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MSK II Exam 1 > 2-15 Dermatoses > Flashcards

2-15 Dermatoses Flashcards

1
Q

What are the major types of dermatoses?

A

Acute inflammatory - urticaria/hives, eczema, and erythema mulitforme

Chronic inflammatory - seborrheaic dermatitis, psoriasis, lichen simplex chronicus, lichen planus, discoid lupus erythematosus, rosacea

Blistering (bullous) disease - pemphigus, bullous pemphigoid, dermatitis herpetiformis

Panniculitis - erythema nodosum & induratum

Infections - viral (verrucae and molluscum), bacterial (acne and impetigo), superficial fungal infections (tinea)

Infestations/parasites: ticks, chiggers, lice, mites

Non-inflammatory - ichthyosis, epidermolysis bullosa, prophyrias

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2
Q

What are the 3 types of acute urticaria?

A

1.Mast cell and IgE dependent

–Acute allergic reaction (minutes) – medical emergency

–Most common onset between ages 20 and 40

–Severe discomfort; profound itching

2.Mast cell dependent but IgE independent

–Drug (#1) or other substance triggers mast cells directly (opiates, contrast media)

3.Mast cell and IgE independent

–Aspirin induced vasodilation

–Hereditary angioneurotic edema (C1-inhibitor deficiency)

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3
Q

What are the complications of acute urticaria? Why so dangerous? What is the tx?

A

All types can cause fatalities

–Systemic anaphylaxis

–Laryngeal edema

–Rx- antihistamines, subcutaneous epinephrine and IM corticosteroids

(With known C1 inhibitor deficiency use C1 inhibitor (C1-INH) concentrates, kallikrein inhibitor or fresh-frozen plasma)

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4
Q

What is the inciting agent for acute urticaria? What does it look like, and how long does it persist?

A

•Inciting agent may be known but frequently inciting agent is not known

–Bee/wasp stings

–Allergic reaction drugs (penicillin, ASA, etc.)

•Abrupt appearance of intensely pruritic wheals +/- bullae

–Wheal: Transient edematous erythematous plaque secondary to an acute allergic reaction

–Bullae: Larger fluid-filled lesions

  • Commonly involves trunk and extremities
  • Usually resolves 24 hrs.
  • May persist days, even months
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5
Q

What is spongiotic dermatitis?

A

Eczema

  • Dermatitis with intercellular epidermal edema and prominent lymphocytes in dermis and epidermis
  • Usually driven by T cell mediated type IV hypersensitivity inflammation
  • Includes numerous pathologic and clinical conditions
  • Usually an acute onset of red, papulovesicular lesions (“boiling over” appearance) which may ooze or crust
  • Acute lesions may evolve into raised, scaling plaques
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6
Q

What is erythema multiforme? What are some causes?

A

•Hypersensitivity (CD8+ cytotoxic T cells) reaction to drugs, infections, malignancy, collagen vascular disorders

–Infections: herpes simplex, deep fungal (histoplasmosis), Salmonella typhi, leprosy

–Drugs: antibiotics, salicylates, anti-malarials

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7
Q

Why is erythema multiforme named ‘multiforme’?

A

•“Multiforme” = wide variety of clinical appearances in addition to characteristic “target” lesions (red-pale-red)

(–Other skin disorders have targetoid lesions but not the classic red-pale-red pattern)

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8
Q

What are some pathological similar conditions to erythema multiforme?

A

•Pathophysiologically similar conditions

–Stevens-Johnson syndrome: Severe, systemic disease with atypical targetoid skin lesions that become bullous +/- oral and ocular involvement

–Toxic epidermal necrolysis: has diffuse necrosis and sloughing of skin and mucosae

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9
Q

What does erythema multiforme look like on gross and histo? How is it different from hives?

A

gross: central blister or necrosis, surrounded my variable redness
histo: necrotic keratinocytes and basal layer liquifaction that can lead to blisters

Urticaria has an opposite pattern - central clearing from edema, not central redness.

