Dermatology Flashcards
Know Dermatology
Skin has 3 layers, what are they?
Epidermis
Dermis
Subcutaneous Tissue
Atopic Dermatitis
Eczema
Relapsing inflammatory skin disorder
ITCH THAT RASHES
Atopic Dermatitis characterized by?
Pruritus that leads to lichenification
Atopic Dermatitis Hx/Pe
Associated with:
Asthma
Allergic Rhinitis
Risk of bacterial and viral infections
Atopic Dermatitis Triggers
Climate Food Allergens Physical / Chemical irritants Emotional Factors
Macule
Flat lesions that differers in colour from surrounding skin
<1 cm diameter
Papule
Elevated solid lesion <5mm
Patch
Small circumscribed area differing in colour from surrounding surface >1cm
Plaque
Elevated solid lesion >5mm
Cyst
Epithelial lines sac containing fluid
Vesicle
Fluid filling, very small <.5mm elevated lesion
Bulla
Large vesicle >5mm
Wheal (hive)
Area of localized edema that follows vascular leakage and usually disappears within hours
Lichenification
Thickening of the epidermis
Scar
Healing defect of the dermis
The Epidermis alone heals without a scar
Hypersensitivity Reaction
Type I
Anaphylactic or Atopic
- Antigen cross-links IgE on PREsensitized mast cells and basophils
Triggers release of vasoactive amines (Histamine)
First and Fast
Examples- Anaphylaxis
- Asthma
- Wheals
Types I, II and III are all antibody or B-cell mediated
Hypersensitivity Reaction
Type II
Cytotoxic
- IgM and IgG bind to antigen on “enemy cell” leading to Lysis (by compliment) or phagocytosis.
Examples- Autoimmune Hemolytic Anemia
- Rh Disease
- GoodPastures
- Rheumatic Fever
CY-2-Toxic
Antibody and complement lead to MAC
Hypersensitivity Reaction
Type III
Immune Complex
Antigen-Antibody complex activate complement which attracts Neutrophils. Neutrophils release lysosomal enzymes
Examples: Polyarteritis nodosa
SLE
Rheumatoid Arthritis
Serum Sickness (Blood)
Arthus Reaction (Vaccines)
Hypersensitivity Reaction
IV
Delayed (Cell Mediated)
Sensitized T lymphocytes encounter antigen and then release lymphokines (macrophage activation).
Examples: TB skin test
Transplant rejection
Contact dematitis
Atopic Dermatitis Dx
Made clinically
Mild eosinophilia
Increase IgE
Atopic Dermatitis Tx
Prophylactic measures
- non-drying soap
- Apply Moisturizers
Treat with topical steroids (don’t use longer than 3 weeks)
Contact Dermatitis
Type IV hypersensitivity Reaction
Results from contact with allergen which the pt has had previously been exposed and sensitized too
Contact Dermatitis Hx / PE
rash and pruritus
Allergens frequently include:
- poison ivy
- poison Oak
- Nickel
- Soaps
- Detergents
- Cosmetics
- Rubber Latex
Occurs where allergen touches
Contact Dermatitis Tx
Prophylaxis consists of Avoidance
Give- Topical or systemic steroids as needed
- wet, cool compresses to relieve and debride the skin
Seborrheic Dermatitis
Caused by Pityrosporum Ovale
A harmless yeast found in sebum and hair collicles
Predilection for areas with Oily skin such as
(Scalp, eyebrows, nasolabial folds and mid chest)
Seborrheic Dermatitis Hx/PE
Rash varies with Age
Infants- Red diaper rash
- Yellow scale
- thick crust (cradle Cap)
Children / Adults- Red, Scaly Patches
- ears, brows, scalp, chest
Seborrheic Dermatitis Dx
Clinical impression
Rule out Contact dermatitis and psoriasis
Seborrheic Dermatitis Tx
Selenium Sulfide
or
Zinc Pyrithione shampoo
Psoriasis
T-cell mediated inflammatory dermatosis
Character:
- Erthematous patches
- Silvery Scales
- 5% have seronegative arthritis
