Disease of Skin Flashcards
Functions of the skin
- Barrier—impermeable to water and
electrolytes, inhibits infection and drying - Temperature regulation
- Respiration
- Electrolyte balance
- Protection against toxicants, UV radiation, most chemicals
- Sensation
- Immune recognition and processing
- Hormonal—vitamin D synthesis, sex hormones
Largest organ—8 pounds; 22 sq ft
Skin Structure
- Epidermis: Thin 2-5mm (most outer area)
- Dermis: Variable thickness, Collagen,..
- Subcutaneous tissue: Hypodermis connects to bone
Components are found in the dermis and hypodermis
Hypodermis
Can be very thick
- Epidermis is stable
- Dermis got a stable thickness
Stratum Basale
Structum dermatoten
- Stem cells are here
Stratum Corneum
Variable Thickness; Stimulate mytosis by physical activity
- Dead cells is under it
1-2 month surface of skin gets replaced
Stratum Spinosum
Thickest area
Stratum Granulosum
Asymetric mytosis
Away from nutrient => apoptotic cell death => morphologic shape, lose nucleis, flaky dead cells => gonna go up further and further to the upper layer and lose the potential to mytosis
Epidermis
Major Cell Type: Keratinocyte
- 0.3-1.4 mm thick; life span 1w to several month
Basal Layer:
- Undifferentiated
- Mitotic
- Asynchronous division
Upper Layers:
- Terminal differentiation
- Accumulation of keratin, lipids
- Formation of tight junctions (keep skin in place)
- Development of stratum corneum
- Rete pegs anchor epidermis to dermis. Depth reflects amount of trauma a skin region receives
Cells of the Epidermis
- Keratinocytes: Primary barrier function derived from the ectoderm
– Related to nervous system; contain all keratin in skin - Melanocytes: Pigment cells from neural crest; # is the same in all races
– Melanosomes differ in numbers
– Doesn’t migrate at all - Langerhans Cells: immune cells for antigen processing
– Rashes, poison ivy, Tcell interaction - Merkel Cells: Neuroendocrine cells from neural crest/neuroepithelial cells
- T-lymphocytes (sparse)
Epidermis absorbs 99.5% of UV radiation
Primary barrier of skin?
́Keratinocytes
Immune cell for skin
́Langerhans
Same number of cells across all races
́Melanocytes: Pigment cells
A skin cell that comes from neural crest/neuroepithelial cells?
́Merkel cells: neuroendocrine cells
Dermal/Subdermal Structures
- Papillary dermis and reticular (thicker; more collegen) dermis
- Sebaceous gland: secrete sebum, form part of the pilosebaceous complex (hair follicle, sebaceous gland, arrector pili mucle)
– Oil help lubricate skin and may be bactericidal - Nerves and blood vessels
- T-lymphocytes, mast cells
Sweat Glands:
- Simple (eccrine): temperature control, weakly antibiotic
– surface of skin
– 90% water, 10% salt and electrolyts
- Apocrine: axilla, groin-open through hair follicle
– Used in olfactory recognition, also perfumes
Skin Pathology Terms
- Hyperkeratosis: Increased thickness of the stratum corneum
– Usually because of aggitation rise to callus) - Parakeratosis: Hyperkeratosis with retention of nuclei in stratum corneum
– Cells pushed up faster; increased rate mitotic cycle - Acantholysis: loss of cohesion between epidermal cells
- Spongiosis: Intracellular edema with epidermal blister
loss of cohesion between epidermal cells
Acantholysis
Hyperkeratosis with retention of nuclei in stratum corneum
Parakeratosis
Intracellular edema with epidermal blister
Spongiosis
Increased thickness of the stratum corneum
Hyperkeratosis
Etiology of Skin Diseases
- Congenital- eg., congenital nevus, hemangioma
- Chemical or physical trauma—burns, caustic chemicals, frostbite, radiation
- Infectious agents—viruses, bacteria, fungi, insects
- Inflammatory—urticaria (‘hives’), eczema, psoriasis
- Immunological—poison ivy, autoimmunity
- Idiopathic—etiology unknown
- Premalignant lesions—actinic keratosis, lentigo
- Neoplastic—basal cell ca., squamous cell ca., melanoma (melanocarcinoma)
ALL LESIONS OF CONCERN SHOULD BE SEEN BY DERMATOLOGIST
Skin Trauma
- Abrasions and burns compromis epidermal barrier
- Skin trauma may result in SIGNIFICANT loss of fluid
- Breach of epidermal barrier (leak fluid plasma and bacteria on surface of skin)
- Secondary infections common
- Healing often by second intention and may result in scarring
Bruises and Hemorrhage
- Occurs from release of blood into dermis or subdermis (no direct blood supply in epidermis)
- Generally resolve without complication; sequence of color change: red–blue—pale green—-Brownish/yellow
Classified based on size:
- Petechiae: Small size, arise from small vessels (mostly capillary); <3mm