Also, hives tend to be evenly red, not the target lesion of erythema multiforme

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10
Q

What is psoriasis, how common is it, and what does it look like?

A
  • Affects 1-2% of the US population
  • Systemic disease causing a chronic skin condition

–Typical lesion: well-demarcated, pink- to salmon plaque

–Involves elbows, knees, scalp, lumbosacral area, intergluteal cleft, and glans penis

–Koebner phenomenon – trauma can induce skin lesions

–Auspitz sign – scrape off scale and get punctate hemorrhages (YouTube link)

–May involve nails

–Also have psoriatic arthritis and can involve other organs

•HLA-Cw*0602 association – increased CD4+TH1 sensitized cells set off other T-cells causing increased cytokines leading to epidermal proliferation.

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11
Q

What are some buzzwords associated with psoriasis?

A

silvery-gray scaly pink plaques, Koebner phenomenom, Auspitz sign, munro microabscess

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12
Q

What is lichen simplex chronicus?

A

A callus, basically

  • From chronic rubbing or scratching
  • If nodular = Prurigo nodularis

(Chronic trauma – psoriaform hyperplasia – hyperkeratotic reaction)

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13
Q

How common is seborrheic dermatitis? How does it present? Does it represent an intrinsic abnormality?

A
  • Common chronic dermatitis (5% of population)
  • Involves skin regions with high density of sebaceous glands (oil or sebum production)

–Scalp, forehead, especially glabella (space between eyebrows), nasolabial folds, auditory canals, intergluteal fold

  • Excessive dandruff on scalp common
  • Infection with superficial yeast (Malassezia furfur) may play important role since condition is improved by use of topical antifungal agents
  • Not an intrinsic sebaceous gland abnormality
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14
Q

What is lichen planus? How does it present?

A
  • Self-limiting chronic inflammatory condition of skin and oral mucous membranes
  • Multiple plaques that are symmetrically distributed, often on wrists and elbows and on the glans penis, + Koebner phenomenon
  • Usually resolves 1-2 years after onset, but may persist for years in oral cavity
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15
Q

What are some buzzwords to associate with lichen planus?

A

Koebner phenomenom - induced by trauma

Wickham striae - areas of hyperpigmentation and hyperkeratosis in the mouth

Sawtoothing and lichenoid infiltrate - band along dermal, epidermal jxn

Civatte/colloid bodies

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16
Q

What is the relationship between CLE and SLE?

A

•Localized cutaneous manifestations like those of systemic lupus erythematosus (SLE) but with no SLE systemic manifestations

–Patients who present only with symptoms and signs of CLE usually do not subsequently develop systemic symptoms and signs (SLE)

–However, 1/3 of all SLE patients will have cutaneous findings identical to those found in discoid lupus erythematosus or more severe skin lesions

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17
Q

What are the major cutaneous findings for CLE? What are the subtypes?

A

•Major Cutaneous Findings: Excessive sun exposure may trigger cutaneous lesions or exacerbate them

–Malar erythema (also a characteristic of SLE)

Chronic subtypes:

  • Discoid - coin-like scaling plaques
  • Tumid – juicy red papules and plaques
  • Lupus panniculitis/profundus – painful subcutaneous nodules
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18
Q

What can chronic plaques associated with CLE cause? What are the histo findings?

A

Chronic plaques show thinned glistening (atrophic) epidermis & areas with dilated, tortuous dermal vessels

Note the central hypopigmentation surrounded by peripheral hyperpigmentation

Histo: Infiltrate of lymphocytes within the superficial and deep dermis, marked thinning of the epidermis with loss of normal rete ridges, and hyperkeratosis

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19
Q

What is a band test?

A

Granular deposits of antigen-antibody complexes and complement at dermoepidermal junction constitute a positive “band test”, dx for lupus erythematosus

Test for presence of anti-ANA Ab IgG or C1q activation, should show granular pattern at basement membrane jxn if positive

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20
Q

How common is rosacea? What are the stages?

