Top to bottom:

corneum

lucidum

granulosum

spinosum

basale

Mutation in Collagen VII gene

- causes poor anchoring fibrils ->sub-epidermal skin blisters that scar

Plectin

BPAg1

BPAg2

α6β4

Laminin isoforms

BPAg2

α6β4

α3β1

Type IV collagen

HSPG

Entacin/Nidogen

Type VII collagen

Microfibrils

others

EB simplex w/ pyloric atresia / muscular dystrophy

mutation involves:

Plectin

BPAg 230

• Occurs in elderly
• IgG ab binds to BP 230 + Type 17 collagen
• Sub-epidermal blisters

Plectin

BPAg1 (aka BP 230)

BPAg 2 (aka BP 180 + type 17 collagen)

Alpha 6 beta 4 integrins

type 4 collagen, laminin, heparin sulfate proteoglycan, nidogen

(Vessel BMZ lacking BP antigens - type 17, bp230,  type 7 / anchoring fibrils)

IgG autoantibodies to desmoglein 3 (in desmosomes)

Intra-epidermal blister

IgG autoantibodies (develops in adult pts) to type VII collagen

Sub-epidermal blister

intra-epidermal autoimmune bullous disease

Desmoglein 3

In prickle cell layer - no desmosomes so cells cant adhere together

Desmoglein 1 mutation

Intra-epidermal autoimmune bullous dz

very superficial

CP (?)

conjunctival pemphigous - blisters in mouth and mucosa

can cause blindness

dermatitis herpetaformous

makes IgA antibodies & has deposits at dermal/epidermal jxn - itchy, small blisters

Human Beta defensins (HBD2)

Cathelecidins

--Produced by keratinocytes & phagocytes to directly kill

O2-dependent (respiratory burst): H202, hydroxyl radicals, singlet oxygen

O2-independent: myeloperoxidase, lysozyme

Express high affinitiy FCεRI IgE receptor --> Degranulation -> release of histamine & serotonin (preformed) + PGs, LT's, PAF

-> Causes enhanced vasc permeability, bronchoconstriction, inflammatory response

Recognize micmrobial & viral components

Bridge gap b/w innate & adaptive

Immature dendritic cells in epidermis

(derived from bone marrow)

• Have Birbeck granules (ID'd w EM or histochemical analysis)
• CD1a = useful marker for ID

• LC meets antigen in epiderms
• Travels to regional lymph node
• T cells recognize MHC I/II
• **UV radiation depletes LC's in epidermis

CD4/8 -- MHC II/I

Results in anergy / apoptic cell death

CD80/CD86 (B7-1/2) -- CD28

-> Clonal expansion, T cell differentiation

IFNγ

TNFβ

IL-2

(induces cell-mediated response)

(Psoriasis has Th1 profile)

IL-4, IL-5, IL-6, IL-10 -- favor antibody  

production (atopics, allergy)

• IL-4: B cells make IgE
• IL-5: eosiophils
• IL-10: inhibits Th1

Insert perforins into membrane

Activate Fas (death receptor) -> apoptosis

CD19, CD20, CD22

**CDR recognizes epitopes so does NOT require antigen presentation

Pentamer

Activates classic complement pathway

Most abundant

Activate classic complement pathway (IgG1, IgG3)

Autoimmune antibodies

Mucosal Ig

Activates Alternate complement pathway

Invovled w bullous autoimmune dz

B cell acts as APC to T cell (MHC-II)

Activated by CD40 (B) --CD40L (T)

--> Induces IgG response

-Specific pattern of skin inflammation with epidermal changes resulting from scratching & rubbing

-Pattern of tiny fluid collections in epidermis

- Freqently in Peds

- Itching, dry skin, erythema, edema, scaling, oozing, lichenification

10-20% prevalence in western countries

Genes+environment (family history, fillagrin mutations)

75% of cases start <6 months of age

60% clearance by 16, with relapses in adulthood

Begins with face (cheeks, chin) & scalp involved (~3-6 mos), then limb folds & hands

-spares perioral & perinasal areas)

- Red, scaly, crusted, weeping patches w/ Excoriations (usually bilateral)

