Skin Flashcards
Folliculitis
Inflammation of the hair follicle
Superficial: Development of pustule but should not scar.
Deep: Whole follicle is affected (base is in vascular dermis) so this may produce scarring.
Bacterial: Usually Staphylococcus Aureus
Atopic: non-pustular bumps on back of arms and buttocks - non-infectious form but may lead to infectious form if scratched.
Pseudofolliculitis Barbae
Known as shaving bumps; occurs due to irritation of the follicle. Common in African American men.
Sequelae: pustules/abscess may occur d/t secondary infection.
Postinflammatory pigmentation and keloids are possible.
Acne Vulgaris
Form of folliculitis that affects pilosebaceous glands
Etiology: adolescence and women
Open Comedomes: non inflammatory with black keratin plug
Closed Comedomes: inflammatory, trapped keratin plug
Relation to androgens –> pilosebaceous glands have androgen receptors and they cause increase production of sebum and upregulate production of keratin.
Insulin has similar effects
Furuncle
Abscess/boil that is the progression of folliculitis
Typically involves only one follicle
Common in post-pubescent people and those who are immunocomprimised
Causative Factors: trauma to follicle, occlusion, diabetes, HIV, obesity, poor circulation.
Carbuncle
Similar to furuncle but multiple follicles will be involved. Much larger.
Abscess - walled off collection of pus, paiful firm mass, systemic symptoms are possible.
Tissue destruction d/t ATP depletion, free radical damage, membrane disruption.
Cellulitis
Progression of carbuncle - fingers of granulation tissue extend subcutaneously. Dermis + Subcutaneous Involvement Medical EMERGENCY Causes: 2dary to Tissue Trauma Broup A Strep or Staph Aureus (adults) Haemophilus Influenza B (children)
Sx’s - d/t neutrophilic infiltrate of tissues
Systemic - fever, chills, malaise
Erythema with ill defined, non-palpable borders
Extreme pain, warmth and inflammation
Possible lymphangitis and lymphadenopathy
Dermatophyte Infections
Typical Presentation: Scaling d/t necrosis of epithelial cells (usually the stratum corneum involved) Erythema Central clearing of lesion is common May be vesicular Itching
Tinea Capitus: Ringworm - hair is broken in lesions on scalp, scaling, lymphadenopathy (triad of sx) - also itching present
Tinea Corporus: anywhere on the body
Tinea Cruris: Jock Itch - present in crural folds (ddx with candidiasis - cruris will not affect scrotum and will not be the ‘beefy red’ like candidiasis.
Tinea Manuum - hands
Tinea Pedis - Athletes Foot - painful
Tineas Unguuim - Onychomycosis (nails)
Diagnostics: Woods Light, KOH skin scraping.
Onychomycosis
Tinea Unguium - affects toenails more than fingernails.
Distal Sunungal most common - distal nail plate + nail bed (trichophyton rubrum - causative agent)
Proximal Sunungal - least common
Infection of nail bed –> hyperkeratotic debris –> separation of nail from nail bed; may see crumbling of nail itself.
Ddx - psoriasis; must use KOH to be sure.
Candidiasis
Ubiquitous, opportunistic.
Mucus Membranes: oral thrush, vulvovaginitis etc.
Epithelium: usually intertriginous areas
SX
erythematous maculopapular lesion, well demarcated, ocassionally satellite lesions; maceration in moist areas.
Mild to intense pruritis.
Herpes Simplex Virus
HSV-1 and HSV-2 (both can affect oral/genital mucosa)
4-10 day incubation
30-100% carrier rate; 20-40%recurrence
Go dormant in nerve ganglion; this is why the prodrome is tingling/itch before recurrence - the virus is travelling along the nerve.
Sx:
Vesicles that are single or grouped with erythematous base, later form crusts that are well demarcated.
Soreness + Pain
Human Papilloma Virus
Affects nuclei of BASAL epithelial cells causing verrucous hyperplasia and epidermal masses.
2-6 month incubation
HPV 6, 11 - non oncogenic, cause genital warts
HPV 16, 18 oncogenic
Will NOT go beneath basement membrane; black dots in the wart are blood vessels that have undergone thrombosis.
Varicella Zoster Virus
Causes Chicken Pox and Shingles (Herpes Zoster)
Virus infect mucosal membranes, epithelium and neurons.
Evades immune response by latency in sensory ganglia (dorsal root).
Transmission: respiratory droplets
Chicken Pox: URTI 2 weeks prior to rah Rash presents on torso and moves outward Dew drop on a rose petal lesion Fever + Malaise No scarring unless secondary lesions. Self-limiting -- though secondary impetigo may result
Shingles:
Travels back along sensory ganglion and affects certain dermatomes.
Infection of keratinocytes.
Intense pain and burning is typical prodrome.
Lesions are similar to chicken pox but in a distinctly dermatomal pattern.
Impetigo
Very CONTAGIOUS
Bacterial infx with Staph or Strep
Bacterial toxin causes breakdown of keratinocyte adhesion molecules (desmosomes) and causes the pustules.
Sx
superficial pustular, bullous or non-bullous eruption, followed by honey coloured crusts.
Typically the face is affected but may appear anywhere there is excoriation.
Diagnostic - bacterial culture
Allergic Dermatitis
Type 4 Hypersensitivity; mediated by sensitized T cells.