Psoriasis Hx / PE
Lesions
- Round, sharp boardered
- Erthematous patch with silvery scales
- Found on Extensor surface
- elbows
- knees
- scalp
Other causing Reasons
- BB
- Lithium
- ACE-I
- Strep infection
- Trauma
Psoriatic Arthritis
- Begins with hands “sausage digits”
- HLA- 27 for spinal involvement
Psoriasis Dx
- Clinical impression
- Auspitz sign (bleeding when scale is scraped)
- Histo shows thickend Epidermis and infiltrate in stratum corneum
Psoriasis Tx
Topical steroids combined with Keratolytic agents and UV therapy
Methotrexate for severe cases
Retinoids may also be used
Arthritis treated with NSAIDs
AVOID Systemic steroids
Urticaria (Hives)
Superficial, Intense Edema in a localized area
Usually acute
Type I Hypersensitivity
Urticaria (Hives) Hx / PE
Range in severity
- few itch bumps
- life threatening anaphylaxis
Lesion
- Elevated papule or plaque
- Reddish or white
Severe Rx
- swelling of tongue
- AngioEdema
- Asthma
- Fever
- GI Issues
Urticaria (Hives) Dx
Clinical impression
Urticaria Tx
Systemic Antihistamines
Topical medications have NO Benifit
Drug Eruption
Eruptions like rashes, SLE like symptom
Happens after 7-14 days of starting new drug
If happens <7 days probably not drug
Tx- Antihistamines
Erythema Multiforme
Classic targetoid lesions
Erythema Multiforme Hx / PE
Lesion has Target Appearance
Occurs on Mucus Membrane where erosions are seen
Palms and soles also affected
Erythema Multiforme Dx and Tx
Clinical impression
History of recurrent labial herpes
Tx- symptomatic tx ONLY
HSV- suppressive acyclovir may decrease the rash
Stevens-Johnson Syndrome (SJS)
Toxic Epidermal Necrolysis (TEN)
SJS & TEN constitute two different points on the spectrum of life threatening
SJS = 30% of BSA
SJS and TEN Hx
Preceded by Erythema Multiforme
Painful mouth rash
Maculopapular drug rash
- Penicilin
- Sulfonamides
- Seizure meds
Exam reveals
- Mucosal erosions
- Cutaneous Macules
- Atypical Targetoid Leions
+ Nikolsky’s Sign = Epidermal detachment
SJS & TEN Diagnosis
SJS= Biopsy shows Degeneration of basal layer of epidermis
TEN= Biopsy shows full-thickness eosinophilic epidermal necrosis
SSSS- ONLY is SUPERFICIAL damage
SJS & TEN Treatment
Same complications as burn victims
Thermoregularory difficulties
Electrolyte disturbances
TX- skin coverage
- maintain fluid and electrolyte balance
High risk of mortality
Erythema Nodosum
Panniculitis whose triggers include
- Infections
- Drug Reactions
- Chronic inflammatory disease
Erythema Nodosum Hx
Painful erythematous nodules on lower legs
Spread slowly
turns brown or gray
Fever and joint pain
Erythema Nodosum Dx and Tx
Clinical impression
Workup
- ASO
- PPD
- CXR to rule out carcoid
- Small Bowl (rule out IBD)
Tx- Remove trigger factors
- NSAIDs
Pemphigus Vulgaris
LIfe Threatening Autoimmune Disease
Intraepidermal Blister Leading to Widespread Painful erosisons
Antibodies directed at DESMOGLEIN molecules
Usually 40 - 60 years old
Pemphius Vulgaris Hx / PE
Mucous Membrane involvement (mouth ulcers) with progress to skin
Gets crust and weeping and 2 infection
Pemphius Vulgaris Dx
+ Nikolsky’s Sign (ability to produce a blister by rubbing skin adjacent to natural blister)
Skin Biopsy with immunofluorescence confirms
Biopsy shows acantholysis (intraepidermal split with free-floating keratinocyctes in blisters)
Pemphius Vulgaris Tx
Long term needed
- Steroids at high doses
Bullous Pemphigoid
Acquired blistering disease
Seperation of epidermal basement membrane