Flexoral regions involved

Rubbing & scratching leads to lichenification (thickening of skin)

- hypopigmentation

Flexural lichenified eczema

Facial involvment = periorbital regions

Truck, shoulders, scalp - chronic remissions / excacerbations (with stress, anxiety)

- hands/wrists frequently involved

Ichthyosis vulgaris - dry, rectangular scales

 accentuated palm creases

(X-linked ichthyosis)

Dennie-Morgan folds (double crease below eyelids in children - nonspecific)

Hertoghe's sign (alopecic lateral eyebrow)

cataracts, keratoconus

• Th2 profile - activate eos, suppress macrophages, IgE isotype switching
• Decreased antimicrobial peptides

Must have 3+

- Pruritis

- Lichenification

- Chronic/relapsing course

- peronal/family history

1. Avoid triggers

2. Control dry skin

3. Treat inflammation

Treat itch with moisturizer & oral antihistamines

- Antibiotics if infected with staph aureus

Oral + Topical antibiotics

Bleached bath (reduces colonies on skin - addresses problem of reduced antimicrobial peptides)

Anxiety / stress

Climate

Irritants

Allergens

Food (eggs, peanuts, milk, fish, soy, wheat)

Infections

Glucocorticosteroids (Class 1 = most potent, class 6 = OTC)

systemic steroids

immunosuppressives (phototherapy)

Atrophy

Telangiectasia (dilated vessels)

Striae

Perioral dermatitis

Risk of cataracts

Cushing syndrome

HPA-axis suppression

1. Anti-inflammatory

2. Antiproliferative

3. Atrophogenic

Nummular ezcema

Asteototic Eczema / Eczema Craquele

Winter itch, dry skin -> fissures, inflammation, crusted dermatitis

Eczema herpeticum

HSV spread on atopic skin

Monomorphic crusted / eroded papules

Eczema vaccinatum

Vaccinia virus

Keratosis pilaris

monomorphic peri-folicular keratotic papules

Rx w keratolytics

Pityriasis Alba

post-inflammatory hypopigmentation

Often on face / upper extremities

Dishydrotic eczema

Molluscum contagiosum

Pox virus (okay in children, means HIV in adults)

Rx w liquid nitrogen, imiquimod, etc

Non-immunologic inflammatory response when normal epidermal barrier disrupted

no prior exposure

Direct toxic effect of irritant on skin

(accounts for 90% of contact dermatitis)

Skin previously sensitized

Type IV cell-mediated delayed hypersensitivity

TH1 profile

Diagnose w patch testing

TRUE test (thin-layer rapid use epicutaneous test)

aka 'patch test'

multiple surgeries in infancy (spina bifida)

Frequent latex (glove) exposure

Area of previous contact with jewelry

Well-demarcated

contact with keys, safety pin, pant buttons, glasses

Urushiol (Anacardiaceae family)

appears in linear fashion

inflammation of skin from contact of plants and then go to sun

celery, lime juice

Tosylamide formaldehyde resin allergen

common presentation

In nail polishes

most common cause of eyelid dermatitis

FLAT, circumscribed legion that differs in color from surrounding area

- any size / shape

ex: melanoma, treated psoriasis, solar purpura

Small (<.5 cm diam), solid, circumscribed, elevated lesion

Can be umbilicated, verruciform

eg: molluscum contagiosum, Verruca vulgaris

palpable, solid, circumscribed, elevated

>.5 cm in diameter

Ex: cyst, abscess, basal cell carcinuma

circumscribed, elevated lesion with a pocket of fluid

Vesicles = <.5 cm

Bulla = >.5 cm

intra-epidermal, sub-epidermal

papule with purulent exudate

Elevation that occupies a large surface area (compared to height above surface)

ex: psoriasis

rounded, flat-topped papule or plaque

epidermis not affected

ex: urticaria

Superficial epithelial loss (only epidermis)

heal without scarring

loss of epidermis + portion of dermis

heals with scarring

Crust = made by exudate that dries on skin surface

Scaling = abnormal shedding of stratum corneum in flakes (no exudate, infection, injury)