- Ecchymosis >1cm (traditional bruise)
- Purpura: 3-10mm
A bruise that is <3mm
Petechiae
A bruise >1cm
Ecchymosis
3-10mm bruise
Purpura
A bruise that arise from small vessels
Petechiae
Burns
Skin is the site of thermal, chemical, electrical and UV burns
Classified by thickness:
-1st degree—damage limited to epidermis
- 2nd degree: damage extending into superficial dermis
- 3rd degree: full thickness
3rd degree burns
what to expect
- anesthesia
- loss of fluid
- 3rd spacing (fluid build up in interstitum)
- Prone to infections, esp Pseudomonas
- No regeneration of structure
- Heat loss
- Hyper metabolic state
- Hypovolmeia
The Rule of 9’s
Baux index = % of Body burned + age + 17
- if >140 likely to die
Each part equal 9% of total SA
- Head
- Right arm
- Left arm
- Chest
- Abdomen
- Upper back
- Lower back
- Right thigh
- Left thigh
- Right leg
- Left leg
This rule applies to people over 15 and less than 75 of age
- All children should be treated (may die with an index of 20)
Surface hyperemia
Sun burns basically
Third-Degree Burn Scars
Treatment involves recurrent debridement to reduce scaring, skin-grafts and cosmetic reconstruction
- Underlying replacement by scar-formation
- Injured area lose sensation, and dermal structures
- Burned area are predisposed to develop squamous cancer later in life
Hypothermia/Frostbite
- Frostnip (red)
- Superficial frostbite (gets whitish blister/pimple)
- Deep frostbite (turn dark and black)
Skin Infections
Skin infections may access blood vessels and
become disseminated.
- Angio-invasive infections, particularly by fungi (eg., Aspergillus, Fusarium, Rhizopus, Mucor) are exceptionally common in immuno- compromised patients (eg., following hematopoietic stem cell transplants, severe burns, or traumatic debridement), and can have mortalities of ~90%
Skin infections are virtually universal and represent an under-appreciated source of morbidity and mortality
- All skin infections should be treated as potentially serious
Skin Infections Types
Viruses: Relatively common
- Herpes simplex, chickenpox/shingles, warts, measles
Bacteria: Extremely common and of variable severity
- impetigo, acne vulgaris, erysipelas, cellulitis, abscess)
- Most skin bacteria are anaerobic
Fungi: Often opportunistic
- Tinea, superficial and/or deep infections
Parasites: (worms, fleas, scabies)
Bites and venoms
Verruca (Warts)
Infectious lesions caused by human pailloma virus
- Infectious and can be transmitted & acquired by contact
- Warts-associated HPVs have low oncogenic potential
- Most are self-limiting and disappear within a year
Form of wart depend upon which HPV
- V. vulgaris—HPV 2 and
- V. plantaris—HVP 1 (bottom of foot)
- Condyloma acuminatum—HPV 6 and 11 (80%)
Herpes Simplex Type I
Cold sore
- Very Infectious
- Self limiting
Herpes zoster
Caused by DNA virus (chicken pox)
- Until recently, common childhood infection (chicken pox); now most children vaccinated
- Natural disease in children (‘chicken pox’)
– relatively benign and self-limited; results in immunity. Infection of adults can have significant adverse consequences
Following acute infection; virus becomes latent in nerve cell bodies
- re-activation of infection in adult (shingles) show PAINFUL eruption along dermatomes
- May result in persistent post-herpetic neuralgia
Adults having disease or vaccination during childhood may lose immunity and should consider re-vaccination
Impetigo
Highly infectious: occurs mostly in young children
- Primary cause is Staph. aureus; may be caused by Group A Strep
- Appears as red lesions around nose and mouth; soon develop yellow-brown (honey-colored) crust from dried serum
- Highly responsive to antibiotics
- May rarely develop into cellulities
- Persistent impetigo may lead to immune complex GN
Persistent impetigo may
lead to
immune-complex
GN
Tinea Cruris
Skin Fungus; near genital, inner thighs, and buttocks
- itchy, red, often ring-shaped rash in the groin area.
Tinea Corporis
Ringworm of the body; rash caused by fun
- t’s usually an itchy, circular rash with clearer skin in the middle
Tinea Capitis
Ringworm of the scalp
- Is a skin disorder that affects children almost exclusively
- Itching, scaly, inflammed balding
- Persistent and very contagious.
Candidiasis
Diaper Rash (not changed regularly)
- Fungal infection caused by a yeast (a type of fungus) called Candida
Fungal Infection of IV Catheter Site
Looks very very clear. God it’s stuck in my brain now
Scabiese
- intense itching and a pimple-like skin rash.