A
  • Fairly common in 30-60 y/o females
  • Stages

–Pre-rosacea (flushing)

–Erythematotelengiectatic

–Papulopustular

–Phymatous

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21
Q

What is the pathophys behind rosacea?

A

•Pathophysiology uncertain

–Numerous triggers

–Abnormal cathelicidin may lead to inflammation

•Perifollicular inflammation with changes similar to acne vulgaris microscopically

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22
Q

What are the bullous diseases that affect the skin?

A

•Common friction blister

–Intraepidermal blister usually just beneath the stratum granulosum with scant or no inflammation in papillary dermis.

•Immune-mediated

–Pemphigus group of diseases

–Bullous pemphigoid

–Dermatitis herpetiformis

•Genetic-congenital

–Epidermolysis bullosa- inherited defects in collagen, laminin, etc leading to several disorders with weak skin and blistering

–Porphyrias

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23
Q

Describe the location of different bullae in blistering diseases.

A

detachment at:

superficial desmosomes = subcorneal blister

deeper desmosomes = suprabasal blister

hemidesmosomes = subepidermal blister

24
Q

Where are adhesion molecules attacked in immune-mediated bullous diseases?

A

Attack at:

superficial desmosomes, desmoglein 1 = pemphigus foliaceus (subcorneal blister)

deeper desmosomes, desmogleins 1 & 3 = pemphigus vulgaris (suprabasal blister)

hemidesmosomes, BPAG1 & BGA2 = bullous pemphigoid (subepidermal blister)

hemidesmosomes, reticulin in anchoring fibers = dermatitis herpetifomes (subepidermal blisters)

25
Q

What is the primary pathophys behind the pemphigus group of disease?

A

•Autoimmune skin diseases: IgG autoantibody to desmosomes (spinous processes) of squamous epithelial cells

26
Q

What are the 5 clinical and pathological types of the pemphigus group of diseases?

A

–Pemphigus vulgaris (80%): Involves mucosa and scalp, face, axilla, groin and other pressure points; classic bullous disease

–Pemphigus foliaceus: more benign course; involves face, scalp, chest and back and spares mucous membranes

–Epidemic form occurs in South America (fogo salvagem)

–Pemphigus erythematosus: mild localized form of foliaceus which involves primarily malar area of face

–Pemphigus vegetans (rare): verrucous plaques instead of blisters involving axilla, groin, and flexural surfaces

–Paraneoplastic pemphigus – with malignancies (lymphoma)

27
Q

What is the target and course of pemphigus foliaceus?

A

Dsg1 in superficial desmosomes

More benign course, involves face, scalp, chest and back and spares mucous membranes

28
Q

What is the pathophysiology, appearance and location of bullous pemphigoid?

A

Bullous Pemphigoid
BPAG1 & BPAG2 in hemidesmosomes

•Autoantibody to hemidesmosomes

  • Primarily older individuals
  • Occurs on inner aspect of thighs, flexor surfaces of arms and axilla (areas more prone to rubbing
  • Bullae with clear or hemorrhagic fluid
  • Bullae smaller (<2cm) than in pemphigus

•Subepidermal blister more resistant to rupture than pemphigus

•Less involvement of mucosa than in pemphigus vulgaris

29
Q

What are the demographics, targets, associations and appearance of dermatitis herpetiformis?

A

Dermatitis Herpetiformis
IgA to gliadin attacks reticulin in dermal papillae fibrils

•Rare skin bullous disorder

–M>F

–Onset in 3rd and 4th decades

•Major association with celiac disease (non-tropical sprue, gluten-sensitive enteropathy)

–Anti-gliadin antibodies cross-react with reticulin in the anchoring fibrils in dermal papillae

•Intensely pruritic plaques and vesicles

–Extensor surfaces, elbows, knees, upper back and buttocks

30
Q

What is panniculitis? What are the types?

A

•Inflammation of the subcutaneous fatty tissue

–Septal

–Lobular

31
Q

What is erythema nodosum, and what is it associated with?