Psoriasis epidemiology

incidence, age, gender

2% of population

150,000 new cases/yr

Any age of onset

Same in men & women

multi-locus inheritance

Family hx exists in 30-50% of cases

Certain HLA genes involved (B13, B17)

plaques, silver scaling, with red background

often on knees and scalp

hyperkeratosis - hyperproliferation

parakeratosis (nucleated keratinocytes at surface)

shortened cell cycle length (30x as many cells produced per day)

Psoriasis - inflammatory response

Cell surface receptor expression

CD4 (dermis) + CD8 (epidermis) cells have CD45 RO+

Increased ICAM-1 expression in endothelial cells

Increased T cell receptors, CD-2, LFA-1 costimulatory molecules

IL-1 (from keratinocytes) & TNF-a (from dendritic & T cells)

- increases ICAM 1

IL-12 (dendritic cells)

- increases CD-2, LFA-1

Rx for psoriasis (withdrawn)

Attaches to and inhibits LFA-1 on T cells

blocks T cell activation/reactivaton and traficking to cutaneous sites

Rx for psoriasis

Attaches to CD-2 on T cell -- blocks T cell activation (caused trigger of NK response -- killed all CD45RO+)

Inflixamab, Adalimumab, Etanercept

Rx for psoriasis

Work by inhibiting TNF-alpha effects (which normally maintains plaques)

Rx for psoriasis

Blockade of IL-12, IL-23 (common p40 subunit)

--inhibits T cell activation

coarse, pigmented hair

scalp, beard, pubic, axillary areas

2nd most superficial region of hair shaft

erector pili muscle -> sebaceous gland

2nd deepest part of hair shaft

from erector pili --> top of bulb

Deepest part of shaft

Includes dermal papilla and hair matrix

A: sebaceous gland

B: erector pili muscle

C: hair bulb

Anagen - growing (3-5 yrs, 85-90% of hairs)

Catagen - involution (2-3 wks, 1-3% of hairs)

Telogen - resting (3-5 mos, 10-15% of hairs)

Depends on melanosomes in hair shaft --> transfer melanin to keratinocytes

dark hair = large, oval melanosomes

light hair = small melanosomes

graying of hair

(melanocytes produce less melanin with age)

Alopecia Areata

Etiology

Autoimmune dz against follicle

Localized -> diffuse areas of hair loss

regular, geometric nail pitting in 10%

Exclamation point hairs

Androgenetic alopecia

etiology

- Polygenic inheritence

- Terminal hairs transition to vellus hairs

- Due to increased Type II 5-alpha reductase activity & increased dihydro-testosterone

androgenetic alopecia

treatment

Topical (minoxidil - rogaine)

Finasteride - only works in men

hair transplant

Androgenic alopecia

Presentation in men vs women

Men: vertex or fronto-temporal regions of scalp

Women: X-mas tree pattern, spares frontal hairline

Diffuse shedding of hair (>100/day) in response to systemic insult to body (1-3 mos after event)

Dx: >4-6 telogen hairs out of 40

Generalized, diffuse loss of 90% scalp hair, in response to trigger

hair formed incorrectly and breaks at surface (due to chemo)

Impulse control disorder

characterized by irregular, bizarre pattern

Scalp biopsy shows RBCs & pigment cast

non-scarring

Due to secondary syphilis

Diffuse, 'moth-eaten' appearance

Dermatophyte infection

Presents with alopecia + erythema + scale

broken hairs = 'black dots'

A: Lateral nail fold

B: onychodermal band

C: nail plate

D: proximal nail fold

E: cuticle

F: Lunula (part of nail matrix)

Tender, deep, boggy, erythematous plaque with with papules, pustules and crust

- Deeper tinea capitis

.1mm/day

4-6 mos to replace fingernail

12-18 mos to replace toenail

• Pitting
• Oil spots - yellow/brown underneath nail- specific
• onycholysis
• Subungal thickening

Pterygium - nail fold attaches to nailbed

Anonychia: atrophy of nailbed -> loss of nail

thinning, fragility, rigidity

Geometric pitting

Trachonychia (rough nails in all 20)