- Show up in the flectur point
Brown Recluse (Loxosceles reclusa)
Venom of a brown recluse can cause a severe lesion by destroying skin tissue (skin necrosis)
- There is no antivenom for it
Brown Recluse (Loxosceles reclusa)
Venom of a brown recluse can cause a severe lesion by destroying skin tissue (skin necrosis)
- There is no antivenom for it
Allergic Dermatitis & Hypersensitivity
- Type I hypersensitivity—hay fever, bee sting
- Type II hypersensitivity—cytotoxic cell
reactions (eg., bullous pemphigoid) - Type III hypersensitivity—deposition of pre-existing antibody-antigen complexes at basement membrane
- Type IV-hypersensitivity—contact dermatitis (poison ivy, jewelry, clothes)
Allergic Contact Dermatitis
Cell-mediated delayed hypersensitivity
- Acquired through exposure
- Based on specific immunologic alteration requiring an incubation period of several days
- About eight to ninety six-hours required after exposure for reaction in already sensitized tissue
Cross Sensitization
Sensitization by A broadens and brings on sensitivity to other materials B and C
- They may seem dissimilar but are related through some chemical group that acts as common denominator
Dermatographia
A condition in which lightly scratching your skin causes raised, red lines where you’ve scratched.
Cyanosis
bluish color in the skin, lips, and nail beds caused by a shortage of oxygen in the blood
Carbon Monoxide Poisoning
skin is cherry red
If any sliver metal goes to the dermis
gonna result in argyria; which is discolorlation
- Will not go away
Neoplasia and Tumor-like Conditions
Benign
- Warts
- Seborrheic keratosis
- Nevi
- Angioma
Malignant
- Basal cell carcinoma
- Squamous cell carcinoma
- Malignant melanoma
- Angiosarcoma
- Lymphoma
Congenital Nevi
Will stay benign; Change in the pigment of skin (discoloration of some areas)
Solar Keratosis
Also called ‘actinic keratosis’
Premalignant lesion caused by UVA and UVB-induced mutations of p53 tumor suppressor gene
- Actinic damage is cumulative with large mutational burden
- Occurs primarily of body parts with high sun exposure
- Lesions have a sandpaper-like feel when rubbed
- 20% of untreated lesions progress to squamous Ca
- Primary treatment in US is cyrotherapy or 5-FU (cannot go out in sun)
Basal Cell Carcinoma
most common malignancy worldwide
Occurs primarily on sun-exposed skin, most commonly on the face; UV etiology (actinic)
- Associated with loss-of-function mutation of PTCH1 (not important)
- Appears as raised, ‘WAXY’ lesion with small blood vessels (telangiectasias) over it’s surface; may be pigmented
- Central erosion and jagged margin (‘rodent ulcer’)
- Arises from basal cell layer of epidermis and invades LATERALLY; Locally aggressive
- Rarely metastasizes
- Surgery with wide margins is usually
curative (Mohs surgery), but >40% will have another BCC within 5 years
> 1M BCCs treated in US annually; BCC is 40-fold more common near the equator
Squamous Cell Carcinoma
Relatively common on sun-exposed skin, X-radiation and with chronic arsenic poisoning.
- Incidence increase with immuno suppression (eg.organ transplant recipients)
- Can happen following burns or chronic ulcers (increased potential for metastasis in this setting)
- Mutation in genes affecting orderly maturation of keratinocytes (TP52, Notch)
Most found on face, particularly lower lip
- When occurring in mucosal membranes—tobacco, chronic alcohol consumption. Metastasis from this location is frequent
- <1% have metastasized at time of discovery
Treatment is surgical. May require adjuvant therapy such as radical lymph node dissection
Malignant Melanocarcinoma
Arises from melanocytes (neural crest cells) either de novo or from premalignant condition. Can have in situ stage
- Initiating lesion appears to be activating mutation of BRAF and loss of the tumor suppressors p16 and ultimately p53
- Most commonly dx’ed cancer in women aged 25-29 years. Peak incidence ~50 year of age
- Can occur wherever pigmented cells are present.
– Most common in skin, but also eye, vaginal and rectal mucosa, mouth and nasal mucosa.
– Melanomas in on-UV sites usually have gain-of-function mutations of the KIT tyrosine receptor kinase
- Selective inhibitors of mutant BRAF and KIT have induced remarkable tumor
responses in appropriate patients. Immune checkpoint inhibitors (eg, Keytruda) alos efficacy
- May be pigmented or non-pigmented (amelanotic)
Malignant Melanocarcinoma
Prognosis
Prognosis depends upon depth of invasion (Breslow thickness).
- <0.75 mm has excellent prognosis.
- Radial growth becomes vertical growth before invasion and prognosis decreases rapidly
Early diagnosis and surgical treatment is essential; prognosis of advanced melanoma is generally bleak unless it is carrying on of the mutation activating genes, in which case remission is possible
Malignant Melanocarcinoma
Arises from?
Arises from melanocytes (neural crest cells) either de novo or from premalignant condition. Can have in situ stage
Melanoma Risk Factors
- Light skin and blue eyes
- Frequent and prolonged actinic exposure
- Severe sunburns early in life (can have up to 50% increase)
- Premelanotic lesions
– Dysplastic nevi
– Lentigo maligna
Recognizing Malignant Melanoma
- Change in size
- Change in color
- Change in shape
- Increase in elevation
- Change in surface
- Change in surrounding skin
- Bleeding
- Change in texture
Malignant Melanoma Survival
Level 1: will survive
Level II: 75% survival
Level III 50% survival
Level IV and V: 10% survival