Seen 60 - 80 year olds
Pathology is antibodies by the basement membranes
Bullous Pemphigoid Hx / PE
Nikolsky’s Sign -
Blisters form crusts and erosions
No mouth ulcers
Leaves Mucous Membranes alone
Bullous Pemphigoid Tx
Systemic Steroids
Topical Steroids can prevent blisters if started early
Bullous Pephigoid Diagnosis
Dermal-Epidermal junction
Herpes Simplex Virus Dx
Multinucleated Giant Cells on Tzanck Smears
VZV has same appearance on Tancks so Direct Fluorescent antibody staining needed for definitive diagnosis
HSV Tx
Oral or IV Acyclovir reduct severity or recurrences
Acyclovir ointment reduces duration of cirual shedding but not recurrence
Varicella-Zoster Virus (VZV)
2 Diseases associated?
Transmits how?
Incubation period?
Contagious for how long?
Causes 2 different diseases
Varicella (Chicken Pox) Herpes Zoster (Shingles)
Transmit via respiratory droplet or direct contact
VZV incubation - 10 - 20 days
Contagious 24 hr before eruption and lasts until lesions crusted
Molluscum Contagisum
Pox Virus in young children and in AIDS pt.
Rash is composed of tiny waxy papules with central umbilication
Kids- Found on face, trunk
Adults- on Genitalia and perineal region
Molluscum Contagiusm DX & Tx
Clinical picture
Local Destructive method- curetting, freezing or trichloracetic acid to lesion
Lesions resolve spontaneously over months to years and left untreated in children
Verrucae (Warts)
Which cause cancer and what type?
how spread?
Subtypes of HPV 16 and 18 lead to squamous malignancies
Spread by direct contact
warts and Genital Warts Tx
WARTS:
Curettage
Cryotherapy
Acid Keratolytics
Gential - Podophyllin Ticholoacetic acid Imiquimod 5-FU Genital
Impetigo
What bacteria?
How transmitted?
2 types?
Group A strep and Staph
Transmitted by direct contact
Types:
- Common
- Bullous
Impetigo Hx / PE
Common- pustules and honey coloured crusts usually on face
Bullous- Acral, large stable blisters (always caused by S. Aureus)
Scarlet Fever
what it look like?
Caused by?
Tx?
“Sunburn with goosebumps”
Strawberry tongue
Caused by S. Pyogenes
Tx- PCN
Cellulitis
Deep, local infection involving connective tissue, subQ tissue or muscle and skin
Cellulitis caused by what organisms (2)
Risk factors?
Staph
Group A Strep
Risk factors:
- DM
- IV drug use
- Venous Stasis
- Immune compromise
Cellulitis
Tx:
7 - 10 days oral antibiotics (Mild cases)
IV Antibiotics (systemic toxicity or comorbid conditions, orbital or hand involvement)
Acne Vulgaris
Cause?
Endogenous skin disease in adolescents
Hormonal activation of sebaceous glands
develops comedo or plugged sebaceous follicle
Acne Vulgaris
HX / PE
Comedo (Open- Blackheads) or (Closed- whiteheads), large numbers but no inflammation
Inflammatory- Comedo ruptures creating pustule thats large and nodular
Scar- inflammtion heals and scars
Acne Vulgaris Tx
Comedones- Topical TRETINOIN (Retin-A) and Benzoyl Peroxide
Inflammatory- Topical antibiotics (erythromycin, clindamycin) or
- Systemic Agents- Tetracycline or erythromycin
Pilonidal Cysts
How does it start then what microbe happens
Abscess in sacrococcygeal region, near top of natal cleft
Repetitive trauma plays a role
Starts as folliculitis and abscess from perineal microbe- bacteroides
Occurs 20 - 40 year old
Pilonidal Cyts Tx
Incision and Drainage ( I & C ) under local anesthesia then
Steile Packing of wound
Abcesses should be healed by 2nd Intention
No Antibiotics since abcess are anerobic
Tinea Versicolor
What bacteria causes it?