Due to soft tissue inflammation

Usually because of cardiovascular or bronchopulmonary disorders (80%)

"Spoon nails"

Sign of iron deficiency anemia

(can be idiopathic / normal in children)

Blood / hemosiderin - doesn't blanch

most common cause: trauma

Can also be connective tissue dz

Yellow nail syndrome

associations

Pulmonary lymphedema

pleural effusions, pulmonary infections, chronic sinusitis

-Transverse furrow in nail plate from temporary arrest of growth

- usually due to systemic event or local trauma

Proximal 2/3rds of nail bed appears whiter

due to edema, resolves with blanching

Associated with cirrhosis

parined, transverse, narrow, white bands

hypoalbuminemia

single/multiple transverse white bands

arsenic poisoning, thallium poisoning, chemotherapy

Proximal half is white

hemodialysis / renal transplant

Whole nail plate - due to medications (chemo, 5-FU, AZT, etc)

Lunulae only - Argyria (excess silver exposure), Wilson's dz

Longitudinal band of black/brown color

tumor of nail matrix/melanoma

Hutchinson's sign - if proximal/lateral nail fold is also darkened

can be normal if on multiple nails in darker people

Epidermal Melanin Unit 

structure + function

Melanocyte in basal layer + ~30-35 keratinocytes reached by dendrites

Melanocytes transfer melanin to keratinocytes to protect

Junctional - only epidermis

         - not raised

Compound - includes migration to dermis

         - slightly raised + dark color

Intradermal - only in dermis

         - more raised + skin color

incidence increasing (overdiagnosis?)

mortality staying the same

1. Superficial Spreading - intermittantly sun damaged skin

2. Lentigo maligna - chronically sun damaged skin (long radial growth phase)

3. Nodular - all areas of skin, no radial growth phase

4. Acral lentiginous - dark skinned ppl, non-sun exposd skin

Assymetry

Border irregularity

Color variation / change

Diameter

Evolution (change)

Familial Melanoma Syndrome

Genetics & presentation

- CDKN2A gene

- Many (50-100) atypical nevi

- Increased risk of melanoma

Breslow's depth

- deeper mole into dermis = poorer prognosis (based on histology)

Surgical excision

(in situ = .5cm margins, up to 2 cm margins for >2mm Breslow)

Not very effective, last resort

- Chemotherapy

- IFN-alpha 2b, IL-2 (aim to ramp up immune system)

- Ipilimumab - activates cytotoxic T cells

- PLX4032 - targets BRAF mutation

UV radiation / Immunocompromised

Dysplastic / atypical Nevi

Personal & Fam hx of melanoma

Light skin

Older

Male

 UVB
    - shorter wavelength (290-320)
    - Causes erythema
    - Absorbed by epidermis
    - Direct DNA damage
UVA
    - Longer wavelength (320-400)
    - Does not cause sunburns
    - Penetrates all the way to SubQ fat
    - Causes photoaging (wrinkly, blotchy skin)
    - Indirect DNA damage

    - immediate pigment darkening

1. UV causes pyrimidine dimers (CPDs) & 6-4 photoproducts & ROS (ss breaks, DNA adducts - indirect)

2. Repair: Photolase enzymes, Nucleotide Excision Repair

       C->T mutations = bad repair, indicative of UV damage

3. P53 recognized CPDs & activates repair enzymes

UVB-DNA damage -> p53 activated -> stimulates MSH production -> stimulates MC1R (->tyrosinase activity) -> melanin concentrates above nuclei

side effect = endorphin production :)

Vitamin D

Circulating form?

Biologically active form?