A

•Erythema nodosum

–Acute septal panniculilits associated with infections (e.g. Beta-strep, TB), sarcoidosis, inflammatory bowel disease, malignancies and drugs (e.g. sulfonamides, oral contraceptives)

32
Q

What is erythema induratum, and what is it associated with?

A

•Erythema induratum

–Uncommon lobular panniculitis and of unknown etiology (vasculitis?)

33
Q

What is Weber-Christian disease?

A

•Weber-Christian disease

–Idiopathic relapsing febrile nodular lobular panniculitis in children and adults

34
Q

What is factitial panniculitis?

A

•Factitial panniculitis

–Self induced lobular panniculitis traumatic injury (injections)

35
Q

What is the association between lupus and panniculitis?

A

•Lupus may have a lobular panniculitis (cutaneous lupus profundus/panniculitis)

36
Q

What are the demographics, cause, and appearance of verruca vulgaris?

A

•Common in children and adolescents

–Generally self-limited (6 months - 3 years)

–Distinct, gray-white to tan 0.1 to 1.0 cm papules or plaques in skin

–Due to human papillomavirus (HPV)

–Most commonly HPV subtypes 2 & 4 in cutaneous warts

–Firm consistency, “cobble-stone” (roughed surface), firm to palpation

37
Q

How are the characteristics of verruca vulgaris determined?

A

•Characteristics determined by skin location

–Verrucae plantaris (sole of foot) and palmaris (palm of hand) tend to be elongated, broad and flat and larger 1-2 cm plaques

–Condyloma acuminatum of the anogenital region are 1 to 4 cm cauliflower-like growths and mainly contain HPV subtypes 6 & 11

38
Q

What is molluscum contagiosum?

A
  • Common self-limited viral disease caused by poxvirus
  • Spread by direct contact
  • Primarily seen in young children and adults
  • 0.2 -0.4 cm nodules on face, trunk and anogenital area
39
Q

What is acne vulgaris? How is it treated?

A
  • Life-long disease most despised during teenage years (zits)
  • Chronic smoldering infection of the hair follicle by lipase producing Propionibacterium acnes
  • Rx

–Retin-A - alters the chemical composition of the sebum of hair follicle so that P. acnes cannot thrive on sebum as a nutrient source

–Antibiotics - P. acnes eradicated (e.g. minocycline, a tetracycline that is incorporated into hair shaft)

40
Q

What is impetigo? Where does it tend to occur?

A
  • Common superficial infection of skin
  • Highly contagious
  • Tends to occur predominately on hands and face
41
Q

What are the 2 forms of impetigo?

A

•Two forms

–Impetigo contagiosa (non bullous)

–Impetigo bullosa

(differ predominately in the size of the pustule)

42
Q

What are the agents responsible for impetigo? How is it treated?

A

•Currently Staphylococcus aureus #1 in both subtypes

–Bacterial toxins cleave desmoglein 1

  • Infection localized subjacent to stratum corneum
  • Honey-colored crust (highly infectious)
  • Historically beta-Streptococcus in contagiosa or Staphylococcus aureus in bullosa
  • Treat with anti-bacterial soap and topical antibiotic (occasionally along with systemic antibiotics)
43
Q

What causes superficial fungal skin infections? Where is the infection confined to?

A
  • Infections by dermatophytes (Microsporum sp., Epidermophyton sp., Trichophyton sp. and Malassezia sp.) present in soil & on animals
  • Infection confined to the stratum corneum of the epidermis

–Dermatophytes grow in the keratin of the cornified layer

–May have a mild inflammatory reaction to fungal products

44
Q

What are the predisposing conditions for skin infection?

A
  • High moisture content of immediate skin environment
  • Lack of exposure to sunlight
  • Increased temperature of skin region

–enclosed space such as shoes or groin

•Use of communal shower or bathing facilities (athlete’s foot)

45
Q

What is tinea? What is it caused by?

A

Tinea = superficial fungal infections

  • Tinea versicolor: Yeast infection by Malassezia sp.
  • Other tinea are by fungi producing yeast and hyphae and are named by location
46
Q

Name as many tinea infections as you can!