Why does it go out of control?
Caused by Malassezia Furfur (yeast of normal skin)
Hot, humid and oily skin causes it to overgrow
Tinea Versicolor HX / PE
Small, scaly patches of varying color on chest or back
Lesions hypopigmented as a result of interference with melanin production
Hyperpigmented due to thickened scale
Tinea Versicolor Dx
Clinical Impression
Confirmed by Potassium hydroxide (KOH) preparation of scale “Speghetti and meatball pattern”
Tinea Versicolor Tx
Topical Selenium Sulfide daily for 1 week
Then applicaiton once weekly for prophylaxis
Dermatophyte Infections
Live where?
Organisms?
Risk factor?
Live only in tissue with keratin (Skin, nails, hair)
Organisms
- Microsporum, Trichophyton, Epidermophyton
Risk Factors
- Pets reservoir for Microsporum
- DM
Dermatophyte Infections
HX / PE
Tinea Corporis
Tinea Pedis / Manuum
Tinea Curis
Tinea Capital
Tinea Corporis
- scaly
- Pruritic eruption
- Sharp, irregular boarder with central clearing
Tinea Pedis / Manuum
- interdigital scaling
- Erosions between toes
- Tick scaly skin on soles
- Asymmetric involvement of hands
Tinea Cruris
- Jock Itch
- Sparms scrotum
Tinea Capitis
- Ringworm
- Scaly scalp eruption
Lice
Head
Body
Pubic
How spread?
Live off Blood
Head louse
- lives on scalp
- lays eggs “Nits” attached to hair
Body Louse
- Lives in clothing and bites ONLY body
Public Louse
- Lives on pubic hair
- “Crabs”
Spread through body contact or sharing bedclothes and garments
Secrete toxin that creates pruritis
Lice HX / PE
Crabs- contain anticoagulant in Saliva so bites turn blue
Body Lice- from inadequate hygene or crowded living
Lice Tx
Head- OTC Pyrethrin and mechanical removal of nits
Body- Wash body, clothes and bedding
- body gets permethrin or Pyrethrin (RID)
Pubic- Treat with Pyrethin (RID)
Scabies
Organism
Spreads?
What causes pruritis
Organism- Sarcoptes Scabiei
Mates on skin after which the female digs passage into Stratum Corneum and lays eggs
Burrowing leads to pruritus
Spead by close contact
Scabies Hx / PE
Intense pruritus at night or hot showers
Affected- Hands, axillae and genitals and Creases in skin
Scabies Tx
1 - 2 applications of 5% Permethrin from neck down
Oral Ivermectin also effective
Itching lasts 2 weeks after treatment
Lichen Planus
What is it?
Chronic inflammatory dermatosis involving the skin and mucous membranes
Extremely Pruritic
Lichen Planus Hx / PE
Presents with:
- Violaceous, flat opped, polygonal papules
- White stripes
- Initial lesions appear on the genitalia- ulcerated
Lichen Planus Dx
Histology reveals Lichenoid pattern
- band of T-lymphocytes at the epidermal junction with damage to the basal layer
Lichen Planus Tx
Resolves in 12 months
Mild cases- topical steroids
Severe- Systemic steroids
Pityriasis Rosea
what is it?
Acute dermatitis that is pink and scaly
Occurs in young adults
Pityriasis Rosea
Hx / PE
Initial lesion is herald patch that is several cm.