UVB + precursor -> Cholecalciferol (25OH) - major circulating form

-> activated by kidney -> 1,25OH

Diet

Skin exposure to UVB

Supplements

Type I - tyrosinase negative

Type II - P gene/protein negative (can't transport tyrosinase)

Type III - TRP1 neg (further down enzyme pathway, more pigment)

Peutz-Jeghers Syndrome

Presentation

• GI polyps (begin age 10-40)
• Small intestine
• Abd pain, GI bleeding, anemia
• Periorificial lentiginosis (pigment spots
• Begin as child, worsen over lifetime
• skin, lips, buccal mucosa, digits, palms, soles
• Increased pancreatic, breast, ovarian ca 

Peutz-Jeghers Syndrome

Mechanism & Genetics

Autosomal Dominant

Defect in STK11/LKB1 tumor suppressor gene (threonine kinase)

Gardner Syndrome

Presentation

Multiple Epidermal Cysts

Osteomas

Supernumerary teeth

CHRPE (retinal pigment)

High colon cancer risk (prophylactic colectomy)

Xeroderma Pigmentosum

Genetics

Autosomal Recessive

Gene defect in XPA-G

Affects DNA excision repair, DNA helicase

Gardner Syndrome

Genetics

Autosomal Dominant

APC gene mutation (tumor suppressor gene)

Xeroderma Pigmentosum

Presentation

Infancy: Acute sun sensitivity

Toddler: mottling & freckling on face

Childhood: narrowing of nares & mouth

1000x increased skin ca risk (age 8=mean)

Also affects vision, neurology

Neurofibromatosis I

Genetics

Autosomal Dominant (50% somatic mutation)

NF1 gene (c17)

Neurofibromatosis

Presentation

Need 2 of these (including 1st degree relative)

- Cafe-au-lait macules (6+)

- Neurofibromas (buttonhole phenom) or  

  Plexiform NFs (Bag of worms)

- Crowe's Sign (axillary freckling)

- Lisch nodules (pigment of iris)

- Optic gliomas

- Bone changes (bowing)

Neurofibromatosis II 

Genetics

Autosomal Dominant

Schwannomin (merlin) gene - c22

Neurofibromatosis II

Presentation

Bilateral acoustic neuromas (hearing loss)

Neurofibromas (no freckling/cafe au lait)

Tuberous Sclerosis

Genetics

Autosomal Dominant (50% spontaneous)

TSC-1, TSC-2 gene

Tuberous Sclerosis

Presentation

Adenoma Sebaceum

  - yellow/red papules on cheek, nose, forehead

Mental deficiency

Epilepsy

Shagreen patch - connective tissue nevus, rough

Koenen's Tumors - periungal fibromas

Hypolemanotic granules (ash-leaf, confetti)

Marfan Syndrome

Genetics

Autosomal Dominant

Fibrillin mutation - component of sheath around elastin

Marfan Syndrome

Presentation

Striae distensae, Elastosis perforans serpiginosa (elastin thru skin)

Musculoskeletal

Cardiovascular

Ocular

Ehlers-Danlos Syndrome

Genetics

Group of many genetic disorders w/ similar phenotype

Mutation affecting collagen 

Ehlers-Danlos

Presentation

Excessive skin stretchin

Hyperextensible joints

Gorlin's sign (tongue to nose/elbow)

Atrophic scarring

Molluscoid pseudotumors

Fabry disease

Genetics

X-linked recessive

Heterozygous females have variable expression

Deficiency of α-galactosidase A gene --> buildup of glycosphingolipid

Fabry disease

Presentation

Angiokeratomas - hard red-black bumps b/w umbilicus - knees

hypo/anhidrosis (don't sweat)

Also - PNS, Cardio, Kidney (maltese crosses), CNS, eyes, ears

Dystrophic Epidermolysis Bullosa

Genetics

Autosomal dominant & recessive types

COL7A1 gene

Encodes for Type VII collagen in the BMZ --> mutation = subepidermal blisters

Dystrophic Epidermolysis Bullosa

Presentation

subepidermal blisters/erosions

fragile skin

mitten deformity

potential mucosal involvement

increase squamous cell ca risk

Melanocytes

Development

Toda Stages (4)

Development of melanosomes

I. Spherical, contains tyrosinase

II. Oval w/ filament periodicity

III. Like stage 2 but w more melanin

IV. Opaque with melanin (little tyrosinase)

Tyrosinase

Structure

Contains Cu

Rate limiting step of melanin production

UV light / heavy metals --> cause dissosiaction of SH group --> activation

Immediate vs Delayed Pigment Formation

Timing, etiology, melanocytes

Seconds vs days

I = melanosome migration to dendrites

D = increased melanosome production

D = increased # of melanocytes

Collagen

Skin pigment manifestations

Melanin

 skin pigment manifestations & diseases

- Increased in Addison's disease (ACTH similar to MSH -> melanin production)