A

–Tinea capitis: scalp in children

–Tinea corporis (ringworm): trunk and extremities in all ages but more in children

–Tinea cruris: inguinal skin adjacent to genitalia

–Tinea pedis (athlete’s foot): feet between toes

–Tinea barbae: beard area in men

–Onychomycosis: fungal infection of nail beds

47
Q

What are arthropods and insects?

A
  • Arthropods: invertebrate animals of the phylum Arthropoda (e.g. insects, spiders, crustaceans)
  • Insects: arthropods with three-part body, three pairs of jointed legs, compound eyes and one pair of antennae (e.g. bedbugs, wasps, bees, flies and mosquitoes)
48
Q

How do arthropods or insects cause pathology?

A

Injury to skin and/or other organ systems

1.Direct injury by insect part/secretions

–Mosquitoes, chiggers, et.

2.Acute or delayed hypersensitivity reaction

–Bee/wasp stings, etc.

3.Direct toxin effect

–Brown recluse spider, etc.

4.Vector for other disease transmission

–Mosquitoes: malaria, West Nile virus, dengue, etc.

–Ticks: Lyme disease, Rocky Mountain spotted fever, etc.

49
Q

What diseases are caused by chiggers/mites?

A

Demodex folliculitis, trombiculosis, scabies

50
Q

What diseases are caused by lice?

A

pediculosis capitus, pubis or corporis

(FYI, pediculosis corporis is a vector for typhus)

51
Q

What are some non-inflammatory dermatoses?

A

Ichthyosis vulgaris:

hyperkeratosis with “fish-scaling”, usually genetic abnormalities

Epidermolysis Bullosa:

genetic abnormalities in structural proteins leading to massive bullae

Porphyrias:

usually autosomal dominant defects in heme synthesis leading to urticaria and subepidermal vesicles

52
Q

What is epidermolysis bullosa? What are the types?

A

Epidermolysis bullosa: genetic abnormalities in structural proteins leading to massive bullae

I.Simplex type: keratin 14 or 5 mutation

Intraepidermal (suprabasilar) blisters

II.Junctional type: defect at lamina lucida (laminin or BPAG2 defects)

Intra-lamina lucida subepidermal blisters

III.Dystrophic types: anchoring fibril defect (type VII collagen, etc.)

Sub-lamina densa blisters

IV.Mixed types: defects in multiple regions

Variable lesions depending on defects

53
Q

What are the complications from epidermolysis bullosa?

A

Patients have numerous complications from rupture of blisters (infections, disfigurement, adhesion of adjacent skin areas, etc.) and growth inhibiton from increased energy needs to combat complications of disease

54
Q

What is porphyria? What are some of the symtpoms?

A

I.Usually autosomal dominant defects (congenital erythropoetic is recessive) in heme synthesis leading to increased intermediates somehow causing urticaria and non-inflammatory subepidermal vesicles (especially with sun exposure skin leading to light absorption by porphyrin ring)

  • PBG (porphobilinogen) in urine may become red or dark or with light exposure

(acute intermittent porphyria, variegate porphyria and hereditary coproporphyria)

55
Q

What are the types of porphyrias?

A

I.Acute neurovisceral with GI and neural symptoms

I.Acute intermittent (porphobilinogen deaminase)

II.Aminolevulinic acid dehydratase deficient (=Doss=plumboporphyria)

II.Acute neurovisceral with cutaneous problems

I.Variegate (protoporphyrogen oxidase)

II.Hereditary coproporphyria (coproporphyrinogen oxidase)

III.Non-acute (cutaneous with light induced lesions)

I.Congenital erythropoetic (uroporphyrinogen III synthase)

II.Erythropoetic (=erythrohepatic protoporphyria) (ferrochelatase)

III.X-linked protoporphyria (over-activity of amino-levulinic acid synthase )

IV.Cutanea tarda (uroporphyrogen III decarboxylase)

  • Associated with hypertrichosis

MSK II Exam 1 (4 decks)

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