Common in teens/adults
NON-SYMMETRICAL
Primary Exposure: activation of niave CD4+ T cells in LN’s
Secondary Exposure = REACTION
Memory T cells –> cytokine release –> activation of endothelial cells + inflammatory infiltrate into dermis/epidermis –> fluid separates keratinocytes –> dermal edema + vesicle formation –> Hyperkeratosis (thickened stratum corneum) and Acanthosis (thickened malpighian layer) –> possible lichenification + excoriation.
Note the mechanism of vesicle formation - it is physical stress d/t infiltrate NOT destruction of cellular components (i.e. desmosomes, hemidesmosomes) as in some viral, bacterial or autoimmune condx.
Atopic Dermatitis
Typ I Hypersensitivity; Ig E mediated. Risk Factors: Not breastfed Urban Environment Diet Tendency to Histamine Release Emotional/Stress
Sx:
Eryhtematous macules, papules and vesicles that occasional weep and or crust. Skin may become hyperkeratotoic and lichenified.
SYMMETRICAL
Major Diagnostic Criteria: Pruritis Flexor surfaces Spongiosum Lichenification Family Hx Minor Diagnostic Criteria: Xerosis - dry skin Pityriasis Alba - hypogigmented macules Keratosis Pilaris - keratotic papules with follicular base Ichthyosis Vulgaris - sclay extensor surfaces Occular Finding - allergic shiners, lichenification of eyelids.
Psoriasis
Autoimmune Condition that enhances the turnover time of epidermal cells.
HOW?
T cell infiltrate –> Cytokines TNF-alpha and NF-kB increase the cGMP:cAMP ratio –> increased keratinocyte replication and thinning stratum granulosum occurs –> Acanthosis + Hyperkeratosis ensue – Pt may experience Auspitz sign; pinpoint bleeding.
cGMP is the proliferative molecule
cAMP is the maturation molecule
This means that in psoriasis you have more proliferation and not enough maturation; leads to the typical scaling and itch.
Sx
erythematous plaques, patches, papules with typical silvery scales.
Extensor surfaces, scalp and gluteal folds - also hands + nails.
CoMorbidities: Arthritis (25%), IBD, MS, Metabolic Syndrome, Depression –> related to the pro-inflammatory markers?
Psoriatic Nails
Hyperkeratosis –> shedding –> punched out lesions –> pitting
Hyperplasia of nail bed –> debris –> lifts nail plate –> irregular nail separation
Oil Spot (typical) –> serum of nail bed looks oily under nail plate - bc psoriasis is affecting nail bed.
Ddx: Onychomycosis - Do KOH skin scraping.
Urticaria
Type 1 Hypersensitivity; Histamine Mediated
ONLY in the epidermis - contrast to dermatitis which is also in dermis.
Wheals (last 24h) and Pruritis
Typically asymmetrical distribution
Ag sensitization IgE–> Mas Cell Degranulation –> Histamine –> Dermal Vascular Hyperpermeability
Melanocytic Nevi
Benign tumours derived from melanocytes
ACTH and Estrogen both connected to increased melanocytes
Junctional Nevi: at dermoepidermal; macular at this stage
Compound Nevi: some migration into dermis - nests/cords of melanocytes
Dermal Nevi: midration of all nevus cells into dermis; some degeneration = maturation; will be quite elevated.
Atypical Nevi
Tend to be compound with atypical growth + see an immune response: lymphocytic infiltrate loss of melanin phagocytosis of melanin by macrophages linear fibrosis
Tend to have irregular borders and be large.
Actinic Keratosis
Pre-malignant condition assx with chronic sun exposure and common in fair skinned people.
Processes:
Basal Cell Hyperplasia –> atypia and dyskeratosis (abnormal keratinization)
Fibroblast Damage –> Abnormal fibers synthesis and thickened dermis
Parakeratosis (retention of nuclei in cell sof stratum corneum – only normal in mucous membrane epithelium) —> thickened stratum corneum.
Usually removed bc of the potential to develop malignancy
Squamous Cell Carcinoma
SECOND MOST COMMON
White Male +55 = higher risk
Epithelia Keratinocyte
Assx Chronic Skin damage – this is what Actinic Keratosis usually develops into.
LOW invasive potential though risk of metastisis increases with size of lesion + degree of dermal invasion.
Spreads laterally under skin - may get into mm and bone.
Related to SUN EXPOSURE + sun exposed areas
Metastasis: Lymph –> Blood –> lungs, liver, brain, skin, bone.
SX
indurated plaque, papule or nodule with thick scale that is eroded, crusted or ulcerated.
Lip/Mouth/Ears may be assx with regional lymphadenopathy.
95% cure rate if found early.
May be assx with HPV infection
Basal Cell Carcinoma
MOST COMMON
White Male 40-80 = higher risk
SLOW growing and RARELY Metastisize
BUT - local destruction and invasion of tissue
ONLY found on epidermal or follicular epithelium NOT MUCOSA bc requires local stroma to support growth
Not typically following Sun Exposure patterns
SX
Flashy nodule with a waxy/pearly appearance and central lesion/depression. May have multiple telangiectasias.
Cure rate is 95% when properly treated.
Malignant Melanoma
Not common but AGGRESSIVE
High mortality rate due to metestasis
Risk Factors
Sun exposure
Family Hx/genetics
Large or lots of Nevi ( Vertical Growth –> Metastasis
Carcinoma and Melanoma in biopsy:
Lots of mitotic Events (unlike nevi)
No Maturation (unlike nevi)
Cells Look Atypical (unlike nevi)