--> darker skin (especiallys hands)

Drugs -> bind melanin @ blood vessels -> appear blue (melanin in dermis)

Argyria

skin pigment manifestations

Lipids / cholesterols

skin pigment manifestations

Appears yellow

In Xanthomas

Carotene

skin pigment manifestations

Carotenemia

Appears orange/yellow

Bilirubin

skin pigment manifestations

Appears yellow

Jaundice -- from liver disease

Keratin

skin pigment manifestations

Seborrheic keratosis (in x-mas tree shape on back)

Appears brown/black

Triglycerides (mostly)

Squalene

Cholesterol + Esters

Hormonal - Androgens (dihydroxytestosterone / 5-a-reductase)

larger glands in areas w finer hairs

1. Excess sebum

2. P. acnes - bacteria cleave tg's to FFAs -> inflammatory response

3. Genetics

4. Hyperkeratosis of pilosebaceous epithelial lining (improper differentiation - Acutane target)

5. Inappropriate cytokine release (affects androgens)

6. Androgen excess (as in PCOS)

Epidermal dysplasia - Precursor to SCC

sun exposed areas

feels like sandpaper

Skin colored projection on face

20-30% overly SCC or BCC

Rapid growing nodule with central crater of keratin

considered well-diff SCC (can metastasize)

Induced by sun exposure, trauma

Develops alongside AK's

Scaly, eczematous patch in areas of chronic sun exposure

Assoc w HPV, chronic scarring

Perineural involvement = greater recurrence, met rate

SCC in epiderims

erythematous, scaly & crusted, sharply demarcated

Most common skin cancer

Risk factors - prior sunburns, radiation, immunosuppression

Gorlin's Syndrome 

(BCNS)

2+ BCCs in people <20 yrs old

palmar/plantar pits, fused/splayed ribs

Unilateral, sharply marginated, erythematous, crusted plaque on nipple

nests = internal malignancy

Affects apocrine glands (vulva, scrotum, axillary)

sign of underlying malignancy

Red, violaceous nodule with shiny surface

Rare

Rapidly progressing

Poor prognosis

bulky, protuberant mass

17/22 translocation

slow progressing, low mets potential

CDKN2A

p53 point mutations

Pityriasis (tinea) versicolor

Fungus

Pityriasis versicolor

presentation

scaly, non-pruritic macules on trunk & limbs

hyper/hypopigmentation

(Wood lamp)

Tinea negra

fungus

Tinea negra

presentation

White piedra

fungus

White piedra

presentation

cream-colored nodules on hair shaft

(potentially STD)

dx w KOH prep

Black piedra

fungus

Black piedra 

presentation

black nodule on hair shaft

dx w KOH prep

Trichophyton - skin/hair/nails - microconidia

Microsporum - skin/hair - thick-walled

                    macroconidia

Epidermophyton - skin/nails - thin-walled

                     macroconidia

Cutaneous candida syndrome (trichophyton)

-vesicopustules rupture into maceration & fissuring - white rim of necrotic epidermis

1. adheres to skin

2. invades skin (keratinase)

3. Host-pathogen interactions

Impetigo

Cause & presentation

Superficial skin infection caused by strep pyogenes (group A)

vesicopustular lesion --> golden crust

Abscesses

bacteria

Usually Staph aureus

Can be others (esp drug users)

Cellulitis

Cause & presentation

S aureus, group A strep

acute, spreading infection of subQ tissues (deeper than erisipelas)

Necrotizing soft tissue infections

key signs

Edema extends beyond area of erythema

Skin vesicles / bullae

Subcutaneous gas

no lymphadenitis

Clostridial cellulitis

cause & presentation

Cause: c perfringes

thin, foul-smelling drainage w/ gas

Fever & scrotal edema/necrosis

anaerobic strep

Strep (NOT group A) or G- bacilli

deep layer of superficial fascia (spares deep fascia / muscle)

