Disease of Skin Flashcards

(65 cards)

1
Q

Functions of the skin

A
  • 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

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2
Q

Skin Structure

A
  • 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

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3
Q

Hypodermis

A

Can be very thick
- Epidermis is stable
- Dermis got a stable thickness

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4
Q

Stratum Basale

A

Structum dermatoten
- Stem cells are here

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5
Q

Stratum Corneum

A

Variable Thickness; Stimulate mytosis by physical activity
- Dead cells is under it

1-2 month surface of skin gets replaced

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6
Q

Stratum Spinosum

A

Thickest area

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7
Q

Stratum Granulosum

A

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

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8
Q

Epidermis

A

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

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9
Q

Cells of the Epidermis

A
  • 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

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10
Q

Primary barrier of skin?

A

́Keratinocytes

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11
Q

Immune cell for skin

A

́Langerhans

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12
Q

Same number of cells across all races

A

́Melanocytes: Pigment cells

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13
Q

A skin cell that comes from neural crest/neuroepithelial cells?

A

́Merkel cells: neuroendocrine cells

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14
Q

Dermal/Subdermal Structures

A
  • 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

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15
Q

Skin Pathology Terms

A
  • 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
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16
Q

loss of cohesion between epidermal cells

A

Acantholysis

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17
Q

Hyperkeratosis with retention of nuclei in stratum corneum

A

Parakeratosis

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18
Q

Intracellular edema with epidermal blister

A

Spongiosis

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19
Q

Increased thickness of the stratum corneum

A

Hyperkeratosis

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20
Q

Etiology of Skin Diseases

A
  • 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

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21
Q

Skin Trauma

A
  • 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
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22
Q

Bruises and Hemorrhage

A
  • 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

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23
Q

A bruise that is <3mm

A

Petechiae

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24
Q

A bruise >1cm

A

Ecchymosis

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25
3-10mm bruise
Purpura
26
A bruise that arise from small vessels
Petechiae
27
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
28
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
29
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)
30
Surface hyperemia
Sun burns basically
31
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
32
Hypothermia/Frostbite
- Frostnip (red) - Superficial frostbite (gets whitish blister/pimple) - Deep frostbite (turn dark and black)
33
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
34
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
35
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%)
36
Herpes Simplex Type I
Cold sore - Very Infectious - Self limiting
37
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
38
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
39
Persistent impetigo may lead to
immune-complex GN
40
Tinea Cruris
Skin Fungus; near genital, inner thighs, and buttocks - itchy, red, often ring-shaped rash in the groin area.
41
Tinea Corporis
Ringworm of the body; rash caused by fun - t's usually an itchy, circular rash with clearer skin in the middle
42
Tinea Capitis
Ringworm of the scalp - Is a skin disorder that affects children almost exclusively - Itching, scaly, inflammed balding - Persistent and very contagious.
43
Candidiasis
Diaper Rash (not changed regularly) - Fungal infection caused by a yeast (a type of fungus) called Candida
44
Fungal Infection of IV Catheter Site
Looks very very clear. God it's stuck in my brain now
45
Scabiese
- intense itching and a pimple-like skin rash. - Show up in the flectur point
46
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
46
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
47
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)
48
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
49
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
50
Dermatographia
A condition in which lightly scratching your skin causes raised, red lines where you've scratched.
51
Cyanosis
bluish color in the skin, lips, and nail beds caused by a shortage of oxygen in the blood
52
Carbon Monoxide Poisoning
skin is cherry red
53
If any sliver metal goes to the dermis
gonna result in argyria; which is discolorlation - Will not go away
54
Neoplasia and Tumor-like Conditions
Benign - Warts - Seborrheic keratosis - Nevi - Angioma Malignant - Basal cell carcinoma - Squamous cell carcinoma - Malignant melanoma - Angiosarcoma - Lymphoma
55
Congenital Nevi
Will stay benign; Change in the pigment of skin (discoloration of some areas)
56
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)
57
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
58
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
59
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)
60
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
61
Malignant Melanocarcinoma | Arises from?
Arises from melanocytes (neural crest cells) either de novo or from premalignant condition. Can have in situ stage
62
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
63
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
64
Malignant Melanoma Survival
Level 1: will survive Level II: 75% survival Level III 50% survival Level IV and V: 10% survival