- Days / weeks later, got a christmas tree pattern on patients back
- usually asymptomatic
Pityriasis Rosea
Dx and Tx
clinical impression
confirmed by KOH exam to rule out fungus
Tx- no treatment, heals in 2-3 weeks
Vitiligo
Depigmentation pathogenesis is unknown
Vitiligo Hx / PE
develop small, sharply demaracted depigmented macules or patches on normal skin.
usually chronic and progressive
Many have serum markers of autoimmune disease (thyroid, dm, pernicious anemia)
Vitiligo
DX & Tx
History and clinical
Tx- topical or systemic Psoralens
- exposure to light
Seborrheic Keratosis
Skin tumor, in all people after 40 y/o
Lesions have NO malignant potential
Seborrheic Keratosis
Hx / PE
Exophytic
Waxy brown papules and plaques
“stuck on appearance”
usually comes in bunches
Seborrheic Keratosis
Dx & Tx
Clinical
Histology shows Hyperplasia of benign, basaloid epidermal cells with horn pseudocyts.
Tx- Cryotherapy or curettage curative
Actinic Keratosis
Precursor of SCC in Situ
Lesions caused by exposure to sunlight
Actinic Keratosis
HX / PE
Appear on sun-exposed area (face and arms)
Affect older pt.
Rare to have solitary lesion
Actinic Keratosis
Dx & Tx
Clinical
Biopsy- intraepidermal atypia over sun damaged dermis
Tx- Cryosurgery
Topical 5-FU
Use Sun Protection
Squamous Cell Carcinoma (SCC)
Second most common skin tumor
Locally destructive effects and potential for metastasis and death
UV Light most common cause
SCC
Hx / PE
Arises from Actinic Keratoses rarely metastasize
Those around lips are more liekly to do so.
SCC occurs on the lip more commonly than BCC
SCC Dx & Tx
Biopsy confirms
Histology- Intraepidermal atypical keratinocytes with penetration of basement membrane by malignant epidermal cells growing into dermis
TX- Surgical excision
Basal Cell Carcinoma (BCC)
Most common malignant skin tumor
Slow growing
Locally destructive
NO Metastatic potential
Chronic UV light is risk factor
Most appear on face
BCC
Hx / PE & Tx
Isalnds of proliferating epithelium resembling the basal layer of the epidermis
Pearly papule
Tx- Excision
Melanoma
Most common life threatening dermatologic disease
Risks- Short intense burts of sun exposure
Melanoma
Hx / PE
Malignant melanoms usually begin in Epidermal Basal layer where melanocytes found
1st growth- horizontal intraepidermal
Presents with lesion that is flat but increase diamter
2nd growth- vertical with dermal invasion
Melanoma
ABCDE
Asymmetric irregular Boarder irregular Colour Diameter > 6mm Evolution- change or new lesion
Melanoma
DX
Adutls should be examined for lesions
Onset of puritis is also an early sign of malignant change
Excisional biopsy should be done on any suspicious lesions
Stage
Melanoma Stage
Breslow’s Thickness (depth of invasion in mm)
TNM Staging
1- 1st skin melanoma 70% survival 5 years
2- local or regional 30% survival 5 years
3- Distant Metastisis 0 % survival 5 years
Melanoma Tx
Potential to relapse after several years
Early melanoma are low risk for relapse but high risk for subsequent melanoms
Pt Surveillance is essential
Chemo and Radiation aren’t likely to be successful
Mycosis Fungoides
Cutaneous T-cell Lymphoma
NOT A FUNGUS
Slow, progressive neoplastic proliferation of T-cells
Industrial exposure increases risk
Chronic disease
Mycosis Fungoides
Hx / PE
Early lesion is non-specific
Psoriatic appearing plaque that is palpable and prutiric
Mycosis Fungoides
DX / Tx
Clincial
Tx-
Stage 1 - Topical Steroids
II- Systemically with netinoids
Photopheresis is mainstay of treatment