Group A strep

fever, erythema, rapid-onset, blisters, dishwater-like fluid

gangrene @ 4 days

causes necrotizing cellulitis

found in water & shellfish

high mortality rate

synergy b/w anaerobes & enterobacteriaceae

gas formation

necrosis of the muscles

gas gangrene

wound pain, swelling, systemic toxicity

mostly C. perfringes

S aureus

Dogs & cats - pasturella

Dogs - wide teeth, rip open skin

Cats - sharp teeth, puncture wounds

Higher complication rate than animals

cause cellulitis & necrosis

polymicrobial 

Porphyria cutanea tarda

associated disease

Porphyria cutanea tarda

Appearance

Fragile skin on hands & sun-exposed areas

Erosions from ruptured bullae

Hypertrichosis

Porphyria cutanea tarda

Etiology

Defect in uroporphyrinogen decarboxylase enzyme (inherited)

Elevated serum porphyrin 

cryoglobulinemia II & III

associated condition

cryoglobulinemia II & III

Lichen planus

associated disease

Lichen Planus

Presentation

Purple

Pruritic

planar

Polygonal

Papular

Erythema nodosum

associated condition

Erythema nodosum

presentation

Pyoderma gangrenosum

associated disease

Pyoderma gangrenosum

presentation

pustule with inflammatory base

undermined edge

Dermatitis herpetiformis

associated disease

Dermatitis herpetiformis

presentation

herpes-like rash on extensor surfaces

vesicles w/ erythematous base

Hyperpigmentation

associated disease

Hyperpigmentation

presentation

hyperpigmentation in hand creases, oral mucosa, sun-exposed areas

(also severe hypotension)

Diabetic dermopathy

presentation

hyperpigmented macules in extremeties

(extravasated RBCs -> hemosiderin)

mostly type 2

Sclerederma

associated disease

Sclerederma

presentation

Thickening of skin ~ orange peel that starts on face & moves down to neck/trunk

pebbling of knuckles

skin tightens so much can't put palms together

Necrobiosis lipoidica diabeticorum

associated disease

Necrobiosis lipoidica diabeticorum

presentation

well-demarcated, erythematous plaque, waxy, yellow in middle

then plaques turn brown (ulcered)

Calciphylaxis

associated disease

Calciphylaxis

presentation

nephrogenic systemic fibrosis

associated disease

nephrogenic systemic fibrosis

Dermatomyositis

associated disease

Dermatomyositis

presentation

Heliotrope (pink/purple 'eyeshadow' rash on eyelids)

Gottron's papules

Mechanic's hands

Photosensitivity

Nail-fold telangiectasia

muscle findings 2-3 mos after skin findings (bilateral)

can be underlying cancer

Carcinoid syndrome

associated disease

Carcinoid syndrome

rosacea

signifies appendix tumor

Pediculosis

etiology & diagnosis

head, body, pubic lice

ID adult lice / filled nits

Papular urticaria

presentation

allergic response to flea/bedbug bites

pruritic, urticarial papules sometimes w vesicle

scabies

presentation

pruritic, elevated, pink/white lesions on finger webbings, elbows, axilla, belt line, feet, scrotum

Burrows = pathognomonic

Mites

presentation

Non-painful bite -- erythema w/ central ischema & surrounding edema

ischemia --> necrosis, fever, arthralgia, vomiting, DIC, shock

black widow

(Latrodectus mactans)

Systemic symptoms, GI cramping, chest pain

presents as acute abdomen

Fleas 

diseases caused

Cimex lectularius

life cycle / presentation

Bed bugs

inject anticoagulant & anasthetic and feed at night --cause papular urticaria

have to wash all linens, clothes, etc

lymphatic filariasis, onchoceriasis, leishmaniasis, leprosy, buruli ulcer, Chagas' disease

Together affect >1 billion people

Myiasis

cause & presentation

Infestation of skin by botfly larvae

furuncle-like lesion with open center (allows larvae to get O2)

Cutaneous larva migrans

Hookworms

Happens when walking barefoot on ground w/ feces

serpiginous skin lesions, very pruritic