due to increasing melanocyte # and size of melanosomes, increase transfer of melanin
    • Minor role in drug-induced photosensitivity
    • Major role in carcinogenesis!
    • Major role in vitamin D metabolism
    • NO glass penetration
87
Q

Common site for Juvenile Spring Eruption?

A

Helices

*PMLE variant in boys

88
Q

What are findings of photo testing in PMLE?

A

React to UVA > UVB

MEDB and MEDA are normal!

89
Q

What differentiates Actinic Prurigo from Juvenile Spring Eruption?
– Treatment

A
  • Cheilitis and Conjunctivitis seen in Actinic Prurigo; typically Native Americans; lips can have lymphoid nodules
  • Thalidomide is only effective systemic agent
90
Q

Which drugs can cause photo recall reaction?

A

MTX, doxorubicin, daunorubicin, idarubicin, 5-FU, etoposide, taxanes, hydroxyurea

91
Q

Phototesting findings for Chronic Actinic Dermatitis? Typical patient?

A

Most sensitive to UVB > UVA > visible light

*Older men of darker skin types

92
Q

UVA blockers (4)?

A

Avobenzones
Benzophenones (oxybenzone)
Ecamsule (Mexoryl SX)
Meradimate

93
Q

UVB Blockers (7)?

A 
PABA
Padimate O
Cinnamates
Salicylates
Octocrylene
Ensulizole
Mexoryl XL (drometrizole trisiloxane)
94
Q

UVA and UVB Blockers (4)?

A

Titanium dioxide
Zinc oxide
Mexoryl XL
Oxybenzone

95
Q

What does SPF mean?

A

MED with sunscreen / MED without sunscreen

Amt UVB absorbed by skin with SPF 50 on…
UVB = 100 - (1/SPF)

96
Q

Fitzpatrick Skin Types

A 
I = always burns, never tans
II = usually burns, rarely tans
III = rarely burns, usually tans
IV-VI = never burns, always tans
97
Q

To be diagnosed with PCOS a patient must have 2 of the following 3 criteria…

A
  1. Amenorrhea or oligomenorrhea ( 3 in most patients
  2. Ultrasound findings consistent with PCOS
    - - Antral follicle count > 12, ovarian volume > 10 ml
98
Q

Endocrine labs to check if concerned for PCOS and expected results

A
  • Testostorone (free and total): > 200 ovarian tumor; > 150 hyperandrogenism
  • DHEA-S: subset of patients have normal testosterone but elevated DHEA-S (thinner patients typically)
  • 17-OH-progesterone > 200 in PCOS
  • Androstenedione
  • LH:FSH > 3:1 is suggestive of PCOS
  • Prolactin
  • TSH - rule out thyroid disease as cause of menstrual irregularities
99
Q

Clinical phenotype of someone with anti-155 (TIF1-gamma) antibodies.

A

Dermatomyositis with cutaneous ulcerations, oral pain/ulcerations, hand/foot swelling and rapidly progressive ILD

100
Q

Clinical phenotype of someone with antisynthetase antibodies.

Name an anti-synthetase antibody?

A

anti-Jo

raynaud’s, mechanic’s hands, pulmonary fibrosis (ILD), arthritis, myositis

101
Q

Clinical phenotype of someone with antiMi-2 antibodies?

A

Classic skin findings: gottron’s papules, shawl sign & good prognosis

102
Q

What antibodies is associated with cardiac involvement of dermatomyositits?

A

Anti-SRP

103
Q

What are dermatoscopic features of melanoma (8)?

A 
Blue-white veil
Pseudopods
Radial streaming
Scar-like depigmentation
Peripheral black dots/globules
Broad network
Negative network
Irregular vascularity
104
Q

What is Darrier-Roussy Disease?

A

Sarcoidal panniculitis – no epidermal involvement. Presents with painless subcutaneous mobile nodules.

Differentiated from Lofgren’s syndrome, which is acute sarcoidosis w/ erythema nudism, hilar adenopathy, iritis, polyarthritis and fever

105
Q

What is Heerfordt’s syndrome?

A

Uveoparotid fever – form of sarcoid with fever, parotid gland enlargement, anterior uveitis, facial nerve palsy

106
Q

What wavelengths are UVA1, UVA2, UVB, UVC?

A

UVA1: 340-400 nm
UVA2: 320-340 nm
UVB: 290-320 nm
UVC: 200-290 nm

107
Q

UVB induced sunburn reaches peak when? What is chromophore?

A

6-24 hours after exposure. Note that UVB does not cause immediate erythema. DNA is chromophore. UVB is major cause of sunburn!

108
Q

Does UVA cause immediate / delayed erythema?

A

Both – immediate erythema can occur; delayed erythema can occur 6-24 hours after exposure. Note that doses of UVA in natural sunlight are not sufficient to induce a sunburn.

109
Q

Immediate pigment darkening is caused by? Delayed tanning is caused by?

A

Immediate pigment darkening: UVA-induced, oxidation and redistribution of existing melanin.
Delayed pigment darkening: UVB-induced, peaks 3 days after sun exposure – increased number of melanocytes, increased melanin synthesis, increased arborization of melanocytes, increased melanosome transfer to keratinocytes

110
Q

How does UVB make vitamin D?

A

UVB converts epidermal 7-dehydrocholesterol –> previtamin D3 –> isomerization to vitamin D3 (cholecalciferol) –> converted to 25-hydroxyvitamin D in liver –> 1,25 dihydroxyvitamin D in kidneys

111
Q

What are the 3 key features of actinic prurigo? HLA association? tested treatment?

A

3Cs: crusting, cheilitis, conjunctivitis
HLA-DR4
Treatment: thalidomide

112
Q

Patients with chronic actinic dermatitis may have positive patch test results to…(3)

A

Compositae, musk ambrette, sunscreen

Also have positive photo patch test results (atopic dermatitis would not)

113
Q

What is the action spectrum of solar urticaria?

A

Most often visible light but can also be UVA, UVB or a combination. This is why sunscreen is often not helpful – it does not block UVA or visible light.

114
Q

What is the most common cause of photo allergic reaction in the United States?

A

Sunscreen, specifically Benzophenone

115
Q

What conditions are associated with erythema nodosum (10)?

A

“SHOUT BCG”

  • Strep / Sarcoid / Sulfa
  • Histoplasmosis
  • OCP
  • Ulcerative colitis
  • TB
  • Behcet’s
  • Crohns (more often than UC)
  • Gastroenteritis
116
Q

Which medications are associated with pseudoporphyria (many)?

A

NSAIDS (naproxen classically but nearly all reported), diuretics (furosemide, HCTZ, torsemide, butamide, others), retinoids (isotretinoin, etretinate), UV light (sun, phototherapy, tanning bed), antibiotics (tetracyclines, cipro, others), random meds (dapsone, cyclosporine, B6, IV 5-FU, OCPs, coca-cola, voriconazole, imatinib)

Dermatology (11 decks)

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